Parasites of the Liver

By | 2011-11-06

Trematodes

FASCIOLA HEPATICA

• Worldwide distribution in ruminants, pigs, and horses; occasionally in humans; distribution in North America centers on the Gulf Coast/southeastern states, Pacific Northwest (including Montana), and eastern Canada; highly significant to veterinary medicine; low significance to public health.

• Common name: liver fluke.

Life Cycle

• Indirect.

• Intermediate host: lymnaeid snails; require neutral, poorly drained soil.

• Eggs are passed with bile to intestine and out with the feces; miracidia develop in 10-12 days; require water to hatch; penetrate snail, undergo asexual development and produce cercariae in 1-2 months; one miracidium into a snail equals several hundred cercariae out of snail; leave and attach to vegetation where encyst becoming metacercariae; cercariae may also overwinter in snail.

• Definitive host acquires infection by ingesting metacercariae on vegetation; fluke penetrates the small intestine to abdominal cavity, migrates to and penetrates liver in 4 — 6 days; migrates throughout liver for 4 — 7 weeks and then enters bile ducts and matures.

• Prepatent period is 8-12 weeks; may live for several years.

• In temperate regions, carrier animals important in contaminating pastures in the spring; metacercariae appear during late summer into fall.

• In mild regions, infected snails may overwinter; metacercariae may appear during spring to early summer; spring occurrence depends on moisture and snail activity the preceding fall; carrier animals also important in maintaining pasture contamination.

Pathogenesis and Clinical Signs

• Migration of immature flukes causes traumatic hepatitis and hemorrhage; anemia may result; migratory tracts eventually heal by fibrosis.

• Adults ingest blood and may also cause anemia; presence of adults causes extensive proliferation of the bile duct epithelium, cholangitis, and necrosis of the ductal wall; fibrosis of the lamina propria of the bile duct occurs that may eventually calcify.

• Clinical disease occurs in four forms:

1. Acute — caused by short-term intake of massive numbers of metacercariae that invade the liver all at once; clinical signs include inappetence, weight loss, abdominal pain, anemia, ascites, depression, sudden death; course is only a few days; occurs primarily in sheep and goats.

2. Subacute — also caused by intake of massive numbers of metacercariae, but over a longer period of time; clinical signs include inappetence, decreased weight gain or weight loss, progressive hemorrhagic anemia, liver failure, and death; course is 4 — 8 weeks.

3. Chronic — caused by intake of moderate numbers of metacercariae over an extended period of time; clinical signs include decreased feed intake and weight gain, reduced milk yield, anemia, emaciation, submandibular edema, ascites; cattle tend to exhibit chronic disease.

4. Subclinical — caused by intake of low numbers of metacercariae over a long period of time; moderate cholangitis occurs without apparent clinical signs.

Diagnosis

ANTEMORTEM

• May find eggs on fecal sedimentation during chronic and subclinical infections, possibly subacute infections also.

• Eggs are oval, operculate, yellow, 130-150 x 65-90 um.

POSTMORTEM

• Mature flukes may be found within the bile ducts; flukes are leaf-shaped, greenish-brown, 2-4 x 1-1.5 cm; with conical anterior end and shoulders.

• Immature flukes (up to 7 mm in length) may be difficult to find within the liver parenchyma; requires sequential slicing of the liver and expressing flukes from cut surfaces.

Treatment and Control

• See Table 4-3 for treatment of cattle; albendazole at 7.5 mg per kg in sheep and 15 mg per kg in goats has been used.

• Strategic use of anthelmintics is cornerstone of control programs; purpose is to remove parasites before animal productivity is affected and to prevent egg shedding that subsequentiy contaminates pastures; the timing, frequency, and choice of anthelmintic vary based on the transmission patterns in each geographic region.

• Grazing management should avoid high-risk areas during periods of transmission; may need to fence off areas of snail habitat; control of snails themselves through draining of habitat or use of molluscicides is impractical in most cases.

FASCIOLOIDES MACNA

• Distributed in North America, central Europe, Mexico, and South Africa; cervids are the usual definitive hosts; catde, sheep, and goats may be accidentally infected; low to moderate significance.

• Common name: large American liver fluke.

Life Cycle

• Indirect.

• Intermediate host: freshwater lymnaeid snails.

• In cervid definitive host, life cycle is essentially as for F. hepatica.

• Prepatent period is approximately 8 months.

• Patency is generally not achieved in catde or sheep (see Pathogenesis and Clinical Signs).

Pathogenesis and Clinical Signs

• Cervids: infections are inapparent; flukes are encapsulated by a thin-walled cyst with channels to the bile ducts; eggs leave the cysts via these channels.

• Cattle: infections tend to be inapparent; flukes reach the liver and are encapsulated in cysts that usually do not communicate with the bile ducts; eggs generally are not passed out of cysts.

• Sheep, goats: flukes tend to migrate continuously within the liver as well as to ectopic sites such as the lungs; traumatic hepatitis results, which is fatal before flukes mature.

Diagnosis

ANTEMORTEM

• May find eggs on fecal sedimentation of deer feces; eggs are oval, operculate, yellow, 110-160 x ~ 75 um.

