care and diseases of trout - Native Fish Lab of Marsh & Associates

CARE AND DISEASES OF TROUT By H. S. DAVIS Revised edition, 1946

RESEARCH REPORT 12

Fish and Wildlife Service, Albert M. Day, Director

United States Department of the Interior, J. A. Krug, Secretary

UNITED STATES GOVERNMENT PRINTING OFFICE: 1947

For sale by the Superintendent of Documents, United States Government Printing Office,

ABSTRACT

HIS IS the third and most extensive revision of Care and Diseases

of Trout. Care of trout at the hatchery, including the care of ponds

and raceways, is treated at some length. This is followed by a general

discussion of trout foods and methods of feeding, special attention being

paid to the use of dry products for supplementing fresh meat in the diet.

Some consideration is given to the improvement of brood stock and its

practical value.

A general discussion of parasites and diseases of trout, and their control,

is followed by a detailed account of each disease, including the character-

istic symptoms, etiology, pathology, and methods of control. The figures

include drawings and photomicrographs of the more important organisms

that cause trout diseases and their effects on the tissues.

CARE AND DISEASES OF TROUT1

By H. S. DAVIS. PH.D., In charge, Aquicultural Investigations, Fish and Wildlife Service

CONTENTS

Page Introduction ................................................................... 1 Care of fingerling trout ............................................ 2 Care of ponds and raceways ..................................... 10 Trout foods ..................................................................... 11 Feeding methods ............................................................ 18 Improvement of stock ................................................ 19 Parasites and diseases ................................................ 22

General considerations ......................................... 22 General principles of disease control .............. 23 Sterilization of ponds and raceways ................ 27 External animal parasites ..................................... 28

Trematoda .............................................................. 28 Gyrodactylus ................................................... 28 Discocotyle salmonis ..................................... 30

Parasitic copepods .............................................. 31 Mussel glochidia ................................................... 33 Protozoa ................................................................... 35

Costia ................................................................... 35 Chilodon .............................................................. 37 Trichodina ....................................................... 39 Ichthyophthirius .............................................. 41

Internal animal parasites ..................................... 45 Parasitic worms ................................................... 45 Protozoa ................................................................. 49

Octomitus salmonis ....................................... 49

Page Internal animal parasites—Continued

Schizamoeba salmonis ................................... 53 Myxosporidia ................................................... 54 Coccidia in trout ............................................ 55

Bacterial diseases ..................................................... 55 Furunculosis .......................................................... 55 Ulcer disease ....................................................... 61 Peduncle disease ................................................ 63 Fin rot ................................................................... 66 Gill disease ............................................................ 68 Western type of gill disease .......................... 73 Cytophaga columnaris ..................................... 74

Miscellaneous diseases, including those of uncertain origin ................................................... 77

Fungus diseases ................................................... 77 Popeye ..................................................................... 82 Thyroid tumor or goiter ................................... 84 Intestinal inflammation ................................... 85 Fatty degeneration of the liver ..................... 85 Acute catarrhal enteritis ................................... 87 Anemia ................................................................... 88 White-spot disease ............................................ 89 Blue-sac disease ................................................... 89 Soft-egg disease ................................................... 91

Literature cited ............................................................ 92

INTRODUCTION

During recent years there has been a constantly increasing demand for larger trout for stocking purposes. At one time, most of the trout were planted as ad-vanced fry or, at least, before they reached a length of 3 to 4 inches. Except in commercial hatcheries few fingerling trout were fed for more than 2 or 3 months. At present, most fingerlings are held for much longer periods and large numbers of trout from 6 to 12 inches or more in length are planted each year.

This change in stocking policy is due to the fact that in thickly populated sections, where the streams are fished intensively, even moderately good fish-ing can be maintained only by liberal plantings of large trout. Our streams can produce only a small part of the food required to support a trout population large enough to satisfy the demand in heavily fished waters. Either large trout must be supplied by hatcheries or fishing must be greatly curtailed.

It is a comparatively simple matter to produce advanced fry in large num-bers with little loss, but if trout are to be held through the summer the trout culturist will be confronted with difficulties of various kinds, which must be met and overcome if the fish are to be kept healthy and growing rapidly during the summer.

There is every reason to believe that heavy losses are unnecessary and, to a considerable extent, can be prevented. There are well-authenticated in-stances of small lots of trout that have been carried through the first year with

Approved f or publication June 1945.

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2 RESEARCH REPORT 12, FISH AND WILDLIFE SERVICE

a total loss of less than 10 percent from the time the eggs were taken. No doubt this represents an exceptional condition that cannot be duplicated on a large scale, but, the fish culturist should try to approach this record.

There is always some loss among the eggs, especially before they are "eyed," which in many cases reaches 20 to 30 percent or more. From the time the eggs are eyed, however, until the young fish begin to feed, there is usually very little loss. The final absorption of the yolk sac, which compels the advanced fry to seek its food from other sources, marks a critical period in the life of the young trout, which is sometimes attended with heavy losses. From this time until late summer or fall the mortality is often heavy and it is during this period that there is the greatest opportunity to cut down losses through the adoption of better methods of caring for the fingerlings. Usually, little difficulty is ex-perienced in carrying the trout through the ensuing winter if they are carefully graded according to size, so as to allow no opportunity for cannibalism.

CARE OF FINGERLING TROUT

Before discussing the conditions under which fingerling trout can be reared to best advantage, it is advisable to consider the natural habitat of young trout during the first few months of their lives. As is well known, trout normally spawn in the riffles of comparatively small, swiftly flowing streams. The young remain near the spawning grounds or work their way into even smaller streams during the first summer. In some instances, especially in northern localities, trout may spawn in ponds or lakes; but in such cases they usually seek gravel beds that are infiltrated with ground water from springs or seepage.

Small brooks in which trout normally spawn usually contain but few large pools; consequently, there is a perceptible current almost everywhere. Even in the larger streams the small fingerlings are almost invariably found in shallow riffles or small side channels where there is a decided current and the water is well aerated. This fact is emphasized as it is believed that the more nearly natural conditions can be approximated in rearing fingerling trout, the better will be the chances of success. This means that the fish should be held where there is an abundant supply of well-aerated water and a perceptible current.

Frequently, fingerling trout are held during their first summer in the troughs in which they were hatched. At many hatcheries, especially in the West, large troughs or tanks are provided to which fingerlings are transferred when the hatching troughs become too crowded. Unquestionably, these are superior to the standard hatchery troughs for rearing fingerlings and very good results are often obtained. Nevertheless, it is believed that there are several serious ob-jections to rearing trout in either troughs or tanks, and that much better re-sults would be obtained if the fish were moved outdoors early in the season. Standard hatchery troughs provide an ideal means of hatching eggs and hold-ing the fry, but after the fish begin feeding, other factors must be taken into consideration. In the first place, the rapidly growing fish constantly require additional space if they are to be kept in vigorous condition. Consequently, if they are to be held for several months it will be necessary to have many times the number of troughs that were required to hold the eggs and fry. Troughs and tanks are expensive to build and to provide a sufficient number of these to hold the fingerlings throughout the summer will greatly increase the over-head. In fact, if the fish are given sufficient room, for best results, the cost of rearing them would be increased out of proportion to the results attained. Moreover, troughs and tanks are wasteful of water since they require a rela-tively large volume of flow for the number of fish carried. At hatcheries with a

CARE AND DISEASES OF TROUT 3

large water supply this may not be an objectionable feature, but where the supply is limited and it is necessary to utilize the water to best advantage, other methods of rearing fingerlings should be seriously considered. Owing to their limited capacity, troughs are usually overcrowded, with the result that the fish are stunted and not infrequently contract diseases which result in heavy mortality.

The number of f.sh that can be held in a trough without detriment to their growth or health will depend, of course, primarily on their size, and on the volume and temperature of the water. There is no general agreement among trout culturists as to the proper number of fingerlings of various sizes that can be safely carried in the standard hatchery trough. At some hatcheries, two or three times as many fish are habitually carried in the troughs as in others where conditions are very similar.

The results of an experiment to determine the effects of overcrowding of fingerlings in hatchery troughs are shown in figure 1. These experiments were carried on with rainbow fingerlings in 4 standard hatchery troughs. The dimensions of the space in which the fish were confined were 12.83 by 1.135 by 0.442 feet, equivalent to 6.436 cubic feet or 48.27 gallons of water. The troughs were supplied with slightly over 5 gallons of water per minute, thus, about 9 minutes were required for a complete change of water.

The experimerit was started on March 1, 1933, with 500 rainbow fingerlings in the first trough, 1,000 in the second, 2,000 in the third, and 3,000 in the fourth. These trout were all from the same lot of fingerlings and the average individual weight of the fish in all four experimental lots was the same. Need-less to say for all lots the diet and other conditions remained identical except for the number of fish present. It will be noted that up to April 26 when the fish reached an average weight of about 2.5 grams, there was very little dif-ference in the average individual weight of the different lots. From that time on, however, the slower growth of the larger lots became more and more noticeable until July 19, when it became necessary to discontinue the lot con-

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FIGURE 1.—Growth curves showing the effect of overcrowding on fingerling rainbow trout. The figures 500, 1,000, 2,000, and 3,000 indicate the number of trout in the troughs.


taming 3,000 fish owing to an outbreak of gill disease. At that time, both this trough and that containing 2,000 fish appeared overcrowded, and the dorsal fins of the fish were worn from constant milling in massed schools at the head or foot of the trough. The 2,000 lot was discontinued on August 2, but the 2 other lots were continued on an experimental basis until August 30. By that date, the fish in the smallest lot had far outgrown all the others. The rapid growth of the fish in this experiment was due to the comparatively high tem-perature of the water, which ranged from 54° to 56° F.

It is apparent from this experiment that when conditions are favorable for rapid growth, 1,000 trout is the maximum number that can be successfully held in a standard hatchery trough through the summer. At hatcheries where the growth is slower, because of lower temperatures, two or three times this number can be safely held in a single trough.

A series of experiments conducted by E. W. Surber at the Leetown (W. Va.) station to determine the amount of oxygen removed by trout from the water in troughs containing various numbers and sizes of fingerlings is also of interest in this connection. The troughs were similar to those used in the preceding experiment, with the same volume of water (48.27 gals.), and were supplied with water having a temperature of approximately 54°F. at the rate of 5.17 gallons per minute. The results of a few typical experiments will be sufficient for our purpose. It was found that 1,500 brook trout, averaging about 14 grams each, removed about 45 percent of the available oxygen from the trough. In a trough containing 17,680 rainbow trout fingerlings with an average weight of 0.26 grams, the amount of oxygen removed was only 24 percent of the total amount; while in another trough containing 16,735 fish, averaging 0.24 grams in weight, only 14.4 percent of oxygen was removed. In another experiment 9,975 rainbow fingerlings (average weight 0.59 grams) removed 34.89 percent of available oxygen, while in a later experiment 8,410 fish of the same size re-moved 27.22 percent.

In an experiment with black-spotted trout, 3,900 fingerlings, averaging 2.30 grams in weight, removed 18.02 percent of the total amount of oxygen. In another trough 41,600 Loch Leven trout fry 1-day old consumed only 3 per-cent of the available oxygen.

Feeding greatly increased the consumption of oxygen as shown in the case of a trough containing 1,500 brook trout with an average weight of 13.45 grams. On the morning of November 28, these fish were found to consume 3.07 parts of oxygen per million parts of water, or 29.63 percent. After the fish were fed 300 grams of food, 7.26 piarts of oxygen per million of water or 70.08 percent of the total amount present was consumed in this trough. At 4:05 p.m., several hours after feeding, the consumption of oxygen in the same trough was only 4.72 parts per million, or 44.74 percent. At this time the fish were again given 300 grams of food and the oxygen consumption rose to 8.55 parts per million, or 81.04 percent of the total amount present. It is evident from these experiments that in overcrowded troughs there is a distinct possi-bility that during or shortly after feeding the oxygen content of the water may drop to dangerously low levels, even though at other times the supply may be more than sufficient for the needs of the fish.

It is believed that raceways (fig. 2) will provide a much more satisfactory means of holding trout than troughs. Obviously the raceway is only a devel-opment of the fundamental idea embodied in the hatchery trough, but con-sidering the number of fish that it will support, it is much cheaper to build and operate. It has the further advantage, if properly constructed, of provid-ing an environment closely simulating that of fingerlings in nature. This is


especially true if the raceway has a sand or gravel bottom, as it should have wherever practicable.

Raceways may vary widely in size, depending on local conditions, but in any event they should be much longer than wide, and supplied with sufficient water to insure good circulation. Unless an exceptionally large flow of water is available, raceways intended primarily for fingerling trout, should not be over 3 to 5 feet wide, with a maximum length of 50 to 75 feet. Where the soil is light and porous, wooden or concrete sides for the raceways are usually nec-essary, but, unless essential in order to retain the water, a dirt bottom is to be preferred, although it is usually best to cover this with a layer of sand or gravel. Only a slight slope of the bottom is necessary, and ordinarily the water in the lowest part should not be over 20 or 25 inches deep. For small fingerlings the depth should be considerably less. The proper depth of water in the race-way is dependent to a large extent on the volume of flow. Where a large flow is available, the depth of the water may be greater than with a small flow. The important consideration is to have good circulation with an appreciable cur-rent in all parts of the raceway. It is also well to remember that the higher the temperature, the greater should be the volume of flow with the same depth of water and poundage of fish.

Many trout culturists use much deeper water than is advocated in the pre-vious paragraph, and where there is a sufficient volume flowing through the raceway, this may prove satisfactory; but it is believed that with a relatively small supply more fish can be held safely in shallow than in deep raceways. This is due to the fact that it requires a greater flow to produce a current in a deep than in a shallow raceway. It is true that in a shallow raceway it may not be possible to hold quite as many fish per unit area of water surface, but, on the other hand, it requires less water to provide a satisfactory circulation.

After the fingerlings reach a length of 4 or 5 inches, they may be held safely in small pools in which there is a less rapid circulation than raceways. Finger-lings smaller than this are of ten held in pools successfully if given plenty of room, but our experience indicates that, in most cases, it will prove more economical to hold such fish in raceways and, if thought advisable, remove

FIGURE 2.—Raceways for fingerling trout at the Pittsford (Vt.) Experimental Hatchery.


them to pools later in the season. A very good arrangement is to provide pools to which the surplus fish can be transferred when the raceways become over-crowded.

The type of pools or raceways to be employed will, of course, depend more or less on local conditions. Where there is danger of the water becoming over-heated, this fact must be taken into consideration and the pools so constructed that there will be no possib lity of such an occurrence. In rapid, well-aerated streams brook trout can withstand temperatures as high as 80°F. for a short time without serious injury. Under similar conditions rainbow and brown trout can survive somewhat higher temperatures. However, such high tem-peratures may produce disastrous results in hatchery waters. Where the fish are crowded together in small pools there is likely to be a deficiency in dis-solved oxygen when the water becomes warm, and under such circumstances high temperatures are much more injurious. Furthermore, hatchery fish are usually not so strong and vigorous as those living in a natural environment and consequently succumb more quickly to adverse conditions.

Ordinarily, a temperature higher than 65°F. should not be allowed in rear-ing pools, and, where practicable, the water should be kept below that tem-perature. Trout appear to grow most rapidly at 55° to 60°F., and at higher temperatures their vitality is lowered and they are more liable to contract some disease.

Overheating of the water can often be prevented by partially shading the pools and raceways. In fact, this is advisable even where there is no danger of overheating, as it has been found that small fingerlings usually do better when given an opportunity to escape from the intense light of the midday sun.

In addition to providing more natural conditions for young trout, raceways have a distinct advantage over troughs in that they require much less atten-tion. Troughs must be cleaned at least once a day, but even heavily stocked raceways usually need not be cleaned of tener than once or twice a week. In-stances are on record where the fish apparently suffered no ill effects even though the raceways were left for several weeks without any attention other than to clean the screens so that the water could circulate freely. In an ex-periment conducted at the Service's Pittsford (Vt.) experimental hatchery, fingerling brook trout were allowed to remain in a raceway from April to Octo-ber without cleaning, and there was virtually no mortality during this period. Moreover, the fish were more vigorous, better colored, and made more rapid growth than those held in troughs. There were about 6,000 fingerlings in the raceway, which was 4 feet wide, 37 feet long, with a depth of 10 to 12 inches. The water supply fluctuated from 20 to 30 gallons per minute. This experi-ment is mentioned not with the intention of advocating that raceways should not be cleaned frequently, but simply to show that extreme cleanliness is un-necessary under such conditions.

As a matter of fact, raceways, like polluted streams, have a remarkable capacity for self-purification, which is accomplished in much the same way. The excrement accumulates on the bottom and supports a luxuriant growth of small organisms, including bacteria, algae, protozoa, and insect larvae, which quickly causes its distintegration, so that the organic compounds are reduced to nontoxic, inorganic substances. The decaying excrement contains large numbers of chironomid larvae, that trout eat readily, and these, together with algae, form a not inconsiderable portion of the food of the young finger-lings. It is not improbable that this "natural" food is largely responsible for the greater vigor of fish reared under such conditions.

CARE AND DISEASES OF TROUT- 7

During recent years the circular pool has been growing rapidly in favor and, for fingerlings at least, promises largely to supplant the orthodox type of pool and the raceway described previously. The superiority of the circular pool for yearling and larger trout is not so evident, and it is probable that for fish of this size the older type of pool will still retain its popularity.

FIGURE 3.—Circular rearing pools at the Leetown (W. Va.) Experimental Hatchery.

FIGURE 4.—Near view of circular rearing pools at the Leetown Experimental Hatchery.

The construction of a circular pool (figs. 3 and 4) sists essentially of a basin-shaped excavation with t

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is very simple. It con-e bottom sloping grad-


ually toward the center. Various types of circular pools are in use, but ex-perience has indicated that a relatively shallow pool, 15 to 25 feet in diameter, is most satisfactory. In these pools the water is not over 18 or 20 inches deep at the center and 8 or 10 inches deep at the margin. The bottom should have a gradual slope toward the outlet at the center, and both the sides and bottom should be of concrete, since it is not possible with a dirt bottom to maintain such a slope for any length of time. The water may enter through the open end of the supply pipe, but a better circulation is obtained by boring several small openings on the side of the pipe that projects over the pool as shown in figure 4. With this type of inlet it is surprising how little water is required to maintain a good circulation. The water, preferably under considerable pressure, enters tangentially at one side of the pool and flows out through an outlet pipe at the center. It travels in a circular pith and makes a number of circuits before leaving through the overflow pipe. Consequently, there is a nearly uniform circulation of water throughout the pool, and the fish are evenly distributed instead of massed near the outlet as so frequently occurs in raceways and pools of the older type. The fish have a better chance to ex-tract oxygen from the water, and consequently a circular pool will carry sev-eral times the number of fish that can be held in a long pool of the same vol-ume of flow. The fish also have more opportunity for exercise, and they can frequently be seen swimming around and around the pool in orderly succes-sion. Another distinct advantage of this type of pool is the fact that there is nothing against which trout can jump and injure themselves, as is frequently the case in raceways unless special precautions are taken.

To one who has had experience only with raceways, the number of fish that can be carried in a circular pool is almost unbelievable. At the Leetown sta-tion, 20,000 rainbow fingerlings, with an average weight of 2.3 grams, were placed on June 11 in a pool 15 feet in diameter. The pool was 18 inches deep at the center and received 12.4 gallons of water per minute. These fish re-mained in the pool with practically no mortality until September 6, at which time the average individual weight was 8.8 grams. 'The total weight of the fish in the pool at this time was approximately 387 pounds. A second pool of the same size was stocked on June 2 with 15,000 rainbow fingerlings, aver-aging 1.9 grams in weight. These fish remained in the pool with practically no losses until September 2, when the average individual weight was 11.5 grams. It is of interest to note that the total weight of the fish in this pool was practically the same as in the pool containing the larger number of fish. Although both pools were fully exposed to direct sunlight, the highest tem-perature recorded was 64°F. at 4:25 p.m., July 28, when the air temperature was 100°F. The temperature of the water as it entered the pool was about 56°F.

One of the great advantages of the circular pool is that the excrement and other wastes collect at the base of the outlet pipe in the center where they can be easily removed by a siphon. A self-cleaning device has been developed at the Leetown station, which automatically removes all waste material and greatly simplifies the operation of this type of pool. This device consists of a large sleeve which is attached to the outlet pipe and extends for a short dis-tance above the surface of the water. At the bottom there is a narrow open-ing between the sleeve and a sloping flange which rests on the bottom of the pool. The width of this opening can be easily adjusted according to the size of the fish in the pool. Excrement and other waste materials are drawn into the opening by water flowing through the outlet pipe, thus keeping the pool clean.


There is considerable difference of opinion among trout culturists with re-spect to the age at which the fingerlings should be removed from the troughs. Probably under ordinary circumstances the sooner the fish are removed to raceways after they begin to feed the better.

Apparently, the most common practice is to hold the fish in troughs for several months and in early summer transfer them to raceways or pools. This practice appears to be predicated largely on the fact that while in the troughs the fish are under more immediate control and can be watched more carefully than when in raceways. While this is undoubtedly true, it is questionable that this outweighs the obvious advantages that fish in raceways enjoy.

It is held by those who believe in keeping the fish in troughs for the first few months that when they are transferred to raceways early in the season, there is always considerable loss which cannot be accounted for by the num-ber of dead fish recovered. Consequently, when the fish are finally removed, their number is always much less than is indicated by the mortality record. This is undoubtedly true, but if the raceways are properly constructed, and the fish graded frequently (as they should be) and protected from enemies, it is believed that this discrepancy will be not much greater than if the fish were held in troughs over the same period. In virtually all cases the so-called "uncounted mortality," which has been emphasized so much, is due, either to improper construction of the raceways, so that many of the fish are able to escape; to the attacks of enemies, such as fish-eating birds; or to cannibalism. The first two of these factors can be virtually eliminated by proper construc-tion at comparatively small expense. It should be remembered that young fingerlings can wriggle their way through an almost inconceivably small open-ing, and all head and foot screens should be constructed accordingly. Protec-tion from birds and other enemies can be assured by covering the raceways with wire netting.

In many cases it is probable that most of the "uncounted losses" are due to cannibalism, wh:ch is doubtless more rampant in raceways or pools than in troughs. It may seem paradoxical, but experiments have shown that canni-balism is greatest among well-fed, rapidly growing fish, not among those that are weak and underfed. Fortunately, cannibalism can be prevented by grad-ing the fish at frequent intervals, so that only those of approximately equal size are held in the same compartment.

It seems to be best in most cases not to transfer the fish to raceways until after they have learned to feed, although experimental work has shown that they can be taught to take food in raceways nearly as readily as in troughs. As previously pointed out, when the fingerlings reach a length of 3 or 4 inches they may be removed to pools which should be so designed as to simulate natural conditions as closely as possible. Pools with dirt bottoms are much superior to those with bottoms of concrete, and unless the soil is of such a nature as to require wood or concrete sides, these should be dispensed with.

The size of rearing pools is dependent largely on local conditions, but gen-erally speaking, comparatively small pools are preferable. Also they should be quite shallow, with a maximum depth of 2 or 3 feet, unless it is necessary to use a greater depth to prevent the water becoming too warm during hot weather. Needless to say, it is essential that the ponds have a copious supply of pure, cold water, and that they should be so constructed as to insure a good circulation throughout. The deepest part of the pond should be at the outlet, toward which the bottom should slope gradually from all sides, so that the pond can be easily drained and the fish removed with little trouble.


When the water supply is limited, the ponds may be arranged in series, one below another, which allows the same water to be used several times. Of course, this is objectionable from the sanitary standpoint, since any disease in the upper ponds would be transmitted immediately to fish in those below. For this reason, it is not advisable to resort to such an arrangement unless it is necessary. However, with the exception of furunculosis, yearlings and older fish are seldom seriously affected by infectious diseases, and therefore the dan-ger is not so great as would at first appear. It is well to bear in mind that, whenever ponds are arranged in series, fingerlings should never be placed in those receiving the drainage from ponds containing older fish. Yearlings and brood fish often harbor parasites, which, while not seriously affecting them, may produce disastrous results when transmitted to fingerlings.

CARE OF PONDS AND RACEWAYS

It is scarcely necessary to point out that raceways and rearing ponds should always be kept in good sanitary condition. No food should be allowed to col-lect on the bottom, and the excrement should be removed frequently enough to prevent the water from becoming polluted. It is difficult to give detailed advice, s:nce the care necessary to keep pools and raceways in sanitary condi-tion will vary widely with conditions.

As pointed out, ponds and raceways do not require such close attention as troughs, because a certain amount of filth is automatically taken care of with-out detriment to the fish. The efficiency of self-purification naturally will vary with the number of fish contained in the pools. If the fish are relatively few, it may be necessary to clean the ponds at only infrequent intervals. In-stances are known of fish kept in ponds with dirt bottoms which were cleaned only at intervals of several months. Although there was an average of one 6- to 8-inch fish per square foot of surface area, there was no evidence that the fish were affected unfavorably. Under ordinary conditions, however, the accumulated filth should be removed more frequently to prevent any injurious effects from the decaying excrement. When cleaning the pools, every precau-tion should be taken to avoid injury to the fish. The practice of going over the bottom with a broom or some similar implement and thus stirring up the material that has accumulated is highly objectionable, as it always results in considerable injury to the fish. Moreover, this practice necessarily removes most of the algae, which is in itself inadvisable. Unless unduly abundant, algae have a beneficial effect, and their growth should be encouraged. There are no more efficient agents in keeping the ponds in a sanitary condition than the algae and associated organisms. Not only do they aid in aerating the water and keeping it free from objectionable substances, but trout feed on them to a considerable extent, and they, no doubt, perform much the same function in the trout's metabolism as do vegetables in the human diet.

A much better and more logical way to remove the excrement and other filth on the bottom of the pools and raceways is to employ some suction device that will avoid stirring up the material or injuring the fish. If this is not feasible, the lowest part of the pool should be connected with a drain, through which most of the filth can be drawn off with little trouble.

In this connection a word of caution should be addressed to those who are about to clean pools in which excrement and, more especially, surplus food has been allowed to accumulate for a considerable time. Under such circum-stances a layer of decomposing material may form on the bottom, which does not appreciably affect the overlying water as long as it is undisturbed. This


layer has a high oxygen demand, contains noxious gases and other toxic sub-stances, which are liberated as soon as the material is moved, and if the fish remain in the pool, there is danger that they may be killed. In such cases the fish should be removed from the pond before any attempt is made to dis-turb the filth on the bottom. Even after the pond has been cleaned, it is best to allow the water to flow through it for a short time before the fish are re-turned. When practicable, it is best to drain all ponds occasionally and allow them to remain dry for several days. If this is done once or twice a year, the Ponds will be in better condition than if kept filled continuously.

TROUT FOODS

There is probably no question on which fish culturists differ more widely than in regard to what constitutes the most satisfactory food for trout. During recent years this problem has received much attention, and diets greatly superior to those formerly used have been developed, but, nevertheless, there is still no general agreement as to the best and most economical diets to use under all circumstances.

It is safe to say that, with the exception of the water supply, no single factor is of more importance in determining the success or failure of a hatchery than the daily diet of the fish. If strong, healthy fish are to be developed, they

.must be provided with suitable food, and it is no small problem to determine what food or what combination of foods may be relied on to give the best results under average conditions.

In any consideration of trout foods it should be remembered that rapidity of growth is not the only factor of importance. Too often in the past this has been virtually the only criterion used in evaluating a trout food. Rapid growth is very desirable, but it should not be procured at the expense of the health and vigor of the fish. The Federal and State hatcheries are raising fish to be liberated in natural waters where they will be obliged to fend for them-selves. It is very doubtful that the fat, lazy, pot-bellied fish so often seen in hatcheries are as well able to care for themselves when thrown upon their own resources, as are fish which have not been pampered or subjected to an abnormal forcing process. For stocking purposes there are needed hardy, vigorous fish that can adapt themselves quickly to their new environment.

It is important to bear in mind that the trout culturist does not have an unlimited number of foods at his disposal, from which to choose. He is, in fact, bound hand and foot, since any food to be considered seriously must be obtained at a reasonable cost, and there must be an adequate supply available at all times.

Available trout foods may conveniently be divided into three groups. In the first group are fresh meats such as horse meat, and the liver, lungs, and spleen of cattle, sheep, and hogs. The second group embraces various dried animal meals; while the third group includes plant products, such as wheat middlings, low grades of flour, shorts, cottonseed meal, soybean meal, and peanut meal. In a Federal fisheries survey conducted in 1935, it was found that sheep plucks were used to a greater extent than any other food. Other products that were fed in large quantities were beef, sheep, and pig liver, horse meat, cereal products, and fish. Since that time, extensive changes have been made in trout diets, with resultant greater emphasis on dry products.

As in the case of higher animals, fish require a certain amount of proteins, carbohydrates, and fats in their diet as well as various inorganic substances, such as lime and salt. These mineral constituents, of which there are a large


number, are just as necessary as the fats and proteins. In addition, fish, like higher animals, require vitamins, even though these are present only in very minute quantities.

Recent experiments have greatly increased our knowledge of the vitamin requirements of trout. A deficiency of vitamin B1 where fresh or frozen fish are fed to trout has been shown to result in serious mortality by several workers. (Wolf, 1942; Tunison et al, 1942; Woodbury, 1942.) Tunison and his coworkers (1943) found that 3 vitamins of the B-complex were involved in the production of anemia in trout on a synthetic diet. On the other hand Simmons and Norris (1941) reported that lack of xanthopterin was respon-sible for the anemia which developed when no raw meat was included in the diet. Wolf (1944) and Tunison et al (1944) found that pantothenic acid deficiency was responsible for a form of gill disease. That still other vitamins are essential to trout is indicated by the benefits derived from the addition of yeast and cod liver oil to the diet which are far greater than can be accounted for on the basis of their calorific value. It is evident that despite our in-creased knowledge of the value of vitamins in the nutritional economy of trout, much work remains to be done before it will be possible to complete the story of their vitamin requirements.

It has been common knowledge among fish culturists for years that trout could not be reared successfully without the inclusion of raw meat in the diet. This fact, which has been demonstrated time and again, led McCa3i and Dilley (1927) to postulate a hypothetical factor H which is present in virtually all raw meats, but is found to only a very limited extent in cooked or dried products. All efforts by McCay and his coworkers to isolate factor H have been unsuccessful, which is not surprising, since it now appears that in all probability there is no such substance. Recent experiments indicate that the beneficial effects attributed to factor H result from several vitamins, all of which must be present at the same time and that one of the first indi-cations of a deficiency of these vitamins is the appearance of an anemic con-dition. All workers, however, are not agreed as to the vitamins that together constitute factor H. Simmons and Norris (1941) believe xanthopterin to be the principle constituent, but Bridge (1943) concludes that factor H contains both a growth factor and an anti-anemic factor and that these are distinct and separate. Tunison et al (1943) believe that at least 3 vitamins —pantothenic acid, riboflavin, and pyridoxine—are concerned in the factor H complex.

