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Infectious Diseases of the Dog and Cat, 3rd Edition
CHAPTER 81 Enteric Coccidiosis
J.P. Dubey
Craig E. Greene
Coccidia are obligate intracellular parasites normally found in the intestinal tract. They belong to the phylum
Apicomplexa, class Sporozoasida, order Eucoccidiorida, and depending on the species, familyEimeriidae,
Cryptosporidiidae, or Sarcocystidae. Coccidian genera that infect cats and dogs areIsospora(also called
Cystoisospora),Hammondia, Besnoitia, Sarcocystis, Toxoplasma, andNeosporaspecies (see Chapter 80), as well as
Cryptosporidiumand Cyclosporaspecies (see Chapter 82).5Caryosporainfections are also discussed in this chapter.
Another coccidian genus,Eimeria, found commonly in herbivores, birds, lagomorphs, and rodents, is found only in
feces of dogs and cats after they ingest intestinal contents or feces from these animals. The oocysts pass unchanged
through the feline or canine intestine. Some coccidians of dogs remain unclassified.
Intestinal coccidia discussed in this chapter are host specific. Infections of definitive or intermediate hosts generallyonly occur in cycles established by evolution. Some aberrant cycles exist, such as with Sarcocystis neurona
infections in horses. Human health risks from these parasites are considered minimal to nonexistent, even in
immunosuppressed humans.
INTESTINAL COCCIDIOSIS
All coccidians have an asexual and a sexual cycle. In some genera, such as Sarcocystis, the asexual and sexual
cycles occur in different hosts, whereas inIsosporaboth cycles may occur in the same host (Table 81-1and Fig.
81-1). The oocyst is the environmentally resistant stage in the life cycle of all coccidia and is excreted in feces of
the definitive host.
A representative coccidian life cycle is best described as follows. Oocysts are passed unsporulated in feces and
contain a single nucleated mass called a sporont, which almost fills the oocyst (Fig. 81-2). After exposure to warm(20 C to 37C [68 F to 98.6 F]) environmental temperatures and moisture, oocysts sporulate, forming two
sporocysts. Within each sporocyst are four sporozoites (Fig. 81-3). The sporozoites have a banana shape and are
the infective stage (Fig. 81-4). They can survive environmental exposure, protected inside the oocysts for many
months. After the ingestion of sporulated oocysts by cats or dogs, sporozoites excyst in the intestinal lumen, and
the sporozoites initiate the formation of schizonts or meronts. During schizogony or merogony, the sporozoite
nucleus divides into two, three, or more nuclei, depending on the parasite and the stage of the cycle. After nuclear
division, each nucleus is surrounded by cytoplasm, forming a merozoite. The number of merozoites within a
schizont varies from two to several hundred, depending on the stage of the cycle and the species of coccidia.
Merozoites are released from the schizont when the host cell ruptures. The number of schizogonic cycles varies
with the parasitic species. First-generation merozoites repeat the asexual cycle and form second-generation
schizonts or transform into microgamonts (males) and macrogamonts (females). The microgamont divides into
many tiny microgametes. A microgamete fertilizes a macrogamete, and an oocyst wall is formed around the
zygote. The life cycle is completed when unsporulated oocysts are excreted in feces.
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IsosporaSpecies
Members of the genusIsospora, the most commonly recognized coccidians infecting dogs or cats, are species
specific for the definitive host. At least four speciesIsospora canis,Isospora ohioensis, Isospora burrowsi,
andIsospora neorivoltainfect dogs, and two speciesIsospora felisandIsospora rivoltainfect cats.
Epidemiology
The life cycle ofIsosporainfecting dogs and cats is similar to the basic coccidian intestinal cycle, except an
asexual cycle can also occur in the definitive or intermediate host. On ingestion by definitive or suitable
paratenic (intermediate) hosts, oocysts excyst in the presence of bile, and free sporozoites invade the
intestine. Some sporozoites penetrate the intestinal wall and enter mesenteric lymph nodes or other
extraintestinal tissues, where they form enlarging unicellular cysts (Fig. 81-5). If no replication occurs, the
host is called aparatenic hostrather than an intermediate host. Monozoic cysts ofIsosporamay remain in
extraintestinal tissues of definitive and paratenic hosts for the life of the host. In dogs and cats, these cysts
may serve as a source of intestinal reinfection and relapse of enteric coccidiosis. Ingestion of monozoic cystsin paratenic hosts leads to intestinal infection in the definitive dog and cat host. The life cycle after the
ingestion of paratenic host is the same as after the ingestion of sporulated oocysts from feces.
