Medical/Veterinary Parasitology Exam 2

double check Anki deck/lecture slides. for some of them go back in and add the common name. patent/prepatent/clinical incubation

What animals, and where in the animal, do Trichostrongyles and Strongyles live?

They are gastrointestinal parasites, living in ruminants and horses (ruminants = cows, sheep, goats)

Trichostrongyles species

Ostertagia spp. → cattle
Haemonchus spp. → sheep & goats
Trichostrongylus spp. → cattle, sheep & goats
Cooperia spp. → cattle
Nematodirus spp. → sheep & goats

What organ are each of the Trichostrongyles species found in?

• Ostertagia spp → abomasum

• Haemonchus spp → abomasum

• Trichostrongylus spp → abomasum and small intestine

• Cooperia spp → small intestine

• Nematodirus spp → small intestine

(the abomasum is the fourth and final stomach compartment in ruminant animals like cows, sheep, and goats)

Life Cycle of Trichostrongyles

• Adult worms live in the animal's GI tract and produce eggs.

• The eggs leave the animal in the feces.

• Outside the animal, the eggs hatch and develop into L1, then L2, in the feces/soil.

• They then become L3, which is the infective stage. L3 move onto pasture vegetation.

• A cow, sheep, or goat eats the L3 while grazing.

• The L3 penetrate the GI mucosa and develop into L4.

• The L4 then come back out into the GI lumen and develop into adult worms.

• The adults produce eggs, which are passed in feces, and the cycle repeats.

  • This is a DIRECT life cycle

What is hypobiosis (arrested development)?

A temporary cessation of nematode development at a specific stage in its life cycle. The larva remains dormant until conditions become favorable.

What can cause a nematode to come out of hypobiosis?

Favorable environmental conditions, such as improved weather, or host-related cues such as improved nutrition can signal the arrested larva to resume development and mature.

What is premunition (concomitant immunity)?

An existing adult parasite infection gives the host resistance to establishment of a new or superinfection by additional parasites.

What is self-cure?

Sudden expulsion of established parasites after the host ingests a large number of infective L3 larvae.

What is spring rise?

A sudden increase in parasite egg output in sheep during the spring.

What is periparturient rise?

A sudden increase in parasite egg output in lambing ewes (adult female sheep) around parturition (giving birth).

What are the general clinical signs of trichostrongyle infection?

Diarrhea, emaciation (extreme, unhealthy thinness and physical weakness), and poor haircoat or wool production.

What normally happens on the arterial side of a capillary?

Hydrostatic pressure is greater than colloid pressure, so water and small dissolved substances such as oxygen and glucose are pushed out of the bloodstream into the tissues.

What is hydrostatic pressure?

The pressure of blood pushing outward against the capillary wall, which tends to force fluid out of the bloodstream.

Artery vs vein

Arteries carry blood away from the heart

Veins carry blood toward the heart

What normally happens on the venous side of a capillary?

Colloid pressure becomes greater than hydrostatic pressure, so water is drawn from the interstitial space back into the bloodstream.

What is colloid pressure?

The osmotic pulling force created mainly by blood proteins, especially albumin, that draws water into capillaries.

What is hypoalbuminemia?

An abnormally low level of albumin in the blood.

Why is albumin important for fluid balance?

Albumin helps create colloid pressure, which keeps water inside the bloodstream and helps pull fluid back into capillaries.

Why can hypoalbuminemia cause edema or bottle jaw?

If albumin is too low, colloid pressure decreases, so less water is pulled back into the bloodstream and more fluid remains in the tissues, causing edema.

Why is this physiology relevant to trichostrongyle disease?

Some trichostrongyles cause blood or protein loss. This can lower albumin, reduce colloid pressure, and cause edema such as bottle jaw.

Why this colloid pressure stuff matters

Parasite causes protein loss → albumin drops → colloid pressure drops → fluid stays in tissues → edema/bottle jaw.

What is Ostertagia ostertagi?

A trichostrongyle parasite of cattle that infects the abomasum and causes ostertagiasis.

What is the normal pH of the abomasum?

About 2

What do chief cells produce?

Pepsinogen

What do parietal cells produce?