In any consideration of trout foods, it is well to bear in mind that there is evidence that the nutritional requirements of the various species of trout may differ in some respects. Rainbow trout, for instance, appear to be more susceptible to dietary deficiencies than are brook trout. This opinion, based on hatchery experience, receives additional support from the fact that all food studies of wild fish have shown that a considerable percentage of the food of rainbow trout consists of algae; while in the case of brook trout the occurrence of these plants in the stomach contents appears to be entirely ac-cidental. Nevertheless, it is undoubtedly true that diets which have been found to give excellent results with one species of trout will in all probability give good results with other species.

Another essential in any trout food is its palatability. Obviously, if a food is to produce rapid growth it must be taken readily by the fish; for, while hunger may drive them to eat unpalatable foods in small quantities, such a diet will never produce vigorous, rapidly growing fish. Experience has shown that this is the reason for the failure of some apparently good foods to yield


satisfactory results. They may contain the proper proportions of proteins, carbohydrates, and fats, as well as sufficient vitamins, but if they are not palatable, the fish will suffer from partial starvation even though there is always a supply of the food available.

It has been the universal experience of fish culturists that trout can be reared successfully on a straight meat diet, although there is much difference of opinion as to which meat gives the best results. Everything considered, probably no meat has proved more satisfactory for young fingerlings than beef liver, and undoubtedly this would be used much more extensively were it not for the fact that its cost has increased greatly in the past few years. However, experiments with both brook and rainbow fingerlings have shown that, in general, a mixed diet is preferable to one composed of a single meat product, and that better results are obtained when beef liver is mixed with beef heart than when it is used alone.

There can be little doubt that the results attained with various meat products are dependent on both their chemical and physical structure, and the latter should not by any means be ignored. This probably accounts for the fact that beef heart has been found superior to beef liver as a food for advanced fry and very young fingerlings. The heart can be ground into very fine particles, which are easily swallowed by the young fish, while the liver forms a thick, mush-like material not so readily separable into discrete par-ticles. Furthermore, a considerable percentage of the ground liver is readily soluble in water, and there is, therefore, from this source an appreciable loss in food value.

As the fish increase in size they are naturally able to ingest larger particles, and to devour the food more quickly. Consequently, there is less loss from solution, and liver will thus produce a faster growth than heart, although there is usually a higher mortality. By combining heart and liver in a mixed diet the growth is virtually as great as with liver alone, while the mortality is comparable to that of fish kept on a straight heart diet.

In our experiments pig liver and sheep liver, when fed straight to young fingerlings, have not given good results. However, sheep liver produced a better growth with rainbow than with brook trout, although even with the former species the results were not so satisfactory as with beef liver and beef heart. Both pig and sheep liver give better results when mixed with other products than when fed alone.

Beef and pig melts, or spleen, are among the cheapest foods available to fish culturists, and for that reason are used extensively at many trout hatch-eries. In our experiments these products have always produced relatively slow growth as compared with liver and other superior diets. The mortality, however, was low, and owing to their lower cost, it may be advisable where rapid growth is not essential to include these products in the diet. Later experiments indicate that beef melts are definitely superior to pig melts.

Melts should always be supplemented by some otber meat or by dry meal, since Hess (1937) has shown that when fed alone, a considerable percentage of the fish after a time develop cataract. The disease appears as a distinct opaqueness in the lenses of both eyes. Hess believed the development of cataract was due to a vitamin deficiency, and McCay and Phillips (1940) have shown that it is caused probably by a deficiency of vitamin A.

While only a few meats have been successfully fed to small fingerlings, a considerably greater variety is available for fish 3 to 4 inches long and larger. Fish of this size do much better on pig and sheep liver than do very young fingerlings, and beef lungs and sheep plucks may also be fed. Here again,


however, a mixture of two or more kinds of meat usually gives better results than one meat alone.

Fresh fish of the coarser and cheaper grades have been utilized to a con-siderable extent for trout food, but in most cases the results have not been entirely satisfactory. It usually requires about twice as much fish as meat to produce an equal growth, and the trout are often not as healthy as those on a meat diet. Furthermore, it is much more difficult to keep fish in fresh condition than it is to keep meat, and the eating of decayed fish is liable to kill trout. It has been shown by Gutsell (1940) that frozen fish, when fed to trout continuously for several months in a proportion greater than 20 percent, may cause serious losses. After a time, the fish become much darker than normal, lose their balance and swim on one side. This condition is frequently followed by blindness, and eventually the fish die. Later Wolf (1942) showed that the trouble is caused by a vitamin B1 deficiency due to the presence of an enzyme in fish flesh that destroys the vitamin in substances mixed with it.

According to Deutsch and Hasler (1943) the following species of fish contain the enzyme that destroys vitamin B1: whitefish, smelt, carp, goldfish, creek chub, fathead minnow, buckeye shiner, sucker, channel catfish, bull-head, mudminnow, white bass, sauger, burbot, and salt-water herring. Species of fish which do not contain the enzyme include garpike, dogfish, Lake Superior herring, lake trout, rainbow trout, brown trout, pickerel, wall-eyed pike perch, bluegill sunfish, rock bass, cod, haddock, mackerel, whiting, sole, redsh, and dabs. In order to avoid any possibility of B1 deficiency fish should be fed separately and not mixed with other constituents of the diet.

Owing to the high cost of fresh meats, it is not in most instances economical to keep trout on a diet composed of only fresh meat after they reach a length of about 2 inches. Up to that time, the cost of food is a relatively unim-portant factor, but as the fish increase in size, one of the greatest problems of the trout culturist is to find a diet that will produce large, healthy fish at the lowest possible cost. This has led to the extensive use of dry products, which are not only more economical than meats, but if fed properly, will produce fully as good, if not better, fish than can be grown on a straight meat diet.

The dried products that have given the best results as substitutes for part of a fresh-meat diet are those of animal origin. A variety of such products are now available and ordinarily are obtainable in any quantity desired. Among the animal meals that have proved most satisfactory are salmon meal, white fish meal, sardine meal, meat meal, dried skimmed milk, and dried buttermilk. The fish meals should be vacuum dried and the dried milk manu-factured by the spray process.

When dry meals are included in the diet of small fingerlings, it is best to start with a limited amount say from 10 to 20 percent, and gradually increase the percentage as the fish grow and become accustomed to the food. Experi-ments have shown that after the fish reach a length of 4 or 5 inches, as much as 70 percent of the better meals may be included in the diet without injurious effects. However, when dry meals are fed at a level higher than 50 percent, the food is utilized less efficiently than at lower levels. Nevertheless, owing to the lower cost of dry feeds, it may be economical to use them at higher levels even though the waste may be somewhat greater.

In general, it is advisable to use a mixture of dry feeds rather than one alone. A mixture which produced good results in experiments is composed


of equal parts of meat meal, salmon-egg meal, white fish meal, and dried buttermilk (Gutsell, 1940). In later experiments, a mixture composed of 2 parts of white fish meal, 1 part meat meal, and 1 part dried buttermilk gave somewhat better results at a lower cost. The addition of 3 percent of cod liver oil to various meals and meal mixtures used by Gutsell and 3 percent kelp meal resulted in a considerable increase in fingerling growth and a more economical utilization of the food.

In preparing mixtures of fresh meat and meals it has been found best in most cases to mix the meat directly with the meal without preliminary moistening. After roughly mixing the meat and meals together in the proper proportions, it is best to complete thF; operation by forcing the mixture through a grinder or a mechanical mixer. This results in a more complete mix than can be produced by hand, and there is consequently less loss in feeding. Liver, on account of its consistency, is more satisfactory for use with dry meals than heart or plucks. This is especially true of pig liver, which when ground is more sticky than either beef or sheep liver. For small fingerlings, however, beef liver will probably be found better, despite its greater cost. For large fingerlings and older fish, either sheep or pig liver appears to be satisfactory. In some sections melts are popular as the meat constituent of the diet. They are not only cheaper than most other meats, but when mixed with 2 percent salt, have a very sticky consistency and thus make an excellent binder for dry meals. To obtain the best consistency, the salt should be added to the melts while they are partially frozen.

Some trout culturists feed dry foods alone instead of in mixture with fresh meat. In such cases it is, of course, necessary to give the fish a meal of fresh meat occasionally to counteract the ill effects of an all-dry diet. While this method of feeding permits the use of a large percentage of dry foods, there is always much more waste than when a mixture is used, and for that reason, it is not recommended.

In comparing the cost of fresh meats and dry animal meals, it may appear at first glance that the latter are more expensive, but it must be remembered that fresh meats contain 70 percent or more of water, while dry meals con-tain only about 10 percent. This means that the price of all fresh meats should be multiplied by three in order to obtain a fair cost comparison with that of dry products. Table 1 shows the results obtained at the Leetown station with some of the better experimental diets. The list is far from com-plete, but will give some idea of the comparative value of various food mixtures. In order to avoid any misunderstanding, it may be well to point cut that the weight of food required to produce a pound of fish is the actual weight of the mixture as fed. For example, 5 pounds of a mixture of 60 percent liver and 40 percent white fish meal would contain 3 pounds of ground liver and 2 pounds of dry fish meal.

The vegetable products that have been used in trout diets include cereals and the so-called protein concentrates. Wheat middlings and low grades of flour are probably fed to a greater extent than other cereal products, although bran, shorts, and other meals are also utilized. The protein concentrates are cottonseed meal, soybean meal, and peanut meal, which differ from cereals chiefly in their high protein content.

There is much difference of opinion regarding the relative value of plant and animal meals in the diet of trout. Experiments have been unfavorable to the use of vegetable products, since fish maintained on diets containing considerable amounts of cereals or protein concentrates have consistently made a much slower growth than those on diets containing the same amounts of

742482°--47----3


TABLE 1.—Comparative growth and mortality of fingerling trout on experimental diets, Leetown (W. Va.) station MAY 6 TO SEPTEMBER 23, 1932

Species Diet (percentage each constituent)

Fin

al

awveei

rgrte

Incr

ease

in

aver

age

wei

ght

Fee

d to

p

rod

uce

1 lb.

of g

row

th >,

...-'.. I':

A Grams Percent Pounds Percent

Rainbow Trout Beef liver 100 ...................................................................... 13.9 900 4 2 6.4 Do Beef liver 70, salmon-egg meal 30 ................................ 17.4 1,239 3.29 1.6 Do Beef liver 60 meat meal 40 .............................................. 16.4 1,071 2 88 1.7 Do Beef liver 60, dried buttermilk 40 ................................ 13.7 878 2 14 2.3 Do Beef liver 70, cottonseed meal 30 .................................. 9 543 5.18 9.8

Brook Trout Beef liver 70, salmon-egg meal 30 ................................ 23.4 2,027 2 06 4.2

MAY 23 TO OCTOBER 11, 1939

Brook Trout Sheep liver 60, white fish meal 40 ................................ 48 1,043 2.78 .2 Do Sheep liver, 58.2, white fish meal 38.8, cod liver oil 3 53.8 1,279 2 60 .8 Do Sheep liver 58.2, white fish meal 38.8, kelp meal 3 .. 51.6 1,223 2.65 .7 Do Sheep liver 58, white fish meal 36, kelp meal 3,

cod liver oil 3 ............................................................. 54.8 1,342 2 61 .5 Rainbow Trout Sheep liver 60, white fish meal 40 ................................ 41.7 1,091 2.97 0

Do Sheep liver 58, white fish meal 36, kelp meal 3, cod liver oil 3 ............................................................. 49.2 1,267 2.77 0

Do Sheep liver 50, white fish meal 50 ................................ 43 1,032 2.91 .8 Do Sheep liver 48.5, white fish meal 48.5, cod liver oil 3 45.1 1,153 2.74 0

JUNE 10 TO OCTOBER 29, 1940

Rainbow Trout Do

Sheep liver 60, L-40-A dry mixture° 40 ..................... Sheep liver 58.2, L-40-A dry mixture 38.8. cod

liver oil 3 ......................................................................

54.6

61.8

1,170

1,337

2.80

2.63

.3

0 Do Sheep liver 58.2, L-40-A dry mixture 38.8, kelp

meal 3 ........................................................................... 50 1 1,065 2.88 .7 Do Sheep liver 60, meat meal 40 ......................................... 48.5 1,055 2.75 3.7 Do Sheep liver 58, L-40-A dry mixture 36, kelp meal 3,

cod liver oil 3 ............................................................. 60 8 1,348 2 59 0


Rainbow Trout Sheep liver 50, L-40-B3 dry mixture 48, salt 2 ....... 44.7 964 3.00 4.9 Do Sheep liver 25, pork melts 25, L-40-B dry mixture

48, salt 2 ...................................................................... 42 3 907 3 03 2.1 Do Pork melts 50, L-40-B dry mixture 48, salt 2 ......... 37.9 824 3.28 6.7 Do Sheep liver 50, No. 12 Cortland dry mixture, 48,

salt 2 ............................................................................... 34.4 739 3.26 .3 Do Sheep liver 25, pork melts 25, No. 12 Cortland dry

mixture 48, salt 2 ....................................................... 34.4 739 3.25 0 Do Pork melts 50, No. 12 Cortland dry mixture 48,

salt 2 ............................................................................. 29.9 612 3.49 1.8


Rainbow Trout Beef melts 50, cottonseed meal 48, salt 2 .................. 16.8 380 4.75 4.9 Do Beef melts 50, soybean meal 48, salt 2 ....................... 26 4 654 3 81 30 3 Do Beef melts 50, peanut meal 48, salt 2 ......................... 28 700 3.52 16.5 Do Beef melts 50, cottonseed meal 16, soybean meal 16,

white fish meal 16, salt 2 ......................................... 33.8 866 3.33 8.8 Do Beef melts 50, cottonseed meal 16, peanut meal 16,

white fish meal 16, salt 2 ....................................... 30.4 744 3.35 4.2 Do Beef melts 50, soybean meal 16, peanut meal 16,

white fish meal 16, salt 2 ....................................... 38.3 994 3.06 18.6

°The D-40-A dry mixture was composed of 2 parts white fish meal, 1 part Valentine's meat meal and 1 part dried buttermilk.

3The L-40-B dry mixture was like the L-40--A dry mixture except that instead of Valentine's "meat meal", a beef scrap meal of high protein content (60% or higher), from a large packing house, was used.

3No. 12 Cortland dry mixture is composed of 1 part white fish meal, 1 part cottonseed meal, 1 part flour middlings, and 1 part of roller dried skim milk.

animal meals. Of course plant meals are much cheaper than animal meals and that appears to be the principal reason for their extensive use.

Cereals, especially, have a high starch content, and it still remains to be proved that diets rich in starch are satisfactory for trout. Recent experiments by Phillips (1940; Phillips and Tunison, 1940) are inconclusive. It was found

CARE AND DISEASES OF TROUT

17

TABLE 2.—Comparative growth and mortality of fingerling trout, with cost of feed to produce 1 pound of trout, Leetown (W.Va.) hatchery

JUNE 7 TO SEPTEMBER 29, 1944

Species Diet (percentage each constituent) 0 7, bj „•a' .r. t, . Ef

Fina

l av

erag

e w

eigh

t

Incr

ease

in

aver

age

wei

ght

Feed

to

prod

uce 1

lb.

of g

row

th

b i t' A Co

st o

f fee

d to

pro

duce

1 lb. o

f gro

wth

Grams Grams Percent Pounds Percent Dollars Rainbow Trout Beef melts,- 50, salt 1, white fish

meal 49 10 0 43 1 331 2.97 .5 $ .103 Do Beef melts 50, salt 1, white fish meal

39.2, dried yeast 9.8 10 2 49.6 386 2.66 1 .136 Do Beef melts 50, salt 1, white fish meal

36.75, dried skim milk2 12.25 . 9.9 44.1 345 2 87 .124 Do Beef melts 50, salt 1, white fish meal

24.5, dried skim milk 12.25, beef scrap meal (60 percent protein- 12.25 10.2 42.0 312 3.10 0 .138

Do Beef melts 50, salt 1, white fish meal 24.5, dried skim milk 12.25, peanut meal 12.25 10 2 41.0 318 3 02 .129

Do Beef melts 50, salt I, white fish meal 24.5, dried skim milk 12.25, cottonseed meal 12.25 10 0 39 3 293 3.18 .5 .136

Do Beef melts 50, salt 1, white fish meal 24.5, peanut meal 12.25, bran 12.25 10 0 40.0 300 3.16 .5 .104

Do Beef melts 50, salt 1, white fish meal 24.5. cottonseed meal 12.25, flour middlings 12.25 9.6 41.0 327 2.92 0 .094

Do Beef melts 50, salt 1, white fish meal 12.25, dried skim milk 23.25. cottonseed meal 12.25. wheat flour middlings 12.25 10 0 38.1 281 3.20 0 .134

'The very low prices of beef melts in 1944 helped keep cost charges down. 2Dried milk so expensive as to make cost of production from diets containing it unnecessarily expensive.

With milk at "pre-war" prices, cost of production would have been under eleven cents with this diet, and more competitive in other instances.

that under the experimental conditions as high as 59 percent of raw starch might be digested. The experiments also showed that about 20 percent more of cooked starch was utilized under similar conditions. It is probable, how-ever, that a much smaller percentage of either raw or cooked starch would be digested under ordinary feeding conditions.

An interesting result of the experiments was the discovery that after 16 weeks the bodies of brook trout maintained on diets rich in sucrose, dextrin, or cooked starch were greatly swollen and the fish behaved listlessly. On dissection, the livers were found to be several times their normal size and very light in color by reason of excessive amounts of glycogen present. Later experiments led these workers to conclude (Tunison et al 1943) that in addition to their effects on the liver "carbohydrates not only interfered with digestion but did not materially improve protein utilization. The trout's body is apparently better adapted to use protein for satisfying its energy requirement."

Extensive use has been made of cottonseed meal in trout rations, while soybean meal and peanut meal have been fed very little. Experiments at Leetown by J. S. Gutsell (unpublished) indicate that both soybean meal and peanut meal are better growth producers than cottonseed meal, but are less satisfactory from the standpoint of fingerling survival (table 1). When combined with white fish meal, the growth is increased and the mortality reduced. These results agree with McCay's (1940) findings that animal pro-tein is superior to protein from plant sources,


It is believed that the use of plant meals in the diet of young fingerlings is inadvisable. This opinion is based on experimental evidence and also on the experience of years at the Federal hatcheries. With the better grades of fish meals and dried milk available at reasonable cost, it probably will not prove economical in the long run to feed plant meals to small fingerlings. Such rapidly-growing fish need relatively large quantities of food rich in proteins which can be easily digested and assimilated. With respect to older fish, the evidence regarding the value of plant meals in the diet is not so conclusive. Many hatcheries are said to be feeding such rations with satis-factory results, but there is still room for doubt whether ultimately anything is gained by such a diet. There is evidence, moreover, that fish reared on a 'meat and animal meal diet are more healthy and vigorous and presumably better suited for stocking purposes.

The use of fillers or bulk foods in the trout ration is now being advocated in some quarters, especially in the western United States (Donaldson and Foster, 1941). Several products are being used for this purpose, such as apple flour, citrus flour, and alder sawdust. These products have very little or no food value and are used in the trout ration for a two-fold purpose: (1) to prevent overfeeding and (2) to serve as roughage.

There is reason to doubt that overfeeding is as injurious as it was once thought to be, although there is no question that food is utilized more effi-ciently if fed in moderate amounts. Experimental lots of rainbow trout at the Leetown station have been overfed continuously for several years without any ill effects, except that the fish were exceptionally fat and the eggs of poor quality (Gutsell, 1940). In experiments by Gutsell (unpublished) using apple flour, citrus flour, and tomato flour as fillers, the fish made a much slower growth than on the same diet without the bulk foods. It is evident that fillers should not be used when rapid growth is desired, but it must be conceded that the use of bulk foods may be desirable in some cases, especially in rearing salmon fingerlings in which rapid growth is of secondary importance.

The use of roughage in the trout diet is by no means new, having been advocated by trout culturists for years. This is based on the well-known fact that the natural food of trout, consisting principally of insects and crustaceans contains a large percentage of indigestible material. It is only natural to assume therefore that artificial diets should contain a similar amount of roughage. This assumption, however, is not borne out by feeding experi-ments, which have failed to yield any clear evidence that roughage is neces-sary in the trout ration. It should be pointed out in this connection that certain products, such as cereals, shrimp bran, and similar foods, which have been much used in trout rations do furnish considerable roughage. It is possible, also, that further studies may show that roughage has a more im-portant function than available information indicates.

FEEDING METHODS

Meat and other foods should always be ground fine enough to be readily swallowed by the fish, but this is a matter that can be easily overdone. When the advanced fry begin feeding, there is little danger of getting the food too fine, and it should be forced through the finest plate of a grinder several times in succession. As the fish increase in size they are able, of course, to swallow larger particles, and, if the food is not ground so fine as at first, they will take it more readily and lose less in the surrounding water.

In feeding small fingerlings most fish culturists add a small amount of


water to the food, so that the particles will separate readily in the water. However, some insist that it is better to place small portions of food at intervals on the bottoms of the troughs, where the fish can break it up at their leisure. If carefully done, there is probably less loss by the" latter method, but it is questionable whether all the fish have an equal opportunity to obtain food.

When the fish begin to take food, it is customary to feed them 5 or 6 times a day, but as they grow older, the number of feedings may be decreased gradually, and 2 meals a day are sufficient for the larger fingerlings. Older fish are usually fed once a day, although when very rapid growth is desired, it is probably better to feed both in the morning and in the evening. Of course, when the fish are fed twice a day, it is not advisable to feed as much at one time as when they receive only 1 meal in 24 hours. Needless to say, the food should always be distributed over a considerable area, so that all the fish will have an equal opportunity to get a share In feeding fish of any age, it is always a good rule to give them only as much food as they will eat readily. It is poor practice to allow food to accumulate on the bottom of the trough or pool, because not only is such food a total loss, but it will soon begin to decay and cause trouble.

When trout are to be handled or transported, it is always advisable not to feed them for some hours previously. This serves a twofold purpose: there will be less excrement to accumulate in the cans and cause trouble, and the fish will stand handling better.

IMPROVEMENT OF STOCK

One of the most important phases of trout culture and one that, remark-ably enough, has received relatively little attention, is the necessity for improvement of the brood stock in order to obtain the best results. Everyone recognizes that continuous and rigid selection is necessary in the case of domesticated animals and plants, but few seem to have realized the im-portance of this principle in trout culture. Indeed, the tendency in many cases has been in the opposite direction, for some of our commercial growers have marketed their best and largest fish and saved the remainder for breed-ing purposes. On the other hand, some trout culturists have taken pride in building up a superior stock of brood fish, but usually they have not system-atically carried on the selection over a term of years, as must be the case if permanent results are to be obtained.

According to Hayford and Embody (1930) breeding experiments with brook trout started in 1919 at the New Jersey State Hatchery at Hacketts-town, resulted in a marked increase in the rate of growth and in egg pro-duction, as well as greater resistance to disease. In four generations the maximum length of fish at the end of the second year increased from 10 inches to 13.75 inches, while the minimum length increased from 7 to 10.5 inches. They state that it is now possible at the end of the first year to have trout for stocking purposes which average between 6 and 7 inches long, instead of the usual 3-, 4-, or 5-inch fingerlings. These results were accom-plished by selecting for breeding purposes a small percentage of the most rapidly growing fish in each generation.

The breeding experiments with brook trout conducted at the Pittsford (Vt.) Experimental Hatchery for several years were carried on in a some-what different manner. Each season, selected fish were mated and the progeny of each pair reared separately during the following summer. In selecting these


fish, special emphasis was placed on rapid growth, vigor, fecundity, body symmetry, and coloration. Owing to the lower temperature of the water the fish did not grow so rapidly or mature so quickly as at Hackettstown, and progress therefore was considerably slower.

It was found that the young from a single pair are usually much more uniform in size than fish of mixed parentage; and that the offspring of different pairs showed marked differences in the rate of growth under practi-cally identical conditions. In some lots the growth during the first summer was two or three times that of other lots. This was true even though the parent fish might differ but little in size or other characteristics. It is also worthy of note that the young of certain parents showed much smaller losses than the young of other pairs which seemed to be equally vigorous.

Several lots of fingerlings representing the third generation of selected fish showed a more rapid growth than those of the 2 preceding generations, and also greatly outgrew fingerlings from the general brood stock. The best fish from the latter showed an average individual weight on September 3 of 6.09 grams, while 1 lot of selected fish on the same diet averaged 12.7 grams in weight on September 7; another lot had an average weight of 12 grams and several lots averaged 10 grams or more. These results are the more striking when it is considered that the general brood stock had been improved by mass selection during this time so that the average weight of fingerlings kept on a diet of beef liver through the summer had more than doubled.

In order to obtain a fair comparison of the growth of selected and non-selected fish, 3 lots of brook trout fingerlings were reared at the Leetown Station under as nearly identical conditions with respect to food and water supply as possible. Each lot contained 1,200 fingerlings and was placed in a standard hatchery trough on March 1, where the fish remained until the experiment was discontinued. Two lots of fish were from eggs taken at the York Pond (N. H.) Station. One lot of these eggs was from fish that had been reared from wild stock; the second lot from fish still farther removed from their original wild ancestors. The third lot of eggs was taken from selected stock at the Pittsford Station. The results of this experiment are shown in figure 5.

It will be noted that from the beginning of the experiment the fish from the Pittsford stock grew much more rapidly than those from the York Pond Station, but there was practically no difference in the growth of the 2 lots of fish from the latter station. The experiment was discontinued in August, when the fish in each lot were 29.5 weeks old. At this time the average weight of the Pittsford fish was 14.7 grams, while that of the 2 lots from York Pond was 4.9 grams and 4.6 grams, respectively. There was also a marked differ-ence in mortality in favor of the Pittsford fish, although the losses were abnormally high in all 3 lots. This was no doubt largely due to the fact that no attempt was made to lessen the mortality by the use of control measures.

The increase in egg production as a result of selective breeding is equally gratifying. The average number of eggs produced at the end of the third summer (that is, from fish commonly known as 2-year-olds) was 958 in 1928, and after selective breeding, 1,779 in 1932. These fish were selected as the best available fish of their age.

An unexpected result was the accumulation of data showing that the date at which trout spawn is primarily determined by heredity. It was also found that while mixed lots of fish continued to spawn for several weeks, those with a common ancestry usually had a much shorter spawning season and in some instances were all ready to spawn at practically the same time (Davis, 1931).


14 21 ............ Salootod

13

12

11

10

5

0

7

6

5 rut R 1 —

4 LOG 70ND

3 /7

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1 10 IT 15 12 10 MARSH APRIL LAY JUNG J517 AUGUST

FIGURE 5.—Growth curves showing the effect of selective breeding on brook trout.

Moreover, these fish continued to spawn on the same date in each succeeding year.

Evidence has also been obtained indicating that it will be possible to develop a strain of brook trout more resistant to furunculosis than are the average fish of this species. Two lots of fish from mated pairs have shown a marked resistance to the disease, the percentage of survivals being much greater than in any other lots. Owing to the fact that it is very difficult to eradicate furunculosis after it has become established at hatcheries, the devel-opment of a resistant strain of fish offers one of the most promising means of combating the disease.

There is considerable evidence to show that, in general, much better results can be obtained when a hatchery produces its own eggs than when the eggs are obtained from outside sources. This appears to be due to differences in the environment and indicates that eggs produced under certain conditions will develop much better and produce more vigorous young under the same conditions than when transferred to a different environment. Conditions at trout hatcheries vary widely as regards temperature of the water, dissolved minerals and gases, and other factors. In spite of such variations, experience has shown that most of them provide favorable conditions for trout, and it would be impossible in many instances to say which conditions are best for trout culture. Undoubtedly, trout can flourish under a wide range of environ-mental conditions, but it does not follow that fish which have become accli-matized to one set of conditions can withstand an abrupt change to a quite different environment without detrimental effect. This has been very notice-able at the Pittsford Experimental Hatchery, where eggs of brook trout from several sources have been hatched in adjoining troughs and the young reared under virtually identical conditions. In nearly every instance the local fish have suffered much smaller losses from various diseases than those hatched from eggs produced elsewhere. There have also been noticeable differences


in this respect among fish hatched from eggs from different outside sources. There is no reason to believe that the diseases in question were brought in with the eggs, as they have been prevalent at this hatchery for years. The most logical explaination is that the vigor and vitality of the fish were affected by the changed conditions.

In view of these facts, it is evident that for best results the trout culturist should produce eggs from carefully selected stock in his own hatchery. Of courses it is recognized that in many instances this, for one reason or another, may be impracticable. In such cases it will probably be found that eggs from certain sources usually do better than those from others, and the trout cultur-ist can govern himself accordingly.

PARASITES AND DISEASES GENERAL CONSIDERATIONS

The parasites and diseases of trout constitute one of the most important problems with which the fish culturist has to deal. Wild trout are but seldom seriously affected by disease caused by the presence of parasitic organisms. No doubt this is due primarily to the conditions under which they live. The swift, cold waters of the typical trout stream are about as poorly adapted to the development and diffusion of trout parasites as could be imagined. The wild trout that are injured by parasites and infectious diseases are ordinarily fish living in ponds or lakes, where conditions are more conducive to the spread of parasites. There is no reason to believe that the various parasites and diseases that are found at hatcheries have developed as a result of the domestication of trout. Undoubtly they all occur to some extent in wild fish, to which they ordinarily cause little or no injury; but when the fish are crowded together in hatchery troughs or pools, there is every opportunity for the rapid increase and spread of parasitic organisms and diseases to which trout are susceptible, resulting in the outbreak of epidemics with consequent heavy losses. Of course, this is simply another application of the well-known principle that in the domestication of animals and plants man is, to a certain extent, running counter to natural laws, with the penalty of eternal vigilance that this entails.

The control of these parasites and diseases is a problem of the greatest importance, and no trout culturist can hope to cope with them successfully unless he is familiar with the more essential facts. In the following pages, no attempt has been made to deal with the subject in a technical or exhaustive manner. On the contrary, the sole object has been to give the essentials regarding each disease in terms as nontechnical as possible, so that the fish-culturist may be prepared to deal with it intelligently should the necessity arise, as no doubt will frequently be the case.

The great majority of the infectious diseases of trout are caused by either bacteria or protozoa. As is well known, the bacteria are very minute organ-isms classified as plants although they possess many characteristics which differ widely from those that in the popular mind are commonly associated with plants. On the other hand, the protozoa are regarded as animals; but here, again, one must note that they are very different from the popular con-ception of an animal. The protozoa are all very small, although larger and more highly organized than the bacteria. Some of the larger protozoa are visible to the naked eye, but the great majority are strictly microscopic, and some are visible under only a comparatively high magnification. The only characteristic that the protozoa can be said to possess in common is that they are all composed of only a single cell, although even in this respect, as


in the case of the Myxosporidia which are characteristic fish parasites, the distinction sometimes breaks down. Of more importance from the practical standpoint is the fact that the protozoa are usually very delicate organisms easily killed by drying or by chemical agents. Many of them have a very complicated life history, a knowledge of which is essential to the devising of effective methods of control.

In addition to bacteria and protozoa, the parasites of trout include several species of worms, but these are usually not as injurious as the former. In fact, Gyrodactylus is the only parasitic worm that ordinarily has to be con-sidered by the trout culturist. Belonging to quite a different group is the parasitic copepod Salmincola, which is a member of the great group of crus-tacea, a group that includes the waterfleas, crabs, crawfishes, and shrimps.