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Fig 81-1 Life cycle of I. felis, which is typical of the Isosporaspp. The mode of
transmission may be direct, via ingestion of sporulated oocysts from
the environment, or indirect via ingestion of cysts in prey animals. A,Either sporulated oocysts or monozoic tissue cysts are ingested. B,
These excyst in the intestine. C, They undergo asexual
(endodyogeny) and (D)sexual (merogony and gametogony)
reproduction with the formation of a zygote. E, The zygote becomes
an (F)unsporulated oocyst that is shed in the stool (G). This matures
into the infectious sporulated oocyst which can be ingested by the
definitive or intermediate host. H, In the intermediate host, the
excysted sporozoites migrate to tissues and form cysts. (Courtesy
University of Georgia, Athens, Ga.)
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Table 81-1 Comparison of Selected Coccidial Genera That Infect Dogs and
Cats
GENUS DIRECT
TRANSMISSION
POSSIBLE?
SEXUAL CYCLE: INTESTINAL
REPLICATION
ASEXUAL CYCLE: EXTRAINTESTINAL
REPLICATION
DEFINITIVE
HOST
FORM OF
OOCYST PASSED
INTERMEDIATE OR
PARATENIC HOSTS
LOCATION OF TISSUE
CYSTS
Isospora Yes Dog and cat U Dog, cat, many other
mammals
Extraintestinal or
lymphoid tissues
(monozoic)
Besnoitia No Cat U Many vertebrates Fibroblasts
Hammondia No Dog and cat U Herbivores, rodents Skeletal muscle
Sarcocystis No Dog and cat Sa Many vertebrates Cardiac and skeletal
muscle
Cryptosporidium Yes Dog and cat Sb None None
Toxoplasma Yes Cat U Many vertebrates Many tissues
U,Unsporulated;S,sporulated.
a Free sporocysts.
b Naked sporozoites.
Fig 81-2 Unsporulated oocysts of Isospora canis (C), Isospora ohioensis (O),
and Hammondia heydorni (H)and sporulated sporocyst of
Sarcocystisspecies (S)from canine feces (unstained, 1700). (From
Dubey JP. 1976. A review ofSarcocystisof domestic animals and of
other coccidia of cats and dogs, J Am Vet Med Assoc169:1061-1078.)
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Clinical Findings
Diarrhea with coccidiosis in immunocompetent animals probably represents incidental or concurrent
infections with coccidia and other infectious agents because coccidial infection can be present in the absence
of clinical illness. Enzootic infections are frequently found in catteries or kennels where animals congregate.
Clinical signs are most apparent in neonates. Experimental studies have shown that clinical signs of intestinal
disease are uncommon unless large numbers of oocysts are fed to very young (younger than 1 month) or
immunosuppressed animals. Clinically, severe diarrhea has been associated with naturally occurring
coccidiosis in immunosuppressed dogs and cats. German shepherd dogs may have an increased susceptibility
to clinical infection.27,41
Diarrhea with weight loss and dehydration and, although rare, hemorrhage is the
primary sign attributed to coccidiosis in dogs and cats. Anorexia, vomiting, mental depression, and
ultimately death may be seen in severely affected animals. Severely immunosuppressed dogs and cats may
have extraintestinal stages in macrophages of the lymphocyte-depleted mesenteric lymph nodes or
extraintestinal tissues.
Fig 81-3 Sporulated oocysts of I. canis (C), I. ohioensis (O), and H. heydorni (H)
(unstained, 1700). Compare with Fig. 81-2. (From Dubey JP. 1976. A
review ofSarcocystisof domestic animals and of other coccidia of
cats and dogs,J Am Vet Med Assoc169:1061-1078.)
Intestinal coccidiosis may be manifest clinically when dogs or cats are shipped or weaned or experience a
change in ownership. Diarrhea might result from the extraintestinal stages ofIsosporareturning to theintestines. Monozoic cysts do not cause clinical disease in paratenic hosts.
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Fig 81-4 I. canissporulated oocyst treated with 5.25% sodium hypochlorite
solution to dissolve part of oocyst wall (OW). Two sporocysts occupy
most of oocyst. Each sporocyst has a thin sporocyst wall (SW), fourbanana-shape sporozoites (S), and a sporocystic residual body (SR).