Hydrochloric acid

What happens to pepsinogen in the normal abomasum?

Hydrochloric acid helps convert pepsinogen into pepsin.

What does pepsin do?

Pepsin digests dietary proteins.

Why does Ostertagia damage normal abomasal function?

The larvae develop in the gastric glands and damage the cells responsible for normal acid and digestive-enzyme function.

What happens to abomasal acidity in ostertagiasis?

Acidity decreases and the pH can rise from about 2 toward 7.

What happens to pepsinogen production/function in ostertagiasis?

Pepsinogen production and normal activation are disrupted, reducing protein digestion.

What happens to the bacteriostatic effect of the abomasum in ostertagiasis?

It is reduced because the abomasum becomes less acidic.

What happens to abomasal mucosal permeability in ostertagiasis?

It increases because the damaged mucosa becomes more permeable.

What leaks where because of increased permeability in ostertagiasis?

Serum albumin leaks into the abomasum, while pepsinogen leaks into the circulation.

Why does albumin leak into the abomasum in ostertagiasis?

Damage to the mucosa and loss of normal barrier integrity allow plasma proteins to escape into the stomach.

What is “Morocco leather” in ostertagiasis?

The characteristic rough, raised, nodular appearance of the abomasal mucosa caused by coalescing lesions.

What is Type I ostertagiasis?

The “summer” form in which larvae do not undergo hypobiosis; it occurs mainly in young cattle during their first year on pasture.

What is Type II ostertagiasis?

The “winter” form in which larvae have undergone hypobiosis and later resume development; it is seen in cattle during their second year on pasture.

What are the major clinical signs of ostertagiasis?

Chronic abomasitis, profuse watery diarrhea, hypoalbuminemia, submaxillary edema, malnutrition, and failure to thrive.

Why can ostertagiasis cause submaxillary edema?

Loss of serum albumin lowers blood oncotic pressure, allowing fluid to accumulate in tissues under the jaw.

What can severe ostertagiasis lead to?

Extreme malnutrition, failure to thrive, and potentially death.

What is Haemonchus contortus, and what animals does it primarily affect?

Haemonchus contortus is an abomasal trichostrongyle and voracious blood-feeding parasite that is especially important in sheep and goats.

What disease and clinical signs are caused by Haemonchus contortus?

Blood feeding causes multifocal hemorrhagic abomasitis, leading to anemia and hypoproteinemia. The protein loss can cause submandibular edema ("bottle jaw").

Why can Haemonchus contortus cause clinical disease before the infection becomes patent?

L4 larvae already feed on blood, so significant blood and protein loss can occur before adult worms begin producing detectable eggs.

Why are adult Haemonchus contortus called "barber-pole worms"?

Adult females have a characteristic red-and-white spiraled appearance resembling a barber pole.

What are the two major groups of horse strongyles?

Horse strongyles are divided into large strongyles and small strongyles (cyathostomes).

What species are considered the major large strongyles of horses?

Strongylus vulgaris

Strongylus equinus

Strongylus edentatus

What are the small strongyles of horses called?

Cyathostomes (cyathostomins)

Why have large strongyles historically been more troublesome?

Their larvae migrate through host tissues, including the walls of blood vessels rather than simply staying in the intestinal lumen. This migration can cause severe vascular damage, including inflammation and aneurysms.

What is characteristic of large strongyle morphology and feeding?

Large strongyles have large buccal cavities and are plug feeders, meaning they use the mouth to take in pieces of intestinal lining.

What is the life cycle of Strongylus vulgaris?

L1 hatch in feces/soil → develop into L2 → infective L3 are ingested → larvae develop and migrate from the large intestine into arteries as L4, causing inflammation → eventually mature into L5/adult worms.

What is the infective stage of Strongylus vulgaris?

L3, which is ingested from the environment.

What disease does Strongylus vulgaris cause?

Larval migration causes inflammation and aneurysms of the cranial mesenteric artery and its branches. This can lead to colic, intestinal necrosis, and sometimes cerebrospinal nematodiasis.

What is cerebrospinal nematodiasis in Strongylus vulgaris infection?

