Worm infection treatment and control in cattle

10/09/2022

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 f***s 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.
For diagnosis, treatment, and control, see Gastrointestinal Parasites of Ruminants et seq.
Bunostomum sp
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 pe*******on; the latter is more common in animals kept in poor conditions.
Larval pe*******on 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 f***s.
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 pe*******on of larvae into the skin of resistant calves.
For diagnosis, treatment, and control, see Gastrointestinal Parasites of Ruminants et seq.
Strongyloides sp
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 f***s, 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 pe*******on 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 f***s. Large numbers of worms in the intestine produce catarrhal enteritis with petechiae and ecchymoses, especially in the duodenum and jejunum.
For diagnosis, treatment, and control, see Gastrointestinal Parasites of Ruminants et seq.
Nematodirus spp
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 s*xually 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. F***l 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.
For diagnosis, treatment, and control, see Gastrointestinal Parasites of Ruminants et seq
Toxocara canis, egg
COURTESY OF DR. MARK FOX.
The ascarid Toxocara vitulorum is a stout, whitish worm (males 20–25 cm, females 25–30 cm) found in the small intestine of calves

10/09/2022

Haemonchus, Ostertagia, and Trichostrongylus spp
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). 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.
Abomasal lesions, Ostertagia
Abomasal lesions, Ostertagia
COURTESY OF DR. SAMEEH M. ABUTARBUSH.
The preparasitic life cycles of the three groups are generally similar. Larvae hatch shortly after the eggs are passed in the f***s 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 f***s 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.
Clinical Findings:
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.
Lesions:
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.

10/09/2022

When to Worm Young Cattle
Calves under one year of age are more susceptible than older cattle. Older cattle frequently have been exposed to the parasites and developed a degree of immunity.
Adult worms in the gut of cattle produce eggs that are passed in the f***s. The eggs hatch, producing immature larvae that develop and move up onto the pasture grasses. Infective larval forms of the worms may be present in large numbers on the growing forage. Some of the eggs can survive the winter and hatch out with warm weather. Temperatures between 60° and 80°F. and at least 2 inches of rainfall per month provide excellent propagation conditions. Feed bunks or waterers contaminated with f***s can be a source of exposure to the larvae.
The need to worm calves during the summer depends strictly on the degree of contamination of pastures or lots. Use of the same pastures year after year or high densities of grazing cattle can result in heavily contaminated forage. The number of times calves should be wormed during the spring and summer depends on the level of exposure and reinfection. Dairy calves confined to small lots around the farmstead may need to be wormed several times during the summer.
Feeder Cattle
Worming of cattle at the time they enter the feedlot is cost-effective only if the load of parasites they are carrying is great enough to reduce the rate of gain. The decision to worm cattle can be based on finding large numbers of worm eggs by microscopic examination of f***s. Alternatively, cattle from the southeastern United States can generally be expected to have a heavier load of parasites than western cattle. The parasite load of cattle from the Midwest will be variable.
Internal parasites have the greatest impact on rate of gain when cattle are on low energy levels which are typical of receiving or backgrounding rations. Therefore, worming feedlot cattle when they are processed into the feedlot will give the best returns.
Beef Cows
The cow herd is the major source of initial exposure of the calves. One of the most important worms in cattle lives in the abomasum, the true stomach. The stomach worms are active during the grazing season busily laying eggs. At the end of the grazing season they bury themselves in the stomach wall and are dormant until spring when they emerge and start egg laying. Timely deworming prior to the grazing season will greatly reduce the subsequent contamination of pastures during the grazing season.
The pregnant cows can be dewormed in the fall. The cows can be expected to winter better, have a higher conception rate the next breeding season, and wean heavier calves.
Dairy Cows
Dairy cows kept in drylots or semi-confinement have access to f***l contaminated feed or water; this practice results in a detrimental load of internal parasites. Mature cows should be wormed at the end of lactation to avoid discarding milk, or wormed at any time with Morantel tartrate, because this product does not require discarding of milk. Replacement heifers should be wormed as yearlings and again prior to entering the milking herd.
Dairy Calves
Dairy calves confined to small lots frequently carry heavy loads of worm parasites. It may be necessary to worm them twice or more during warm weather to maintain desired growth rates.
General Use Dewormers
Deworming with one of several anthelmintics (wormers) approved for use in cattle is an effective preventive practice. Consult your veterinarian concerning strategic worming; timing the deworming to be the most cost effective.
Fenbendazole (Panacur) is available as a stable suspension or granules. It is effective against roundworms in the gut, larval forms in the tissues, and lungworms. Withdrawal time to slaughter is 8 days.
Ivermectin (Ivomec) for cattle is an effective medication against the internal worm parasites including lungworms as well as cattle grubs and sucking lice. It is available in injectable or pour-on formulations. Withdrawal time to slaughter is 35 days.
Levamisole (Levisol, Tramisol) is available in boluses, a paste for oral administration, as a pour-on or an injectable form. Levamisole is effective against roundworms and lungworms. Withdrawal time is (orally) 2 days and (injected) 7 days.
Morantel tartrate (Rumatel) comes in boluses or crumbles for oral use. It is effective against roundworms, and has a 14-day withdrawal time to slaughter.
Thiabendazole (Omnizole, TBZ) for oral administration is available in paste, boluses, suspension, or crumbles. It is effective against roundworms. Thiabendazole is approved for use in lactating cows and has a 96-hour milk discard time. Withdrawal time to slaughter is 3 days.
Albendazole (Valbazen) is available in paste or suspension. It is effective against all intestinal worms including tapeworms, and lungworms as well as liver flukes. It has a 27-day withdrawal for slaughter. It should not be used in animals during the first 45 days of pregnancy.
Oxfendazole (Synonthic) is a new wormer that is effective against intestinal parasites including tapeworms. This wormer has a unique delivery system in that the wormer is injected directly into the rumen. Oxfendazole is also available in the drench form.
Fenbendazole, Ivermectin, Levamisole, Albendazole and Oxfendazole are not approved for use in dairy cattle or dairy heifers of breeding age.
Methods of Administration
Administering a wormer to individual animals is the only way to be sure that each one is getting the required amount of active material relative to its body weight. This section describes the various methods of administration, their advantages, the drawbacks, and suggestions to ensure "success."
Orally
Wormers in liquid form, or suspension can be administered by drenching, with a dose syringe or with multiple dose equipment with a backpack reservoir. Avoid getting any of the wormer into the lungs where it could initiate pneumonia. Pour-on fomulations are absorbed following direct application to the skin.
Boluses should be given with a balling gun to get them past the base of the tongue. It is not uncommon for cattle to hold a bolus in the mouth for some time and then spit it out. Always observe an animal to be sure it has swallowed the boluses before releasing it.
The paste formulations of wormers are given with special guns, comparable to a caulking gun, designed for each individual product. The tip of the tube is placed in the corner of the mouth, and the paste deposited on the back of the tongue. Do not force the gun deep into the mouth as the paste can cause difficult breathing or the gun can cause injury to soft tissues of the mouth. Good restraint, preferably a squeeze chute, is essential to successful oral administration of wormers. Most cattle are head shy and will resist the operator's attempt to treat them orally.
Injections
Injections should be made with clean equipment and sharp needles. Withdraw the wormer through the rubber diaphragm stopper. Never open the bottle to fill the syringe; this increases the chances for contamination and post injection abscesses. The injections should be under the skin of the neck, not into the muscle. Never inject in the rear quarters. Do not inject more than 10 ml of drug in a single site.