SR may be compact or dispersed (unstained, 1600). (From
Kirkpatrick CE, Dubey JP. 1987. Enteric coccidial infections. Isapora,
Sarcocystis, Cryptosporidium, Besnoitia, and Hammondia, Vet Clin
North Am Small Anim Pract 17:1405-1420.)
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Fig 81-5 Tissue cyst of I. ohioensisin smear of mesenteric lymph node of an
experimentally infected mouse. The sporozoite (S)is surrounded by
a thick cyst wall (CW). Vacuole around cyst wall is fixation artifact(PAS stain, 1250).
Diagnosis
Intestinal coccidial infection in dogs and cats is diagnosed by identification of the oocysts with any of the
fecal flotation methods commonly used to diagnose parasitic infections (see Fecal Examination, Chapter 70).
Shedding of oocysts by some animals may be erratic, therefore repeated examinations are recommended. In
dogs, onlyI. caniscan be identified with certainty by oocyst size and shape (see Fig. 81-2). The two species
ofIsosporafound in cats can be readily distinguished by oocyst size (see Fig. 80-9). Oocysts ofI. felisin
cats andI. canisin dogs are large and easily distinguished from small oocysts, whereas it is almost
impossible to distinguishI. rivolta, I. burrowsi, andI. ohioensismorphologically (Fig. 81-6; see also Fig.
80-9). AlthoughI. felis-, I. rivolta-, I. canis-, andI. ohioensis-like oocysts are passed unsporulated in freshly
excreted feces, they sporulate partially by the time a fecal examination is made. Partially sporulated oocysts
contain two sporocysts without sporozoites.Isosporaspp. may sporulate within 8 hours of excretion, and
theseIsosporaare highly infectious.
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Fig 81-6 Unsporulated oocysts of I. ohioensis (O)and H. heydorni (H)
compared with eggs of nematodes Toxocara canis (C)and
Ancylostoma caninum (A)in flotation of canine feces (unstained,385). (From Dubey JP. 1976. A review ofSarcocystisof domestic
animals and of other coccidia of cats and dogs,J Am Vet Med Assoc
169:1061-1078.)
Therapy
The presence of underlying disease or host immunosuppression should be suspected when coccidial
infections persist for extended periods in older animals or when associated with chronic diarrhea. Treatment
is often indicated in bitches and their newborn puppies because of the severity of clinical signs at this age. If
diarrhea or dehydration is severe, parenteral fluid therapy must be considered as a supportive measure. Blood
transfusion may be required when severe intestinal hemorrhage results in anemia.
Specific therapy involves the use of drugs that are coccidiostatic rather than curative (Table 81-2). However,
as with many protozoal diseases, the presence of low-level infection may lead to premunition. The drugs
shorten the prepatent period and may shorten the course of the disease.
Sulfonamides have long been the drugs of choice for the treatment of coccidiosis. Rapid-acting
sulfonamides, such as sulfadimethoxine or sulfaguanidine, can be given alone or in combination with otherantifolate drugs such as trimethoprim. Trimethoprim-sulfonamide offers the advantages of being readily
available and being less toxic than other drugs. It should be considered a drug of first choice. Nitrofurazone
can be administered alone or in combination with sulfonamides. Nitrofurazone is also available as a 4.59%
soluble powder that can be added to drinking water (up to 1 g/2 L) for 7 days.
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Amprolium is considered an effective preventive and treatment for coccidiosis in kenneled puppies.
Although it is not currently approved for use in dogs, it can be administered as an undiluted liquid and a
paste, but it is unpalatable in these forms (see Drug Formulary, Appendix 8).
Table 81-2 Anticoccidial Drugs for Dogs and Cats
DRUGa SPECIES DOSE (mg/kg)
b ROUTE INTERVAL
(HOURS)
DURATION
(DAYS)
Sulfamethoxinec B 5060 PO 24 520
Sulfaguanidine B 100200 PO 8 5
Trimethoprim- D 3060d PO, SC 24 5
sulfonamide B 1530e PO, SC 1224 5
Ormetoprim-sulfadimethoxineD 66f PO 24 723
Furazolidoneg B 820 PO 1224 5
Amprolium D 300400 (total)h PO 24 5
D110200 (total)
i PO 24 712
C 60100 (total) PO 24 7
Quinacrine B 10 PO 24 5
Spiramycin H 50100 (total)j PO 24 5
Toltrazuril D 15 PO 24 36k
Ponazuril B 7.515l PO 24 28
Roxithromycin H 2.5 PO 12 15
B,Dog and cat; D,dog; C,cat; H,human; PO,by mouth;SC,subcutaneous.