Among the plants the only common parasites, aside from bacteria, that affect trout are the water fungi (Saprolegniaceae) which, under certain con-ditions, may attack fishes. As fungus is always easily recognized, infections by this parasite have assumed an importance among fish-culturists out of proportion to its actual potentialities for harm. Usually the appearance of fungus is an indication of the presence of some less conspicuous and more insidious agent, which is the real cause of the trouble. In other words, the appearance of fungus is a warning signal that no fish-culturist should dis-regard, but which in itself may be relatively unimportant.

It not infrequently happens that fish are affected at one time with two or more entirely distinct diseases. This, of course, complicates the situation, and results not only in a much higher mortality than would otherwise be the case, but also greatly increases the difficulties of control.

GENERAL PRINCIPLES OF DISEASE CONTROL From the practical standpoint, whether any particular parasite is external

or internal is of the greatest importance. If it is an external parasite — that is, lives on the body, fins, or gills of the host — it is possible in most cases to apply some chemical that will destroy the parasite without serious injury to the host. Many substances have been employed for this purpose, the most widely used being a solution of common salt (sodium chloride). This is a fairly effective treatment for such delicate organisms as protozoa and fungi, but even under the most favorable conditions, a few of the parasites survive and the treatment must be repeated at frequent intervals. In common hatch-ery practice, the salt is simply distributed throughout the trough, the water supply having previously been cut off. When the fish begin to show signs of distress and turn on their backs or sides, the water is again turned on and the fish quickly recover. As it is impossible to control accurately the strength of the solution under such conditions, a better method is to dip the fish for a short time in a 3 percent solution. This method requires less salt and the treatment is easier to control. The solution should be renewed frequently, since it soon loses its effectiveness.

Other chemicals used extensively for killing external parasites are copper sulphate, potassium permanganate, acetic acid, and formalin. Copper sul-phate and potassium permanganate are especially indicated when dealing with bacterial infections, but the latter is also effective against protozoa and flukes (Trematoda). Formalin and acetic acid are of value in treating fish infected with animal parasites, but are not effective in bacterial infections.

The most common method of treating fish for external parasites is the dip-ping method, in which fish are immersed in a relatively strong solution of the chemical for a very short time. To use this method most efficiently, the fish

742482° 47-4


should be removed from the trough or pool in a net and turned into a tub or similar vessel containing the solution. This allows the fish to swim about freely in the solution and all parts of the body are equally exposed to the chemical. If large numbers of fish are treated at one time, the solution should be frequently aerated. After the fish have been exposed to the solution for the required length of time, the contents of the tub should be poured through a net and the fish placed immediately in running water. In this way the maximum effect of the treatment is obtained with the least injury to the fish.

In treating trout with copper sulphate a solution of 1 part copper sulphate (by weight) is dissolved in 2,000 parts of water. The fish should be dipped in the solution for 1 or 2 minutes and then transferred at once to running water. They will at first show very evident signs of distress, but in most cases will fully recover in a short time. Even small fingerlings, unless they have been previously weakened by disease, are not permanently injured by the treatment if it is carried out properly. If the disease is well established, many of the fish may be so weakened as to be killed by the treatment, but such fish would undoubtly have died in any event. Healthy, vigorous trout will survive for several minutes immersion in a 1 to 2,000 solution of copper sulphate.

According to Ellis (1937), copper sulphate and salts of other heavy metals as well as certain acids injure fish by combining with the mucus covering the body and gills to form an insoluble compound which seriously interferes with respiration. Consequently, the fish die from asphyxiation, and not from toxic poisoning. Since salt is effective in removing mucus, it is frequently used in connection with the copper sulphate treatment to lessen its injurious effects. For this purpose the salt may be added to the copper sulphate solu-tion or the treatment may be followed by a salt bath.

If a galvanized vessel is to be used for the solution, it should first be painted on the inside with asphaltum or some similar substance to prevent any chemical action between the copper sulphate and the walls of the vessel. It is more convenient to use the pulverized form of copper sulphate, which dissolves very rapidly, so that the solution is immediately ready for use. To guard against deterioration it is always advisable to make up a fresh solution just before it is to be used. The solution rapidly becomes weakened with use and consequently should be renewed frequently.

Copper sulphate will quickly precipitate out of solution in hard water and its efficiency as a disinfectant is thus greatly impaired. This can be pre-vented by adding acetic acid drop by drop after the white flocculent pre-cipitate has formed until the solution regains its clear blue color. Care should be exercised to prevent the addition of any excess acid.

The strength of the copper sulphate solution that can be used with safety varies considerably in different types of water. For this reason, if one has had no previous experience with this chemical in the water in which the fish are to be treated, it is advisable to experiment first with a few fish to deter-mine the strength of the solution that they can withstand without serious injury. In most waters a 1 to 2,000 solution will not seriously injure healthy fish, but in some very soft waters copper sulphate in this proportion is said to have caused excessive losses. It should also be remembered that chemical solutions act more quickly at high temperatures, and the length of the treat-ment should be shortened accordingly. In any event the fish will probably be "off their feed" for a day or so following the treatment.

While the dipping method is efficient and not unduly laborious for the treatment of fish in the hatchery, it nevertheless involves much handling,


which, especially where several treatments are required, may be decidedly injurious. The evil effects of handling are much more pronounced when the fish are held in pools or raceways from which they must be removed by a seine. In fact, dipping the fish under such circumstances is so difficult and injurious that in many instances it is doubtful if it is worth while. This difficulty of treating fish in raceways or pools is one of the strongest argu-ments that has been advanced against their use for young trout.

For these reasons, methods for the treatment of fish without removal from troughs or pools have received much attention. Kingsbury and Embody (1932) have devised a method whereby a very dilute solution of potassium permanganate or copper sulphate is allowed to flow through the hatchery troughs for a period of 1 hour or more. This method, of course, obviates all handling of the fish, but is complicated and does not lend itself readily to the treatment of fish in pools or raceways.

Fish (1933) has devised a much simpler method, which is especially applicable to raceways and pools. The essential part of this device is a U-shaped siphon mounted on a block of wood which floats on the surface of the water. The length of the arms of this siphon should be about 12 and 14 inches, respectively. The shorter arm is inserted in a hole in the float, while the longer arm hangs down outside the container. Variations in the amount of water delivered by the siphon are obtained by using glass tubing of dif-ferent diameters. In most cases it is necessary to use only one siphon, and proper concentration of the chemical in the pool is obtained by adjusting the strength of the original solution to the volume of flow. An even simpler device is to immerse the neck of a large bottle filled with the solution in a shallow pan in which the solution is automatically kept at a constant level. This is the principle employed in the ordinary kerosene cooking stove with which everyone is familiar. To obtain a uniform flow of the solution at the required rate it is necessary only to attach a tube with the required diameter to the pan. The dilutions to be used are those recommended by Kingsbury and Embody, that is, 1 part copper sulphate to 100,000 parts water, or a 1 to 150,000 solution of potassium permanganate. The fish should be exposed to the disinfecting solution for 1 hour, after which it should be washed out as quickly as possible by increasing the flow of water through the pool.

The application of chemicals to ponds or troughs while water is allowed to flow through them in the usual manner presents many difficulties, and it is almost impossible to insure that all the fish will be exposed to the proper con-centration of the chemical for the required length of time. This objection can be avoided by stopping the flow of water during the treatment. In that case it is necessary only to determine the volume of water in the pond and to add the amount of chemical required to produce the desired concentration. There is the disadvantage, however, that when the fish are crowded the oxygen may be exhausted before a full hour has elapsed, but it appears that this danger is not so great as is generally believed. If a deficiency of oxygen does occur, k may be corrected by artificial aeration or by circulating water through the pond by means of a pump.

The formalin treatment as developed by Fish (1940, 1940a) is especially designed for treating fish, after the flow of water has been stopped and is undoubtedly the most effective means yet devised for ridding fish of external protozoan parasites and gyrodactylid worms. It should be emphasized, how-ever, that it is of little or no value in combating bacterial infections. The con-centration recommended by Fish is 1 part formalin to 4,000 parts water. The


fish should be kept in the solution for 1 hour, which is sufficient to kill all the parasites. This treatment will not injure the fish to any extent unless they are already in a greatly weakened condition. According to Fish, infection with animal parasites can be prevented by treating the fish for 1 hour with a 1 to 6,000 solution of formalin at bi-weekly or possibly monthly intervals.

The formalin treatment is not only more effective, but it is also much cheaper than the ordinary salt treatment. The only drawback is that formalin diffuses very slowly through the water and special precautions must be taken to obtain a uniform concentration. This can be done by first diluting the formalin with water in a pail or tub and then spreading the mixtures as evenly as possible over the surface of the pond. Fish has found that the best results are obtained by first diluting the formalin 1 to 100 and then applying with an ordinary spray pump.

The control of diseases caused by internal parasites presents a very dif-ferent problem, because in most cases it is impracticable to attempt the use of medicines. Good results sometimes follow a change in the diet or the addition of some such substance as cod-liver oil to the food, but in general the successful control of such diseases must depend almost entirely on prophylactic measures. It is most important to keep the fish in as healthy and vigorous a condition as possible by providing suitable quarters with an abundant supply of cold, well-aerated water. Overcrowding should be avoided, and, of course, the greatest care should be exercised to provide a suitable diet. Every pre-caution should be taken to guard against infection from any source, and any implements or vessels that might possibly carry infection should never be used with healthy fish, unless they have been thoroughly sterilized.

If possible, fingerling trout should not be held in water that has previously come in contact with older fish. Yearling and older trout are usually not so seriously affected by parasites as are fingerlings, and thus may act as carriers without showing any evidence of infection themselves. For this reason, from the standpoint of disease, a spring-water supply which contains no fish is greatly to be preferred. In many sections of the country, however, there are no springs of sufficient volume to supply a hatchery, and the water must be taken from a stream. Of course, stream water can be sterilized before use, but in most cases, owing to the large amount required, this is not practicable. The danger of infection from a stream supply can be lessened, to some extent at least, by using a larger flow of water than is otherwise necessary, which tends to reduce the effects of overcrowding and to keep the fish in a more vigorous condition. Moreover, there is some evidence that stream and lake water may have desirable qualities, especially for brown trout and land- locked salmon, which are not present in water taken directly from springs. This brings up the problem of so-called "conditioned water," which has re-ceived very little attention from fishery biologists. The term "conditioned water" has been given to water in which animals have lived and which con-sequently contains various products, largely excretory, contributed by the conditioning animals. Such waters have been shown (Allee et al, 1934; Evans, 1936) to contain some growth-promoting factor that was absent in water which had not been biologically conditioned.

Of course, the precautionary measures just mentioned are fully as important in the case of external parasites as in combating diseases caused by internal parasites, but they are emphasized here because they are virtually the only measures known for dealing with diseases of the latter type. In treatment of diseases the trout culturist must exercise eternal vigilance and be quick to recognize the first indication of an outbreak. Half the battle lies in the


ability to diagnose a disease in its early stages and to adopt appropriate meas-ures for its control before it is too late.

STERILIZA1 ION OP PONDS AND RACEWAYS

For the sterilization of ponds and raceways when large quantities of disin-fectant are required, freshly slaked lime (calcium hydroxide) is, if properly applied, both cheap and effective. It can be used in the form of a powder, or preferably as "milk of lime" (1 part slaked lime to 4 parts of water). In disinfecting with lime, the pond should first be drained and the milk of lime applied as a spray over the bottom and sides. Special attention should be given to the inlet and outlet of the pond to make sure that the solution is forced into all cracks and crevices. If possible the pond should be allowed to dry in the sun for several days after being sprayed with lime. It should be emphasized that calcium hydroxide unites with carbon dioxide in the air or water to form calcium carbonate which has no antiseptic value, and for that reason should be freshly prepared shortly before it is to be used.

There are obvious advantages in sterlizing a pond while it is filled with water. For this purpose it is necessary to use some powerful disinfectant which is effective in a very dilute solution. Copper sulphate and potassium permanganate are frequently used, but under ordinary conditions it is be-lieved that chlorine is much superior (Connell, 1939; Davis, 1938; Hagen, 1940). However, if exceptionally large amounts of organic matter are present, creating a high chlorine demand, copper sulphate may prove more effective.

Tithe ponds or raceways to be disinfected are small, the most convenient source of chlorine is calcium hypochlorite (bleaching powder) which comes in the form of a manufactured powder guaranteed to contain not less than 70 percent of available chlorine. The chlorine is released when the powder is dissolved in water. For use in sterilizing ponds, the pond should first be drained and the powder spread on the bottom near the inlet so that the water passes over it as the pond is filled. The amount of clorine dissolved in the water can be determined by a Hellige chlorine comparator using orthotolidine as the indicator. The addition of a solution of orthotolidine to water containing free chlorine produces a colored solution extending through different in-tensities of yellow to a clear reddish brown. Since the intensity of the color is proportional to the amount of chlorine present, the chlorine content can be determined by comparison with color standards. Ordinarily, 5 p.p.m. (parts per million) should be sufficient to kill all harmful bacteria and other organ-isms if the solution is allowed to remain in the pond for several hours.

The Hellige comparator is somewhat expensive, and if only a small amount of disinfecting is to be done, its purchase may not be justified. In the absence of a comparator, a rough method is to add a few drops of orthotolidine solution to the water in a test tube or small bottle. A deep yellow or reddish brown indicates the presence of sufficient chlorine to kill bacteria in a few minutes.

When a large amount of chlorine is required, liquid chlorine is more eco-nomical than calcium hypochlorite. Liquid chlorine can be obtained in iron cylinders containing 50 to 100 pounds of chlorine. The liquid is under great pressure and is converted into gas as it escapes from the cylinder. The gas is introduced into the water through a garden hose attached to the outlet valve of the cylinder. A section of iron pipe, closed at the free end and perfor-ated with a large number of very small holes, is attached to the other end of the hose. In this way the gas is broken up into small bubbles which are more readily absorbed by the water. If the water enters the pond through a pipe


under pressure, it is a simple matter to get the necessary amount of chlorine into solution. The hose with the perforated iron pipe is inserted into the pipe line and the required amount of chlorine is released as the water flows into the pond. The pond should, of course, have been previously drained. When the pond is supplied through a ditch or open flume, it is more difficult to get the chlorine into solution without the loss of a large percentage of the gas. If the gas is forced to bubble up through several feet of water, much of it is absorbed, but even under such conditions, it is impossible to avoid consider-able waste.

According to Connell (1939) the difficulty of getting chlorine into solu-tion in open water without excessive waste can be overcome by use of an outboard motor which churns up the water in which the chlorine is being re-leased, breaking the gas into minute bubbles which are quickly absorbed. The outboard motor is clamped to a plank extending over the pool and the propeller should be submerged as deeply as possible. The chlorine gas is di-rected against the propeller from the open end of the hose.

The chlorine disappears quickly from the water, especially in direct sun-light, and if the solution is held in the pond for 24 hours before being re-leased, it should not be injurious to fish. However, it is advisable first to test the water with orthotolidine, the absence of color indicating that no free chlorine is present. If for any reason it is desirable to drain the pond before the free chlorine has disappeared, it can be neutralized by adding a 5 percent solution of sodium thiosulphate ("hypo") to the water. The orthotolidine test will show when the chlorine has been completely neutralized.

When ordinary precautions are taken, liquid chlorine can be used with little danger, nevertheless, the operator should be provided with a gas mask for use in case of accident.

EXTERNAL ANIMAL PARASITES

TREMATODA Gyrodactylus

One of the most common external animal parasites of trout is the small trematode worm, or fluke, belonging to the genus Gyrodactylus. These worms occur at virtually all hatcheries and, when abundant, may seriously injure the fish and even cause considerable mortality, especially among small finger-lings. In exceptional cases they may be present in such numbers that every part of the body is fairly covered with parasites. Usually, however, they are not sufficiently abundant to cause a heavy mortality, their presence being in-dicated by frayed fins and evidences of physical discomfort. It is possible that more than 1 species of these worms may infect trout, but, unfortunately, little attention has been paid to their specific characters. According to Muel ler (1936) the common species on trout in this country is Gyrodactylus elegans, which is found also on trout in Europe. A very similar, possibly identical, species occurs on the goldfish. From the practical standpoint it is of little importance whether one or several species infest trout, for there is no reason to believe that they differ essentially in their habits or in their effects on the host. Similar parasites are common on other species of fish and may be an important factor in the propagation of warm-water fishes.

DESCRIPTION OF PARASITE The fluke Gyrodactylus may occur almost anywhere on the host, but is

usually most abundant on the fins, especially the dorsal and caudal fins. The affected surfaces become covered with a bluish-gray slime due to an in-


creased secretion of mucus. Later, if the parasites are very abundant, the fins become badly frayed and may eventually be worn down to mere stubs. These lesions often become infected with fungus, so that in late stages of the disease there is frequently a considerable growth of fungus on the fins and body. Gyrodactylus can be easily found by scraping off some of the slime from the affected parts and examining it under the microscope. The worms will be seen in rapid movement, twisting and squirming about in every direction.

If the fish is examined in water with a hand lens, the worms can usually be seen without difficulty attached by one end to the fish and waving the body back and forth, or they may be slowly crawling about in the same manner as a measuring-worm. Fish infested with Gyrodactylus can often be seen rubbing themselves against the sides or bottom of the pond in an evident ef-fort to rid themselves of the worms. In fact, this is one of the most reliable in-dications of the presence of the parasite.

When examined under a low magnification (fig. 6) the worm appears as a small, transparent object armed at one end with a pair of large recurved

FIGURE 6.—Photomicrograph of Gyrodactylus from trout. Magnified 85 diameters.

hooks. Surrounding the paired hooks is a flattened, disk-shaped structure bearing a number of small hooks on its outer margin. It is by means of these hooks at the posterior end of the body that the worm is able to cling to the host, the hooks becoming embedded in the epithelium. At the anterior end the body terminates in two short lobes.

Unlike most parasitic worms, Gyrodactylus does not lay eggs. On the con-trary, it gives birth to living young, which are already well developed and im-mediately attach themselves to the host. The young in various stages of development can usually be seen within the body of the mother, the large paired hooks being especially prominent.

CONTROL MEASURES

Although Gyrodactylus probably occurs at all trout hatcheries, for some unexplained reason many hatcheries seem to experience little trouble from the parasite while others suffer from frequent outbreaks. Fortunately, the para-site can be easily controlled and no hatchery should suffer serious losses from Gyrodactylus.


Dipping the fish for 1 minute in a 1 to 500 solution of acetic acid, as first recommended by Embody (1924), is effective in ridding fish of the parasite, and was in almost universal use until recently. An even better method, how-ever, is to dip infested fish in a 1 to 4,000 solution of formalin for 1 hour; as the fish are less injured by this treatment and all worms are destroyed. With the acetic acid dip a few worms, which are not fully exposed to the acid in the short time allowed for dipping, may survive and make necessary a repeti-tion of the treatment within a short time.

Treatment with a dilute solution of potassium permanganate has been found also very effective in ridding fish of Gyrodactylus. For this purpose Kingsbury and Embody (1932) recommend a concentration of not less than 1 to 150,000 nor greater than 1 to 100,000. These concentrations will kill other external parasites such as Chilodon and Trichodina.

Discocotyle salmonis

The trematode worm, Discocotyle salmonis, is somewhat similar to Gyro-dactylus, but is readily distinguishable by its much larger size and dark brown color. Unlike Gyrodactylus, it occurs only on the gills, and is usually crowded in among the filaments, where it is not easily seen unless a careful examination is made. The worm, which is 3 to 5 millimeters long is, however, readily visible to the naked eye. Its posterior end is modified into a flattened disk, which bears on each side a row of four suckers armed with small hooks, and thus forms an efficient attachment organ, by means of which the parasite clings to the gills and is very difficult to dislodge.

The parasite injures the fish by sucking blood from the gills and through irritation of the tissues at the point of attachment. The gills of infested fish are usually light colored, with an excessive secretion of mucus. When abundant the parasite may cause an acute anemia, which eventually results in the death of the host.

Nothing is known of the life history of this worm, but from analogy with related forms, it is probable that the eggs, surrounded by a tough resistant shell, are laid between the gill filaments of the host, where they remain until hatched. There is no evidence that Discocotyle has an intermediate host, as is the case with internal parasitic trematodes. It is not impossible, however, that the eggs may occasionally drop from the gills and develop on the bottom of the pond. The worms apparently develop very slowly, since trout do not become infested to any extent until they are 2 years old.

This parasite was first described by Elmer Schaffer in 1916 from rainbow trout at the State hatchery, Cold Spring Harbor, N. Y. Later it was found on brook and rainbow trout at other hatcheries, but so far as the writer is aware, it has been reported only from Long Island, where it is evidently firmly established.

CONTROL MEASURES

The acetic-acid treatment, which is so effective in the case of Gyrodactylus, is of no value in combating Discocotyle. The latter is much more resistant to the acid solution than the former and a solution strong enough to kill it usually causes the death of the host as well. Furthermore, the great majority of the worms lie between the gill filaments, where they are more or less protected from contact with any solution.

According to Laird (1927), the parasite can be successfully controlled by the use of Zonite. A solution composed of 1 part Zonite to 5 parts of water


is sprayed directly on the gills of infested fish by means of an atomizer. In using this treatment it is necessary to handle each fish individually and to bend the lower jaw back so that the gills are separated. If this is not done, many of the worms will not be reached by the spray.

In Europe it has been found that a closely related species occurring on the gills of trout can be destroyed by immersing the fish for 1 to 172 minutes in a saturated solution of common salt. It is claimed that the worms are virtually all killed, while the fish are not seriously injured by the short immersion in the salt solution.

PARASITIC COPEPODS

The copepods are small crustaceans, the majority being free-living forms abundant in both fresh and salt water, where they form an important item in the diet of many food and game fishes.

Several species of parasitic copepods are found on trout and Qalmon, but by far the most common form is Salmincola edwardsii, which is widely distributed throughout the east and middle west. This species is the only one whose life history has been worked out, but since the other species occurring on trout are very closely related, it is not probable that their behavior and life history are essentially different from those of Salmincola edwardsfi.

DESCRIPTION AND LIFE HISTORY

The copepod, Salmincola edwardsii occurs only on brook trout—rainbow and brown trout being immune. The parasite is attached to the gills or fins where it can be easily seen with the naked eye (fig. 7). It is relatively large, measuring several millimeters in length, and is yellowish white in color. Its anterior end is attached to the gills by means of a special organ developed from the mouth parts. The end of this attachment organ bears a bulb-shaped enlargement, which is inserted in the gill filaments, firmly anchoring the parasite in place. Posteriorly each copepod bears a pair of long egg sacs, within which the embryos undergo complete development. The parasite ordinarily seen attached to the gills is a female. The male is much smaller and is ususally not noticed except after special search.

FIGIME 7.—Parasitic copepods (Salmincola edwardsii) attached to gill filaments of adult trout. Magnified 7 diameters.

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When the young are fully developed the egg sacs break open and the larvae escape into the water as minute, free-swimming organisms closely resembling the free-living copepods, which form such an important constituent of the plankton. They are less than a millimeter in length, very active, and swim about with rapid, darting movements. They may remain in this free-swim-ming state for about 2 days, constantly searching for trout on which to attach themselves. If a suitable host is not found within this time, they are unable to develop further and soon perish.

Each larva possesses powerful mouth parts and a peculiar attachment fila-ment, by means of which it is able to rasp a hole in the gill tissues, into which the enlarged end of the filament is inserted and soon becomes embedded. After attachment, the parasite undergoes rapid degeneration through which it loses its swimming feet and all evidence of segmentation, the abdomen be-coming converted into a rounded, sac-like structure.

About 2 or 3 weeks after attachment the parasites become sexually mature. Mating then takes place, after which the diminutive males drop off and die. The females, however, live on for several weeks, increasing enormously in size and undergoing still further degeneration. . The young are liberated in about a month after the eggs are fertilized. Each female ordinarily lays 2 batches of eggs, after which she dies and gradually disintegrates. Under ordinary conditions, the entire life cycle is completed in about 272 months.

While attached to the gills, the parasite injures the fish by sucking large quantities of blood and also by mechanical injuries to the tissues, which some-times result in secondary infections by fungus. When only a few parasites are present, they do comparatively little harm, but when they become very abun-dant, as is likely to be the case under the crowded conditions in hatchery ponds, the fish are greatly weakened and large numbers eventually succumb.

Usually adult fish are more heavily parasitized than fingerlings or yearlings, and the heaviest losses occur during the spawning season, when the vitality of the fish is low and they are consequently unable to resist the heavy drain on the system caused by the presence of the parasites.

Copepod parasites have been found frequently on wild trout in various parts of the country, but are apparently seldom abundant enough to cause serious injury. This can be readily understood, since under natural conditions, it is evident that only a very small percentage of the larvae would be able to attach themselves to the proper host. In hatchery ponds, conditions are differ-ent. Here the fish are crowded closely together in a limited area with a relatively small flow of water, so that there is every opportunity for the free-swimming larvae to find a suitable host, even though this must be accomplished within a short time.

CONTROL MEASURES

When once firmly established at a hatchery, this parasite is very difficult to control. The chief difficulty lies in the fact that, like most crustaceans, the copepods are covered with a tough, resistant, chitinous membrane, which is not easily penetrated by chemicals. Consequently, the parasites are uninjured by solutions that seriously affect the more delicate gill tissues to which they are firmly attached. It is, therefore, impossible to kill them by treating the fish with chemical solutions, as can be done with most external parasites. There is one exception to this statement which may be utilized to advantage: the larvae are comparatively delicate and are killed in a few minutes by a strong salt solution; consequently, they can be destroyed while in the free-swimming stage or shortly after becoming attached, without injury to the


host, but this treatment is obviously of only limited application. Owing to the large volume of water flowing through trout ponds, the cost of treating them with salt is usually prohibitive, since to be effective the treatment must be continued for some time. In the case of fingerlings frequent salt baths may be used successfully to prevent the fish from becoming parasitized, but even this can be considered only a temporary expedient.

Fasten, to whose investigations we are indebted for most of our knowledge cf this parasite, strongly recommends the installation of sand filters in all cases in which the parasites occur in the water supply. This will effectually prevent the larvae from being carried into the ponds. As adult trout are most heavily parasitized, Fasten also recommends that in badly infested hatcheries only 2-year-old fish be used for egg production, and that these fish be discarded immediately after spawning. Of course, this would necessitate rearing a new lot of brood fish each year, which would greatly increase the cost of the eggs. The introduction of predacious minnows into the brood ponds has also been recommended. These fish feed on the larvae of the parasite before they have an opportunity to become attached to a host.

Since in most cases, at least, such methods would be only palliative and would not result in the eradication of the parasite, it would seem in the long run less expensive to get rid of all parasitized fish and start anew. Of course, in the case of hatcheries having a contaminated water supply, such extreme measures would not be justified, unless at the same time an efficient sand filter should be installed.

References: Fasten, 1912, 1918, 1921; Savage, 1935.

MUSSEL GLOCHIDIA

Although the glochidia of fresh-water mussels are frequently found attached to the gills and fins of various species of fish, trout were thought until recently to be entirely free from such infestations. However, in July 1932 the writer found rainbow fingerlings in rearing pools on the Truckee River in California seriously infested with the glochidia of Margaritif era margaritifera falcata (Gould). This mussel is abundant in certain sections of the Truckee River, and the glochidia had evidently been carried into the pools in the water supply which was obtained from the river. Practically every fish was infested with several glochidia, which appeared as small, rounded, translucent bodies at-tached to the gill filaments. The glochidia were easily visible to the naked eye and in some instances were so abundant as to prevent the gill covers from closing.

The fish were suffering a heavy mortality, evidently due to the presence of the glochidia. A wild rainbow trout about 6 inches long, with the gills heavily infested, was found dead in the river. The fish in the rearing pools were said to have suffered heavy losses each year at this time which in all probability were due to infestation with glochidia.

Extensive studies of this mussel and its effects on trout were conducted at the above-mentioned rearing station by Murphy (1942) during the summer of 1941. This investigator found that the glochidia could live for 11 days after extrusion from the parent mussel without becoming attached to a fish. With heavy infections (600 to 1,200 glochidia per fish) rainbow fingerlings 42 milli-meters in length suffered a heavy initial mortality within a day or two, due to interference with the circulation of blood in the gills. Deaths among rain-bow fingerlings infected with less than 400 glochidia were usually the result of secondary infections by fungus or bacteria. These infections probably


FIGURE 8.--For description, see opposite page.


started in lesions produced when the glochidia left the fish. At an average daily temperature of 57.5°F. the glochidia remained attached to the gills fur 36 days and during this time increased approximately 660 percent in length.

The mussel, Mar garitif era mar garitif era falcata is found in North America west of the Rocky Mountains and other subspecies are widely distributed throughout the northern hemisphere. Murphy found that rainbow and brown trout are more susceptible to infection with this parasite than is the brook trout. Slight experimental infections were obtained in one species of sucker and two minnows, but the whitefish and sculpin were immune. In 1941 the writer found the glochidia abundant on the gills of fingerling chinook salmon (Oncorhynchus tschawytscha) at the Leavenworth (Wash.) hatchery. Fingerlings of the blueback salmon (Oncorhynchus nerka) in the same water were not infected.

CONTROL

It is impossible to destroy the parasite while on the gills with a chemical treatment, since it is entirely covered by the gill epithelium within 2 to 4 hours after attachment. Most of the glochidia can be removed by running the supply water through a filter or a settling basin, but this may be too expensive to be practicable. If possible, the water should not be used for rearing trout while glochidia are present. In most localities this period will probably include June and July.

PROTOZOA

Costia

Two species of Costia are known to occur on trout. The most common form is Costia riecatrix, which was first described from European fishes, but is widely distributed also in the United States. It is not uncommon on pond and aquarium fishes and occurs rather frequently on trout as well. When abun-dant, it produces a disease known as costiasis, which may be quickly fatal.

According to Fish (1940), Costia necatrix is the most destructive of the ectoparasitic protozoans found on trout and salmon, but owing to its small size is frequently overlooked. The disease is most common where fingerling trout are overcrowded or fed an unbalanced diet, and Benish (1937) states emphatically that a severe attack of costiasis occurs only when fish have been weakened by bad living conditions.

Protozoan parasites of trout: A. Costia necatrix viewed from ventral side. The wide ventral groove leads to the mouth which is located near the base of the flagella. The small, rounded nucleus and the larger contractile vacuole can be seen just above the ventral groove. The short flagella lie on the floor of the groove and are difficult to dis-tinguish. x 1,500. B. Similar to A, but viewed at an angle to the ventral side. The internal structure is not shown. Both A and B were drawn from unstained specimens killed in osmic vapor. x 1,500. C. Stained specimen of Costia necatrix viewed from the ventral side to show internal structure. The nucleus contains a rounded nucleolus and chromatin granules attached to the nuclear membrane. The cytoplasm contains large numbers of small, rounded granules. x 2,000. D. Side view of Costia pyriformis drawn from a stained specimen. The short, rod-shaped chromatoid bodies are probably bacteria. The blepharo-plast which is much larger than in C. necatrix can be seen at the right. x 2,250. E. Side view of C. pyriformis. Drawn from unstained specimen killed in osmic vapor. x 2,250. F. C. pyriformis turned slightly toward the dorsal side to show ventral groove. In both E and F the blepharoplast appears as a clear, rounded vesicle on the dorsal side. Abbreviations: bl. blepharoplast ; ch. chromatoid bodies; c.v. contractile vacuole ; n. nucleus.


