Phylum Ashelminthes:SubPhylum Nematoda

Class: Rhabditea

Subclass: Rhabditia

(Phasmidea, Secernentea)

Order: Ascaridida

Super Family: Ascaridorea

Family: Ascarididae

Ascaris lumbricoidesCommon Name: Large intestinal roundworm

Disease: Ascariasis Morphology:

Creamy white or pinkish yellow when freshly expelled

Elongated, cylindroidal, tapering bluntly anteriorly

Provided with pair of lateral line Genital ring

Adult male: smaller, curved posteriorly with 2 spicules > 30 cm X 3 mm

Adult female: large, tapered posteriorly > 20 – 25 cm X 5 mm (*45 cm)

Female and male Ascaris lumbricoides

Morphology: (cont.) In both sexes the mouth is surrounded by one dorsal and 2 ventrolateral lipsThe female is prodigious in egg production, depositing about 200,000 – 240,000 eggs daily!Uterus may contain up to 27 million eggs at one time!!!1 Ascaris female produces approx. 65 – 75 M eggs during its life span of about 12 months.

The “tri-lipped/ trilobed” anterior end of Ascaris lumbricoides.

Ascaris lumbricoides

Fertilized ova Ovoidal with thick

transparent shell Golden brown in color; 45

– 75 X 35 – 45 um Egg shell consist of 3

layers: 1. Vitelline membrane 2. Glycogen membrane 3. Albuminous layer

The outer, albuminous coat of the egg is brown in color due to bile pigment absorbed from the feces

Ascaris lumbricoides

Unfertilized ova88 – 94 um by 39 – 44 umLarger, narrower & more

elongated than the fertilized ova

Shell is thinner w/ an irregular coating of albumin

Inside the eggs are highly refractile granules

First 2 layers are absentSometimes eggs may be

decorticated

Question:

Is it possible that only unfertilized Ascaris ova are seen in the stool?

Explain.

Ascaris lumbricoides(large intestinal roundworm) Largest nematode

adult males ( 200-300 mm)

• If no male present in small intestine, female will lay bizarre shaped unfertilized eggs

• No intermediate host

A large mass of Ascaris lumbricoides that was passed from the intestinal tract.

Typical fertilized ova

Ascaris lumbricoides

developing embryo

lips and face

Ascaris

Life Cycle

Life Cycle• After being ingested, infective eggs hatch in the duodenum• Larvae actively burrow into the mucosal lining, enter the circulatory system, and are carried to the liver, through the right side of the heart, and on to the lungs by way of pulmonary arterial flow•Larvae remain in the lungs several days, but eventually rupture from the pulmonary capillaries and enter the alveoliFrom here they move up the lungs and trachea to the epiglottis, are coughed up, swallowed, and passed into the small intestine After molting the worms grow to sexual maturity

Life Cycle • Adult worms live in the lumen of the small intestine and get nourishment from semidigested food in the host• Copulation occurs here and eggs are passed with the feces•The zygote does not begin development until the egg has reached the soil•Eggs are fairly resistant to desiccation and low temperatures•With proper temperatures and oxygen levels the embryo molts at least once in the shell and develops to an infective larva•Eggs can remain viable in the soil for 2 years

Epidemiology

• Distribution of A. lumbricoides is worldwide, but it is prevalent in warmer climates• It depends upon poor sanitation for its proliferation• It is most prevalent in children:

• they are exposed to contaminated soil, • do not wash before eating, •put hands in mouth, etc.

Pathogenesis & Symptomatology2 Types:1. Produced by migrating larva2. Produced by the adult worms

• Most cases of ascariasis are asymptomatic• The most frequent symptom is upper abdominal discomfort• Little damage results from larval penetration of the host’s mucosa• However, aberrant larvae migrating in such organs as the spleen,

liver, lymph nodes, and brain usually result in an inflammatory response

• Also, larvae escaping from capillaries in the lungs and entering the respiratory system cause small, hemorrhagic foci accompanied by coughing, fever, and difficulty in breathing

Pathogenesis & Symptomatology, cont.

2. Due to adult worms:

Worms sometimes cause mechanical blockage of the intestinal tract

Also, worms may penetrate the intestinal wall or appendix causing local hemorrhaging

Overcrowding may also lead to wandering; worms can enter the appendix and cause blockage; worms have been known to migrate all the way to the anus

Some worms migrate anteriorly and have been known to block pancreatic and bile ducts; others have gotten into the stomach and some even as far as the esophagus and tracheae

Diagnosis Finding the characteristic ova in the stool

of a patient: DFSKato Thick Smear TechniqueKato Katz Technique – quantitative method

Treatment

2 ways:1. Mass treatment2. Selective treatment

DOC: Mebendazole Pyrantel pamoate

Toxocara canis

• Found in the small intestine of dogs and other canines• Causes visceral larval migrans among humans (an accidental host); most common among children• It usually results from the ingestion of eggs and the subsequent migration of second stage larvae within the internal organs • The second stage larvae hatching from the eggs penetrate the intestinal wall and quickly invade the liver• Although a majority of these larvae remain in the liver, some pass on to the lungs and, sometimes, the CNS and eyes• Although most of the larvae eventually gravitate to a single location and become encapsulated by host tissues, for a period of time they actively migrate through the tissues, leaving long trails of inflammatory reaction cells

Visceral Larval Migrans Case Study

• A previously healthy 37-year-old black man had fever, abdominal cramping, vomiting, and diarrhea. After 1 week of symptoms, a chest radiograph showed multiple noncavitating pulmonary nodules• On further questioning, the patient stated that he had acquired a puppy 1 month before onset of the abdominal pain. The puppy was being house-trained, and the patient had had no previous household exposure to dogs. Subsequently, tests for serum antibodies against • T canis IgG and IgM were obtained and were positive at 11.5 and 9.3 standard deviations above the mean of a reference group of normal subjects. The Toxocara IgM titer indicated acute infection with T canis.

A chest radiograph showing multiple noncavitating pulmonary nodules