a See Appendix 8, Drug Formulary, for additional information.
b Dose per administration at specified interval.
c Other sulfonamides, such as sulfadimidine and sulfaguanadine, can be used, but sulfaquinoxaline
should not be used because it interferes with ditamin K synthesis and may result in hemorrhagic
complications.
d Greater than 4kg body weight.
e Less than 4kg body weight.
f 11 mg ormetoprim and 55 mg of sulfadimethoxine.
g When furazolidone is combined with sulfonamides, 50% of this dose is used.
h Total dose per day. Lower dose recommended for puppies, with a maximum of 300 mg total per
day (see Drug Formulary,Appendix 8).
i Total dose per day. Combine 150 mg amprolium and 25 mg sulfadimethoxine per kilogram per
day for 14 days (see Drug Formulary, Appendix 8).
j Total dose per day. Dose on a mg/kg basis is listed in Drug Formulary,Appendix 8.
k Doses of 30 mg/kg have been used for 1 day; however treatment at half that dose for at least 3
days with repeating if needed, has been more effective in treatment of pups and kittens with
coccidiosis without relapses.
l Dose extrapolated from use in horses and mice for treatment of Sarcocystis neuronainfections.
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Quinacrine, spiramycin, toltrazuril, tetracycline, and roxithromycin have been used on a limited basis to treat
canine and feline coccidiosis.4Their use might be considered if more established treatment regimens fail or
protozoal resistance develops.
Prevention
Coccidiosis tends to be a problem in unsanitary environments. The fecal shedding of large numbers of
environmentally resistant oocysts makes infection likely under such conditions. Animals should be housed in
a way that does not allow contamination of food and water bowls by oocyst-laden soil or infected feces.
Feces should be removed daily and incinerated. Oocysts survive freezing temperatures. Runs, cages, food
utensils, and other implements should be disinfected by steam cleaning or immersion in boiling water or by a
10% ammonia solution. Animals should have limited access to intermediate hosts and should not be fed
uncooked meat. Insect control is essential in animal quarters and food storage areas because cockroaches and
flies may serve as mechanical vectors of oocysts. Coccidiostatic drugs can be given to infected bitches before
or soon after whelping to control the spread of infection to puppies.
HammondiaSpecies
Two species ofHammondiaexist in domestic animals:Hammondia hammondi, with cats as definitive hosts,
andHammondia heydorni, with dogs and other canids as definitive hosts.5,25
UnlikeIsosporaspecies,H.
hammondiandH. heydornihave obligatory two-host life cycles (see Chapter 80and Table 81-1). Goats and
rodents are natural intermediate hosts forH. hammondi, and the domestic cat (Felis catus)and the European
wild cat (Felis sylvestris)are the definitive hosts.H. hammondidoes not invade extraintestinal tissues of the
cat, and cats are infected only by eating tissue cysts. Experimentally, many warm-blooded animals, including
monkeys, sheep, goats, pigs, rabbits, guinea pigs, and mice, can serve as intermediate hosts. Intermediate hosts
become infected by ingesting sporulated oocysts, which resemble those of T. gondii. Sporozoites excyst in the
intestinal lumen, invade the intestinal wall, and multiply as tachyzoites in the intestines, mesenteric lymph
nodes, and other tissues. The parasite eventually encysts principally in muscles (Fig. 81-7).
H. heydorni'slife cycle is not fully known but seems to be similar to that ofH. hammondi. Dogs and other
canids are definitive hosts, and cattle, sheep, goats, buffaloes, camels, moose, and deer serve as intermediate
hosts.14,26a
The structure of the parasite in the intermediate hosts is not known.H. hammondiandH. heydorni
are nonpathogenic, therefore no treatment is necessary.
BesnoitiaSpecies
Cats, not dogs, are definitive hosts for three species ofBesnoitia:Besnoitia wallaceiof rats and mice,Besnoitia
darlingiof opossums and possibly lizards, andBesnoitia oryctofelisiof rabbits.18,26
The life cycle ofBesnoitiais similar to that of T. gondii(see Table 81-1). Cats become infected by ingesting
tissue cysts, and schizonts (Fig. 81-8) and gamonts are formed in intestinal goblet cells or lamina propria.