SYMPTOMS

Probably the most characteristic symptom of costiasis is the appearance of a light bluish or grayish film, which spreads over the body and fins. The fish lose their appetite, become rapidly weakened, and die in a short time. These symptoms, however, are not sufficiently distinctive to enable one to recognize the disease with certainty without a microscopical examination. This can easily be made by scraping a small quantity of slime from the body and exam-ining it in a drop of water under the miscroscope, using a comparatively high magnification. The parasites, if present, can be seen as minute oval bodies darting here and there with great rapidity.

DESCRIPTION OF COSTIA NECATRIX

Although very small, this parasite has a complex structure which can be made out only with considerable difficulty. The body is flattened, having definite dorsal and ventral surfaces. It is from 10 to 20 microns in length and about 10 microns broad. When viewed from the flat side it is oval in shape (fig. 9, A) with rounded anterior and posterior ends. While attached to the skin or gills it is more pyriform in shape as shown in figure 9, B.

The ventral surface is concave with a deep oral groove extending from left to right across the body (figs. 8, A and 8, B). This groove is much deeper on the left side where it leads into the gullet at the anterior end. Two pairs of flagella are usually present although some individuals may have only 1 pair. One pair of flagella is much shorter than the other, extending only a short distance be-yond the posterior margin of the body. The longer pair is usually 2 or 3 times the length of the body and usually unequal, 1 flagellum being about two-thirds the length of the other. These flagella are used for propelling the animal through the water and also for clinging to the epithelium of the host, while the short flagella are used for feeding. Within the body is a small contractile vacuole and a rounded vesicular nucleus which in stained specimens has a spherical, deeply staining, central body, the karyosome, surrounded by a clear unstained area (fig. 8, C).

The parasites live on the skin and gills of the fish, where they destroy the epithelial cells, apparently feeding on the fragments. Usually they are not uniformly distributed over the body, but are especially abundant near the base of the dorsal fin (fig. 9B) and on the gills, although in heavily infected fish they may be found on almost any part of the body. The peculiar distribu-tion in patches over the body and gills may be due to the fact that as they multiply by division, the daughter individuals tend to remain attached to the epithelium and to move about very little. It is evident, however, that the parasites must break loose occasionally and thus infect other fish. They may also form resistant cysts which enable them to live for some time off the host.

During the winter of 1940 several outbreaks of costiasis at the Lcetown (W. Va.) hatchery were found to be due to an undescribed species of Costia. This species which is described below, is more common at the Leetown sta-tion than Costia necatrix, and differs from the latter in several important respects.

Costia pyriformis

Costia pyriformis (Davis 1943) is smaller than Costia necatrix, the length varying from 9 to 14 microns and the width from 5 to 8 microns. It is distinctly pear-shaped and moves with a characteristic spiral movement which is very different from the movements of C. necatrix. Many individuals bear 2 long


and 2 short flagella (figs. 8, E and 8, F) , but frequently only 1 long and 1 short flagellum can be distinguished. A spiral groove, starting on the dorsal side at the anterior end, extends along the ventral surface, becoming wider and shal-lower toward the posterior end. The flagella arise dorsally at the anterior end of the groove and when the organism dies, they frequently lie along the floor of the groove. In this position the short flagella are difficult to distinguish, since they do not extend beyond the body as does the longer pair.

Stained specimens of C. pyrif ormis differ even more strikingly from C. necatrix. They are rounded at the anterior end, tapering posteriorly, and con-tain a number of rod-shaped bodies that stain deeply with chromatin stains (fig. 8, D). The nucleus can be easily distinguished as a rounded, deeply-staining body on the ventral side about midway between the anterior and post-erior ends. Near the anterior end on the dorsal side is a large blepharoplast flom which the flagella arise. It usually stains deeply with chromatin stains, but may stain lightly or not at all. The blepharoplast may be as large as the nucleus and can frequently be distinguished in the living organism as a clear vesicle at the base of the flagella.

In addition to the nucleus and blepharoplast, there are several deeply staining bodies which are usually distinctly rod-shaped and frequently ar-ranged in pairs (figs. 8, C and 8, D). The bodies can be distinguished in the liv-ing animal as bright refringent granules, usually in active motion. They are probably bacteria such as are known to occur in many protozoans. A con-tractile vacuole is present near the nucleus.

This species attaches itself to the epithelial cells of the body and gills of the fish in the same way as Costia necatrix, and probably does not differ materially from the latter in either habits or life history.

CONTROL

The same methods of control can be employed with either species. It is difficult to control Costia with the ordinary salt bath, but good results have followed dipping in a 1 to 500 solution of acetic acid. The most effective treatment is the use of formalin as described by Fish (1940). He found that all Costia on the fish were destroyed by 1 treatment with a 1 to 4,000 solution of formalin for 1 hour, and that weekly treatments with a 1 to 6,000 solution of formalin were effective in preventing the fish from becoming infected with this parasite.

References: Andai, 1933; Benish, 1937; Davis, 1943; Fish, 1940, 1940b; Plehn, 1924; Savage, 1935.

Chilodon

This is a large genus containing many species, several being parasitic on fish. They occasionally occur on trout and have been known to cause serious injury to fingerlings. They are more common parasites of pond fishes than of trout and are frequently abundant on goldfish, causing heavy losses among both young and adults. The best known species is Chilodon cyprini which is a common parasite of gold fish. Infected fish show little evidence of the presence of the parasites until they become abundant, when the fish lose their appetite and show a tendency to lie on one side. They may also show a slight cloudiness over the surface of the body.

When an infected fish is examined with a hand lens the parasites can be seen as minute, colorless, flattened organisms creeping rapidly about over the sur-face of the fins, body and gills. Under a higher magnification, they appear


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FIGURE 9.—For description, see opposite page.


more or less heart-shaped (figs. 10, B and 9, E). The ventral side is flat with cilia arranged in parallel rows. They are longer at the anterior end and are located in narrow grooves which appear as fine lines under the microscope. The number and arrangement of these grooves varies in different species. The dorsal surface is slightly convex and lacks cilia except in the oral groove at the extreme anterior end.

The mouth is located on the ventral side near the anterior end and is sur-rounded by a number of horny rods which extend for some distance into the body and gradually disappear. There is a large ovoid macronucleus in the posterior third of the body and a small micronucleus which is probably en-closed in the macronucleus in some species. Two contractile vacuoles are present about one-third of the distance from each end of the body, but on op-posite sides.

Although these parasites are often abundant over the entire body of a gold-fish, on trout they appear to be confined largely to the gills and fins. They do not appear to injure the host appreciably unless present in large numbers, but when numerous, may be the cause of serious mortality among small fingerlings.

Chilodon can easily be controlled by dipping the fish for a short time in a 3 percent solution of common salt or in a 1 to 500 solution of glacial acetic acid. An even more effective treatment is a 1 to 4,000 solution of formalin for 1 hour. One treatment by the formalin solution is sufficient, but if salt or acetic acid is used, it may be necessary to give a second treatment on the following day. Since the parasites readily leave the host, the trough or pond should be sterilized if the fish are removed for treatment.

References: Moore, 1924; Plehn, 1924. Trichodina (Cyclochaeta)

These parasites were formerly assigned to the genus Cyclochaeta, but as pointed out by Mueller (1932), should be included in the genus Trichodina, since, so far as is known, they all lack the ring of cirri that characterizes the former genus. These protozoans are common parasites of fish and occur on a great variety of species. They are more common on warm-water fishes than on trout, but nevertheless are abundant at many trout hatcheries and may cause serious injury to fingerling trout.

Photomicrographs of protozoan parasites of trout: A. Costia necatrix photographed from whole mount. Each contains a nucleus with large, rounded endosome. x 860. B. C. necatrix attached to skin of channel catfish. Photographed from section. x 680. C. and D. Costia pyriformis. The saddle-shaped blepharoplast can be seen on the dorsal side near the anterior end. The rounded nucleus is located near the ventral side with rod-shaped chromatoid bodies between it and the blepharoplast. Photographed from whole mounts. x 1,270. E. Chilodon sp. from smallmouth black bass viewed from ventral side. The striations can be seen indistinctly on each side of the deeply stained macronu-cleus. The cytopharynx is visible near the anterior end at the right. x 680. F. Cross-section of Chilodon cyprini attached to gill of goldfish. The alternating ridges and fur-rows which appear as parallel striations can be seen on the ventral side at the right of the macronucleus. x .680. G. Young stage of lchthyophthirius multifilis which has been dis-lodged from its position in the epithelium. The minute micronucleus can be seen attached to the lower side of the macronucleus. Photographed from a whole mount. x 340. H. Sec-tion of skin of bluegill sunfish with I. mu/tifills in the epithelium. The wrinkled surface of the body is characteristic. Sections of 2 scales can be seen just below the parasite. I. Small I. m2s/tigis which has recently penetrated into the gill epithelium. Note the small deeply stained micronucleus which at this stage is not attached to the macronucleus. x 330. J. Somewhat later stage with a large, U-shaped macronucleus. The parasite has greatly increased in size and is forcing the lamellae aside. The micronucleus is now located within the macronucleus. The ectoplasm can be seen as a dark line surrounding the endoplasm which is filled with rounded metaplastic bodies. x 170.

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It is evident that several species of Trichodina occur on trout, most of them undescribed. It is also apparent that they are not always restricted to a single kind of host fish, the same species of Trichodina, in some instances at least, being found on very different hosts. For instance, the one shown (fig. 12, I) occurs on black bass and other warm-water fishes, but has also been found on trout. Trichodina truttae (fig. 12, J) described by Mueller (1937), occurs on the gills of cut-throat trout at various Oregon hatcheries, and is probably the species found by Richardson (1937) on brook trout from a Canadian hatchery.

Trichodina myakkae (figs. 10, E, 10, F, and 12, G) was described by Mueller (1937) from the largemouth black bass, but has been found on the gills of trout at the Leetown (W. Va.) hatchery.

DESCRIPTION AND I.IFE HISTORY

The trichodinids have a very complicated structure, the details of which can be made out only after careful preparation and under a high magnifica-tion. In general the body is saucer- or bell-shaped, the concave lower side being used for attachment to the host. The convex adoral side is smooth and bears 2 parallel rows of cilia known as the adoral spiral (fig. 10, C). The adoral spiral usually makes a complete circuit of the adoral surface and leads into the mouth at one side. Around the margin of the disk-shaped body is a band of long cilia known as the ciliary girdle. It is by means of these cilia that the organism moves over the surface of the body and gills.

The adhesive disk on the lower or aboral side is a holdfast organ by means of which the parasite clings to the host. It is composed of a complicated skeletal structure (fig. 12, E) arranged in the form of 3 concentric rings. The inner and most conspicuous is the denticulate ring which is made up of a series of horny elements or denticles arranged like beads on a necklace. Each denticle is shaped like a hollow cone with the smaller end inserted into the cavity of the adjacent denticle, an arrangement admirably adapted to provide both strength and flexibility. On the outer side each denticle bears a flattened blade-like structure known as the hook. On the inner side of the denticle is a tooth-like process, the ray, which projects toward the center of the disk. There is great variation in the number and shape of the denticles and, conse-quently, they are of great value in differentiating between the various species. Overlapping the hooks on the aboral side and extending toward the margin of the disk is a circular, ribbon-like structure known as the striated band. When viewed from the lower surface of the disk it appears as a series of radiating lines extending from the denticulate ring to near the edge of the disk. In sec-tions it can be seen that these lines are in reality long slender rods (fig. 10, C). External to the striated band is a thin striated border membrane which is usually bent downwards so that its edge is in contact with the surface of the host (fig. 12, F).

Within the body is a large horseshoe-shaped macronucleus, a small, rounded micronucleus, a large contractile vacuole, and several food vacuoles.

The parasite multiplies by binary fission which results in the formation of 2 daughter individuals like the parent. The skeleton, of course, contains only one-half the number of parts present in the parent and the original number is restored by an interesting and complicated process. Figure 12, I shows the adhesive disk of a young individual just formed by binary fission. The denticulate ring and striated band are just closing. The series of overlapping plates in the striated band is the beginning of a new denticulate ring which will replace the old as it is resorbed. Each plate will develop into a denticle and


since there are two plates for each denticle of the old ring, the original number will be restored. The original number of rods in the striated band is restored by a different method. Figure 12, H is the adhesive disk of a young trich-odinid in which new rods can be faintly seen between the old rods. The ad-hesive disk of an adult of the same species is shown in figure 12, E. Sexual reproduction by conjugation is common among trichodinids.

PATHOLOGY

The trichodinids are among the most common protozoan parasites of fish and have been the cause of serious mortalities among trout and pond fishes at hatcheries. They occur on the body, fins, and gills and under the hand lens appear as small, circular transparent animals moving rapidly about over the surface by means of the cilia at the margin of the disk.

Trichodiniasis, the disease caused by these parasites, is characterized by the appearance of white, irregular blotches on the head and dorsal surface of the body. The fins may also become badly frayed in heavily-infected fish. This is accompanied by sluggishness and a partial or complete loss of appetite. When an infected fish is viewed in a bright light at the proper angle, a white translucent covering or film can be seen extending over the body which in places reaches a considerable thickness, forming the white blotches previously mentioned. This film is composed of cells produced by hyperplasia of the epidermis. The scales become loosened and the skin may show a reddish tinge due to congestion of the blood vessels. This thickening of the epidermis, which is a protective reaction on the part of the host, actually benefits the trichodinid parasites, since they feed on the cells thus formed. Some of the smaller species, such as T. myakkae are too small to ingest epithelial cells and appear to feed largely on bacteria that may be present.

Fish are infected by direct transmission and there is no evidence that the parasites can spread by any other means. Richardson (1937) found that 12 hours after the introduction of an infected trout into a container with 2 clean fish, the latter were as heavily infected as the former. He also found that the length of time the parasite can live off the fish depends upon the temperature. When a fish dies the parasites escape slowly from the host and at room tem-peratures (22°-25°C.) may continue to leave the fish for 8 to 10 hours. At lower temperatures the process was greatly prolonged. At 11°C. live trichod-inids were present on the dead host up to 72 hours and at 4.5° C. they sur-vived for 140 hours after the death of the host.

CONTROL

Control of Trichodina is very easy. A treatment with a 3 percent salt solu-tion or with a 1 to 500 solution of acetic acid is ordinarily sufficient to rid fish of this parasite. Treatment with a 1 to 4,000 solution of formalin is, of course, very effective, and is to be preferred where it is not advisable to handle fish or when other external parasites are present.

References: Mueller, 1932, 1937; Plehn, 1924, Richardson, 1937. Ichthyophthirius

The protozoan, Ichthyophthirius multifilis, usually known as "ich," is com-mon on pond fishes, but is rarely injurious to trout. This is due to the fact that the parasite develops slowly at low temperatures and is unable to complete its life cycle where there is a rapid flow of water. Consequently, it seldom be-comes established at trout hatcheries; but in some instances, where conditions were somewhat unusual, it has caused serious losses among trout of all ages.

E




SYMPTOMS

The most characteristic symptom of ichthyophthiriasis, the disease caused by this parasite, is the presence of small, greyish white swellings or elevations on the body and fins. These swellings are usually sharply defined, but when fish are heavily infected, they may be so close together as to merge into one another, thus forming irregular, light-colored patches. Similar lesions occur also on the gills, but are not so easily seen as those on the body.

In early stages of the disease, the infected fish usually rub against the sides or bottom of the pond in an effort to rid themselves of the parasites. As this is also a characteristic reaction of fish infected with Gyrodactylus, it should not be interpreted as a specific symptom of the disease. Infected trout also show a marked tendency to get into rapidly flowing water, and may leap into the air more than usual, apparently in distress. In late stages of the disease the fish become sluggish and lie around the edges of the pond where they can be easily captured.


The parasite can be identified easily by scraping material from the surface of the body and examining this in water under a low magnification. A fully grown specimen is exceptionally large for a protozoan, reaching a diameter of nearly 1 millimeter, and can be distinguished with the naked eye as a minute, rounded, white body slowly swimming about. Under the microscope the parasite appears spherical or oval in shape and covered with rows of fine, hair-like cilia by which the animal propels itself through the water. There is a small circular mouth opening at one end, while scattered throughout the body are a number of small contractile vacuoles and numerous opaque granulas. Near the center of the body is a large crescent-shaped nucleus (fig. 9, J).

This protozoan has a very interesting and complicated life history (fig. 11), a knowledge of which is essential in order to combat the infection intelligently.

Protozoan parasites of trout: A. Flagellate form of Octomitus salmonis. The deeply stained paired nuclei surrounded by a lighter area can be seen at the anterior end. Extending the length of the body is a pair of axostyles to which are attached 3 pairs of flagella at the anterior end and a fourth pair at the posterior end. x 1,950. B. Ventral view of Chilodon sp. from black bass. The mouth opening into the cytopharynx surrounded by rod-like structures can be seen near the anterior end. On each side of the mouth are several parallel lines or striations bearing cilia. The large macronucleus is located in the posterior half of the body. The micronucleus is not shown. There are 2 contractile vacuoles about one-third of the distance from each end. Drawn from unstained specimen killed in osmic vapor. x 1,000. C. Cross-section of Trichodina sp. from the bluegill sunfish. The adoral spiral, composed of 2 rows of cilia, can be seen above the mouth and at the op-posite side of the adoral surface. On the lower side of the body is the adhesive disk com-posed of the denticulate ring, the striated band, and border membrane. Just above the striated band are the myonemes connecting the band with the ciliary girdle. x 1,340. D. Cyst of Oct omitus saltnonis containing 2 individuals surrounded by the transparent cyst wall. x 1,950. E. Adoral view of Trichodina myakkae. Surrounding the body are the membranelles of the ciliary girdle. The adoral spiral extends only about one-half the dis-tance around the body and leads into the cytopharynx, located between the arms of the macronucleus. In the middle of the body is the contractile vacuole which opens to the exterior at one side of the mouth. x 1,340. F. Cross-section of Trichodina myakkae. The deeply stained macronucleus can be seen at each side of the body. At the margin of the body is the ciliary girdle with the velum and adoral spiral above. There are 2 food vac-uoles in the endoplasm containing partially digested bacteria. x 1,340. Abbreviations: ad.s. adoral spiral; b.m. border membrane ; cil. cilia ; cil.g. ciliary girdle ; c.v. contractile vacuole ; dt. denticulate ring ; m. mouth ; ma. macronucleus; m.c. marginal cilia ; mi. micronucleus; my. myoneme ; str. striations; ve. velum.

A


FIGURE 11.—Life cycle of the Ichthyophthirius multifilis. A. Adult parasite on catfish. B. Parasite after leaving fish as a free-swimming form and settling to the bottom. C. Divi-sion of adult into many smaller individuals after formation of cyst. D. Bursting of cyst, releasing hundreds of minute parasites, which in turn reinfect the fish.

The young parasite is very small and entirely different in appearance from the adult. It swims about actively in search of a host, and when it comes in con-tact with a fish, it bores into the epidermis, attaches itself by one end of the cone-shaped body and rotates rapidly so that it quickly displaces some of the epithelial cells. In this way the parasite gradually works its way into the deeper layers of the epidermis (fig. 9, I) destroying the cells in its path. Wolf (1938) finds that in trout, at least, the parasite eventually comes to rest be-tween the epidermis and the corium. This is undoubtedly often the case in other fishes as well (fig. 9, H). As a result of the irritation caused by the bor-ing of the parasite into the tissues, there is a rapid proliferation of epidermal cells; and in the gills, where there is little connective tissue, the parasite fre-quently appears to be surrounded entirely by the greatly thickened epithelium (fig. 9, J).

Once embedded in the skin or gills of the host the parasite begins to grow rapidly and soon appears to the naked eye as the little white spot or swelling previously mentioned. When full grown, the parasite leaves the fish and drops to the bottom, where it soon forms a cyst by secreting a thin membrane around


itself. Within the cyst it multiplies rapidly by division, and eventually a large number of minute young are produced, which are invisible to the naked eye. When reproduction is completed, the cyst wall breaks open, releasing hundreds (in some instances thousands) of young, which immediately swim off in search of a new host.

CONTROL

Owing to the fact that during most of its life the parasite is surrounded by the living cells of the host where it cannot be reached by chemicals, Ichthy-ophthirius is more difficult to combat than most external parasites. When not embedded in the skin or gills, it is easily killed by various chemicals such as a 3 percent salt solution and exposure for 1 hour to a 1 to 4,000 solution of formalin. In using salt, the fish may be dipped into the solution until they show signs of distress or the salt may be added to the troughs in the usual man ner. Since parasites embedded in the skin are not affected by the solution, it is necessary to repeat this treatment on several succesive days in order to kill them as they emerge. The length of time required to free the fish of parasites will depend on the temperature, for the lower the temperature, the longer the time required. If the fish are retained in the pond after treatment, it should be sterilized each time with quicklime or chlorine. Accordingly to Mac-Lennan (1935) the encysted forms are not resistant to drying or to chemicals and can be easily destroyed. He finds, however, that the encysted stage may last as long as 5 days, and that for an additional 96 hours, the spores are capable of infecting fish. It thus appears that infection is possible for at least 8 days after the fish are removed; and probably a considerably longer time must elapse before it would be safe to use the pond unless it had been thor-oughly dried out or disinfected.

Owing to the difficulty of killing the parasites by the external application of chemicals, a more practical method is to remove them as they leave the fish. This may be done by holding infected fish in swiftly running water which carries the parasites away before they have an opportunity to multiply and reinfect the fish. This method can be applied easily at any trout hatchery as it is necessary only to hold the fish in troughs or raceways through which a good current of water is flowing. There should be a complete circulation with no dead areas in which the parasites can lie until they complete encystment. Naturally, it will be necessary to hold the fish in running water for several days until all parasites on the fish have disappeared.

References: Butcher, 1940; MacLennan, 1935; Prytherch, 1924; Wolf, 1938a.

INTERNAL ANIMAL PARASITES

PARASITIC WORMS

Although many species of parasitic worms are known to occur in trout, they are, fortunately, very rarely so abundant in hatchery fish as to cause appreci-able injury. This is in striking contrast to other types of parasites, which are almost invariably more abundant in trout at hatcheries than in those living under more natural conditions. The answer to this seeming paradox is, no doubt, to be found in the fact that almost all endoparasitic worms require at least two distinct hosts for the completion of the life cycle. The adult worm lives in an animal known as the primary host, whereas the larva is found in a very different animal known as the secondary or intermediate host. In some

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CARE AND DISEASES OF TROUT • 47

cases the worm requires more than one secondary host for its complete de-velopment. The larvae can develop only to a certain stage in the secondary host, but should this animal be eaten by the primary host, they are then able to complete their development in the latter.

Trout may serve either as a primary or as a secondary host, but never as both for the same species of worm. Worms for which trout form the primary host usually in the larval stage inhabit some crustacean, whereas those worms that utilize trout as the secondary host usually occur in the adult stage in fish-eating birds. This being the case, it is easy to understand that there is little opportunity for these parasites to complete their life cycle in hatchery fish that, for the most part, are fed on artificial foods and protected from pre-dacious enemies.

All types of parasitic worms occur in trout (Richardson 1936, 1941), in-cluding flukes (Trematoda), tapeworms (Cestoda), roundworms or thread-worms (Nematoda), and spiny-headed worms (Acanthocephala). The flukes are so small that they are seldom noticed, although they may occur occasion-ally in the intestine. A larval fluke (one of the Strigeidae) may form cysts in the skin. Since these cysts are surrounded with pigment, they appear as minute black spots, which, when abundant, are rather conspicuous. Similar cysts are common in the skin of yellow perch, minnows, and other pond fishes.

The larvae of several species of strigeids occur in the eyes of fish and one has recently caused heavy losses among trout of various sizes at the New Jersey State Hatchery at Hackettstown, (Palmer, 1939; Ferguson and Hay-ford, 1941). Ferguson and Hayford have provisionally identified this par-asite as Diplostomum flexicaudum, described by Van Haitsma from the eyes of the common sucker.

The last larval stage of the parasite (metacercaria) occurred only in the lens of the eye and when ablindant, caused it to become white and opaque, which resulted in partial or total blindness. In extreme cases the lens became soft and eventually disintegrated. The fish died from starvation caused by blindness. Rainbow, brown, and brOok trout were infected, but the flukes were most abundant in rainbow trout, which suffered a heavy mortality. The

Photomicrographs of protozoan parasites: A. Octomitus salmonis photographed from a smear made from the intestinal contents. The paired nuclei with axostyles between can be easily distinguished. The flagella are not visible. x 680. B. and C. Schizamoeba salmonis photographed from sections of a trout stomach. B shows a large ame-bold form with 3 nuclei. The rounded form at the right in C is an early stage in cyst formation. An ameboid form with 4 nuclei can be seen at upper left. x 680. D. Cross-section of a portion of one of the pyloric caeca of trout containing intracellular_ stages (int.) of 0. salmonis in the epithelium. x 330. E. Adhesive disk of an adult Trichodina sp. from the bluegill sunfish. The most conspicuous structure is the denticulate ring with the broad hooks on the outer side and the slender, pointed rays projecting inward. Out-side of the hooks is the striated band composed , of radiating .lines. This in turn is sur-rounded by the delicate border membrane which is also striated. x 680. F. Sections of Trichodina sp. attached to gill lamella of sunfish. The deeply stained macronuclei can be seen above the denticulate ring. x 680. G. Adhesive disk of T. myakkae. Note absence of rays on inner side of denticulate ring. x 680. H. Adhesive disk of a juvenile Trichodina sp. from sunfish. The faint lines in the striated band alternating with those much better de, fined are the new bars which are just beginning to form. Compare with fig. E. x 680. I. Adhesive disk of a juvenile Trichodina sp. from black bass which has just been formed by binary fission. The striated band and denticulate ring have not quite closed. The new denticulate ring is represented by a series of overlapping plates in the striated band. Each plate will develop into a denticle of the new ring. The inner part of the bars in the striated band will be resorbed along with the old denticulate ring. The dark shadow within the denticulate ring is the macronucleus which lies at a lower, level. x 680. J. Adhesive disk of Trichodina truttae. Photographed from a specimen preserved in formalin. x 340.

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eyes of suckers and blackhead minnows also contained large numbers of flukes, though those of the bluegill sunfish were less heavily infected.

Like all strigeids, this worm has a complex life history. The adult worms are found in the intestines of several species of gulls. The eggs pass from the birds with the feces and hatch in water into small, free-swimming larvae (miracidia). These larvae must make their way into snails of the genus Lymnaea within a few hours, otherwise they die. Once in the snail they un-dergo a complicated development, multiply, and form a second free-swimming stage (cercariae) in which they penetrate the tissues of a fish and eventually come to rest in the lens. Cercariae first begin to emerge from the snail about 6 weeks after entrance of the miracidia. Thousands of cercariae may leave the snail in a day and this process may continue for several weeks. Gulls be-come infected by eating parasitized fish.

The most effective method of controlling eye flukes, as well as other species of trematodes with a similar life history, is to destroy the snail hosts. This can be done by the use of chemicals such as chlorine or copper sulphate (p. 27).

Ward and Mueller (1926) have described a form of "popeye" in black-spotted trout at one of the Oregon State hatcheries, caused by heavy infesta-tion with the larvae of a trematode. The larvae formed minute cysts in various parts of the body and were so abundant as to cause heavy mortality. The pro-trusion of the eyes was apparently due to the presence of cysts in the optic nerve, as only those fish in which cysts were found, embedded in one or both of these nerves showed the popeye condition. The enormous number of cysts found in this instance can probably be accounted for by the presence of snails in the nursery ponds. From our knowledge of the life history of closely re-lated worms it seems very probable that this parasite requires two secondary hosts. The first is a mollusk (probably a snail) in which the parasite multi-plies rapidly, after which it becomes encysted in fish, which form the second intermediate host.

A .number of tapeworms have been reported from trout, probably one of the best known being the species described years ago by Leidy under the name Dibothrium cordiceps. The larvae of this species are very common in the muscles and body cavity of trout in Yellowstone Lake and for that reason have attracted considerable attention. The adult tapeworm is found in the white pelican, which is common there. Fasten (1922) has found a similar worm very abundant in trout from certain lakes in Washington.

Another tapeworm, Abothrium crassum, which is common in salmon in both this country and Europe, has been found in considerable numbers at one of the Vermont State hatcheries. Only the adult worm lives in trout and sal-mon, in the pyloric region of the intestine.

McKernan (1940) succeeded in ridding trout of tapeworms in the intestine by the use of kamala. The fish under experiment were badly infected with an undescribed species of Proteocephalus, as many as 5 worms, 50 to 90 mil-limeters long, being found in the intestine of 3-inch trout. Kamala was thor-oughly mixed with the food in the proportion of 172 to 2 percent by weight, and after one week the fish were found to be entirely free from the worms.

Roundworms, or nematodes, are comparatively rare in trout. One species, Cystidicola stigmatura, has been reported frequently in salmonid fishes from the Great Lakes, and has also been found in brook trout from several streams in Pennsylvania. The small, white, thread-like adult worms, about 1 to 172 inches long, live in the air bladder and are sometimes present in large numbers. The larvae occur in the freshwater shrimp (Gammarus).


The spiny-headed worms are characterized by a retractile proboscis, armed with numbers of recurved hooks, which is embedded in the intestinal wall, this sometimes resulting in infection followed by severe inflammation. Like the tapeworms, the spiny-headed worms have no digestive tract, but unlike the former, they have a body that is small and unsegmented. One of these worms is sometimes rather abundant in European trout and is reported to have caused considerable mortality. The riter has seen specimens of brook trout from Newfoundland that were so badly infested with spiny-headed worms that they must have suffered considerable injury.

References: Fasten, 1922; Ferguson and Hayford, 1941; Linton, 1891; McKernan, 1940; Palmer, 1939; Ward and Mueller, 1926.

PROTOZOA

Octomitus salmonis

A small protozoan parasite known as Octomitus salmonis occurs in the in-testine of trout and salmon. This parasite has received considerable atten-tion during recent years because it has proved to be the cause of serious mortal-ity among fingerling trout in our hatcheries.

This parasite is widely distributed throughout the country, having been reported from trout hatcheries in many different localities, and it is probable that there are very few hatcheries at which it does not occur. It has not been found in wild fish except under circumstances which indicate that the infec-tion was probably derived from hatchery fish. There is, however, no reason to doubt that the parasite does occur naturally in wild trout, but under such con-ditions, it is probably seldom sufficiently abundant to cause noticeable injury. It is only when the fish are crowded together in the hatchery that Octomitus becomes a serious problem.

All species of trout and salmon propagated artificially may become infected with Octomitus salmonis. In most cases it is more injurious to brook trout than to either rainbow or brown trout, although at a few hatcheries the rain-bow appears to be more susceptible than the brook trout. It is notable that this is true only at hatcheries where rainbow trout is the principal species reared, and it is not improbable that under such conditions a physiological strain of the parasite has been developed that is more virulent in rainbow than in brook trout.