Aberrant larvae migrate into the central nervous system, causing neurologic disease.

What disease does Strongylus edentatus cause?

Larval migration causes hepatic damage with fibrosis and can cause peritonitis. Infection is usually subclinical unless parasite burdens are heavy.

parasite larvae traveling through the liver cause tissue damage, scarring, and dangerous belly inflammation, though mild infections usually show no symptoms.

What disease does Strongylus equinus cause?

Larval migration through the liver causes hepatic damage and hepatitis.

Why did benzimidazole use become a problem in horse strongyle control?

Repeated use of benzimidazole drugs helped control large strongyles, but heavy repeated use selected for drug resistance, especially in small strongyles (cyathostomes).

How do small strongyles feed, and what general effects can heavy intestinal infection cause?

Small strongyles feed superficially rather than as plug feeders. Heavy infections can interfere with digestion and nutrient uptake, leading to poor weight gain, poor body condition, and poor coat quality.

Why are small strongyles an important cause of diarrhea in horses?

Diarrhea can occur when large numbers of hypobiotic larvae emerge from the intestinal mucosa at the same time, causing sudden mucosal damage and inflammation.

What happens during hypobiosis and emergence of small strongyles?

Larvae can arrest development in the intestinal mucosa during unfavorable conditions, then later resume development and emerge. Mass emergence can severely disrupt intestinal digestion and fluid absorption.

What intestinal lesions can small strongyles cause?

Granulomatous colitis with numerous nodules, eosinophilic inflammation, edema, and interference with digestion.

What is the main goal of controlling trichostrongyles and strongyles?

Reduce pasture contamination with parasite eggs and infective L3 larvae.

How are trichostrongyles and strongyles controlled?

Use strategic deworming together with sanitation and pasture management, including feces removal, composting manure to kill eggs/L3, avoiding overgrazing, and providing safe pasture for mares and foals.

What is Enterobius vermicularis and who does it infect?

Enterobius vermicularis is the human pinworm. It has a direct, one-host life cycle and infects humans, not dogs or cats.

Where do adult pinworms live, and what does the female do at night?

Adults mainly live in the large intestine. At night, the female migrates out through the anus and deposits sticky eggs around the perianal folds.

How quickly do Enterobius eggs become infective?

About 6 hours after being deposited around the anus.

Why are Enterobius eggs usually not found on routine fecal exams?

The female deposits eggs on the perianal skin rather than releasing most of them directly into feces. The slides therefore emphasize the Scotch-tape preparation for diagnosis.

How does scratching promote pinworm transmission and reinfection?

Perianal eggs cause itching, so scratching contaminates the fingers and nails. Eggs can then be swallowed again by the same person or spread onto food, toys, bedding, and other surfaces.

Why can pinworm spread easily through a household or daycare?

Infective eggs contaminate hands, bedding, clothes, carpets, toys, food, and other shared surfaces, allowing rapid person-to-person transmission.

What is retroanal or retrograde infection in Enterobius?

Eggs hatch on the perianal skin and larvae migrate back through the anus into the intestinal tract.

Can Enterobius occur outside its usual intestinal location?

Yes. Although adults usually remain in the large intestine, ectopic worms can occasionally be found in places such as the appendix or female reproductive tract.

Are all pinworm infections symptomatic?

No. Many infected people are asymptomatic, although perianal itching is the classic sign.

What is the geographic distribution of Enterobius vermicularis?

Worldwide

What are common environmental sources of pinworm eggs?

Bedding, clothes, carpets, toys, and other contaminated household or shared surfaces.

Why can pinworm eggs be described as “airborne”?

The eggs are extremely light and can become suspended in dust or blown through the air when contaminated bedding or clothing is disturbed.

Is Enterobius vermicularis zoonotic?

No. Human E. vermicularis is not acquired from dogs or cats; other animals have their own pinworm species.

What animals are commonly infected by Physaloptera spp., and where are the worms found?

Dogs, cats, primates, mustelids, opossums, raccoons, skunks, and occasionally swine. The worms are embedded in the stomach mucosa.

What is the morphology of Physaloptera spp.?