Schizonts may be found in extraintestinal organs.26
Unsporulated oocysts are shed in feces, and they are
difficult to distinguish from those of T. gondii. Intermediate hosts become infected by ingesting sporulated
oocysts. The parasite develops in connective tissue, and cysts may become macroscopic.Besnoitiais
considered nonpathogenic in cats, and no treatment is necessary.
779
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Fig 81-7 H. hammonditissue cyst in skeletal muscle of mouse. Note thin cyst
wall enclosing hundreds of periodic acidSchiff-positive bradyzoites
(PAS stain, 750).
Fig 81-8 B. oryctofelisischizonts in the lamina propria of jejunum of an
experimentally infected cat (H and E stain, 750).
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IntestinalSarcocystisSpecies
Infections resulting from Sarcocystisspp. are ubiquitous in reptiles, birds, and warm-blooded animals.
5
Virtually all cattle and sheep are infected with this parasite. More than 90 species of Sarcocystishave been
identified, and they have an obligatory two-host life cycle (see Table 81-1). Carnivores (predators) are
definitive hosts, and herbivores (prey) are intermediate hosts. As the name implies, the parasite forms tissue
cysts (sarcocysts) in muscles and neural tissues of these intermediate hosts (Fig. 81-9). Sarcocysts are thin or
thick walled, and the zoites are usually separated from each other by septa. Cats and dogs become infected by
ingesting sarcocysts. The life cycle of Sarcocystisis distinct from other coccidians of domestic animals in that
oocysts sporulate within the definitive host and are excreted in the feces in an infective form (Fig. 81-10). The
intermediate hosts become infected by ingesting sporocysts or oocysts. One to three generations of schizogony
occur in blood vessels or hepatocytes (depending on the species of intermediate hosts). Merozoites then invade
skeletal muscles and nerve cells, where they form sarcocysts (see Figs. 81-10and 81-11). Certain species of
Sarcocystis, transmissible via dogs, are pathogenic in cattle, sheep, goats, pigs, and mule deer, whereas species
transmissible via cats are generally nonpathogenic.
Fig 81-9 Esophageal muscle with thick-walled sarcocyst ofSarcocystis hirsute(H
and E stain, 630). (From Gardiner CH, Fayer R, Dubey JP. 1988.An
atlas of protozoan parasites in animal tissues, Beltsville, Md, USDA
Agricultural Handbook No 651.)
More than 20 species of Sarcocystisinfect cats and dogs. It is not possible to differentiate species on the basis
of measurement of sporocysts. Sarcocystisis excreted in feces fully sporulated, often as free sporocysts when
examined microscopically (Fig. 81-12). They are small and not very dense, so they lie at a different plane of
focus than other parasites.
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Sarcocystisspecies are not pathogenic for the intestinal tract of dogs or cats, so no treatment is necessary.
Infections can be prevented by cooking all meat fed to animals. Occasionally, sarcocysts are found in skeletal
muscles of immunosuppressed or wild cats and dogs, but their life cycle is unknown.8,12
ExtraintestinalSarcocystisspp.
Sarcocystis canis Infection
One of the extraintestinal Sarcocystis-like parasites (S. canis)has been found in Rottweiler dogs in the
United States.0a,21-23,48a
Only asexual stages (schizonts) were seen in various cells, including neurons,
hepatocytes, and dermal cells (Figs. 81-13and 81-14). Affected dogs ranged from 2 days old to adult dogs
and had neurologic and hepatic signs and dermatitis. Schizonts were 5 to 25 4 to 20 m and contained 6 to
40 merozoites. Occasionally, merozoites were arranged around a residual body. The parasite was named S.
canisbecause it differed from other species of Sarcocystis. Its life cycle is unknown. An unidentified
Sarcocystissp. caused granulomatous myositis in a dog.2a
FelineSarcocystis Infection
Sarcocysts have been identified in the skeletal and cardiac muscles of 11 free-ranging Florida panthers and
cougars,30
3 domestic cats32
and in hind-limb muscle biopsy specimens of 2 domestic cats.28
The sarcocysts
found in these studies were not specifically identified, and the immune status of the host may have been
compromised. Some of these infections might have been caused by Sarcocystis neurona, which is discussed
in the following section.
