The common stomach worms of cattle are Haemonchus placei (barber’s pole worm, large stomach worm, wire worm), Ostertagia ostertagi (medium or brown stomach worm), and Trichostrongylus axei (small stomach worm, see Trichostrongylus axei Infection in Horses Trichostrongylus axei Infection in Horses The small stomach worm, Trichostrongylus axei, is the only nematode species that occurs in humans, ruminants, and horses. Infection is rarely diagnosed in horses maintained without ruminant... read more ). In some tropical countries, Mecistocirrus digitatus, a large worm up to 40 mm long, is present. H placei is primarily a parasite in tropical regions, whereas O ostertagi and, to a lesser extent, T axei are found in more temperate climates. Adult male Haemonchus are up to 18 mm long, females up to 30 mm. Ostertagia adults are 6–9 mm long, and Trichostrongylus, ~5 mm.
The preparasitic life cycles of the three groups are generally similar. Larvae hatch shortly after the eggs are passed in the feces and reach the infective stage in ~2 wk under optimal temperatures (~75°F [24°C]). Development to the infective stage is delayed during cold weather. In areas with narrow diurnal temperature variations, those months with a mean maximum temperature of 65°F (18°C) and with rainfall >2 in. (5 cm) are favorable for development of the free-living stages of H placei, but where wide fluctuations occur, a mean minimum temperature of 50°F (10°C) may effectively limit development. The preparasitic forms of O ostertagi and T axei develop and survive better in cooler conditions, and their upper limits for survival are lower than those for H placei. If the temperature is unfavorable or drought conditions exist, infective larvae may remain dormant in the feces for weeks until conditions become favorable again, eg, after heavy rainfall, when large numbers of infective larvae emerge onto the surrounding grass.
The prepatent period of O ostertagi is normally ~3 wk. Ingested larvae enter the lumen of the abomasal glands and molt by the fourth day; they remain there during the prepatent period, growing and undergoing a final molt before emerging as young adult worms from the gastric glands onto the abomasal mucosa. During this time, the specialized cells (pepsinogen-producing zymogen cells, acid-producing parietal cells) lining parasitized glands are lost and replaced by hyperplastic, undifferentiated cuboidal cells, resulting in nodules that may be discrete or confluent. Around the time of worm emergence, the changes seen in parasitized glands also appear in neighboring nonparasitized glands, rapidly extending the effects of the parasite burden. As a result, in heavy infections, abomasal pH may rise from 2 to >6; from a clinical viewpoint, when pH rises above 4.5, digestion in the abomasum ceases. A protein-losing gastropathy results and, together with anorexia and impaired protein digestion, leads to hypoproteinemia and weight loss. Diarrhea is persistent. In Type I ostertagiosis, which results from recent infection, most worms present are adults, and the response to anthelmintic treatment is good. Type I disease is seen primarily in calves 7–15 mo old. It is most common from time of weaning and ensuing months in warm temperate regions and in young cattle during summer and early fall in cool temperate regions.
In Type II ostertagiosis, large numbers of larvae, which had become dormant or inhibited in development at the early fourth larval stage, emerge from the glands weeks or months later. This is seen primarily in cattle 12–20 mo old. In warm temperate regions, inhibition-prone larvae are acquired in spring, and disease may result when large numbers of larvae resume development to the adult stage in late summer or fall. In cold temperate regions, inhibition-prone larvae are acquired during late autumn and mature during late winter or early spring.
Larval inhibition in O ostertagi and other nematodes is thought to be analogous to diapause in insects. It has been interpreted as a survival mechanism in which the preparasitic stages on pasture avoid the adverse conditions of winter in cool regions and of hot and dry (or hot and alternately wet and dry) conditions of many warm regions. The factors that cause and later "switch off" inhibition are not completely known, but prolonged experimental cold conditioning of infective larvae was found to be important in a cool temperate region. In warm regions of both northern and southern hemispheres, conditioning of preparasitic stages to inhibition develops principally during spring before the hot and dry conditions of summer. The resumed development or maturation of the parasites is likely to be genetically predetermined and may be influenced by parturition, nutrition, concurrent infection, and host immune response.
H placei may also become inhibited over winter; they then resume development in the spring and infect the pastures with eggs at a time suitable for their development. Both the larval and adult stages are pathogenic because of their blood-sucking ability. T axei causes gastritis with superficial erosion of the mucosa, hyperemia, and diarrhea. Protein loss from the damaged mucosa and anorexia cause hypoproteinemia and weight loss. Inhibition does not occur to the same degree.
