Moniezia (Tapeworm)

Many producers are concerned about tapeworms (Moniezia spp.) because they can see the moving segments (white rice grain-like “worms”) in freshly deposited feces. Tapeworm eggs are ingested by field mites and infection is transmitted when mites are consumed with forage. Adult tapeworms reside in the small intestine (Figure 11), feed by absorbing nutrients from digested feed and cause very little damage. However, growth in kids (not adults) may be somewhat reduced and intestinal blockage may rarely occur. Infection can be controlled with albendazole, fenbendazole, or oxfendazole.

Figure 11. Adult tapeworms in small intestine.

Fasciola hepatica (Liver fluke)

Fasciola hepatica can be a major problem in low lying perennial wet areas of the southeast. This parasite resides in and damages the liver resulting in unthriftiness, weight loss/reduced gains, and sometimes death. The life cycle is indirect requiring an amphibious snail as an intermediate host. Fluke eggs are passed in the feces and a larval stage called a miracidium develops inside the egg over a period of 2-3 weeks. Eggs then hatch releasing the miracidium which infects a snail. Asexual reproduction occurs in the snail over a period of 5-7 weeks and then the mature larval stage called a cercaria leaves the snail and encysts on forage where it develops to a metacercaria. Animals ingest the metacercaria when grazing. Snails are active mainly from January/February through May/June, depending on environmental conditions, providing the source of infection (transmission). Snails burrow into the mud and become dormant the rest of the year, especially the hot summer months. Development to the adult fluke (Figure 12) takes about 6-8 weeks. Because transmission ceases in late spring/early summer, treatment to control flukes can be divided into two periods, one period when immature and adult flukes are present (February-August) and another when adults only are present (September-January).

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Figure 12. Adult liver fluke showing leaf-like appearance.

Diagnosis is by using a sedimentation procedure to find eggs in feces. Regular floatation techniques are not good as the floatation medium induces premature hatching of the eggs and they do not float. Clorsulon (Curatrem) is the only product that is effective against immature flukes. Clorsulon and albendazole are effective against adult flukes. Therefore, selection of either of these depends on the time of year. Another liver fluke, the deer fluke (Fascioloides magna), can kill small ruminants by destroying the liver. Infection is rare, but should be considered where deer have access to pastures grazed by small ruminants. Control is difficult.

Dictyocaulus filaria, Muellerius, Protostrongylus (Lungworms)

Problems with lungworm infection occur sporadically in the southeast. Infection results in respiratory distress (chronic coughing), unthriftiness, and sometimes death. The life cycle of Dictyocaulis filaria is direct and adult worms live in the lungs (Figure 13) with larva being passed in the feces. Transmission usually occurs during the cooler months (November-April) of the year. Because larvae, not eggs, are found in feces, diagnosis is by using the Baermann procedure which extracts the larvae from feces. Infection can be controlled with albendazole, fenbendazole, ivermectin, or oxfendazole. There are 2 other minor lungworms (Muellerius capillaris and Protostrongylus spp.) whose life cycles are indirect requiring land snails/slugs as intermediate hosts. Control is not as easy and fortunately pathogenesis is minor.

Figure 13. Adult lungworms in the bronchi of the lungs.

Parelaphostrongylus tenuis (Meningeal worm)

The meningeal worm (Parelaphostrongylus tenuis), also known as the deer worm or meningeal deer worm, frequently infects llamas, alpacas and sometimes goats. White-tailed deer are the natural host for the parasite, so goats are at potential risk everywhere that white-tailed deer are found. Small ground dwelling slugs and snails are intermediate hosts. Goats, which are not normal hosts, can ingest the slugs/snails harboring the infective form and the larvae migrate into places where they don’t normally reside in the deer. Migration is up the spinal nerves to the spinal cord but then they seem to get lost. The larvae then migrate throughout the spinal cord and the brain (actually around the spinal cord and brain, not in it). This causes damage to the central nervous system which may be severe enough to result in death.

Animals can become infected in the spring, summer or fall. Disease is usually seen in the fall and winter about 3 to 4 months after infection. Often only one animal is infected at a time on a single farm. Infected animals will show a wide variety of symptoms which include, but are not limited to: rear leg weakness and ataxia (uncoordinated walking), paralysis, hypermetria (exaggerated stepping motions), circling, abnormal head position, blindness and gradual weight loss. Generally, animals with more severe symptoms have a worse prognosis.

Diagnosis is difficult in the live animal and is usually made when animals die and the larvae are found on examining the spinal cord and brain microscopically. The use of ivermectin at monthly intervals during the transmission season (spring and summer) has been used in attempts to prevent infection, but this strategy has not been proven. However, this frequent administration interval most likely will have an effect on the development of resistance by the other resident worms.

Eimeria spp. (Coccidia)

Coccidia are protozoan parasites that infect cells in the small intestine and is a disease associated with filth, moisture and times of depressed immunity such as kidding, weaning or during transportation. Infection results in destruction of the intestinal lining leading to scours, unthriftiness, weight loss/reduced weight gains, and sometimes death. Mature oocysts (Figure 14) are passed in the feces and can develop to infective stages (within the oocyst) in 2-7 days. Upon ingestion, infective stages invade the intestinal lining and undergo asexual reproduction producing many more invasive stages. This can occur repeatedly and eventually sexual reproduction occurs forming oocysts to complete the cycle. Devastating losses can occur quickly because of the asexual process and usually is a problem at weaning when kids are stressed. Preventing and/or controlling coccidiosis can be achieved by providing an anticoccidial product in the feed or water. There are several effective products on the market, such as amprolium and monensin. Individual clinical cases can be treated with sulfa products. Fortunately, a solid immunity develops subsequent to infection, however, if infection was severe, stunting usually results.

Figure 14. Coccidia oocysts in fecal exam.

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