780
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Fig 81-10 Life cycle ofS. cruzi, which is typical ofSarcocystisspp. A, Muscle
cyst is ingested by definitive carnivore host. B, These excyst in the
small intestine and penetrate epithelial cells. C, Gametes develop inthe intestinal epithelium and these (D)fuse to form a zygote which
matures into an unsporulated and then a sporulated oocyst. E,
Sporulated oocysts are shed in the feces. F, Oocysts, ingested by
herbivores, excyst in the small intestine to release sporozoites. G,
These penetrate the epithelium and migrate in the blood
vasculature where they replicate in two phases of schizogony. H, In
the final stages, mature schizonts rupture releasing merozoites
which enter the muscles to form sarcocysts which contain many
organisms. (Courtesy University of Georgia, Athens, Ga.)
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Sarcocystis neurona Infection
S. neuronais the principal parasite associated with equine protozoal encephalomyelitis, although a species of
Neosporahas also been incriminated (see Chapter 80). Opossums (Didelphis virginiana)are the definitive
hosts for S. neurona(Fig. 81-15). Animals that ingest oocysts from opossums and serve as intermediate hosts
by developing muscle sarcocysts are the nine-banded armadillo (Dasypus novemcinctus), striped skunk
(Mephitis mephitis), raccoon (Procyon lotor), sea otter (Enhydra lutris), and brown-headed cowbird
(Molothrus ater).19,36
Experimentally and naturally, cats have been shown to be intermediate hosts of S.
neurona, although results have varied with individual isolates.1,19,49
Cats experimentally fed sporocysts shed
by opossums develop schizonts in their tissues and sarcocysts in their muscles, and infected cats develop
high antibody titers (1:4000) as measured by a serum agglutination test.17
Opossums were shown to shed S.
neuronasporocysts after ingesting feline tissues containing sarcocysts.16
Horses are considered incidental or
aberrant dead-end hosts because they only develop lesions within the central nervous system, and muscle
sarcocysts have not been documented. This organism can cause fatal encephalomyelitis in dogs, raccoons,
mink, and cats.
Fig 81-13 S. canisschizonts in section of dermal ulcer from dog. Note
distended macrophages (arrows)with parasites in inflammatory
exudate, mainly neutrophils (H and E stain, 750).
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Fig 81-14 An intactS. canisschizont (arrow)and several merozoites
(arrowheads)released from ruptured schizont in smear of exudate
from dermal ulcer of dog (Giemsa stain, 750).
Sarcocystis-associated meningoencephalomyelitis was described in a 13-week-old Burmese kitten with
lethargy, depression and crying, and progressive upper motor neuron hemiparesis.13
Another 12-week-old
kitten developed progressive neurologic dysfunction 3 days after a routine castration.6Encephalomyelitis
was associated with numerous S. neuronaschizonts and merozoites in the brain and spinal cord. S. neurona
infection was also documented in a 13-year-old captive Canadian lynx (Felis lynx Canadensis).29
Serum
antibodies to S. neuronawere detected in 13% of 310 farm cats from Ohio48
and in 5% of 196 domestic cats
from Michigan whose sera were submitted for T. gondiiantibody testing.43
Diagnosis in horses has involved
immunoblot testing for specific antibodies to S. neuronain cerebrospinal fluid not contaminated with blood.
Use of feline antibody conjugates would be needed to apply this method for use in cats. Treatment of
affected cats has not been attempted because diagnosis of clinically affected cats was made after death.
Effective treatment of horses has involved the use of ponazuril. (See Table 81-2and Drug Formulary,
Appendix 8, for dosage information that has been extrapolated from dosages used to treat horses and mice.)
Other anticoccidial drugs such as clindamycin, tetracyclines, or antifolate inhibitors might also be considered.
782
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Fig 81-15 Life cycle ofS. neurona. Opossums (Didelphis virginiana, D.
albiventris) are its definitive hosts. They ingest organisms from the
tissues of intermediate hosts. A, These excyst in the small intestineand enter the gut epithelium. B, Gametogony occurs followed by
fertilization producing a zygote which eventual forms an oocyst. C,
Sporulated oocysts shed in the feces are ingested by natural
intermediate hosts such as cats, armadillos, raccoons, sea otters,
skunks and possibly other mammals. D, Ingested sporocysts excyst
in the small intestine and (E)replicate to a limited extent within the
vascular endothelium and leukocytes within viscera and then
spread, probably by leukocytes, to other tissues. F, There,
sarcocysts, composed of bradyzoites, develop in the muscle and
neural tissues. Equids are considered aberrant intermediate hosts asdevelopment does not occur beyond schizont and merozoite
stages. (Courtesy University of Georgia, Athens, Ga.)