POSTMORTEM

• Mature flukes may be found in cysts in liver of cervids and cattle or within the liver parenchyma or other organs of sheep and goats; flukes are leaf-shaped with no demarcated anterior cone, thick, up to 10 cm in length by 2.5 cm in width.

Treatment and Control

• Clorsulon at 20 mg per kg in both sheep and cattle has been used.

• Prevention is best achieved by not grazing sheep in endemic areas; avoid grazing cattle in high-risk areas during transmission.

DICROCOELIUM DENDRITICUM

• Worldwide distribution, except Australia, in cattle, sheep, and goats; sporadic occurrence, moderate significance.

Life Cycle

• Indirect.

• First intermediate host: terrestrial snails.

• Second intermediate host: ants.

• Embryonated eggs are passed with the feces and ingested by snails; cercariae develop in 3-4 months, are shed by the snail, and clump together in slime-balls; ants eat slime-balls and metacercariae form in 26-62 days; most develop in the hemocoel, but some lodge in the subesophageal ganglion; this causes tetanic spasms of the mouthparts as temperatures decrease, which locks the ant onto herbage overnight; ants are then available to grazing animals the following morning.

• Definitive host acquires infection by ingesting ant containing metacercariae; flukes enter the liver by migrating up the bile ducts from the small intestine.

• Prepatent period is 47-54 days; may live for 6 years or longer.

Pathogenesis and Clinical Signs

• Pathologic changes increase in severity as infection increases in age; advanced infections can cause hepatic cirrhosis and proliferation of bile duct epithelium.

• Clinical signs in young animals are usually not present; in sheep, may cause anemia, edema, decreased wool production, and lactation.

Diagnosis

ANTEMORTEM

• Eggs may be found on fecal sedimentation.

• Eggs are brown, operculated, oval, 36-46 x 10-20 um, containing miracidia; operculum may be difficult to see.

POSTMORTEM

• The flukes are flattened, leaf-like, 6-10 x 1.5-2.5 mm; found in bile ducts; because of their small size, they may be missed at necropsy.

Treatment and Control

• Generally do not treat domestic animals for infection; if heavy infections are present, can use albendazole at 15-20 mg per kg once or 7.5 mg per kg once and repeated 2-3 weeks later; fenbendazole at 100-150 mg per kg has also been used.

PLATYNOSOMUM FASTOSUM

• Distributed in southern North America through Central and South America, West Africa, Malaysia, and Pacific Islands in cats; usually low significance except in highly endemic areas.

Life Cycle

• Indirect.

• First intermediate host: terrestrial snails.

• Second intermediate host: sowbugs, woodlice, lizards.

• Paratenic host: lizards, frogs.

• Embryonated eggs are passed with the feces and ingested by snails; sporocysts containing cercariae are shed by snail and ingested by second intermediate host in which metacercariae form.

• Cats acquire infection by ingesting infected lizards (hence the name “lizard poisoning disease”); flukes migrate from the small intestine up the common bile duct.

• Prepatent period is 2-3 months.

Pathogenesis and Clinical Signs

• Infections are usually inapparent with only a short-term inappetence occurring.

• Heavy infections can cause proliferative cholangitis and cirrhosis.

• Clinical signs may include anorexia, icterus, enlarged liver, diarrhea, vomiting, and death.

Diagnosis

ANTEMORTEM

• Eggs may be found on fecal sedimentation; fecal flotation may be ineffective.

• Eggs are brown, operculated, oval, 35-50 x 20-35 um, containing miracidia.

POSTMORTEM

• Adults live in bile ducts, gallbladder, and pancreas; worms are very small and generally not seen at necropsy; rather, may find them on histologic section.

Treatment and Control

Praziquantel at 20 mg per kg has been used.

• Prevent predation and scavenging whenever possible.

Protozoa

HISTOMONAS MELEACRIDIS

• Worldwide distribution in gallinaceous birds; locally significant in free-ranging birds.

• Common name: blackhead.

Life Cycle

• Direct; indirect with Heterakis gallinarum or earthworm paratenic host.

• Trophozoites are passed in the feces or in the eggs of H. gallinarum (nematodes ingest trophozoites that infect oocytes); primary means of transmission is ingestion of trophozoites in eggs of H. gallinarum or in eggs of H. gallinarum in earthworms; trophozoites die quickly (within hours) but it is possible they can be ingested with contaminated food or water.

• Remains in flagellated form in cecal lumen approximately 1 week; penetrates subepithelial tissues appearing as a round form without flagellum; carried via circulation to liver 10-12 days postinfection.

• Chickens: nonpathogenic.

• Turkeys: causes inflammation and ulcers in the ceca; cores of necrotic tissue, exudate, and parasites plug ceca; in liver, causes characteristic circular, yellow-green areas of necrosis with a depressed center; clinical signs include depression, inappetence, sulfur-colored droppings, cyanosis of the head (hence the common name), death.

Diagnosis

ANTEMORTEM

• None.

POSTMORTEM

• Examination of fresh or fixed impression smears obtained from the edge of cecal or liver lesions for organisms; may also be able to find organisms in histological sections.

Treatment and Control

• Modern, intensive management has decreased the incidence of this parasite; separate turkeys from chickens and poults from adults; avoid contaminated ground and adhere to strict sanitation; reuse of litter may lead to build-up of H. meleagridis eggs; treat chickens for H. meleagridis.