10/09/2022

The need to control internal parasites will exist as long as cattle are grazing pastures. However, parasite levels are not the same on all pastures or in all cattle. Pastures that are heavily stocked generally have a higher parasite burden than lightly stocked ones. Cattle in a drylot are less likely to have heavy worm infections than those on pastures. Young cattle will typically have more internal parasites than older cattle. Therefore, the methods of controlling internal parasites should be developed to fit individual production situations. Strategic deworming starts with understanding the life cycle of problem parasites, identifying seasonal changes in parasite burdens and implementing cost effective control. A successful deworming program, along with good overall herd management, will increase milk production in cows and thereby increase weaning weights of calves.

Please check this link first if

20/08/2022

Bunostomum
The hookworm Bunostomum phlebotomum is a large (3 cm), robust, white worm capable of causing anemia and black tarry f***s in calves. Infection can occur both by ingestion or skin pe*******on and may be a problem in young calves housed in moist environments, especially in the tropics. The eggs are large, dark, and rectangular, resembling trichostrongyle-type eggs (i.e., thin shelled and segmented [100 × 50 μm]), but they have rough eggshells, often with clinging debris. The prepatent period is 1 to 2 months, and apparently hypobiosis is a strategy for avoiding prolonged drought conditions. Bunostomum can be controlled with anthelmintics, but environmental sanitation with dry bed grounds is more realistic in the long term. Calves establish rapid immunity to reinfection. In geographic areas where anthelmintics are widely used, the parasite has largely disappeared but should be considered a cause of anemia in other areas.