SYMPTOMS

Octomitiasis is not characterized by well-defined symptoms by means of which it can be readily distinguished from other ailments of trout. There are no external lesions, and the most common indication of the presence of the disease is the appearance of very emaciated fish commonly referred to as "pinheads." Many of the pinheads may improve after a time and eventually resume their normal rate of growth, but others gradually grow weaker and weaker until death supervenes.

More rarely the disease occurs in an acute form accompanied by heavy mortality. In such cases the fish may exhibit a whirling or corkscrew motion in the water or may lie on the bottom of the trough and bend the body from side to side with quick, spasmodic movements. Too much emphasis should not be placed on the significance of such movements, however, since they un-doubtedly accompany other intestinal disorders.

Often a prominent feature of the disease is the spotty nature of the out-break. Instead of appearing simultaneously in all the troughs containing a


certain lot of fish, the disease may first break out in one or in several troughs that are not connected in any way. It frequently happens that all the troughs containing fish from the same lot of eggs will eventually show the disease, al-though by the time it appears in the last of the troughs it may already have run its course in the troughs first affected.

The simplest and most reliable method of diagnosing the disease consists of a microscopical examination of the contents of the anterior end of the in-testine. This material should be mounted on a slide in a drop of water, in which the parasites will remain alive and active for 10 to 15 minutes. As no other parasites that could be confused with Octomitus are likely to be en-countered, an examination with the low power of a compound microscope is usually sufficient. At this magnification the parasites can easily be seen as colorless, minute, pear-shaped organisms darting rapidly about in every di-rection. In some instances the parasites do not occur in the cavity of the in-testine, but only in the intestinal lining. This condition, however, is usually found in only very young fingerlings.


The parastic protozoan that causes octomitiasis belongs to the group called Flagellata, the members of which are characterized by the possession of one or more long, whip-like locomotor organs known as flagella. In Octomitus there are 4 pairs of these flagella 3 of which are attached to the broader an-terior end of the body while the four th pair arises from the posterior end. In life it is very difficult to distinguish the flagella, because they are transparent' and usually in rapid motion.

The body of Octomitus is colorless and transparent, and in order to make out the details of its structure, it is necessary to kill and stain the organism (fig. 10, A). It is then found that there is a pair of chitinous rods, known as axostyles, extending throughout the length of the body, to which the flagella previously referred to are attached. On each side of the axostyles near the anterior end is an elongated nucleus, each nucleus being connected with the nearer axostyle.

In the flagellate stage the parasites reproduce by a process known as binary fission, during which the organisms become rounded and the various cell struc-tures, with the exception of the flagella, divide into 2 equal parts. New flagella are quickly developed, so that the daughter flagellates are identical with the mother in every respect but size. Since the process requires but a short time, it follows that under favorable conditions the flagellates may multiply very rapidly.

At certain times cysts are formed, which can live for a considerable period outside the host, and it is probably by this means that the parasites are ordi-narily transmitted from fish to fish. The cysts (fig. 10, D), which are oval to spherical in shape, are formed by flagellates that become surrounded by a thin transparent membrane. Shortly after the membrane is formed the in-closed organism divides into 2, and in this condition the cysts pass out of the intestine in the feces. They can remain alive in the water for days, probably for weeks, and when accidentally swallowed by another fish, may set up a new infection. In this they are aided by the tough, resistant membrane, which enables the cysts to withstand conditions that would quickly kill the flagel-lated forms.

In addition to the flagellates in the intestinal cavity, there is another stage of the life cycle (fig. 12, D) that is found in the epithelial cells that line the


intestine and pyloric caeca. This stage is very different from the flagellated stage previously described. It first appears as a small rounded cell, which in-creases rapidly in size and soon divides into a number of small cells similar to the original. These daughter cells in their turn invade other epithelial cells and repeat the cycle. Under certain conditions these intracellular stages may multiply so very rapidly that a large percentage of the epithelial cells become infected. After a time, some of the intracellular parasites develop into the flagellated form and then quickly emerge into the cavity of the intestine.

PATHOLOGY

The effects of the parasites on the host undoubtedly vary widely under different conditions, and there is still much to be learned in this regard. The evidence at hand is contradictory in some respects, but it is believed that much of this apparent discrepancy can be explained on the basis of the 2 cycles of development within the host.

It is undoubtedly true that fish may harbor large numbers of flagellates with-out exhibiting any noticeable ill effects. This, however, appears to be largely a matter of age and probably also of acquired immunity on the part of the host. Ordinarily, trout over 3 or 4 inches in length show little or no ill ef-fects, even when the parasite is abundant in the intestine, while the younger fish, under the same conditions, may exhibit every evidence of malnutrition.

Among young fingerlings the effects of a severe infestation by the flagellates are, as a rule, decidedly marked. Such fish lose their appetite and become greatly emaciated, the large head and attenuated body suggesting the term "pinhead," by which they are commonly known among fish-culturists. They are usually weak and listless and in late stages of the disease may become too feeble to fight the current and thus, are liable to be swept against the screen, where they soon die.

This chronic form of octomitiasis is ordinarily most prevalent during the spring and early summer, when the fingerlings are from 2 to 3 inches long. Although the mortality is usually not very heavy at any time, the disease may persist for several weeks, so that the total loss may be as high as 50 or even 75 percent. Chronic octomitiasis is probably prevalent to a greater or lesser ex-tent at most trout hatcherieS where the fingerlings are held until summer or later, although the severity of the mortality appears to be dependent on a number of environmental factors, among which unsuitable food and over-crowding appear to be especially important.

Although the chronic wasting disease just described is undoubtedly the most common result of infection by Octomitus, there is another form of oc-tomitiasis, previously referred to, which manifests itself as an acute infection accompanied by a high mortality. Such epidemics occur only sporadically and are normally not of regular recurrence year after year as is the chronic form of the disease. In the majority of cases acute octomitiasis occurs early in the season shortly after the fish begin to feed.

Acute octomitiasis is caused by a rapid multiplication of the intracellular stages of the parasite, the flagellated stages frequently being entirely absent. As a result, there is considerable injury to the intestinal lining, accompanied by more or less inflammation, which quickly causes the death of the fish.

While there are 2 distinct forms of the disease, it is nevertheless true that in most instances we have to deal with a combination of these. It is probable that even in the chronic wasting type of octomitiasis, these parasites in the intracellular stages may sometimes be an important factor, since they are in-


variably present. In fact, a comparison of dying fish with emaciated but fairly vigorous individuals in the same lot has shown that in most instances, para-sites in the intracellular stages were more numerous in the former.

It should be emphasized that loss of appetite and emaciation is not in-variably due to the presence of Octomitus, and there is an all too common tendency to hold this parasite responsible for any sickness or mortality that cannot be easily explained. The presence of Octomitus in the intestine can be readily determined by a microscopical examination and, with the exception of small fingerlings, failure to find the flagellates in numbers may be taken as conclusive evidence that some other agent is responsible for whatever diseased condition may be present.

M'Gonigle (1940) was unable to find any evidence that in the hatcheries of the Maritime Provinces of Canada Octomitus was concerned in the heavy mortalities which frequently occurred among fingerling trout. He concluded that the mortality was due to acute catarrhal enteritis (see p. 87) which had no connection with Octomitus. The writer is in full agreement with M'Gonigle's contention that losses among small fingerlings have often been incorrectlly attributed to infection with Octomitus, but he is unable to follow this investigator in his further conclusion that octomitiasis is always a rela-tively unimportant factor in the mortalities of fingerlings. The evidence of the injurious effects of Octomitus is too conclusive to be thus lightly brushed aside.

CONTROL MEASURES

Because Octomitus salmonis is so widely distributed and may occur in fish of all ages, it appears impracticable to eliminate the parasite from a hatchery. In fact, there is no doubt that many fish harbor small numbers of the parasite and are consequently carriers of the disease.

Since Tunison and McCay (1933) reported that they had been successful in destroying the flagellate stage in the intestine by the addition of 0.2 percent calomel ( mercurous chloride) to the food, this treatment has come into gen-eral use throughout the country. Tunison and McCay found that 0.5 percent carbon tetrachloride and beta napthol were also effective in ridding the fish of the parasites, but these chemicals have never come into general use.

In order to eliminate the flagellate stage, it is frequently necessary to ad-minister calomel for several days in succession. There is evidence that under such circumstances calomel has a definitely toxic effect, and results in increased mortality. Smith and Quistorff (1940) have published results of experiments which indicate that the continued use of calomel in the diet over a long period is not harmful and may even be beneficial. It should be pointed out, however, that these investigators were dealing with perfectly healthy fish and that their experiments were confined to fingerling salmon. Consequently, their results do not necessarily prove that previous views regarding the toxicity of calomel were erroneous.

In view of the shortcomings of the calomel treatment, the experiments of Fish and McKernan (1940) and Nelson (1941) are of special importance. These experiments indicate that in carbarsone, we have a much more effec-tive treatment for Octomitus than in calomel. Carbarsone was thoroughly mixed with the food in the same proportions as calomel (0.2 percent) and in every instance all flagellated forms of Octomitus disappeared within 4 days. Furthermore, there was no evidence of a toxic effect on the fish, even when the treatment was continued for 7 days. Carbarsone is the trade name for para-carbamino phenyl-arsonic acid and has been used with marked success in the


treatment of intestinal amebiasis. It is a white crystalline odorless solid that is stable and practically insoluble in water. It is more expensive than calomel (about $3.00 per ounce), but this is counter-balanced by its greater efficiency and its freedom from toxic action.

As might be expected, none of these treatments is effective against the para-sites during their intracellular stages, which appear to be uninjured. How-ever, the elimination of the flagellates may indirectly affect the parasites in the intracellular stage through improvement in the general physical condition of the fish.

All available evidence points to the conclusion that if the fry and fingerlings can be kept in an otherwise healthy and vigorous condition, there is compara-tively little danger of heavy losses from this disease; but if the vitality of the fish is lowered or they are subjected, even for a short period, to unfavorable conditions, there is great danger of a rapid increase in the abundance of the parasites, with correspondingly detrimental effect on the host.

There are many factors which may directly or indirectly cause an outbreak of octomitiasis. Among those that are most conducive to the development of Octomitus are overcrowding, unsuitable water supply, especially a deficiency of dissolved oxygen and improper food. Owing to the inherent defects of artificial propagation it is almost impossible entirely to avoid the unfavorable effects of these factors, but certainly in most instances much can be done to improve conditions.

It is a natural tendency to attempt to increase the output by overloading the equipment. In some cases this may succeed for a time, but it is likely sooner or later to result in disaster. The evil effects of overcrowding are, no doubt, in part due to an insufficient supply of dissolved oxSigen, and this of course, is especially noticeable when the water is not properly aerated befor e entering the troughs or raceways. Often the water from springs is deficient in this gas, and it should always be made to flow over an efficient aerating de-vice to obviate any danger from this source.

A promising method of control, which has received comparatively little attention as yet, is the production of immune races of trout. There is con-siderable evidence that this is entirely feasible, but it will, of course, require rigid selection for several generations before conclusive results can be ob-tained. As a matter of fact, owing to the prevalence of octomitiasis, there has necessarily been more or less involuntary selection in this respect at many hatcheries which rear their own brood stock. This may be a partial explana-tion of the well-known fact that fingerlings from hatchery eggs usually grow faster and suffer smaller losses than those hatched from eggs obtained from wild fish.

References: Davis, 1924, 1925; Fish and McKernan, 1940; Moore, 1923, 1924; Nelson, 1941.

Schizamoeba salrnonis

This is one of the most common parasites of hatchery trout, but there is no evidence that it is ever seriously harmful to the host. It is usually most abund-ant in healthy, vigorous fish and is ordinarily not common in those that are not in good condition. This is probably due primarily to the fact that the parasite rarely occurs in numbers in fish that have been without food for any length of time.

The parasitic ameba, Schizamoeba salmonis, lives in the stomach and in-testine of all species of trout and salmon, but, like Octomitus salmonis, it has thus far been found only in hatchery fish or fish that might readily have be-


come infected from hatchery fish. The amebae (figs. 12, B and 12, C) occur in the stomach as small, colorless organisms, more or less irregular in shape. The transparent protoplasm has a finely granulated structure containing one or more vesicular bodies, the nuclei. The amebae are found in the mucus that covers the lining of the stomach and are of ten very abundant. This vegetative ameboid stage disintegrates quickly when removed from the stomach and for that reason is rarely seen without special search.

The parasite is most commonly found in the encysted stage, which is fre-quently very abundant in both the stomach and intestine. In the latter the cysts are usually in the core of gelatinous mucoid material that forms the major part of the intestinal contents. The cysts are spherical and vary greatly in size, the average diameter being about 20 to 25 microns. They are sur-rounded by a thin, transparent membrane and, in addition to a number of nuclei, usually contain numerous spherical ref ringent bodies composed of fat. The cysts gradually increase in size and after a time divide into 4 to 11 cells of approximately equal size. At this stage they have a remarkable resem-blance to a segmenting egg, but, of course, this similarity is only superficial.

The cysts provide a means by which the parasite may be transmitted from one fish to another. Protected by the surrounding membrane, they pass out of the intestine in the feces and may live for some time in water. If eventually taken into the stomach of another trout, the life cycle is repeated.

As previously pointed out, this parasite has not been observed appreciably to injure the host although when excessively abundant, it would seem that it must have some deleterious effect, even if this is limited to the consumption of food that would otherwise be utilized by the host.

This ameba is much more common in fingerlings than in older fish, al-though in several instances the writer has found it abundant in adult trout. It is probable that most hatchery fish harbor a few of these parasites, which would explain the ease with which the fingerlings become infected.

Reference: Davis, 1924.

Myxosporidia

The Myxosporidia are typically fish parasites all but a few species, which occur in amphibians and reptiles, being found only in fishes. They may live in the tissues of various parts of the body, but are especially common on the gills where they usually form small, white cysts. Many myxosporidians live in cavities of the body, being found in the gall bladder, kidney tubules, and urinary bladder. They all form great numbers of small, resistant spores by means of which they spread from one fish to another.

Trout undoubtedly are hosts to a number of myxosporidians, but so far they have received little attention. Chloromyxum truttae has been found by the writer in the gall bladder of brook trout in Vermont. The parasite occurred in both wild and hatchery fish and, while sometimes abundant, caused no appreciable injury. Myxosporidians have also been found in the kidney tubules of trout in widely-separated localities. In most cases they were mem-bers of the genus 1171yxidium, although other genera were represented. Figure 13, F, is a section of the kidney tubule of a wild brook trout from a stream near Staunton, Va. Although the parasites were abundant in certain parts of the kidney, there was little change in the appearance of the tubules. Re-cently, several species of Myxosporidia have been described by Fantham, Porter, and Richardson from wild brook trout in Canada.

Although in most cases myxosporidian parasites apparently cause little injury, there is always the possibility that, like many other parasites, they


may at times become exceptionally abundant with serious results to the host. Some species, however, may be injurious, even in small numbers. During the summer of 1940 a species of Myxidium was found by the writer in the kidneys of fingerling cutthroat trout (Salmo clarkii) at an Oregon hatchery. The fish were showing a heavy mortality at the time, but since they were also suffering from gill disease and Octomitus, it is uncertain to what extent, if any, the kidney parasites were concerned in the mortality. A myxosporidian infection of the kidneys of carp is believed by Plehn (1924) to be involved in a dropsi-cal condition of these fish, and the writer has found Myxosporidia in the kidney of fingerling salmon that showed similar symptoms.

Coccidia in Trout

A species of coccidia has been found in wild brook trout from Furnace Brook near Rutland, Vt., but has not been reported in trout from other localities nor has it been found in hatchery fish. In some instances, the fish showed a heavy infection (fig. 13, E) which resulted in extensive destruction of tissue invaded by the parasite.

These parasites occur in the epithelium of the pyloric caeca and to a lesser extent in the intestinal epithelium in the neighborhood of the caeca. Para-sites in various stages of development are usually present in the epithelium, and those in stages immediately preceding sporulation are frequently found in the lumen of the intestine. Four spores are formed in each individual (zygote), each spore containing 2 sporozoites. This would place the organ-ism in the genus Eimeria. It is probably an undescribed species, but has not been studied sufficiently to justify a definite conclusion.

Under favorable conditions coccidia may become very abundant and cause serious injury to the host. Coccidiosis in poultry is a fatal disease, but there is at present no evidence that coccidiosis in trout is particularly injurious. It is possible, however, that if once established at a hatchery, this parasite might cause serious trouble, since it multiplies rapidly and requires no inter-mediate host.

BACTERIAL DISEASES

FURUNCULOSIS

Furunculosis derives its name from the apparent similarity of the most characteristic lesions to human boils and furuncles. This resemblance is only superficial, however, since the structure of the furunculosis lesion is very different from that of a boil. Furthermore, these boil-like lesions are fre-quently absent and it is then necessary to rely on other criteria for diagnosis.

The disease affects chiefly the various species of salmonid fishes although a large number of fresh-water and marine fishes have been infected experi-mentally. It is probable, however, that few of these fishes would contract the disease in nature and it apparently occurs in epidemic form only among the Salmonidae. Of the trouts, the brown and brook trouts are particularly susceptible. The cutthroat trout is less susceptible than the preceding species while the rainbow trout is often considered immune. This is not strictly true, however, since the rainbow trout may contract the disease if continually exposed to sources of infection, or if suffering from injuries or lowered vitality. The results of experiments in Great Britain under the direction of the Furunculosis Committee (1933) agree with the writer's experience that the rainbow trout rarely contracts the disease. The brown trout was


found to be the most susceptible, while the brook trout appeared to be intermediate between that and the rainbow trout.

There is conclusive evidence that individuals of the same species exhibit great variation in susceptibility. Some resist infection entirely, while others readily contract the disease. As previously pointed out, evidence has recently been obtained which shows that this difference in susceptibility is largely a matter of heredity.

The investigations of the Furunculosis Committee indicate also that sus-ceptibility in trout increases with age, young trout under 2 years being less susceptible than 3-year and older fish. This has not been the experience in this country, where fingerlings and yearlings frequently suffer very heavy losses. Among mature trout the disease is usually rare except during and shortly after the spawning season, when the fish are particularly susceptible to infection. In fact, it is at this time that the heaviest mortality ordinarily occurs.

Furunculosis was originally thought to be confined to hatcheries and fish farms, but a number of epidemics have been reported in wild fish during recent years, especially salmon in streams of Great Britain. In this country serious outbreaks of the disease have been confined to trout in hatcheries and rearing ponds. However, Duff (1932) reported the disease in Elk River at Fernie, British Columbia, where it caused serious losses among the Rocky Mountain whitefish (Prosopium williamsoni) and the Dolly Varden trout (Salvelinus malma). An occasional cutthroat trout (Salmo clarkii) was also affected. The disease occurred also in hybrid salmon (Oncorhynchus) in a rearing pond at Cultus Lake, British Columbia.

SYMPTOMS AND PATHOLOGY

The symptoms of the disease are usually well marked. The most charac-teristic one is the presence of open sores on the body. These ordinarily develop in the dorsal muscles, although they may occur on other parts of the body. Sometimes the lesions have a marked tendency to develop at or near the base of the dorsal or pelvic fins, hence, furunculosis has in some cases been confused with the disease known as fin rot, which is caused by an entirely different organism.

Photomicrographs of bacterial and protozoan parasites of trout: A. Section of gill lamella from trout with furunculosis. A large clump of bacteria (bac.) can be seen in a capillary near the edge of the lamella. The presence of the bacteria has resulted in con-siderable distension of the capillary. x 680. B. Section through small lesion of ulcer disease. The epithelium (ep.) is greatly thickened to form the epithelial tufts which are charac-teristic of the disease. Masses of bacteria (bac.) can be seen in the dermis beneath the epithelium. x 85. C. Blood smear from infected fish showing bacteria abundant in the blood plasma. The large oval cells with deeply stained nuclei are crythrocytes or red corpuscles. x 680. D. Section through furunculosis lesion in body muscle of trout. Large masses of bacteria can be seen among the more lightly stained muscle fibers which are in various stages of disintegration. In the upper part of the figure the muscle fibers have been entirely destroyed and only the nuclei (stained black) are left. In the lower left-hand corner is a cross-section of a capillary gorged with blood. x .340. E. Section through the epithelial lining of a pyloric caecum of brook trout infected with coccidia. The epithelium is filled with intracellular stages of the parasite (coc.) with consequent destruc-tion of the epithelial cells. x 340. F. Section of kidney tubule of brook trout infected with Myxosporidia ; probably a species of Leptotheca. The lumen of the tubule is filled with small trophozoites of the parasite. Several trophozoites contain spores which are deeply stained. x 680.


The disease is essentially a generalized septicemia, the bacteria being carried to all parts of the body in the blood stream. As the bacteria thus pass through the capillaries, they may collect here and there in small clumps which multiply rapidly, destroying the wall of the blood vessel and spreading out into the surrounding tissues (fig. 13, D).

The lesions thus formed appear to the naked eye as minute red spots in the subcutaneous tissue or among the muscle fibers. They contain large numbers of the causative bacteria which multiply rapidly, causing disin-tegration of the blood vessels and other tissues in the immediate vicinity. As a result, a swelling is formed which is filled with a deep red pus-like material composed of bacteria, blood, and disintegrated muscle fibers. Some-times soft, blister-like lesions filled almost entirely with blood are formed just beneath the skin. The lesions increase in size and may eventually break through the skin to form an open sore. In many cases, however, death occurs before this happens. Especially is this the case in fingerling trout, in which usually the only evidence of the lesion that can be seen from the exterior is an irregular, dark blotch just beneath the skin on one side of the body. This blotch ordinarily is situated between the dorsal and pelvic fins and in young trout is probably the most characteristic symptom of the disease.

There is frequently a marked congestion of the blood vessels in the ab-dominal cavity. The lining of the intestine may be inflamed and there may be a discharge of blood and mucus from the vent, especially after death. The spleen is commonly enlarged and has a bright cherry-red color. This is decidedly noticeable in fingerling trout and is a very convenient diagnostic character. Tithe spleen is crushed in a drop of water underneath the cover-glass, white clumps of bacteria can usually be seen, even when there is no other indication of thc disease.

Masses of bacteria can also be found in the liver where they develop in much the same manner as in the spleen, but cannot be easily made out with-out sectioning and staining. The kidneys are ordinarily badly diseased and eventually may be converted into a semi-liquid mass. The gills are con-gested and clumps of bacteria can be distinguished in the capillaries (fig. 13, A). In short, the causative bacteria may occur in practically all parts of the body, but show a predilection for the more vascular organs, where they can be found in early stages of the disease before the more characteristic symptoms appear.

According to Plehn, the disease may occur rarely in an entirely different form, in which the causative organism is found only in the cavity of the intestine, at least until a comparatively late stage of the disease. In such cases there are no external symptoms, and recent investigations indicate that in some instances the bacteria may live in the intestine for a considerable time without any apparent injurious effects on the fish.


The bacteria were first described by Emmerich and Weibel in 1894 as the cause of an epidemic among trout in Germany. These authors called the organism Bacterium salmonicida. Later, Marsh, who was evidently un-aware of Emmerich and Weibel's work, described an organism that he had isolated from the blood of diseased trout from Northville, Mich., and which he named Bacterium truttae. There can be little doubt that the bacteria described by Emmerich and Weibel and by Marsh are identical, and accord-ingly the specific name salmonicida takes precedence over the latter name truttae.


The bacterium (fig. 13, C) is a short rod about 2 to 3 microns long, with rounded ends, but may show considerable variation in form, especially when grown in culture media. The most important characteristic of the organism, which makes it easy to distinguish from other bacteria when growing in culture media, is the formation of a pigment which stains the media trans-parent brown.

The bacteria can usually be found in the blood of infected fish, where they are present in large numbers, occurring both singly and in large clumps. They grow best at a comparatively low temperature, the optimum being probably about 10° to 15° C. (50° to 60° F.). They are unable to live for any length of time at 37° C. and for that reason cannot develop in a warm-blooded animal.

The manner in which the disease is transmitted has not been definitely determined, but it seems most probable that the bacteria gain entrance to the body through the walls of the digestive tract or through small wounds on the body or gills. The disease may be readily transmitted experimentally by introducing the bacteria directly into the blood or tissues. After having gained entrance to the blood stream, they multiply rapidly and are carried to all parts of the body. Some of the bacteria may become localized in the muscles, where they produce the small red foci previously mentioned. These foci may eventually form large ulcers filled with a red pus-like material con-taining immense numbers of bacteria. The failure of such ulcers to develop in small fish is probably due to the death of the fish before the bacteria have been able to attack the muscles to any great extent. The dark blotches on the sides of the body, so characteristic of the disease in fingerling trout, are caused by the infiltration of blood among the muscle fibers, accompanied by some disintegration of the tissues; but death supervenes before the breaking of the muscle fibers has become an important feature of the lesion.

Among the visceral organs, the liver, spleen, and kidneys appear to be especially liable to infection. Large masses of the bacteria can usually be found in these organs, and the tissues of the spleen and kidney may be broken down entirely.

CONTROL MEASURES

In considering methods of controlling this disease, it is well to bear in mind that furunculosis is essentially a blood disease, the bacteria developing in tissues and cavities of the body, where they cannot be reached by the external application of chemicals. Consequently, it is idle to attempt to cure the fish by the use of salt baths or disinfecting solutions. Probably a certain percentage of infected fish recover from the disease, but recovery rarely occurs in fish in which the disease is so far advanced as to produce notice-able lesions.

This being the case, control measures must be designed primarily to pre-vent the spread of the infection to healthy fish. This is by no means a simple matter, since it has been shown that apparently healthy fish may act as carriers, which greatly increases the difficulty of control. In some instances the disease has run its course and apparently died out, only at a later time suddenly to break out afresh. In such cases the bacteria may have been carried over in the intestines of apparently healthy fish or possibly in the mud and debris on the bottom of the pond, and later, should the fish become weakened in any way, the bacteria are again able to get the upper hand.

A method of immunizing trout against Bacterium salmonicida by admin-istering a vaccine in the food has been developed by Duff (1942). The


vaccine was prepared by adding chloroform to an actively-growing culture of the bacteria which were killed in a short time. The dead culture was then thoroughly mixed with the food and fed once daily for several weeks, after which the fish were exposed to live virulent cultures of Bacterium salmonicida in water. It was found that after not less than 64 feedings of vaccine, the mortality in vaccinated trout was approximately 25 percent as compared with a mortality of 75 percent in the untreated fish. It is evident that while the results of Duff's experiments are very encouraging, this method of immunizing fish has not yet been sufficiently perfected to justify its general use.

Until some practicable means of immunizing fish has been developed, the only logical method of control is to destroy all infected fish at once. These should be burned, if possible, but if this is not practicable, they should at least be covered with lime and buried in pits at a sufficient distance from the ponds to prevent contamination. Dead fish should never be allowed to lie in the ponds, as putrefaction does not appear to injure the bacteria, which, when the fish decompose, are set free in enormous numbers.

All ponds in which diseased fish have been held should be thoroughly sterilized before being used again. According to German authorities a 1 to 100,000 solution of potassium permanganate will kill the bacteria of furun-culosis if allowed to remain in the pond for a considerable time. Undoubtedly, the most effective method of sterilizing ponds is by use of chlorine (Davis, 1938; Hagen, 1940; Wolf, 1940). A concentration of 3 p.p.m. is sufficient to kill the bacteria, but where much organic matter is present, it is advisable to use a stronger solution. A freshly prepared solution of water-slaked lime is also effective and may be preferable under some circumstances. Needless to say, whatever the chemical used, great care should be exercised to insure that the solution penetrates all cracks and crevices where bacteria may be concealed. If practicable, the pond should be exposed to the sun for several days after disinfection and allowed to dry out as much as possible. Of course, all implements that could possibly carry the bacteria should be disinfected at the same time.

Several investigators have found that pure water is deleterious to the bacteria (Williamson, 1928) and that they die out quickly in water of this type, while they may live for weeks in sewage and in water containing an appreciable amount of organic matter. (Plehn, 1924; Duff et al, 1940). Consequently, it has been held that pollution is a predisposing factor, but Williamson (1928) was unable to find any connection between pollution and the disease. There is conclusive evidence, however, that warm weather and low water favor its development. Possibly the true explanation may lie in the fact that pollution, high temperatures, and low water tend to lower the vitality of trout and salmon and thus make them more susceptible to in-fection.

Of course, every precaution should be taken to prevent the spread of the disease from one hatchery to another through shipments of infected fish. In fact, no such shipments should be allowed from hatcheries in which the disease is known to be present. Fortunately, there appears to be less danger of the spread of the disease by means of eggs. According to Blake (1931) any possibility of the transmission of the disease in this way can be pre-vented by treating the eggs for 20 to 30 minutes with a 1 to 2,000 solution of acriflavine. There is, however, danger that the bacteria may be carried on the packing material or egg cases, and these should be destroyed or


thoroughly disinfected if there is any reason to believe that they may have been contaminated.

References: Blake, 1931; Duff and Stewart, 1933; Furunculosis Com-mittee, 1930, 1933, 1935; Plehn, 1924; Williamson, 1928.

ULCER DISEASE

Ulcer disease is common at many hatcheries in the Northeastern United States, where it has caused high mortalities. According to Wolf (1938) it is primarily an ailment of brook trout though lake and brown trout are also susceptible. Rainbow trout are very resistant, but not immune.

The disease was first described by Calkins (1899) who found it present in epidemic form at a hatchery on Long Island. This investigator believed the disease was caused by a protozoan, but it is now generally recognized that there is little evidence to support this conclusion. Owing to the simi-larity of the lesions to those found in furunculosis, the two diseases were considered identical until Fish (1934) called attention to the fact that ulcer disease differed from furunculosis in several important respects.

SYMPTOMS

As the name signifies ulcer disease is characterized by the formation of open sores or ulcers on the surface of the body which closely resemble those of furunculosis. In its early stages the lesion appears to the naked eye as a small, whitish pimple which may be situated almost anywhere on the surface of the body or head. Under the lens, it is evident that it is formed by a papilla-like outgrowth of the epidermis which later becomes wrinkled and very irregular in shape, frequently dividing into branched finger-like projections. These may reach a length of several millimeters and the whole structure has been appropriately termed an epithelial tuft by Fish. Not infrequently, there is a red discoloration at the base of the epithelial tuft, due to congestion of the blood vessels in the dermis or corium.

In advanced stages of the disease the lesion may be one-half inch or more in diameter

' grayish-white at the center, where the muscle is exposed and

surrounded by a white margin of thickened epithelium underneath which is a distinct reddish area as in earlier stages. Ordinarily the lesions are approxi-mately circular in outline, although they may be irregular or greatly elon-gated.

One of the characteristics of this disease is the frequency with which the jaws and roof of the mouth become infected. Lesions on the jaws develop rapidly and may result in the entire eating away of the bones. The fins, especially the dorsal and caudal fins, are also attacked and the fin rays as well as the soft tissue destroyed. Sometimes the lesions develop first on the outer edge and extend toward the base as in fin rot, but in other cases lesions may appear mid-way or at the base of the fin rays. The fin rays eventually fall out, leaving a notch in the fin which appears as though a piece had been torn out. Not infrequently, the fins may be entirely destroyed.