Young animals are more often affected, but adults not previously exposed to infection frequently show signs and succumb. Ostertagia and Trichostrongylus infections are characterized by profuse, watery diarrhea that usually is persistent. In haemonchosis and Mecistocirrus infection, there may be little or no diarrhea but possibly intermittent periods of constipation. Anemia of variable degree is a characteristic sign of both these infections.
Concurrent with the diarrhea of O ostertagi and T axei infections, and with the anemia of heavy Haemonchus infection, there is often hypoproteinemia and edema (rare in O ostertagi infections), particularly under the lower jaw (bottle jaw) and sometimes along the ventral abdomen. Heavy infections can result in death before clinical signs appear. Other variable signs include progressive weight loss, weakness, rough coat, and anorexia.
Worms can readily be seen and identified in the abomasum, and small petechiae may be visible where the worms have been feeding. The most characteristic lesions of Ostertagia infection are small, umbilicated nodules 1–2 mm in diameter. These may be discrete, but in heavy infections they tend to coalesce and give rise to a “cobblestone” or “morocco leather” appearance. Nodules are most marked in the fundic region but may cover the entire abomasal mucosa and may be accompanied by a rise in gastric pH to 6–7. As a result, pepsinogen will no longer be converted to pepsin and may leak across the damaged epithelium, leading to high plasma levels. There is also evidence that adult Ostertagia can cause direct hypersecretion of pepsinogen. The increased abomasal pH may also stimulate production of gastrin and thus hypergastrinemia, which is closely associated with the inappetence that may accompany infection. This parasite-associated drop in intake has been shown to be largely responsible for impaired weight gain. Edema is often marked and, in severe cases, may extend over the abomasum and into the small intestine and omentum.
In T axei infections, the mucosa of the abomasum may show congestion and superficial erosions, which are sometimes covered with a fibrinonecrotic exudate.
Several species of Cooperia are found in the small intestine of cattle; C punctata, C oncophora, and C pectinata are the most common. The red, coiled adults are 5–8 mm long, and the male has a large bursa. They may be difficult to observe grossly. Their life cycle is essentially the same as that of other trichostrongylids. These worms apparently do not suck blood. Most of them are found in the first 10–20 ft (3–6 m) of the small intestine. The prepatent period is 12–15 days.
The eggs usually can be differentiated from those of the common GI nematodes by their practically parallel sides, but a larval culture of the feces is necessary to definitively diagnose Cooperia infection in the living animal. In heavy infections with C punctata and C pectinata, there is profuse diarrhea, anorexia, and emaciation, but no anemia; the upper small intestine shows marked congestion of the mucosa with small hemorrhages. The mucosa may show a fine lace-like superficial necrosis. C oncophora produces a milder disease but can be responsible for weight loss and poor productivity. It is usually necessary to make scrapings of the mucosa to demonstrate Cooperia spp, which must be differentiated from Trichostrongylus spp, Strongyloides papillosus, and immature Nematodirus spp.
The adult male Bunostomum phlebotomum is ~15 mm long and the female ~25 mm. Hookworms have well-developed buccal capsules into which the mucosa is drawn; cutting plates at the anterior edge of the buccal capsule are used to abrade the mucosa during feeding. The prepatent period is ~2 mo. Infection is by ingestion or skin penetration; the latter is more common in animals kept in poor conditions.
Larval penetration of the lower limbs may cause uneasiness and stamping, particularly in stabled cattle. Adult worms cause anemia and rapid weight loss. Diarrhea and constipation may alternate. Hypoproteinemic edema may be present, but bottle jaw is rarely as severe as in haemonchosis. During the patent period, a diagnosis may be made by demonstrating the characteristic eggs in the feces.
On necropsy, the mucosa may appear congested and swollen, with numerous small hemorrhagic points where the worms were attached. The worms are readily seen in the first few feet of the small intestine, and the contents are often blood-stained. As few as 2,000 worms may cause death in calves. Local lesions, edema, and scab formation may result from penetration of larvae into the skin of resistant calves.
The intestinal threadworm Strongyloides papillosus has an unusual life cycle. Only the female worms are found in the intestine. They are 3.5–6 mm long and are embedded in the mucosa of the upper small intestine. Small, embryonated eggs are passed in the feces, hatch rapidly, and develop directly into infective larvae or free-living adults. The offspring of these free-living adults may develop into another generation of infective larvae or free-living adults. The host is infected by penetration of the skin or by ingestion; infective larvae can be transmitted in colostrum as in other species of the genus. The prepatent period is ~10 days.