Large, about 4–6 cm, white to pinkish worms with a cephalic collarette around the anterior end.

the head or front end of the organism has a ring or collar-like fold of protective skin.

How does Physaloptera(stomach worm) cause gastric bleeding?

The worm attaches to the stomach wall with its anterior structures; repeated attachment and detachment damages the mucosa and can produce bleeding.

What is melena, and why can Physaloptera cause it?

Melena is black, tarry stool caused by digested blood from higher in the GI tract. Gastric bleeding from Physaloptera can therefore produce melena.

What clinical disease can Physaloptera cause?

Multifocal hemorrhagic gastritis, enteritis, catarrhal gastritis, vomiting, anorexia, weight loss, anemia, and melena.

stomach and intestines are inflamed and bleeding, causing a total loss of appetite, throwing up, weight loss, weakness from a low blood cell count, and dark, tarry stools.

What type of life cycle does Physaloptera have?

An indirect life cycle involving an intermediate host and often a paratenic host.

What are the typical intermediate and paratenic hosts for Physaloptera?

Intermediate hosts are usually insects or other arthropods; paratenic hosts are animals that eat those arthropods, such as rodents or birds.

Can Physaloptera worms be seen in vomit?

Yes. In some infected animals, adult worms may be vomited.

What animals are commonly infected by Spirocerca lupi, and where are the worms found?

Canids and wild felids. The worms are associated with the esophagus and stomach.

What is the morphology of Spirocerca lupi?

Large red worms, about 3–7 cm long, with six rudimentary lips and a thick-walled, well-developed buccal capsule.

What type of life cycle does Spirocerca lupi have?

An indirect life cycle involving an intermediate host and potentially a paratenic host.

How do adult Spirocerca lupi worms cause disease?

Adults form nodules in the esophageal wall, which can interfere with passage through the esophagus and contribute to vomiting or regurgitation.

How do migrating Spirocerca lupi larvae cause disease?

Larvae cause tissue damage during migration before reaching the esophagus and forming adult-containing nodules.

What are the two main sources of clinical disease in Spirocerca lupi infection?

Adult worms in esophageal nodules and tissue damage caused by migrating larvae.

What is the basic life cycle and migration route of Spirocerca lupi in dogs?

A dog ingests an infected beetle or paratenic host containing L3 larvae. L3 penetrate the gastric mucosa, migrate within the walls of gastric arteries and the descending aorta, then move to the esophagus where adults form nodules.

How does larval migration of Spirocerca lupi cause disease?

Migration through arterial walls damages tissue and can cause vascular thickening/stenosis, inflammation, aneurysm formation, and potentially rupture.

Where do adult Spirocerca lupi ultimately form nodules?

In the esophageal wall, typically in the thoracic esophagus above the diaphragm.

What are the main Gnathostoma species and their definitive hosts?

G. spinigerum → cats, dogs, mustelids;

G. hispidum → pigs.

Adults form cystic nodules in the stomach wall.

What is the morphology of Gnathostoma spp.?

Stout, pink worms about 1–5 cm long with a characteristic anterior spinous head bulb covered in small hooks.

How does Gnathostoma attach to tissues?

Its anterior head bulb has rows of small hooks that help anchor the worm to host tissues.

What is an important clinical sign of Gnathostoma infection in definitive hosts?

Vomiting, associated with gastric irritation and cystic nodules in the stomach wall.

What happens when humans are infected with Gnathostoma?

Humans do not develop the normal adult gastric infection. Instead, immature larvae migrate through tissues, causing extraintestinal larva migrans.

What forms of larva migrans can human gnathostomiasis cause?

CLM = cutaneous larva migrans; OLM = ocular larva migrans; NLM = neural larva migrans; VLM = visceral larva migrans.

Why can human gnathostomiasis affect many different organs?

Humans are abnormal hosts, so the larvae continue migrating rather than developing normally in the stomach and can travel through skin, viscera, eyes, or nervous tissue.

What is the basic Gnathostoma life cycle?

Unembryonated eggs enter water → L1 hatch → copepod ingests L1 → larva develops to L2 → fish/frog or similar host eats copepod → develops to infective L3 → definitive host eats infected host → adult worms develop in gastric nodules.