While, as previously mentioned, the ulcers are similar to furunculosis lesions, they can usually, with little difficulty, be distinguished from the latter. Ordinarily, a furunculosis lesion appears first as a blister or bladder-like swelling beneath the skin, which eventually breaks through to the sur-face. It is filled with a red, pus-like material composed chiefly of blood and necrotic tissue. A lesion of ulcer disease, on the other hand, develops from the surface inward and does not extend for any distance into the muscles.

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The muscular tissue appears to be eaten away cleanly from the surface and there is little evidence of undermining and the irregular disintegration of the deeper muscles so characteristic of furunculosis. Furthermore, the con-tents of the lesions of ulcer disease are usually light in color and easily washed away, leaving the grayish-white muscular tissue fully exposed.

According to Fish, the lesions of ulcer disease do not normally become fungused during the life of the fish; while in furunculosis, infection of the lesions with Saprolegnia is a common occurrence. Wolf, however, found that this is not universally true and that fungus may occasionally develop on ulcered fish.

PATHOLOGY AND CAUSE OF DISEASE

A typical ulcer starts as a papilla-like outgrowth of the epidermis which later divides into irregular finger-like structures, the epithelial tuft. This breaks down at the center and forms a sore or lesion. Sections through an open lesion (fig. 13, B) show a great thickening of the epithelium around the margin. Underneath, there is a mass of bacteria located in the dermis. As the ulcer grows, the bacteria invade the dermis in an ever increasing circle and cause its complete destruction so that in the center, the body muscles are exposed. Only rarely can bacteria be distinguished in the open part of the lesion, and the body muscle is not invaded as in the case of furunculosis. It is evident that for the most part the bacteria are confined to the dermis, and as this is destroyed, they are washed out of the lesion.

The appearance and development of the ulcers suggest that they are due to an infection which enters through the epithelium, and the experiments of Wolf (1938) support this view. Whether the bacteria are capable of penetrating the normal epithelium or can gain entrance only where it has been injured is still unknown. That the latter occasionally happens is indi-cated by the fact that several lesions may develop in a straight line, as though infection had occurred along a scratch in the epithelium.

The superficial character of the lesions is the most striking difference between ulcer disease and furunculosis. Sections of the liver, kidney, and spleen fail to show any evidence of bacteria as in furunculosis. Furthermore, Fish (1934) was unable to culture any bacteria from the blood or internal organs of diseased fish, but did isolate a bacterium from ulcers which proved to be pathogenic when used to inoculate healthy trout. He was unable to prove, however, that it was the cause of ulcer disease.

Working in the author's laboratory, Mrs. E. C. Lazar has isolated a bacterium from fish with ulcer disease which on inoculation produced lesions indistinguishable from typical ulcers of a natural infection. This organism, however, has the same cultural characters as Bacterium salmonicida, and serological tests by Dr. D. C. B. Duff have confirmed the identification. Brook trout inoculated with this organism by a slight prick with a needle developed a typical epithelial tuft at the site of the inoculation. Similar inoculations with B. salmonicida cultures procured from Dr. Duff failed to produce such a lesion.

After having been run through several fish the culture isolated by Mrs. Lazar increased in virulence and on inoculation into healthy trout, produced lesions indistinguishable from those found in typical cases of furunculosis. When first isolated, only superficial lesions were produced by experimental inoculations and on autopsy, the kidney, liver, and spleen appeared normal. Later inoculations, however, produced deeper lesions more like those of furunculosis and bacteria were found in the kidney, liver, and spleen.


The problem is still under investigation and it is too early to arrive at a definite conclusion, but there is much evidence to support the view that ulcer disease may be caused by a less virulent strain of Bacterium salmonicida, the causative organism of furunculosis. It is significant, for instance, that while a typical ulcer has a very different structure from a typical furun-culosis lesion, there are many border-line cases. Wolf (1938) found in several instances that trout with typical ulcers also showed lesions charac-teristic of furunculosis, which developed internally and did not open on the surface of the body. The writer also has seen fish which showed furun-culosis-like lesions as well as typical ulcers.

In the previous edition of this publication the author called attention to the resemblance between ulcer disease and fin rot and expressed the opinion that both diseases might be caused by the same organism. This theory has not been supported by recent developments, but Wolf (1940) concluded from his experiments that the two diseases are identical and that the term fin rot should be abandoned, since it is properly applicable only to the type of fin infection found in ulcer disease. In the author's opinion, there is no question that infections by different organisms have been called fin rot (see p. 66), but it does not follow that the infections so designated were usually ulcer disease. On the contrary, the original description of fin rot (Davis, 1928) was based primarily on an infection at a hatchery which had no history of the occurrence of either ulcer disease or furunculosis.

CONTROL

Since ulcer disease is evidently contracted by infection through the epi-dermis, there is a possibility that it can be controlled by dipping the fish in a disinfectant such as copper sulphate. Experiments by Wolf, however, indicate that such treatments are of little value, and it is doubtful if the disease can be controlled by such means. Apparently, the only effective measures are to destroy all fish in infected lots and thoroughly sterilize all pools and utensils as recommended for furunculosis .

References: Fish, 1934; Wolf, 1938, 1940, and 1940a.

PEDUNCLE DISEASE

A remarkable disease appeared during June and July 1941 among finger-ling rainbow trout at the Leetown, (W. Va.) hatchery. While invariably fatal, only a small percentage of the fish became infected and consequently the mortality was comparatively light. The disease reappeared during the spring of 1945. So far the disease has not been reported from any other hatchery.

SYMPTOMS

The appearance of the sick fish is so characteristic that there is no possi-bility of confusing peduncle disease with any known ailment. The disease usually appeared first on the adipose fin which became white along its outer edge. This discoloration extended gradually toward the base until it covered the entire fin (fig. 14, A) and then began to spread over the caudal peduncle. Eventually the entire peduncle became a dirty white, but by that time the adipose fin had disappeared and the integument on the dorsal side of the peduncle had disintegrated, exposing the muscle beneath. Fish in late stages of the disease were swimming about with the caudal fin still attached to the


vertebral column which was fully exposed. A few fish survived for a short time after the caudal fin had entirely disappeared.

PATHOLOGY AND CAUSE OF THE DISEASE

There is little doubt that the disease is caused by a bacterial infection which starts in the adipose fin and eventually spreads to the entire caudal peduncle and attached fins. In no case was the infection observed to extend anterior to the anal fin. This was probably due to the fact that the fish died before the infection could progress further. Material scraped from the sur-face of the caudal peduncle contained great numbers of a nearly pure culture of non-motile, slender, rod-shaped bacteria 3 to 5 microns long (fig. 14, B), which are believed to be the cause of the disease. Attempts to culture the bacteria have so far been unsuccessful.

The bacteria apparently first gain entrance through the epidermis of the adipose fin. Having penetrated the epidermis, they multiply rapidly in the dermis which is quickly destroyed, giving rise to the whitish discoloration so characteristic of the disease. Very few bacteria could be found among the epidermis cells although they were very numerous in the dermis. Follow-ing destruction of the integument, the bacteria invade the muscles through the connective tissue surrounding the muscle fibers. The advance of the bacteria among the muscle fibers is usually preceded by congestion of the blood vessels followed by local hemorrhage as the capillary walls are destroyed by bacterial action. This, in turn, is followed by destruction of the muscle fibers by bacteria which enter them from the end (figs. 14, C and 14, D). At first, the bacteria are arranged in parallel rows between the fibrils which soon disappear. As a result of this bacterial activity, the muscle fibers are broken down from the surface inward until the entire peduncle is destroyed. The lesions are always clean and clear-cut, indicating that all necrotic tissue is washed away as soon as formed.

CONTROL

It is evident that, as the tissues of the caudal peduncle are destroyed, the broken-down cells with great numbers of bacteria are continually being

Photomicrographs of bacterial parasites of trout: A. Fingerling rainbow trout show-ing different stages of the peduncle disease. In the upper fish the adipose fin has be-come infected and has turned white as a result. The middle fish shows a considerably later stage of the disease. The muscles of the caudal peduncle have been destroyed ex-posing the vertebrae attached to the caudal fin which has also been partially destroyed. The last stage of the disease with loss of the caudal fin is shown by the third fish. B. Sec-tion through the mucus layer found at the advancing edge of a lesion on the caudal pe-duncle. The mucus is filled with the rod-shaped bacteria which cause the disease. C. Lon-gitudinal section through infected muscle of the caudal peduncle. The section is in the re-gion of the myocommata (the connective tissue partition separating the muscle segments) and shows the bacteria invading the ends of the muscle fibers. A few bacteria are already in the muscle fibers where they can be seen between the fibrils. x 680. D. Cross-section of infected muscle fibers in the caudal peduncle. The small dots scattered through the fibers are sections of bacteria lying between the muscle fibrils. Masses of bacteria can be seen in the connective tissue surrounding the muscle fibers. x 680. E. Gills of fingerling brook trout infected with Cytophaga columnaris. The lesion on the gill at the right is more advanced and is covered with a dirty white material com-posed of bacteria, remains of tissue cells and debris held together by a slimy substance secreted by the bacteria. x 3. F. Characteristic hay-cock like mass of bacteria on the surface of a lesion. This is the form assum'ed by the bacteria when transferred to a slide. In a few minutes they collect to form similar masses on the edge of scales or on bits of debris. x 680.


washed away. Consequently, water containing diseased fish is highly infec-tive and spread of the disease can best be prevented by removing all fish which show any evidence of infection. As such fish will eventually die in any case, there is no reason for not getting rid of them at once. Of course, troughs, ponds and all utensils that have been contaminated should be thor-oughly sterilized.

Overcrowding appears to be a predisposing factor, since the disease was most prevalent in troughs that were badly crowded.

FIN ROT

This disease, which is known also as tail rot, is prevalent at many hatcheries in widely separated localities. It is now evident that several diseases due to different causes have been confused under this term, and in the present state of our knowledge, it is not always possible to separate them. The following account applies to what is believed to be the typical form of fin rot, but until the causative organism has been isolated, it is impossible to distin-guish it in all cases from other fin infections such as ulcer disease and furun-culosis.

SYMPTOMS

As the name indicates, fin rot is characterized by disintegration of the fins which may eventually be entirely destroyed. Usually the infection ap-pears first in the dorsal fin, but later may spread to the other fins. Occa-sionally the infection starts in the caudal fin which may be reduced to a mere stub.

Ordinarily the first noticeable indication of the disease is a more or less distinct white line along the outer margin of the fin. This white streak gradu-ally moves toward the base of the fin, while at the same time the outer margin becomes badly frayed, owing to the disintegration of the tissue be-tween the fin rays (fig. 15). This process continues until eventually the entire fin may be destroyed.

CAUSE AND PATHOLOGY

The causative organism is believed to be a rod-shaped bacterium, which can usually be found in large numbers in the infected fins. The writer has detected this organism in cases of fin rot from several different localities, and apparently it is the only organism that is uniformly present in the diseased tissues.

As previously indicated, the infection normally starts on the outer margin of the fin. As a result of the irritation caused by the growth of the bacteria, there is a rapid proliferation of the epithelial cells, so that the epithelium becomes greatly thickened. This thickened epithelium forms the white streak across the fin that is so characteristic of the early stages of the disease. Later the epithelium is destroyed, exposing the fin rays, which are also attacked by the bacteria and soon are frayed and broken. On the inner side of the infected area the bacteria are continually invading uninfected tissues, which in turn pass through the same sequence of events as those infected earlier.


FIGURE 15.—Dorsal fin of fingerling brook trout infected with fin rot. Magnified 7 diameters.

The bacteria develop not only on the outer surface of the fins but invade also the tissues, chiefly the connective tissues. In their growth through the tissues the bacteria follow the lymph channels and frequently can be seen grouped in great masses around the fin rays. As the cartilages at the base of the fins are less resistant to bacterial action than the denser peripheral portions, they are sometimes destroyed first, and the fins may drop off instead of gradually disintegrating.

The dorsal fins of fingerling rainbow trout frequently show a light-colored, thickened area along the margin that has a superficial resemblance to an early stage of fin rot. Examination with a hand lens will show, however, that the margin of the fin has a smooth contour and lacks the ragged appear-ance and projecting fin rays so characteristic of fin rot. The thickened edge of the fin is composed of scar tissue, apparently the result of irritation, and there is no evidence that any infection is involved. It is most common in pools that are overcrowded.

CONTROL

In view of the method of infection outlined above, control measures obvi-ously must be directed toward destroying the bacteria before they penetrate the tissues. This can be accomplished by dipping the fish for 1 or 2 minutes in a 1 to 2,000 solution of copper sulphate. This treatment has been found effective in early stages of the disease, but after the bacteria have gained entrance to the tissues, they are out of reach of chemical baths. Usually several treatments at intervals of 24 hours are required before the spread of the disease can be effectually checked. As it is impossible to cure fish in the advanced stages of the disease, all such fish should be destroyed before beginning the copper-sulphate treatment. If not removed, they form a con-tinual source of infection, as great numbers of bacteria pass into the water from lesions on the fins and body. It is also essential that the troughs or ponds and all utensils used around the diseased fish be thoroughly disin-fected.

The disease varies greatly in severity; in many instances only a small percentage of the fish die, while in other cases the mortality may be very


high. In the milder form of the disease a large proportion of the infected fish may recover; the lesions heal before the fins are entirely destroyed, and the fins regenerate more or less completely.

Little information has been obtained regarding the factors that tend to bring on an outbreak of the disease. As in the case of so many other trout diseases, overcrowding is undoubtedly an important contributing factor. There is also evidence that sometimes Gyrodactylus may be involved. It is easy to understand how injury to the fins by this parasite might make them more susceptible to infection.

GILL DISEASE The gills of fish are frequently infected by parasites of various kinds,

especially protozoa and gyrodactylid worms. In trout, however, the term "gill disease" usually refers to specific infection characterized by certain effects on the gills. The disease is widely distributed over the United States, but is apparently more common at hatcheries in the eastern States than in the far west where another type of gill trouble is more prevalent. All species of trout and salmon are susceptible to this infection. The same or a similar disease has been observed in largemouth and smallmouth black bass, and in the black crappie.

FIGURE 16.—Gills of fingerling trout affected with gill disease. Note that the gill filaments are enlarged at the ends, and in many instances adjoining filaments have become fused for some distance. Magnified 14 diameters.

SYMPTOMS

Unfortunately, the disease is not characterized by any well-defined symp-toms other than the appearance of the gills and a general sluggishness and loss of appetite on the part of the fish. In fact, loss of appetite, while of course not specific for this disease, is probably, for the average fish cul-turist, the most reliable indication of its presence. Whenever fish of any lot suddenly stop taking food and lose their customary "pep" they should at once be examined for the possible presence of gill disease. In early stages of the disease, the gills are swollen and congested and consequently, appear a deeper red than usual. Later the gill filaments become more or less com-pletely fused, while the tips become enlarged and distinctly lighter in color (figs. 16 and 17). Eventually the gills may become badly fungused, the fungus often spreading from the gills to the top and sides of the head. This


FIGURE 17.—Same as figure 16, but another view.

fungus is purely a secondary infection and, in the case of large fingerlings and yearlings, is almost invariably present before the fish die. Infected fry and small fingerlings, however, rarely show any trace of fungus, probably because the disease is so quickly fatal to small fish that fungus has no opportunity to develop.

Probably the most constant symptom that can be easily recognized is the greatly increased secretion of mucus by the gills. This is usually a prominent feature of the disease in fish of all ages and is particularly noticeable, as debris becomes entangled in the mucus and may so clog the gills as to inter-fere with respiration. It is well to bear in mind, however, that this excessive secretion of mucus by the gills is not distinctive, since it may be due to other causes as well as to gill disease.

The bacteria are most abundant on the outer third of the gill filaments, where, evidently as a result of the irritation set up by their presence, there is a rapid increase in the number of epithelial cells. This results in a marked thickening of the epithelium, especially at the ends of the filaments, which become greatly enlarged (fig. 18, D), accompanied by fusion of the lamellae into a continuous mass of tissue. Later, adjoining filaments may fuse, start-ing at the enlarged ends and extending toward their bases. In extreme cases all filaments on each side of the gill arch may be fused into a continuous mass. Sometimes the gills become necrotic, but as this condition is almost invari-ably accompanied by infection with fungus, it is probable that this organism is chiefly responsible. The fish usually succumb in a short time after the appearance of fungus.

CAUSE AND PATHOLOGY

This disease is caused by infection with bacteria that occur in the form of long, thread-like filaments which usually lie side by side to form a more or less continuous layer on the surface of the gills. These filaments may reach a length of at least 100 microns and are composed of long, rod-shaped bacteria joined end to end (fig. 18, E). They are colorless, transparent, and so difficult to distinguish that it requires very careful focusing under a high magnification to make them out as they lie closely, adherent to the surface of the gills. When an infected gill is examined on a slide the bacteria show no motion at first, but later the filaments begin to exhibit slow sinuous movements which are most marked at the ends of filaments which have


become detached from the gills. These move slowly back and forth, some-times accompanied by a sinuous bending of the entire filament. Attempts to isolate the bacteria in pure culture have so far been unsuccessful, but their general appearance is strongly suggestive of the myxobacteria.

The increased secretion of mucus accompanied by thickening and fusion of the gill filaments must seriously interfere with the circulation of water over the gills. To make matters worse, the mucus may become filled with sand grains and debris which must still further impede the flow of water. The free interchange of gases between the water and the blood is also seri-ously affected by the thickening of the epithelium, the water and blood being separated by many cells instead of 2 thin layers as in the normal gill. The result is serious interference with normal respiration, and it is probable that the high mortality is due primarily to this factor rather than to any toxic action.

Ordinarily, the bacteria are found only on the surface of the gills, but in the case of fry, they may occur also on the body and fins. This may account for the great destructiveness of the disease among fish of this age. In a number of instances the disease, within a few days of its appearance, caused virtually a total loss among fry.

According to Wolf (1944) this disease is caused by a deficiency of panto-thenic acid in the diet and the presence of the characteristic bacteria is purely incidental. While it is possible that a dietary deficiency may be a contributing factor in some instances, the fact that a complete cure has been effected in hundreds of cases by destroying the bacteria without any change in the diet would seem to be a sufficient answer to Wolf's conten-tion. Later, A. M. Phillips (unpublished report) confirmed Wolf's finding that a deficiency of pantothenic acid may cause hyperplasia of the gill epi-thelium but doubts if it has any relation to the bacterial disease (see page 73). Apparently Wolf failed to realize that there are at least two, and possibly more, types of gill disease.

CONTROL MEASURES

Inasmuch as the disease is caused by bacteria, which occur only on the surface of the gills and body, it should be more easily controlled than one that is due to internal parasites. This assumption is borne out by practical experience, as it has been found that the disease yields readily to treatment

Photomicrographs of trout gills infected with bacteria: A. Cross-sections of lamellae of trout gill to show normal structure. Each lamella is composed of a middle layer made up of blood capillaries and supporting cells, covered on each side by a single layer of cells, the respiratory epithelium. x 340. B. Cross-sections of lamellae in early stage of infection by gill bacteria. The outer half of each lamella is fused with adjoining lamellae on both sides. Later they may become completely fused throughout so that the space at the base of the lamellae is obliterated. The epithelium also becomes greatly thickened. Bacteria can be seen indistinctly on the outer surface of the fused lamellae. x 340. C. Cross-section through the edge of lamellae more highly magnified to show presence of bacteria. The bacteria on the middle lamella have become dislodged from the surface, but on the other lamellae they can still be seen in close contact with the epithe-lium. x 680. D. Section through several gill filaments at a later stage of infection. The lamellae at the outer ends of the filaments have become fused into a common mass tr form the enlarged ends so characteristic of the disease. On the lower part of the filaments the lamellae are still separate or fused only at the outer edge. x 25. E. Causative bacteria of gill disease as they appear in a dried smear made of scrapings from the gills. Note that the bacteria are arranged end to end to form long filaments. When living, it is impossible to distinguish the individual bacteria that form the filaments. x 680.


with copper sulphate. On the first appearance of the disease the fish should be dipped in a 1 to 2,000 solution of copper sulphate for 1 minute and then quickly transferred to running water. After the disease has become estab-lished, treatments on 2 successive days may be necessary to destroy all the bacteria. In such cases, it is impossible to avoid considerable mortality since by that time the gills have been injured so badly that many fish die even though the bacteria have been entirely destroyed. In the event that it is impracticable or undesirable to dip the fish in the manner just described, the disease can be controlled by use of a more dilute solution of copper sulphate in which the fish are held for one hour (p. 25) . When properly handled, the treatment of fish in pools and raceways by such dilute solu-tions has been effective. This is especially true if the fish are treated on the first appearance of the disease, but after it has reached a more advanced stage, dipping in a stronger solution may be necessary.

A weak solution of potassium permanganate was recommended by Feustal (1935) as being superior to copper sulphate for treatment of gill disease. This was later confirmed by Frederic F. Fish (unpublished) who used the treatment on salmon fingerlings with marked success. The treatment as used by Feustal was very simple. Sufficient potassium permanganate was put in the head of the trough to make a 1 to 200,000 solution. The crystals were quickly dissolved by the inflowing water which was allowed to con-tinue to flow at the usual rate. Fish lowered the strength of the solution to 1 part potassium permanganate to 400,000 parts water and adjusted the ratio of inflow per minute to volume of water in the trough or pool to 1:25. The treatment was repeated on 4 successive days.

When fish in a pool are to be treated, the chemical should first be dissolved in water and then sprayed over the surface of the pool. If the fish are in troughs, the crystals may be weighed out and added to the water at the head of the troughs, but it is much simpler to make up a stock solution which can be easily measured to provide the required amount for each trough.

Experiments by the writer with the treatment as used by Fish gave some-what different results. The fish showed a noticeable improvement after the treatment, but it appeared that the bacteria were not killed, although they were loosened from their close attachment to the gill epithelium. As a result, most of the bacteria were sloughed off in the mucus, which probably accounted for the improved condition of the fish. It was evident that the number of bac-teria was greatly reduced after each treatment and on the fifth day, only a few remained. Subsequently, however, the bacteria gradually increased until they were as abundant as before and it was necessary, after 2 to 3 weeks, to repeat the treatment. The same thing recurred after the second treatment and it was necessary to give a third or even a fourth treatment.

The results of these experiments indicate that it is possible to keep gill disease under control by flushing the troughs with a 1 to 400,000 solution of potassium permanganate on four successive days, but that it will probably be necessary to repeat the 4-day treatment at frequent intervals.

While it appears that treatments with potassium permanganate must be repeated more frequently than with copper sulphate, the former has the ad-vantage that it can be used with less trouble and the•treatdient is much less toxic to fish. In fact, unless the fish are very weak, there is little mortality and most of them show no signs of injury.

It has been found that fry and fingerlings may contract the disease from older fish that appear to be perfectly healthy. Evidently, the bacteria may live in small numbers on such fish for an indefinite time without produc-


ing any noticeable effects. The fish act as carriers, and it is probable that in this way the disease in a hatchery is carried over from one season to the next. It is evident that the presence of carriers will make it very difficult, if not im-practicable, to completely eradicate the disease from a hatchery.

WESTERN TYPE OF GILL DISEASE

Fish (1935) has called attention to a western form of gill disease which differs in several respects from the disease that is so prevalent at eastern hatcheries. In the last few years this disease has caused severe losses in several western States and is probably the most destructive hatchery disease in that region.

The lesions of the western type of gill disease are very similar to those of the eastern form except that alteration of the gill epithelium is not so exten-sive. The appearance of the gills as described by Fish is almost identical with that of gills in early stages of the eastern disease, but proliferation of the epithelial cells is not so marked and there is very little fusion of the gill fila-ments which is usually so noticeable in advanced stages of the eastern form of gill disease. Furthermore, the thread-like filaments, composed of slender, rod-shaped bacteria, that are always present on the gills in the eastern type of gill disease, have not been found in fish affected with the western variety. Fish has found 2 species of bacteria of very different appearance to be com-monly present on the gills of the diseased fish, but has not yet been able to show that either is the cause of the disease.

Another respect in which the western type of gill disease differs from the common eastern form is that it does not respond to treatment with copper sulphate or potassium permanganate as does the eastern variety. In fact, it has been found that in several instances the loss among treated fish was actually much higher than among the controls that were not treated. Fish believes that the disease progresses relatively slowly at first, and that by the time the presence of the disease is recognized, the gills have become so altered that the fish are unable to withstand the additional rigors of treatment.

A somewhat similar condition of the gills has been described by Wales and Evins (1937). These authors termed the condition sestonosis, and be-lieved that it was the result of irritation caused by diatoms and other small algal forms, bacteria, and protozoa.

Recently, A. M. Phillips (unpublished report) has confirmed an earlier observation by Wolf (1944) that a deficiency of pantothenic acid in the diet of trout may cause a marked hyperplasia of the gill epithelium similar to that found in western gill disease. When fish which had developed the typical lesions were fed a supplement of pantothenic acid, the disease soon dis-appeared. Phillips was unable to find any evidence that bacteria were con-nected with the disease and believed that he was dealing with the western type of gill disease.

To avoid any possible misunderstanding, it should be emphasized that there can be no question concerning the occurrence of the eastern type of gill disease at western hatcheries also, although it may have been introduced from the East. The author has received specimens of trout from hatcheries in the Pacific Coast States and in the Intermountain region that showed typical cases of eastern gill disease, including the presence of the characteristic bac-teria on the gills.

References: Davis, 1926 and 1927; Fish 1935.


Cytophaga columnaris

This interesting species of bacteria was first described by the writer (Davis, 1922) as the cause of serious mortalities among fishes from the Mississippi River. Recently it has been grown in pure culture by Dr. Laura Garnjobst (1945) who has published a complete description of the organism. Her studies show that it is one of the myxobacteria which are characterized by long, slen-der rods surrounded by a slimy material secreted by the bacteria. The rods lack flagella, but nevertheless are actively motile.

Cytophaga columnaris attacks fish only at comparatively high tempera-tures. Garnjobst gives the optimum as 25° to 30° C. (77°-88° F.) and while it will grow at considerably lower temperatures, it is rarely injurious at tem-peratures below 65° F. Consequently, it is not ordinarily found on trout, but during the summer of 1940 an infection appeared among brook trout at the Leetown (W. Va.) hatchery. It reappeared during the summer of 1944 on brook trout in another raceway where the disease caused considerable mortal-ity. In both raceways the temperature at times approached the upper limit for trout and it is evident that under such conditions C. columnaris may cause heavy losses. Infection with this organism has also resulted in serious mor-talities among fingerling and adult salmon at Fish and Wildlife Service hatch-eries at Leavenworth, Wash., and Coleman, Calif.

SYMPTOMS

The first indication of the disease is the appearance of a grayish-white spot on the head, gills fins or some part of the body, which is usually surrounded by a zone with a distinct reddish tinge. Superficially, the spots resemble lesions produced by Saprolegnia, but a close inspection shows that they lack the fuzzy appearance so characteristic of a fungus infection. Infection frequently starts on the fins, the outer edges becoming lighter in color. This lighter area gradually extends toward the base, but there is no marked thickening of the epithelium to form a conspicuous white line as in the case of fin rot. On the contrary, the color appears to fade gradually. Eventually the fins may become frayed and ragged in appearance. Ordinarily, lesions first develop at the site of an injury, and the infection spreads from this point. For example, lesions on the trout at Leetown in 1940 appeared first around the mouth and caudal fin, apparently the result of injuries received in jumping.

CAUSE OF THE DISEASE

If a small amount of material is removed from a lesion and examined under a microscope, it will be found to contain large numbers of bacteria with a very characteristic appearance that makes them easily recognizable. The bacteria are long, slender, rod-shaped organisms 5 to 12 microns long and 0.3 micron wide (fig. 20, B). They are motile and can often be seen to move for a short distance in a straight line, accompanied by a sinuous bending of the body. One of the most characteristic movements is to turn one end slowly in a circle, the other end remaining stationary and forming a pivot on which the entire rod revolves. A modification of this movement can be seen at the surface of any aggregation of bacteria where individual rods wave rapidly back and forth.

One of the striking characteristics of the organism is the formation of columnar or dome-shaped masses of bacteria. When a bit of material, such as a scale, covered with bacteria is transferred to a slide, they soon collect in such masses around the edges, each column being separated a short distance


from its neighbor. The free end of the column is usually rounded and some-times appreciably enlarged. Similar aggregations of bacteria may be found on the surface of lesions, but in such cases they are usually shaped more like a haycock with a broad base (figs. 14, F and 19, B).

PATHOLOGY

As previously mentioned, infections with Cytophaga columnaris usually occur on the surface of the body or on the fins. The bacteria are found in greatest numbers in the connective tissues, but may also attack epithelial and other tissues. In most cases they apparently gain entrance to the dermal and muscular tissues through an injury to the epidermis, although it may be very slight. After reaching the dermis the bacteria multiply rapidly and pene-trate the connective tissues in all directions. They occur in large numbers underneath the scales which drop off as the dermis is destroyed.

For obvious reasons, a study of the effect of C. columnaris on the tissues can be made more easily in scaleless fishes, such as the catfishes. A section through a well developed lesion on the common bullhead for example, shows that in the center the epidermis has been destroyed and the dermis more or less eroded. In late stages the dermis also may be destroyed exposing the muscles underneath. At the margin of the lesion the epidermis is breaking down as the bacteria move out from the focus of infection to invade uninjured tissues. The capillaries in the dermis become congested, followed by disin-tegration of their walls so that the blood fills all interstices in the surrounding tissues.

It is notable, however, that there is no hyperplasia of the epidermis around the lesions which is such a prominent feature of the lesions of furunculosis or ulcer disease. Proliferation of the epithelial cells of the body and gills is one of the most characteristic reactions to irritants of various kinds, but is en-tirely lacking in infections with C. columnaris. It is also of interest that the bacteria spread more rapidly in the dermis than in the epidermis so that the former is frequently heavily infected while the overlying epidermis is still intact. Figure 19, C shows a section of the infected dermis of a bullhead with the bacteria lying between the connective tissue fibers.

From the dermis the bacteria invade the skeletal muscles following the connective tissue (myocommata) between the muscle segments and thence along the connective tissues surrounding the muscle fibers. They may also enter the ends of the fibers, but this appears to be exceptional. As in the dermis, infection of the muscles is accompanied by congestion of the capillaries fol-lowed by hemorrhage. In the hemorrhagic areas large mononuclear leucocytes are especially abundant and there is considerable phagocytic activity. Phagocytes were observed which had ingested several bacteria, but apparently phagocytosis is very ineffective. Even before any bacteria can be found the muscle fibers begin to break down and shortly after the bacteria appear in any numbers all cellular elements, including the phagocytes, are destroyed.