Infections are most common in young calves, particularly dairy stock. Although signs are rare, they may include intermittent diarrhea, loss of appetite and weight, and sometimes blood and mucus in the feces. Large numbers of worms in the intestine produce catarrhal enteritis with petechiae and ecchymoses, especially in the duodenum and jejunum.
Nematodirus helvetianus is generally recognized as the most common bovine species, although other species, eg, N spathiger and N battus, can also infect cattle. The adult males of N helvetianus are ~12 mm long and the females 18–25 mm. The eggs develop slowly; the infective third stage is reached within the egg in 2–4 wk and may remain within the egg for several months. Eggs may accumulate on pasture and hatch in large numbers after rain to produce heavy infections over a short period. The eggs are highly resistant, and those passed by calves in one season may remain viable and infect calves the next season. After ingestion of infective larvae, the adult stage is reached in ~3 wk. Worms are most numerous 10–20 ft (3–6 m) from the pylorus.
Signs, which include diarrhea and anorexia, usually develop during the third week of infection before the worms are sexually mature; clinical infections may be seen in dairy calves from 6 wk onward. Diagnosis is difficult during the prepatent period, but during the patent period it is easily made on the basis of the characteristic eggs. Relatively small numbers of eggs are produced. Fecal sampling of both healthy and sick calves in an affected group will increase the chance of making a diagnosis. Immunity to reinfection develops rapidly. Necropsy may show only a thickened, edematous mucosa.
The ascarid Toxocara vitulorum is a stout, whitish worm (males 20–25 cm, females 25–30 cm) found in the small intestine of calves <6 mo old; older calves are resistant. Larvae hatching from ingested eggs pass to the tissues and, in pregnant cows, are mobilized late in pregnancy and passed via the milk to calves. Eggs appear in the feces of calves from 3 wk of age and are easily recognized by their thick, pitted shells and dark brown center. In some parts of the world, the infection is considered serious, particularly in buffalo calves.
Adults of Oesophagostomum radiatum (nodular worm) are 12–15 mm long, and the head is bent dorsally. Because the eggs are very similar to those of Haemonchus placei, they are often grouped together on routine fecal examination. The life cycle is direct. The larvae penetrate primarily into the wall of the lower 10–20 ft (3–6 m) of the small intestine but also into the cecum and colon, where they remain for 5–10 days and then return to the lumen as fourth-stage larvae. The prepatent period in susceptible animals is ~6 wk. However, in subsequent reinfections, larvae become arrested for some time, and many never return to the lumen (host encystment).
Young animals suffer from the effects of adult worms, whereas in older animals, the effect of nodules enclosing larval worms is more important. Infection causes anorexia; severe, constant, dark, persistent, fetid diarrhea; weight loss; and death. In older, resistant animals, the nodules surrounding the larvae become caseated and calcified, thus decreasing the motility of the intestine. Stenosis or intussusception occasionally occurs. Nodules can be palpated per rectum, and the worms and nodules can be seen readily at necropsy.
Adults of the large-mouth bowel worm, Chabertia ovina, are ~12 mm long and bent ventrally at the anterior end. There is a typical direct life cycle. The larvae penetrate the mucosa of the small intestine shortly after ingestion and later emerge and pass to the colon. The prepatent period is ~7 wk. Larvae and adults may cause small hemorrhages with edema in the colon and passage of feces coated with mucus. Clinical chabertiosis is seldom, if ever, seen in cattle.
Trichuris spp infections are common in young calves and yearlings, but the numbers of worms are seldom large. The eggs are resistant, and infections are likely to persist on problem premises. Clinical signs are unlikely, but in occasional heavy infections, dark feces, anemia, and anorexia may be seen.
The anoplocephalid tapeworms Moniezia expansa and M benedeni are found in young cattle. The worms of this group are characterized by the absence of a rostellum and hooks, and the segments are wider than they are long. The eggs are triangular or rectangular and are ingested by the intermediate host, free-living oribatid mites, which live in the soil and grass. After 6–16 wk, infective cysticercoids are present in the mites. Infection occurs after ingestion of infected mites; the prepatent period is ~5 wk. Moniezia are commonly considered nonpathogenic in calves, but intestinal stasis has been reported.