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Fig 81-16 Section from skin of dog with Caryosporadermatitis. Note
numerous Caryosporastages in dermal cells, including gamonts and
schizonts (H and E stain, 750; bar = 10 m). (From Dubey JP, BlackSS, Sangster LT, et al. 1990a. Caryospora-associated dermatitis in
dogs, Parasitol76:552-556.)
VISCERAL AND CUTANEOUS CARYOSPOROSIS
A Caryospora bigeneticalike organism was isolated from cutaneous nodules in five dogs ranging in age from 2
to 6 months. The dogs were thought to be concurrently affected with a distemper virus-like infection.7The skin
nodules were up to 2 cm in diameter, and some had a central ulcerated area through which serohemorrhagic
exudate could be expressed. Microscopically, the dermatitis was characterized by edema and infiltrations by
polymorphonuclear cells, eosinophils, and macrophages (Fig. 81-16). Schizonts, male and female gamonts,
unsporulated and sporulated oocysts, and caryocysts were seen in macrophages. In one dog, infection had spread
to the lymph nodes.
Members of the genus Caryosporahave an oocyst with one sporocyst that contains eight sporozoites, and they
typically parasitize reptiles and raptors. At least two species, C. bigeneticaand Caryospora simplex, parasitize
rodents and snakes. Caryosporaspp. have a complicated life cycle involving asexual and sexual multiplication in
the prey (rodent) and the predator (snake). In addition to usual schizonts and gamonts, sporulated oocysts and
monozoic cysts (caryocysts) are formed in connective tissue cells of the prey. The caryocysts (unlike sporocysts
and oocysts) have a thin cyst wall enclosing the host cell nucleus. Two unusual features of Caryosporastages are
noted in histologic sections of dog tissue: (1) the small size (less than 15 m) of all developmental stages and (2)
the presence of gamonts, schizonts, and oocysts in a single macrophage.
81.2
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Fig 81-17 Mesenteric artery with multinucleated first-generation meront ofS.
hirsute(synonymS. bovifelis) protruding into lumen (H and E stain,
630). (From Gardiner CH, Fayer R, Dubey JP. 1988.An atlas ofprotozoan parasites in animal tissues, Beltsville, Md, USDA Agricultural
Handbook No 651.)
INTRAHEPATIC BILIARY COCCIDIOSIS IN DOGS
Intrahepatic biliary coccidiosis is a rare condition in dogs.34
Clinical signs associated with hepatic disease include
icterus, weight loss, and vomiting. Small and large bile ducts are enlarged because of inflammation and
desquamation of epithelial cells. Lesions may extend into hepatic parenchyma. Asexual stages (schizonts) of an
unidentified coccidium are found in biliary epithelial cells (Fig. 81-17). These coccida are different from
Toxoplasma, Sarcocystis,Hammondia, and Cryptosporidiumspecies and any other known coccidium found in the
dog.
INTRAPULMONARY COCCIDIOSIS IN DOGS
An adult dog with clinical signs of weakness, fever, diarrhea, dehydration, weight loss, and harsh lung sounds was
found to have canine distemper complicated by pulmonary infection with coccidia-like organisms.38
Asexual
stages of coccidia were observed in cytoplasmic vacuoles of many bronchiolar epithelial cells.
Suggested Readings*
* See the CD-ROM for a complete list of references.
1. Butcher, M, Lakritz, J, Halaney, A, et al.: Experimental inoculation of domestic cats (Felis domesticus)
with Sarcocystis neuronaor S. neurona-like merozoites. Vet Parasitol. 107, 2002, 1142.
81.3
81.4
81.5
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4. Daugschies, A, Mundt, HC, Letkova, V: Toltrazuril treatment of cystoisosporosis in dogs under
experimental and field conditions.Parasitol Res. 86, 2000, 797799.
6. Dubey, JP, Benson, J, Larson, MA: Clinical Sarcocystis neuronaencephalomyelitis in a domestic cat
following routine surgery. Vet Parasitol. 112, 2003, 261267.
Uncited references
45. Schares, G, Heydorn, AO, Cppers, A, et al.:Hammondia heydorni-like oocysts shed by a naturally
infected dog andNeospora caninumNC-1 cannot be distinguished.Parasitol Res. 87, 2001, 808816.
81.6
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