Owing to differences in the structure of the tissues, lesions on the gills fol-low a somewhat different course. Gill lesions frequently start at the distal end of the filaments and extend toward the base. At the same time they spread out laterally until a large part of the gill may be involved (fig. 14, E) . Sometimes the gill cover may also become infected, causing erosion of the soft parts, be-ginning at the outer edge. In striking contrast with the condition in true gill


disease, there is no thickening of the epithelium, but the epithelial cells in the immediate vicinity of the lesion become strongly vacuolated (fig. 19, A). This characteristic reaction occurs before any bacteria can be found on the cells. Later, as the bacteria advance over the epithelium, (fig. 20, A) the lamellae are entirely destroyed, followed by distintegration of the filaments. As in infections of the integument, the blood vessels are greatly congested, resulting in extensive hemorrhage when the filaments break down. In figure 19, D the bacteria can be seen invading the cartilaginous axis of the filament which is being eroded by lytic action. Covering both gill and body lesions is a dirty-white layer composed of bacteria, partially broken down cells and debris held together by the slime secreted by the bacteria. Frequently, the bacteria are aggregated to form the elevated or haycock-like structures (figs. 14, F and 19, B) previously mentioned. These are composed of practically a pure cul-ture of C. columnaris with great numbers of pycnoidal nuclei which appear to be derived chiefly from erythrocytes.

It was formerly believed that healthy, uninjured fish do not become infected with C. columnaris, but evidence is accumulating that this may not be true in all cases. There is no evidence that the trout at Leetown which became in-fected during the summer of 1944 had been injured in any way and except for the presence of the disease they appeared to be in excellent condition, al-though it is possible that the relatively high temperature of the water may have lowered their vitality. Even stronger evidence that the disease may at-tack healthy fish is provided by an outbreak among white crappie (Pomoxis annularis) in Coolidge Lake, Ariz. It was reported that in August 1942, thou-sands of crappies died in the lake although other fishes were not affected. Specimens of diseased fish sent to the writer showed a heavy infection on the gills with C. columnaris which was evidently the cause of the mortality. It appears that in this case the disease reached epidemic proportions and it is not impossible that many mortalities of fish during warm weather may be caused by infection with C. columnaris. Of course, so many parasites occur on the gills that it is always possible that the infection followed some slight in-jury, but in both cases no parasites, other than bacteria, could be found.

Nevertheless, the fact remains that infections are most likely to occur when fish are handled or otherwise injured at water temperatures above 70° F. The lesions usually appear within 24 hours and death follows within 48 to 72 hours. At lower temperatures the danger of infection is much less and the disease develops more slowly. The lesions, however, are liable to a secondary infection with fungus (Saprolegnia) which may prove more injurious than the original infection.

CONTROL

If there is reason to believe that fish may become infected as a result of handling, this can be prevented by dipping the fish at the time in a 1 to 2,000 solution of copper sulphate for 1 to 2 minutes. Where properly done, this will afford almost complete protection from the disease and is routine practice at some warm-water hatcheries when fish are handled during the summer. After evidence of infection appears, fish may be cured by the same treatment if the disease is not too far advanced, but 2 or 3 dippings at 12- to 24-hour intervals may be necessary. It is not possible to cure fish with extensive lesions or in-fected gills and such fish should be destroyed at once. Further progress of the disease can be checked by transferring the fish to cold water, and with trout and salmon this is usually the best method of control.

References: Davis 1922; Garnjobst 1945.


MISCELLANEUOS DISEASES, INCLUDING THOSE OF

UNCERTAIN ORIGIN

FUNGUS DISEASES

Trout, like most fresh-water fishes, are attacked occasionally by fungus or water molds (Saprolegniacea). Probably the species most frequently found in trout is Saprolegnia parasitica Coker which may attack both the eggs and fish. Formerly, it was thought that this was the only species parasitic on fish, but it is now apparent that several species may infect trout and other fishes, although, owing to the difficulty of making specific distinctions, the matter is still far from being settled.

Although Saprolegnia parasitica often causes heavy losses among trout of various ages, it is doubtful whether the fungus is the primary cause of the trouble. Any physical injury or infection by external parasites may enable this fungus to obtain a foothold on the fish and then to spread from the original site of infection. Susceptibility to infection is greatly increased if the fish are suffering from general debility or are living under unfavorable condi-tions. The fungus may develop on any part of the fish, and usually occurs in small patches, but in late stages may cover a large area. Ordinarily the fungus appears as a tuft of white threads which radiate from the body of the fish for a distance of about one-third of an inch or even more. When the water is somewhat roily, sediment and debris may become entangled among the fungal filaments so that the fungused areas may appear a dirty gray or brown. The fungus is attached to the fish by means of small, root-like filaments which penetrate the skin, and in late stages of the disease may invade the underlying subcutaneous muscle. As the filaments grow through the skin, they cause the death of the surrounding tissues and thus form large necrotic areas which may eventually cause the death of the fish.

The eggs of fish are also subject to attack by Saprolegnia, and at most hatcheries the heaviest losses from fungus occur at this stage. There is no evidence that Saprolegnia can begin to develop on a normal, healthy egg un-less there is some foreign organic matter adhering to the surface. However, it develops very quickly on any dead eggs that may be present, and from these the mycelial filaments spread rapidly to adjoining healthy eggs, which are soon killed. Consequently, within a comparatively short time, a large number of eggs may become bound together in a mass by entangling filaments, which continually spread farther and farther from the original site of infection.

The fungus reproduces by means of minute biciliate zoospores which are produced in enormous numbers in enlarged, club-shaped ends of the filaments, known as zoosporangia, and it is these zoospores that enable the fungus to spread from fish to fish. Another method of dissemination of the fungus is by means of resting cells or chlamydospores. These cells, which develop in long chains, readily separate from each other and may then give rise to hyphae or to zoospores. In addition to these methods of asexual reproduction, Sapro-legnia reproduce sexually through the formation of egg-like zoospores which, after being fertilized, develop into mycelia similar to those formed by the zoospores. The sexual type of reproduction occurs very rarely in the fungus found on trout and from the practical standpoint is consequently of little importance.


Another species of fungus which has evidently been confused with Sapro-legnia parasitica in the past has been described by Davis and Lazar (1940). This fungus, which has been named Saprolegnia invaderis, was found in small fingerling trout at the Leetown (W. Va.) hatchery. Infection occurs through the alimentary tract from which the fungus grows out through the abdominal wall to the exterior. In most cases, the fungus first starts to grow in the lumen of the stomach, but occasionally it grows in the intestine as well. In a short time branched hyphal filaments extend throughout the lumen of the stomach and then begin to grow through the stomach wall destroying any tissues that may lie in their path (fig. 20, D). Once through the stomach wall, the hyphae pass through the body cavity and then through the body wall of the fish to the exterior (fig. 20, C). Irritation set up by the fungus as it grows through the tissues causes congestion of visceral blood vessels and accumulation of blood in the infected organs. Ordinarily the hyphae do not reach the exterior until after the death of the host. At this time the appearance of the fish is characteristic, the abdomen being covered with a fuzz-like growth of short hyphae (fig. 20, E) which in a few hours may extend all over the body. Zoo-spores and chlamydospores develop on the emergent hyphae and provide for the dissemination of the parasite to healthy fish. Apparently, no reproduc-tive bodies are formed within the body of the host.

This species has in one instance been found also on the gill of an adult trout where it had formed a small, necrotic area. There was no evidence that the gill had been injured in any way, and it is possible that this fungus may attack other organs besides the alimentary tract. It is evident that, unlike S. parasitica, S. invaderis is able to develop without previous injury to the tissues that are infected.

CONTROL

Consideration of any treatment for the control of fungus must take into account the cause of the infection. If the presence of fungus is due to a second-ary infection following injuries produced by some other parasite, it is obvious that a permanent cure will be impossible unless the cause of the original in-fection is removed by appropriate means. On the other hand, if fungus is the primary cause of the trouble, eradication of this parasite must be the chief concern. The results reported from the use of various chemicals for ridding fish of fungus are frequently contradictory. No doubt this has been due, in

Photomicrographs of Cytophaga columnaris: A. Section of gill lamellae near bac-terial lesion. Although no bacteria can be seen on the lamellae, the epithelial cells are strongly vacuolated. This characteristic reaction to C. columnaris is very different from the reaction of the epithelial cells to gill bacteria. Compare with figure 18B. x 340. B. Section through mass of bacteria covering outer surface of lesion on trout gill. The gill filaments underneath have been destroyed and only the partially disintegrated nuclei of the tissue cells remain. The dark mass at the lower side of the figure is the remains of a blood clot. Note that on the surface the bacteria have collected in chunks with a rounded convex surface. The dark objects at the base of these masses of bacteria are the nuclei of tissue cells. x 340. C. Section of dermis of skin of bulhead infected with C. columnaris. The bacteria have invaded the connective tissue which has not yet begun to break down. Note that the bacteria are arranged with their long axis parallel to the connective tissue fibers. x 680. D. Section through the gill filament of a trout infected with C. columnaris. The epithelium has been entirely destroyed and the bacteria are now invading the car-tilaginous axis of the filament by lysing the cartilage. Note the presence of bacteria be-tween the cartilage cells in the lower left-hand part of the figure. Above this region the cartilage has been entirely destroyed and the space is occupied by masses of bacteria. x. 680.


FIGURE 20.—For description, see opposite page,.


part, to the fact that different species of fungi were involved and also to the stage and degree of infection. After the parasite has penetrated deeply into the tissues, it is obviously much more difficult to eradicate than at an earlier stage. Furthermore, infections of such vital organs as the gills are particularly in-jurious and difficult to combat.

At most hatcheries the usual treatment for fungus has been to expose the fish to a strong solution of salt (sodium chloride), which was accomplished in various ways. Probably the best method is to dip the fish in a 3-percent salt solution until they show signs of distress. In early stages of the disease one such treatment is usually effective, but if the fungus is well established, even several successive treatments may not effect a cure. Dipping the fish for 1 minute in a 1 to 2,000 solution of copper sulphate has proved effective in some instances. Schneberger (1941) reports good results in preventing infection of trout eggs by the addition of an ounce of a saturated solution of copper sulphate to the water entering a battery of eggs. Malachite green is said by several investigators (Foster and Woodbury, 1936; O'Donnell, 1941) to be the most effective agent yet used for the control of fungus. O'Donnell recom-mends that the fish be dipped in a 1 to 15,000 solution of malachite green *(zinc free) for 10 to 30 seconds. He found that this treatment was non-toxic to 18 species of fish (including trout) upon which it was used. In most in-stances, one treatment was sufficient to completely rid the fish of fungus and promote healing, but occasionally it was necessary to give 2 or 3 dips at in-tervals of 2 days.

In dealing with fungus, however, by far the most effective Method is to prevent the development of the disease, and in most cases this is a compara-tively simple matter. As previously mentioned, there is reason to believe that healthy, uninjured fish are not affected by fungus; but infection is very likely to follow any mechanical injury, even though very slight. Once the protective mucous covering of the fish is broken, an opportunity is afforded for the zoo-spores to germinate and penetrate the epithelium at the point of injury. From this focal point the mycelium then invades the surrounding uninjured tissues.

Infection as a result of physical injury is especially liable to occur during or shortly after the spawning season. Not only is it almost impossible to avoid slight injuries to the fish as a result of handling incident to stripping, but the vitality of the fish is usually lower at this time than at other seasons, so that they are especially susceptible to infection. Fortunately, the danger of de-veloping a fungus infection in spawned fish can be greatly decreased by dip-ping them in a 1 to 15,000 solution of malachite green, or in a 3-percent salt solution after they have been stripped.

Photomicrographs of Cytophaga columnaris and Saprolegnia invaderis; A. Section of gill lamellae of trout infected with C. columnaris. The epithelium has been de-stroyed, only the capillary network being left, and this is already beginning to disin-tegrate. The bacteria appear as dark lines or dots on the surface of the cells. Compare with fig. 19, A. x 680. B. C. columnaris, photographed from a dried smear made from a lesion on the surface of the body. x 800. C. Section of the abdominal wall of a fingerling trout infected with Saprolegnia invaderis. The fungus hyphae can be seen growing through the skin. The epithelium is much thicker than normal. x 340. D. Section through wall of trout stomach which has been penetrated by fungus hyphae. The thick, muscu-lar part of the wall is fi.lied with a network of hyphae extending in all directions. Outside the stomach in the body cavity there is a luxuriant growth of branching hyphae. Note the congested blood vessels in the outer layer (serosa) of the stomach wall. x 170. E. Fingerling trout showing fungus hyphae growing out through abdominal wall. The lighter color of the body anterior to the anal fin is characteristic and is caused by hyphae growing through the skin. Somewhat enlarged.


Under ordinary circumstances Saprolegnia can be prevented from causing any considerable injury to incubating eggs by carefully removing all dead eggs at frequent intervals. If this is done, there will be little opportunity for the fungus to become established. Care should also be taken to prevent the eggs from becoming covered with sediment or debris. This not only tends to smother the eggs but also affords an opportunity for the development of bac-teria and protozoa, which may so injure the eggs as to make them susceptible to infection by Saprolegnia.

One of the most effective weapons in combating fungus is to keep the ponds and troughs in a sanitary condition. Any surplus food or dead fish which are allowed to remain in the ponds for any length of time become covered with a luxuriant growth of fungus, which, of course, results in the formation of enormous numbers of zoospores. These are continually being set free in the water, so that the slightest wound on any fish present is very liable to become infected.

The control of S. invaderis is a comparatively simple matter and no special treatments are necessary. Since zoospores and chlamydospores are not formed until 24 to 48 hours after the death of the fish, it is necessary only to remove all fish within a few hours after death, to prevent the infection from spreading to healthy fish. Failure to do this may easily result in a rapid spread of the infection, as the habit fingerlings have of nibbling at their dead comrades, pro-vides an ideal method of infection.

References: Clinton, 1894; Davis and Lazar, 1940; Kanouse, 1932; O'Donne117 1941.

POPEYE

"Popeye" is a popular term applied to fish that show a marked protrusion of the eyeballs, a condition known as exophthalmos. This disease is common among fingerling trout at some hatcheries and may occur also among yearlings and adult fish.

There are undoubtedly several forms of popeye disease, due to causes quite different. One form, caused by a severe infestation with the larvae of a trematode worm, has already been referred to in the section on parasitic worms. Another type of popeye, often called "gas bubble" disease, described by Marsh and Gorham (1905) , may occur when the water supply becomes supersaturated with air. Most spring waters are more or less deficient in dis-solved air, but occasionally the water may be supersaturated. In such cases, there is a tendency for nitrogen gas to collect in various parts of the body, in-cluding the loose connective tissues surrounding the eyeball, causing the latter to protrude from its orbit. This form of popeye can be easily prevented by installing an efficient deaerating device, which will allow excess gas to escape from the water. It is also claimed that in waters supersaturated with oxygen this gas may form bubbles in the tissues and give rise to symptoms similar to those produced by nitrogen (Plehn, 1924; Woodbury, 1941).

Still another form of popeye results from an accumulation of serous fluid in the abdominal cavity and other parts of the body. In this form, the abdomen becomes greatly distended and when opened, is found to be filled with a watery fluid. This is probably the most common form of popeye in trout and in all cases observed by the writer has been found associated with a diseased condi-tion of the kidneys. The kidneys of the affected fish are usually darker in color than normal, due to the accumulation of pigment, and the tubules con-tain casts and crystals, probably of some calcium salt. In places, the epithe-


Hum lining of the kidney tubules may be entirely disintegrated. The cause of of this disease is unknown, no evidence having been discovered that it is due to a specific infection of any kind. Trout showing this type of popeye have in several instances shown a marked improvement following the addition of 172 to 2 percent of cod-liver oil to the diet. This suggests that the disease may possibly be connected in some way with calcium metabolism, especially as it appears to occur only at hatcheries supplied with water having a high cal-cium content.

Recently, the writer observed a fourth kind of popeye in fingerling trout, characterized, as in the previous case, by the accumulation of serous fluid in the abdominal cavity and around the eyeball. Here, however, the resemblance ends, as the kidney tubules do not contain the characteristic casts and crystals observed in previous cases, but on the contrary, show a heavy infection with a myxosporidian parasite. It has not yet been determined whether or not this parasite is the cause of the popeyed condition.

Several writers have held that certain forms of popeye are due to bacterial infections of the eye, but there is still considerable doubt whether this is the case. In a study of popeye by Williamson (1927) the investigator isolated 22 strains of bacteria from the diseased eyes of fishes, but concluded that none of them could be proved responsible for the gas-bubble disease.

A type of popeye quite different from any previously described has been re-ported by Belding and Merrill (1935) as having caused considerable mortality among brook and rainbow trout at a Massachusetts hatchery. In this disease less than half the fish (20-30 percent) show a marked exophthalmos (pro-trusion of the eyeballs). While it may affect practically all tissues of the body, the disease shows a selective affinity for the kidney, and any changes in other tissues may be largely the result of impaired renal function.

The most characteristic symptom of this disease appears to be the accum-ulation of serous fluid in various parts of the body. In addition to exophthal-mos, blisters may form on the surface of the body, which appear as raised circular or elliptical areas of skin, separated by fluid from the underlying tissues. These blisters may appear on any part of the body except the head, tail, and fins, but usually on the sides above the lateral line. They may con-tain a clear amber or reddish fluid, or purulent material consisting of cells, bacteria, and granular debris. Abscesses, filled with a white or bloody turbid fluid may occur deep in the muscles. These are found most frequently in the neighborhood of the kidneys and in the ventral triangle between the pectoral fins.

Practically all the internal organs may be involved, particularly the kid-neys, serous cavities, liver, and pleen. The kidneys are most frequently af-fected, over 50 percent of the cases showing gross lesions consisting of abscesses filled with a grayish-white material. Similar abscesses may occur in other organs.

It is apparently a chronic infectious disease, but the cause has not been definitely determined. • Probably, however, the causative agent is a bacterium which is difficult to cultivate. Bacteria, isolated from the diseased tissues, proved pathogenic to trout, causing death in about 3 weeks; but in no case was the typical disease produced by inoculation with cultures.

The disease is seasonal in character, the mortality being confined to spring and early summer. It affects chiefly adult fish, and brook trout appear to be somewhat more susceptible than rainbows.

References: Belding and Merrill, 1935; Marsh and Gorham, 1905; Wil-liamson, 1927; Woodbury, 1941.


THYROID TUMOR OR GOITER

This disease, which is characterized by enlargement of the thyroid gland, was at one time believed by some investigators to be of a cancerous nature. It is now universally conceded, however, to be analogous to goiter in man and to have no relation to cancer. The belief in the cancerous nature of thyroid en-largement in trout was largely due to the peculiar structure of the gland in fishes. Unlike the thyroid of higher animals, this gland in fishes is not sur-rounded by a definite capsule. On the contrary, the cells form a branching structure, which extends into the surrounding tissues. When the gland be-comes enlarged, it has a striking superficial resemblance to a malignant growth, since it appears to invade the surrounding tissues in a similar manner.

The thyroid is a small, ductless gland that produces an internal secretion essential to the health of the animal. It is situated beneath the floor of the mouth between the first and third gill arches. Owing to its small size and the separation of its units, which are distributed among other tissues, it is not recognizable by the naked eye.

The first external indication of thyroid enlargement is a red streak or spot on the floor of the mouth near the second pair of gill arches. This red area is due to an increased blood supply to the enlarging thyroid and may appear in fish only 2 months old. This is followed by an external swelling, which may become visible as a cone-shaped, reddish tumor on the ventral side of the head just beneath the gills. Sometimes the tumor first appears on the floor of the mouth, and secondary growths frequently occur on the gills and at the anterior end of the lower jaw. The tumors do not become externally visible before the fish are at least 6 months old, and only rarely do they become noticeable before the fish are a year old. The greatest number of goiters are said to appear during the second and third years of life, probably due to the fact that the thyroid is most active in rapidly-growing fish. In older fish the activity of the thyroid decreases, and the tumor may decrease in size and dis-appear, the fish making a spontaneous recovery. Large tumors of ten become abraded, which results in infection by fungus or bacteria.

The primary cause of thyroid tumor is now generally conceded to be a deficiency of iodine, which is essential to the proper functioning of the thy-roid gland. There is also evidence that overcrowding, overfeeding, a limited water supply, and insanitary conditions in the ponds are important contribut-ing factors.

CONTROL

Since the causes of the disease are so Well understood, its control is a comparatively simple matter. Wild trout virtually never show any evidence of goiter, and hatchery fish in early stages of the disease show immediate improvement when liberated in natural waters.

Inasmuch as a deficiency of iodine is the principal. causative factor, it is essential that this condition be corrected at once. This can be done by adding small quantities of a solution of iodine to the water, but the addition of iodine directly to the food is much simpler and apparently gives equally good results. The form in which the iodine is administered appears to make little difference. At the Federal hatcheries, very good results have been ob-tained with the so-called Lugol's solution, which consists of 1 percent iodine dissolved in a 1-percent solution of potassium iodide. A tablespoonful of this solution thoroughly mixed with 50 pounds of ground food is sufficient to keep the fish from showing any trace of thyroid tumor.


When such products as shrimp meal, salmon meal, white fish meal, or kelp meal, which are rich in iodine, are fed to the fish, it is, of course, unnecessary to add iodine to the ration. Even a comparatively small percentage of these iodine-rich products will serve to protect the fish from goiter.

References: Marine and Lenhart, 1910 and 1911; Marine, 1914; Marsh, 1911; Gaylord and Marsh, 1914.

INTESTINAL INFLAMMATION

Trout in rearing pools at times suffer a heavy mortality which is appar-ently due to impairment of the digestive functions. The blood vessels of the intestine become congested, particularly at the lower end; the pyloric caeca may also be similarly inflamed; and the gut becomes filled with mucus and blood. In severe cases, patches of the intestinal lining may be entirely destroyed. The vent is usually enlarged and there is a copious discharge of mucus. Both flagellate and intracellular stages of Octomitus salmonis may be abundant, but it is not believed that this parasite is the primary cause of the disease, as many fish exhibiting these symptoms may be only slightly infected, or not at all. It is probable, however, that infection with Octomitus may frequently be an important contributing factor.

In severe cases of the disease the fish dart rapidly through the water and frequently jump out on the banks. In more chronic cases the fish refuse food; grow dark in color; and become more susceptible to attack by para-sites. In such cases they may lie quietly about the pond, gradually growing weaker, until they succumb.

The disease is evidently caused by an unsuitable diet and is probably the result of a vitamin deficiency. At present, however, there is little evidence available as to the particular vitamins involved.

FATTY DEGENERATION OF THE LIVER

This disease, called also lipoid degeneration, has been known for some time in Europe, where it has caused heavy losses, but apparently has only recently become a serious factor at American hatcheries. It affects chiefly rainbow trout, rarely brook or brown trout.

SYMPTOMS

The diseased fish are usually darker in color than normal and in advanced stages float listlessly at the surface of the water. The gills, on the other hand, are much lighter than normal and in extreme cases may have only a very light pink color. This is due to a marked anemia which is one of the most characteristic symptoms of the disease.

On dissection, the stomach and intestine are usually found to contain little, if any, food, but are filled with a pale yellow fluid. The body cavity is frequently distended with a similar fluid which may result in a noticeable exophthalmos, or protrusion of the eyeball.

The most striking feature of the disease is the appearance of the liver which typically is light yellow or yellowish gray. This coloration may be uniform over the entire organ, but not infrequently, there are scattered, dark red blotches, which give the liver a peculiarly mottled and very characteristic appearance.


PATHOLOGY

The characteristic yellow color of the liver is due to the deposition of lipoids in the liver cells, where they replace the glycogen normally stored in these cells. Lipoid is a general term applied to a number of fat-like sub-stances which differ from true fats in containing nitrogen, as well as in other respects. In severe cases, lipoids may accumulate to such an extent as to cause extensive degeneration of liver cells. Frequently, the lipoids, instead of being evenly distributed throughout the liver, are concentrated in certain areas, causing the mottled appearance. According to Gaschott, who studied the disease extensively in Germany, lipoids may be deposited also on the heart in angular masses.

The appearance of the gall bladder may vary greatly in this disease. In some cases it may be distended by a clear, colorless secretion, in others it may be shrunken and contain only a little orange-yellow liquid. Gaschott states that the disease is frequently accompanied by intestinal inflammation, since the fish eat with unimpaired appetite, but are unable to digest their food.

The pink color of the gills is due to anemia which, in advanced cases, may be so severe that very little, if any, blood flows when the blood vessels are cut. This condition may result in a sudden increase in mortality, when for any reason the oxygen content of the water falls below normal.

CAUSE OF THE DISEASE

The disease is evidently caused by malnutrition as the result of overfeed-ing or the use of unsuitable diets. A deficiency of vitamins in the diet is probably an important factor. German investigators have found that the disease is more likely to result from the use of certain foods, especially from those rich in fats, than from others. The more extensive use of vitamin-deficient dry meals with too little fresh meat in the diet may be responsible for the recent increase in the disease at American hatcheries.

Gaschott found that low temperatures are often an important factor in bringing on an outbreak of the disease, and in this country it appears to be most prevalent during cold weather. This is easily understood, since at low temperatures metabolism is slowed, and fish are unable to utilize their food as rapidly as at higher temperatures.

One of the most remarkable characteristics of lipoid degeneration is that it appears to be confined largely to rainbow trout. However, evidence is accumulating to indicate that brook and brown trout may not be as immune to this disease as was formerly believed. In these fishes the disease appar-ently occurs in a more insidious form and its presence is less easily recog-nized than in rainbow trout. It is well known that both brook and brown trout are frequently injured by improper feeding and, in some cases, at least, may show definite symptoms of lipoid degeneration.

CONTROL

In dealing with lipoid degeneration, it is important to remember that there are reasons for doubting that fish which have suffered from a severe attack of the disease ever fully recover. There is such extensive degenera-tion of the liver that it may not be possible for the organ completely to regain its normal condition. At any rate, it must require time before the organ is able to function again as it should.


Since the disease is a nutritional disorder, it is obvious that prevention and cure depend on the use of suitable foods in proper amounts. Many fish culturists overlook the fact that a considerable percentage of dry meals in the diet makes a more concentrated food and, consequently, there is more danger of overfeeding than with the diets formerly used. However, with proper care in feeding, and the use of balanced diets which have a sufficient vitamin content and are readily digested, there is no reason to believe that the use of dry foods will have any harmful effect.

On the first appearance of the disease, it is advisable to reduce drastically the amount of food fed and, if dry foods are being used, to increase the proportion of fresh meat. The composition of the diet should be carefully scrutinized to determine whether or not it is deficient in any essential element. Gaschott found that periodical changes in the diet were very helpful in con-trolling the disease. He emphasizes the fact that trout should not be fed heavily during the winter, and in times of severe cold, believes it best to stop feeding altogether. Even though this may check their growth, he con-siders it preferable to running the risk of bringing on an outbreak of the disease.

References: Hayford and Davis, 1936; Gaschott, 1929, 1931.

ACUTE CATARRHAL ENTERITIS

M'Gonigle (1940) has called attention to a disease which is the cause of serious mortalities among small fingerlings at Canadian Maritime hatcheries. According to this investigator, enteritis is an exceedingly acute intestinal disease of very young salmonid fishes, particularly brook trout, which have been feeding only about 2 to 3 weeks, although older fingerlings in the hatchery may be attacked at the same time.

SYMPTOMS

The most characteristic symptom of the disease is a very violent whirling and "corkscrewing" of affected individuals which is so violent that the fish appear to be writhing with pain. After two or three of these violent con-tortions, the fish, breathing rapidly, sink quietly to the bottom. Several convulsions may occur in rapid succession followed by the death of the fish. Sometimes the whirling may be less violent and, in cases where "pin heads" are dominant, may be scarcely noticeable. Apparently the largest and finest fingerlings become affected most acutely. No other symptoms were observed by M'Gonigle.

PATHOLOGY AND CAUSE OF DISEASE

Pathological changes are confined to the intestine. There is always a marked increase in the mucus secretion in the anterior part of the intestine and simultaneously a complete stoppage in the flow of bile. As a result, the mucus in the upper gut, instead of being stained a greenish or brownish yellow is clear and colorless. Bacteria may be more abundant than usual in the intestine, but there is no evidence that they have any causal connection with the disease.

Although no definite cause is known, all available evidence seems to indi-cate that foods and feeding are important factors. M'Gonigle believes that the disease is associated with rapid increases in temperature which occur in the spring or early summer at hatcheries which are supplied with water from


streams. Enteritis seems to be more severe in hatcheries having a late hatch followed by rapid and marked warming of the water. It is less common at spring-fed hatcheries where no such changes in water temperatures occur. The disease affects chiefly the eastern brook trout, although it has been ob-served in other species, especially the Atlantic salmon, Saltno solar.

M'Gonigle emphasizes the fact that enteritis has frequently been confused with octomitiasis, but this does not necessarily mean, as M'Gonigle seems to assume, that all mortalities among small fingerlings which have been attributed to infection with Octomitus were, in reality, due to acute enteritis. In fact, many of the hatcheries at which heavy losses from octomitiasis have been reported are spring-fed and, consequently, do not experience the rapid increases in temperature which M'Gonigle found to be ordinarily associated with the disease.

CONTROL

No satisfactory treatment or preventive is known and until more has been learned about the cause of the disease, little progress in that direction can be expected. M'Gonigle recommends that affected fish be planted in small streams where they can get natural food such as insect larvae. Since the disease is not due to infection by animal parasites or by bacteria, liberation of the fish in natural waters can do no harm.

References: M'Gonigle, 1940.

ANEMIA

Anemic trout are not uncommon under hatchery conditions. The gills be-come pale pink or even grayish-white, frequently followed by the death of the fish. The appearance of the gills is due to a great reduction in the number of red blood corpuscles, which give the blood its characteristic color.

According to Tunison and Brockway (1943), different species of trout show considerable variation in the normal number of red blood cells. They found that in healthy hatchery fish, rainbow trout showed the highest count with an average of 1,220,000 red corpuscles per cubic millimeter. Brook trout were second with an average count of 1,032,000 followed by brown trout with an average of 766,000. Lake trout gave the lowest count with an average of only 642,000 red cells per cubic millimeter. Plehn (1924) states that for normal trout the number of red corpuscles is approximately 1,500,000 per cubic millimeter.

Anemia may be due to various causes. It is characteristic, for example, of fatty degeneration of the liver, and may result from heavy infections with animal parasites. There is no doubt, however, that in many instances anemia is primarily the result of dietary deficiencies. When fed a synthetic diet containing no fresh meat, Phillips (1940a) found that the red cell content decreased rapidly and the fish began to die during the sixth week when the count was 710,000 per cubic millimeter. The mortality increased rapidly as the red-cell count continued to decrease. After the blood count reached 557,000, fresh beef liver was added to the diet at a 50 percent level and the mortality gradually decreased as the blood count rose. When the red cells reached 700,000 per cubic millimeter, the mortality ceased. It will be noted that the mortality began and stopped at practically the same red cell content, which would indicate that serious mortality may be expected when the red-cell count drops below 700,000 per cubic millimeter.


It was found that fresh beef liver was an effective cure in all cases of anemia brought on by elimination of fresh meat from the diet. Maggots of the house fly ( Musca domestica) also cured the anemia in a short time. Tunison and his coworkers (Tunison et al, 1943) conducted a series of experiments in which attempts were made to cure anemia with various vitamins of the B-complex. As a result of these experiments it was con-cluded that trout anemia is caused by a 'multiple vitamin deficiency and that a combination of riboflavin, pantothenic acid, and pyridoxine is required to restore a normal blood count. However, later experiments (Tunison et al, 1944) indicate that other factors besides these three vitamins are involved in the anemia picture of trout.

References: Bridge, 1943; Phillips, 1940a; Phillips and Tunison, 1940; Tunison et al, 1943 and 1944; Simmons and Norris, 1941; Wales and Moore, 1943.

WHITE-SPOT DISEASE

The white-spot disease occurs in both eggs and fry and is characterized by the appearance of an opaque or white area in some part of the embryo, usually the yolk. The opaque area is very noticeable in the semi-transparent yolk, so that the disease is easily recognizable even in its early stages. White-spot may occur at any stage of development up to the complete absorption of the yolk sac, but is more likely to appear during the early stages.

There is still considerable uncertainty regarding the cause of this disease, and it seems probable that it is not always due to the same agency. The characteristic white spot in the yolk is due to coagulation of the transparent yolk, causing it to become opaque. In many instances, the coagulated yolk contains one or more kinds of bacteria, but this is by no means always the case. Frequently numbers of the so-called "periblast cells" which are instru-mental in the absorption of the yolk, are present in the white spots.

The evidence points strongly toward the conclusion that white-spot is primarily caused by some injury to the eggs. Such an injury might produce coagulation of the yolk followed by increased activity of the periblast cells. If the egg membrane, or in the case of the fry, the layer of cells surrounding the yolk, is ruptured or perforated, any bacteria present may gain entrance and develop in the yolk, which, of course, is simply non-living organic ma-terial.

The fact that several kinds of bacteria may occur in the white spots and that no one kind appears to predominate is strong evidence that the disease is not due to a specific infection. - Furthermore, there is no indication that the disease is contagious, as is shown by the random distribution of diseased eggs among those that are perfectly normal.

It is well known among trout culturists that white-spot is most likely to occur in eggs that have been shipped a considerable distance or that have been handled roughly. This, of course, is in complete accord with the theory that the disease is usually the result of physical injuries. There is also evi-dence that in some cases the disease may have been the result of the chilling or freezing of the eggs.

Reference: Leach, 1924.

BLUE-SAC DISEASE

The blue-sac disease affects the fry before the yolk sac is absorbed, and usually appears within 1 or 2 days after hatching. The first symptom is an enlargement of the yolk sac which soon becomes so heavy that the fish is


unable to rise to the surface. When in this condition, the fry can no longer maintain an upright position and may be seen lying quietly on its side. In some Lases the sac bursts after a few days, but rupture of the yolk sac appears to be the exception rather than the rule.

The enlargement of the yolk sac is due to accumulation of a serous fluid in the abdominal cavity between the inner and outer walls of the yolk sac. This fluid often has a bluish tinge which has given rise to the name com-monly applied to the disease. The accumulation of fluid is frequently fol-lowed by fusion of the fat droplets of the yolk into a large, plainly visible globule. Later certain areas of the yolk become white and opaque. This condition spreads and may eventually involve the entire yolk. In many instances the affected fish continue to develop, but only the normal portion of the yolk is absorbed.

The cause of the disease is not definitely known, but has been by different authors variously ascribed to rough handling of the eggs, resulting in shocks or jars, to too much pressure during shipping, and to infection by bacteria. In support of the last-mentioned view, it has been discovered by a German investigator, L. von Betegh (1912), that the serous fluid may contain a fmre culture of a diplobacillus. In this country Guberlet, Samson, and Brown (1931) found a pure culture of a diplobacillus similar to that described by von Betegh in the serous fluid of salmon fry suffering from the disease. These investigators were able to infect salmon by placing them for 5 to 30 minutes in water to which a culture of the organism had previously been added. They report that the younger fish exhibited a higher degree of susceptibility than did the older fry. According to Atkinson (1932), treatment of trout eggs with a 1 to 2,000 solution of acriflavine for 25 minutes greatly reduced subsequent loss of fry in an epidemic of the disease caused by a similar diplobacillus.

An epidemic of sac disease at the Springville (Utah) hatchery was found by K. G. Bunnel and C. N. Feast (unpublished report) to be due to a specific infection by bacteria which were identified as Proteus hydrophilus. Experi-mental inoculations with this organism gave positive results in all cases.

On the other hand, an investigation by Frederick F. Fish (unpublished report) of an outbreak of sac disease among brook- and brown-trout fry at the Leetown (W. Va.) station yielded little evidence of a specific infection. Cultures from the serous fluid gave negative results except in a few instances. Sections of the tissues of diseased fish also failed to disclose any evidence of bacterial activity. Furthermore, there was no evidence of the spreading of the disease from one trough to another, as is usually the case with bacterial infections.

Further support of the view that blue-sac may occur in the absence of a bacterial infection is supplied by Schereschewsky (1935), who holds that the dropsical condition is simply the expression of a general sickness. It is, in fact, the result of dilation of the circulatory vessels, which causes general blood congestion. In addition to the accumulation of serous fluid in the yolk sac, this investigator finds that there are marked pathological changes in other parts of the body, especially in the liver and kidneys. The primary cause of the abnormal condition of the various organs is believed by Schereschewsky to be improper functioning of the thyroid glands. In other words, blue-sac is a symptom of a goitrous condition which may appear even in the embryo.


Constriction of the yolk sac is believed by this author to be a secondary symptom of the same pathological condition. The constriction appears at the point in the yolk sac where congested veins cause accumulation of large quantities of blood, which results in the more rapid absorption of yolk in that area.

It seems probable that the term sac or blue-sac disease has been applied to any abnormal condition of the yolk sac which involves the accumulation of serous fluid. It is not improbable that lesions of this nature may at times be due to bacterial infections, while in other cases they may be the result of improper care or handling of the eggs. There is also some evidence that the mineral content of the water may in some instances be an important factor.

References: von Betegh, 1912; Leach, 1924; Guberlet, Samson, and Brown, 1931; Atkinson, 1932; Schereschewsky, 1935; Dieterich, 1939.

SOFT-EGG DISEASE

The soft-egg disease is a peculiar condition of the eggs which has caused very heavy losses at a number of commercial hatcheries in New England. The disease, which does not appear until sometime after the eggs are spawned, is characterized by a soft and flaccid condition of the eggs. The cause of this condition is the formation of minute openings in the egg membrane, which allow the water to pass freely in either direction, thus destroying the turgidity characteristic of normal eggs. If these perforations are formed before the yolk sac has developed, more or less of the yolk may escape into the water, where it immediately hardens.

The openings in the egg membrane are produced by some external agency, which in small localized areas causes disintegration or digestion of the mem-brane. There is no doubt that the perforations are produced by some micro-scopic organism, but the identity of this organism has not been definitely determined. Three types of organisms usually are found in the infected areas —a fungus (Saprolegnia), bacteria of several species, and an ameba. There is little doubt that the primary cause of the disintegration of the egg mem-brane is either bacteria or the ameba, because the fungal filaments seem not to be present until after the perforations have been formed. The filaments then grow through the holes and spread out on the inside of the egg mem-brane. The evidence at hand seems to indicate that the ameba is the primary agent rather than the bacteria, but this evidence is by no means conclusive.

Fortunately, exact knowledge of the source or nature of the causative organism is not necessary for working out efficient methods of control. Since the cause of the trouble is undoubtedly some organism that gets on the eggs after they are removed from the fish, it is evident that rigid sterilization and antiseptic methods are the prime requisites. All pans, and other receptacles, including trays, should be thoroughly sterilized (preferably by boiling) at frequent intervals, and all troughs should be painted each season. Every precaution should be taken to avoid, as far as possible, introduction of in-fection from outside ponds, and in spawning and washing the eggs, clean spring water should always be used. At a number of hatcheries very good results have been obtained by treating the eggs for a short time with a strong salt solution. Where these methods of control have been adopted the loss from soft eggs has been reduced to a negligible quantity.


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1938. The use of chlorine for disinfecting fish ponds. Prog. Fish-Cult., no. 42, No- vember-December, 1938, pp. 24-29. U. S. Bur. of Fish.

1943. A new polymastigine flagellate, Costia pyriformis, parasitic on trout. Jour. Parasitol., vol. 29, pp. 385-386, 4 figs.

DAVIS, HERBERT SPENCER and LAZAR, ESTELLE C. 1940. A new fungus disease of trout. Trans. Am. Fish. Soc., vol. 70, pp. 264-271, 6

figs. DAVIS, HERBET SPENCER and JAMES, MILTON CARL

1924. Some experiments on the addition of vitamins to trout food. Trans. Am. Fish. Soc., vol. 54, pp. 77-85, 3 figs.

DEUTSCH, H. F. and HASLER, A. D. 1934. Distribution of a vitamin Bi destructive enzyme in fish. Proc. Soc. Expt. Biol.

Med., vol. 45, pp. 429-432. DIETERICH, ELIZABETH.

1939. Die Hydrocoele embryonalis (DotterblasenwassersuCht) der Salmoniden. Zeit. f. Fischerei, vol. 36, pp. 605-642, 15 figs.

DONALDSON, LAUREN R., and FOSTER, FREDERICK J. 1941. Bulk foods in the diet of young salmon. Prog. Fish-Cult., no. 53, January-

February 1941, pp. 23-25. U. S. Bur. of Fish. Dun', D. C. B.

1932. Furunculosis on the Pacific Coast. Trans. Am. Fish. Soc., vol. 62, pp. 249-255. Dun', D. C. B., and STEWART, BEATRICE.

1933. Studies on furunculosis of fish in British Columbia. Contrib. Can. Biol. and Fish., vol. 8, no. 8, pp. 103-122.

ELLIS, MAX MAPES. 1937. Detection and measurement of stream pollution. Bull. U. S. Bur. Fish., vol.

48 (Bull. 22, 1937) pp. 365-437, figs. 1-22 (1940). EMBODY, GEORGE CHARLES.

1924. Notes on the control of Gyrodactylus on trout. Trans. Am. Fish. Soc., vol. 54, pp. 48-50.

EMMERICH, R., and WEIBEL, E. 1894. Ueber eine durch Bakterien erzeugte Seuche unter den Forellen. Archiv f.

Hygiene, vol. 21, pp. 1-21. EVANS, GERTRUDE.

1936. The relation between vitamins and the growth and survival of goldfishes in homotypically conditioned water. Jour. Expt. Zool., vol. 74, pp. 449-476.

FANTHAM, H. B.; PORTER, ANNIE; and RICHARDSON, L. R. 1939. Some Myxosporidia found in certain freshwater fishes in Quebec Province,

Canada. Parasitology, vol. 31, pp. 1-77, 10 pls. FASTEN, NATHAN

1912. The brook-trout disease at Wild Rose and other hatcheries. Biennial Report, Comm. of Fish., Wis., 1911 and 1912, pp. 12-22, 5 figs.

1918. Trout and fish lice. Publ. Puget Sound Biol. Sta., vol. 2, 1918-20, pp. 73-76, 1 pl.

1921. Studies on parasitic copepods of the genus Salmincola. Amer. Nat., vol. 55, pp. 449-456.

1922. The tapeworm infection in Washington trout and its related biological prob-lems. Amer. Nat., vol. 56, pp. 439-447, 7 figs.

FERGUSON, M. S. and HAYFORD, ROBERT A. 1941. The life history and control of an eye fluke ; an account of a serious hatchery

disease caused by a parasitic worm. Prog. Fish-Cult., no. 54, August 1941, pp. 1-13, figs. 1-8. U. S. Bur. of Fish.

FEUSTEL, J. G. 1935. Gill disease checked. Prog. Fish-Cult., No. 6, May 1935, pp. 7-8. U. S. Bur.

of Fish. FISH, FREDERIC FORWARD.

1933. The chemical disinfection of trout ponds. Trans. Am. Fish. Soc., vol. 63, pp. 158-163, 3 figs.

1934. Ulcer disease of trout. Trans. Am. Fish. Soc., vol. 64, pp. 252-258, pls. I-IV. 1935. A western type of bacterial gill disease. Trans. Am. Fish. Soc., vol. 65, pp.

85-87, 2 pls.


1935a. The bacterial diseases of fish. Prog. Fish-Cult., no. 5, April 1935, pp. 1-9. U. S. Bur. of Fish.

1935b. The protozoan diseases of hatchery fish. Prog. Fish-Cult., May 1935, no. 6, pp. 1-4. U. S. Bur. of Fish.

1938. Simplified methods for the prolonged treatment of fish diseases. Trans. Am. Fish. Soc., vol. 68, pp. 178-187.

1939. Disease prevention in the trout hatchery. Prog. Fish-Cult., no. 43, January-February, 1939, pp. 1-6. U. S. Bur. of Fish.

1940. Formalin for external protozoan parasites. Prog. Fish-Cult., no. 48, January-February, 1940.1-10. U. S. Bur. of Fish.

1940a. Additional notes on the control of ecto-parasitic Protozoa. Prog. Fish-Cult., 49, March-April 1940, pp. 31-32. U. S. Bur. of Fish.

1940b. Notes on Costia necatrix. Trans. Am. Fish. Soc., vol. 70, pp. 441-445,2 figs. FISH, FREDERIC FORWARD and BURROWS, ROGER E.

1939. Experiments upon the control of trichodiniasis of salmonid fishes by the pro-longed recirculation of formalin solutions. Trans. Am. Fish. Soc., vol. 69, pp. 94-98.

FISH, FREDERIC FORWARD, and MCKERNAN, DONALD L. 1940. Calomel versus carbarsone. Prog. Fish-Cult., no. 51, July-Octobr, 1940, pp.

26-29. U. S. Bur. of Fish. FOSTER, FRED J. and WOODBURY, LOWELL.

1936. The use of malachite green as a fish fungicide and antiseptic. Prog. Fish-Cult., No. 18, May 1936, pp. 7-9. U. S. Bur. of Fish.

FURUNCULOSIS COMMITTEE. 1930. Interim Report March 1930. H. M. Stationery Office, Edinburgh, pp. 1-65. 1933. Second interim report. H. M. Stationery Office, Edinburgh, pp. 1-81. 1935. Final report. H. M. Stationery Office, Edinburgh, pp. 1-67.

GARNJOBST, LAURA, 1945. Cytophaga columnaris (Davis) in pure culture: a myxobacterium pathogenic

to fish. Jour. Bact., vol. 49, pp. 113-128,5 figs. GASCHOTT, OTTO.

1929. Die verlustreichen Lebererkrankungen der Forellenmastbetreibe im Fruhjahr 1929. Algemeine Fischerei Zeitung, Jg. 1929.

1931. Some diseases of trout. (Translated by F. G. Richmond.) Salmon and Trout Magazine, no. 63, pp. 171-188, no. 64, pp. 273-282.

GAYLORD, HARVY RUSSELL and MARSH, MILLARD CALEB 1914. Carcinoma of the thyroid in the salmonoid fishes. Bull. U. S. Bur. Fish., vol.

32, doc. 790, April 22,1914, pp. 363-524, pls. LVI-CX, 53 text-figs. GUBERLET, JOHN EARL.

1926. Ecto-parasitic Infusoria attacking fish of the northwest. Univ. Wash. Publ. in Fish., vol. 2, pp. 1-16,1 pl.

GUBERLET, JOHN EARL; SAMPSON, V. J.; and BROWN, W. H. 1931. A report of hydrocoele embryonalis, or yolk sac disease in salmon fry, with a

note on its cause. Trans. Am. Micro. Soc., vol. 50, pp. 164-167. GUTSELL, JAMES S.

1939. Fingerling trout feeding experiments, Leetown, 1938. Prog. Fish-Cult., no. 45, May-June 1939, pp. 32-41. U. S. Bur. of Fish.

1940. Frozen fish in hatchery diets may be dangerous, Prog. Fish-Cult., no 48, January-February, 1940, pp. 28-32. U. S. Bur. of Fish.

1940a. The feeding of trout brood stock: The diet of rainbow trout in relation to quantity, quality, and cost of eggs. Prog. Fish-Cult., no. 50, May-June 1940, pp. 19-28. U. S. Bur. of Fish.

HAGEN, WILLIAM, JR. 1940. Sterilizing hatchery water supplies: the use of liquid chlorine and powdered

derris root. Prog. Fish-Cult., no. 48, pp. 19-24. U. S. Bur. of Fish. HAYFORD, CHARLES 0.; and DAVIS, HERBERT SPENCER.

1936. The use of dry foods in the diet of rainbow trout and results of overfeeding. Prog. Fish.-Cult., no. 17, April 1936, pp. 7-10. U. S. Bur. of Fish.

HAYFORD, CHARLES 0. and EMBODY, GEORGE C. 1930. Further progress in the selective breeding of brook trout at the New Jersey

State Hatchery. Trans. Am. Fish. Soc., vol. 60, pp. 109-113.


HESS, WALTER NORTON. 1930. Control of external flukes on fish. Jour. Parasitol., vol. 16, pp. 131-136. 1937. Production of nutritional cataract in trout. Proc. Soc. Expt. Biol. and Med.,

vol. 37, pp. 306-309.

KANOUSE, BESSIE B. 1932. A physiological and morphological study of Saprolegnia parasitka. Mycologia,

vol. 24, pp. 431-452, 2 pls. KINGSBURY, 0. R. and EMBODY, GEORGE C.

1932. The prevention and control of hatchery diseases by treating the water supply. N. Y. State Conserv. Dept., pp. 1-16, 4 figs.

LAIRD, JAMES A. 1927. The use of zonite in treating gillworm. Trans. Am. Fish. Soc., vol. 57, pp.

177-179. LEACH, GLEN CLIFTON.

1924. Artificial propagation of brook trout and rainbow trout, with notes on three other species. Rpt. U. S. Comm. of Fish. for 1923, Appendix VI, doc. 955, January 24, 1924, pp. 1-74, figs. 1-22.

LINTON, EDWIN. 1891. A contribution to the life history of Dibothrium cordiceps Leidy, a parasite

infesting the trout of Yellowstone Lake. Bull. U. S. Fish Comm., vol. IX, for 1889 (1891), pp. 337-358, pls. CXVII-CXIX.

MCCAY, CLIVE MAINE. 1937. Observations on the nutrition of trout. Prog. Fish-Cult., no. 30, June 1937,

pp, 1-24. U. S. Bur. of Fish. 1940. Hatchery diets and growth: experimental studies of the growth of brook

trout. Prog. Fish-Cult., no. 49, March-April 1940, pp. 27-30. U. S. Bur. of Fish. MCCAY, CLIVE MAINE and DILLEY, W. E.

1927. Factor H in the nutrition of trout. Trans. Am. Fish. Soc. Vol. 57, pp. 250-260. MCCAY, CLIVE MAINE; and PHILLIPS, ARTHUR MORTON.

1940. Feeds for the fish hatcheries: A summary of research at the Cortland Experi-mental hatchery. Prog. Fish-Cult., no. 52, November-December 1940, pp. 18-21. U. S. Bur. of Fish.

MCKERNAN, DONALD L. 1940. A treatment for tapeworms in trout. Prog. Fish-Cult., no. 50, May-June 1940,

pp. 33-35. U. S. Bur. of Fish. MACLENNAN, RONALD F.

1935. Dedifferentiation and redifferentiation in ichthyophthirius. Arch. f. Protistenk, vol. 86, pp. 191-210, 26 figs.

MARINE, DAVID. 1914. Further observations and experiments on goiter (so-called thyroid carcinoma)

in brook trout (Salvelinus fontinalis). III. Its prevention and cure. Jour., Expt. Med., vol. 19 (1914) ; pp. 70-88, 1 text fig., pls. 13-17.

MARINE, DAVID and LENHART, C. H. 1910. Observations and experiments on the so-called thyroid carcinoma of brook

trout (Salvelinus fontinalis) and its relations to ordinary goiter. Jour. Expt. Med., vol. 12 (1910), pp. 311-337, 3 text figs., pls. XXV-XXVI. (Also published as Penn-sylvania Dept. of Fish., Bull. no. 7).

1911. Further observations and experiments on the so-called thyroid carcinoma of the brook trout (Salvelinus fontinalis) and its relation to endemic goiter. Ibid., vol. 13 (1911), pp. 455-475, 1 text fig., pls. LX-LXI.

MARSH, MILLARD CALEB. 1903. A more complete description of Bacterium truttae. Bull. U. S. Fish Comm.,

vol. XXII, September 11, 1903, pp. 411-415, pls. I-II. 1911. Thyroid tumor in salmonoids. Trans., Amer. Fish. Soc. vol. 40, 1911, pp.

377-391, 1 pl. MARSH, MILLARD CALEB; and 'GORHAM, F. P.

1905. The gas disease in fishes. Report, U. S. Bur. of Fish., for 1904, Aug. 28, 1905, pp. 343-376, pls. I-III.

MELLEN, IDA. 1928. The treatment of fish diseases. Zoopathglogica, vol. 21, pp. 1-31.


MErrAm, A. E. 1915. Report on the outbreak of furunculosis in the River Liffey in 1913. Scientific

Investigations, Dept. of Agr. and Tech. Instruction, Ireland, 1914, II (1915), 19 pp. 3p1s. Dublin.

M'GONIGLE, R. H. 1940. Acute catarrhal enteritis of salmonid fingerlings. Trans. Am. Fish Soc. vol. 70,

pp. 297-303. MOORE, EMMELINE

1923. Diseases of fish in state hatcheries. Twelfth Annual Report, N. Y. Conserv. Comm., 1922 (1923), pp. 66-79, 2 pls.

1923a. A report of progress on the study of trout diseases. Trans. Am. Fish. Soc., vol 53, pp. 74-81, 2 figs.

1924. Diseases of fish. Fourteenth Annual Report, N. Y. Conserv. Comm. 1924 (1925), pp. 83-97, 12 figs.

MRSIC, WILHELM 1933. Die Gasblasenkrankheit der Fische. Zeit. f. Fischerei, vol. 31, pp. 29-65.

MUELLER, JUSTUS F. 1932. Trichodina renicola (Mueller, 1931), a ciliate parasite of the urinary tract of

Esox niger. Roosevelt Wildlife Annals, vol. 5, no. 2c, pp. 139-154, 2 pls. 1936. Studies of North American Gyrodactyloidea. Trans. Am. Micro. Soc., vol. 55,

pp. 55-72, 4 pls. 1937. Some species of Trichodina from freshwater fishes. Trans. Am. Micr. Soc.,

vol. 56, pp. 177-184, 1 pl. MURPHY, GARTH

1942. Relationship of the freshwater mussel to trout in the Truckee River. Calif. Fish and Game, vol. 28, pp. 89-102, 5 figs.

NELSON, E. CLIFFORD 1941. Carbarsone treatments for Octomitus. Prog. Fish-Cult., no. 55, November

1941, pp. 1-4. U. S. Bur. of Fish.

O'DONNELL, D. 1941. A new method of combating fungus. Prog. Fish-Cult., no. 56, December

1941, pp. 18-30. U. S. Bur. of Fish.

PALMER, EDDY D. 1939. Diplostomiasis, a hatchery disease of fresh-water fishes new to North America.

Prog. Fish-Cult., no. 45, May-June 1939, pp. 41-47. U. S. Bur. of Fish. PHILLIPS, ARTHUR MORTON, JR.

1940. Feeding carbohydrates. A study of the digestion and absorption of carbo-hydrates by brook trout. Prog. Fish-Cult., no. 51, July-October 1940, pp. 16-23. U. S. Bur. of Fish.

1940a. Meatless diets and anemia: The development of anemia in trout fed a syn-thetic diet and its cure by the feeding of fresh beef liver. Prog. Fish-Cult., no. 48, January-February 1940, pp. 11-13. U. S. Bur. of Fish.

, PHILLIPS, ARTHUR MORTON, JR.; TUNISON, A. V.; et al. 1940. The nutrition of trout. Cortland Hatchery Rpt. No. 8 for the year 1940,

33 pp, N. Y. State Conserv. Dept. PLEHN, MARIANNE

1924. Praktikum der Fischkrankheiten. 179 pp., XXI col. pls., 173 text figs. E. Schweizerbart'sche Verlagsbuchhandlung, Stuttgart. [Note: This is the most com-plete work published on the diseases of fish.]

PRYTHERCH, HERBERT FRANCIS 1924. The ichthyophthirius disease of fishes and methods of control. Rpt. U. S.

Comm. Fish for 1923, Appendix IX, doc. 959, April 21, 1924, pp. 1-6; figs. 1-10.

RICHARDSON, LAURENCE R. 1936. Observations on the parasites of the speckled trout in Lake Edward, Quebec.

Trans. Am. Fish. Soc., vol. 66, pp. 343-356, 11 figs. 1937. Observations on trichodinid infection (cyclochaetosis) of SalveUnits fontinalis

Mitchell. Trans. Am. Fish. Soc., vol. 67, pp. 228-231. 1941. The parasites of the fishes of Lake Wakonichi, Central Northern Quebec. Trans.

Am. Fish. Soc., vol. 71, pp. 286-289.


SAVAGE, JAMES 1935. Copepod infection of speckled trout. Trans. Am. Fish. Soc., vol. 65, pp. 334-339. 1935a. Notes on costiasis. Trans. Am. Fish. Soc., vol. 65, pp. 332-333.

SCHERESCHEWSKY, HELENE 1935. Die Kinderkrankheiten dergSahnoniden (Dotterblasenwassersucht und Dotter-

blaseneinschnurung). Zeit. f. Fischerei, vol. 33, pp. 474-501. SCHNEBERGER, EDWARD

1941. Fishery research in Wisconsin. Prog. Fish-Cult. No. 56, December 1941, pp. 14-17. U. S. Bur. of Fish.

SHAFFER, ELMER 1916. Discoctyle salmonis nov. spec. em n neuer Trematode an den Kiemen der Regen bogenforelle (Salmo irideus). Zool. Anz. vol. 46, pp. 257-271, 10 figs.

SHILLINGTON, K. G. 1934. Selective breeding of speckled trout. Trans. Am. Fish. Soc., vol. 64, pp. 274-275.

SIMMONS, R. W. and NORRIS, E. R. 1941. Xanthopterin, the fish anemic factor. Jour. Biol. Chem., vol. 140, p. 679.

SMITH, RICHARD T. and QUISTORFF, ELMER 1940. Calomel in the diet of hatchery salmon. Prog. Fish-Cult., no. 51, July-October

1940, pp. 24-26. U. S. Bur. of Fish. SURBER, EUGENE WICKER

1936. Circular rearing pools for trout and bass. Prog. Fish-Cult., no. 21, August 1936, pp. 1-14, figs. 1-12. U. S. Bur. of Fish.

TIFFNEY, WESLEY R. 1939. The identity of certain species of Saprolegniaceae parasitic to fish. Jour. Elisha

Mitchell Sci. Soc., vol. 55, pp. 134-165, 3 pls. TUNISON, A. V.; PHILLIPS, ARTHUR MORTON, JR., et. al.

1939. The nutrition of trout. Cortland Hatchery Report No. 8, for the year 1939, 33 pp., N. Y. State Conserv. Dept.

TUNISON, A. V.; BROCKWAY, D. R.; DORR, A. L.; and McKAv, C. M. 1943. The nutrition of trout. Cortland Hatchery Rpt. No. 11. Fish. Res. Bull. no. 4.

N. Y. State Conserv. Dept., Albany, N. Y. TUNISON, A. V.; BROCKWAY, D. R.; SHAFFER; H. B.; and MAXWELL, J. M.

1943. The nutrition of trout, Cortland Hatchery Rpt. No. 12, Fish. Res. Bull. no. 5. N. Y. State Conserv. Dept., Albany, N. Y.

VON BETEGH, L. 1912. Hydrocoele embryonalis. Centralblatt f. Bakteriologie, Parasitenkunide und

Infectionskrankheiten, erste Abteilung, vol. 66, Originale, pp. 284-286, 1 pl. (Eng-lish translation by Anne L. Massey in Scientific Investigations, 1913, no. III, Dept. of Agr. and Tech. Instruction, Ireland, Fish. Branch, 4 pp., 1 pl.)

WALES, JOSEPH H., and EVINS, DONALD 1937. Sestonosis, a gill irritation in trout. Calif. Fish and Game, vol. 23, No. 1.

January. 1937, pp. 144-146. WALES, JOSEPH H., and MOORE, MYRON

1938. Progress Report of trout feeding experiments, 1937. Calif. Fish and Game, vol. 24, no. 2, April, 1938, pp. 126-132.

WARD, HENRY BALDWIN, and MUELLER, JUSTITS F. 1926. A new pop-eye disease of trout fry. Archiv. fur Schiff s- und Tropen-Hygiene,

Pathologie und Therapie Exotischer Krankheiten, vol. 30, pp. 602-609, 4 figs. WILLIAMSON, ISOBEL J. F.

1928. Furunculosis of the Sahnonidae. Fishery Board for Scotland, Salmon Fish-eries, 1928, no. V, pp. 1-17, pls. I—II.

1929. Further observations on furunculosis of the Salmonidae. Fishery Board for Scotland, Salmon Fisheries, 1929, no. 1, pp. 1-12.

WILLIAMSON, JANE 1927. Bacteriological investigation of the cause of bulging eye in certain marine food

fishes. 46 pp., 12 figs., Aberdeen Press and Journal Office. WOLF, Louis EDWARD

1935. The use of potassium permanganate in the control of fish parasites. Trans. Am. Fish. Soc., vol. 65, pp. 88-100.


1936. An air bladder disease in lake trout fingerlings. Trans. Am. Fish. Soc., vol. 66, pp. 359-363.

1936a. Blood clots in the gills of trout. Trans. Am. Fish. Soc., vol. 66, pp. 369-371. 1938 Observations on ulcer disease of trout. Trans. Am. Fish. Soc., vol. 68, pp.

136-151. 1938a. Ichthyophthiriasis in a trout hatchery. Prog. Fish-Cult., no. 42, November-

December, 1938, pp. 1-17. 1940. The value of disinfection in ulcer disease: sterilizing ponds with chlorine pre-

vents recurrence. Prog. Fish-Cult., no. 49, March-April, 1940, pp. 35-36. U. S. Bur. of Fish.

1940a. Further observations on the ulcer disease of trout. Trans. Am. Fish. Soc., vol. 70, pp. 369-381.

1942. Fish-diet disease of trout. A vitamin deficiency produced by diets containing raw fish. Fish. Res. Bull., no. 2, N. Y. State Cpnserv. Dept., pp. 1-16.

1944. Annual Report Bureau of Fish Culture. N. Y. State Conserv. Dept., 33rd Ann. Rept., pp. 111-112.

WOODBURY, LOWELL A. 1941. A sudden mortality of fishes accompanying a super-saturation of oxygen in

Lake Waubesha, Wis. Trans. Am. Fish. Soc., vol. 71, pp. 112-117, 1 fig. 1942. Vitamin B1 deficiency in hatchery reared rainbow trout. Trans. Am. Fish. Soc.,

vol. 72, pp. 30-34. WRIGHT, ALICE

1936. A report of four years' experience with fin rot and some remarks on octomitiasis. Prog. Fish-Cult., no. 24, November 1936, pp. 1-26. U. S. Bur. of Fish.

S. GOVERNMENT PRINTING OFFICE: 1947

care and diseases of trout - Native Fish Lab of Marsh & Associates

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