17/09/2021

11/07/2021

Harm caused by Bunostomum worms symptoms and diagnosis
The strong mouth capsule of adult worms causes heavy lesions in the intestinal wall, often with rupture of intestinal blood vessels, with the subsequent blood loss. Larvae that pe*****te the skin (mainly through the feet and limbs) can be highly irritating for livestock. Bunostomum worms belong to the most harmful in warm and moist regions. Unweaned calves and lambs are particularly at risk during the rainy season: already 50 to 200 worms can cause anemia. Over 2000 worms can be fatal for calves, and over 300 worms for lambs.
Typical symptoms are diarrhea (often mucous or hemorrhagic), dehydration, loss of appetite, weakness, weight loss or reduced growth, bottle jaw (submandibular edema). Larvae that pe*****te the skin can cause dermatitis (including itching, swelling, redness, thickening), hair loss, rough coat and damaged hooves. Affected lungs can cause coughing.
Since most infections are mixed with other gastrointestinal roundworms (e.g. Cooperia spp, Haemonchus spp, Ostertagia spp, Trichostrongylus spp, etc.) it is often difficult to ascribe the damage to Bunostomum or to other worms.
Diagnosis is based on the clinical signs and confirmed after detection of characteristic eggs in the f***s. However, it is difficult to distinguish the eggs of Bunostomum from other gastrointestinal roundworms. L3 larvae obtained after in-vitro culture of eggs may be required for specific diagnosis.
Prevention and control of Bunostomum infections
In contrast with other gastrointestinal roundworms, tall pasture favors transmission of Bunostomum worms. This is due to the fact that tall grass retains more moisture, which allows infective larvae to swim to the tip of the grass blade, from where it is easier to reach the skin of their hosts. Therefore it is very important to keep livestock away from moist pastures.
Indoor transmission is possible and therefore facilities have to be kept as dry and clean as possible, because humid bedding and dirt favors the development and survival of infective larvae.
Bunostomum worms are quite species-specific and larvae do not survive longer than about 2 months on pasture. Consequently, alternate grazing (e.g. cattle followed by sheep or horses with 2-3 months interval) can help reduce pasture contamination with Bunostomum worms. However, this may be unadvisable for the prevention of other gastrointestinal worm species that infect both cattle and sheep.
As a general rule, whatever reduces pasture contamination with infective larvae (e.g. adequate pasture rotation) or exposure of livestock to such larvae will diminish the impact on the herd. Such preventative measures are the same for all gastrointestinal roundworms and are explained in a specific article in this site (click here).
Livestock exposed to these worms often develop natural resistance progressively and may recover spontaneously. Such resistant animals do not become sick if re-infected, but continue shedding eggs that contaminate their environment.
Numerous broad spectrum anthelmintics are effective against adult worms and larvae, e.g. several benzimidazoles (albendazole, febantel, fenbendazole, mebendazole, oxfendazole, etc.), levamisole, as well as several macrocyclic lactones (e.g. abamectin, doramectin, eprinomectin, ivermectin, moxidectin).
A few other narrow-spectrum anthelmintics such as closantel, nitroxinil are effective against adult worms but may not control larvae and other roundworm species that often infect livestock simultaneously with Bunostomum worms.
Depending on the country most of these anthelmintics are available for oral administration as drenches, feed additives and/or tablets. Levamisole and most macrocyclic lactones are usually also available as injectables. A few active ingredients are also available for livestock as pour-ons and slow-release boluses.
Numerous commercial products contain mixtures of two or even more active ingredients of different chemical classes. This is done to increase the chance that at least one active ingredient is effective against gastrointestinal worms that have become resistant, or to delay resistance development by those worms that are still susceptible.
Excepting slow-release boluses, most wormers containing benzimidazoles (e.g. albendazole, febantel, fenbendazole, flubendazole, mebendazole, oxfendazole, etc.), levamisole, tetrahydropyrimidines (e.g. morantel, pyrantel) and other classic anthelmintics kill the worms shortly after treatment and are quickly metabolized and/or excreted within a few hours or days. This means that they have a short residual effect, or no residual effect at all. As a consequence treated animals are cured from worms but do not remain protected against new infections. To ensure that they remain worm-free the animals have to be dewormed periodically, depending on the local epidemiological, ecological and climatic conditions. An exception to this are macrocyclic lactones (e.g. abamectin, doramectin, eprinomectin, ivermectin, moxidectin), that offer several weeks protection against re-infestation, depending on the delivery form and the specific parasite.
There are so far no true vaccines against Bunostomum worms. To learn more about vaccines against parasites of livestock and pets click here.
Biological control of Bunostomum worms (i.e. using its natural enemies) is so far not feasible. Learn more about biological control of worms.
You may be interested in an article in this site on medicinal plants against external and internal parasites.
Resistance of Bunostomum worms to anthelmintics
There are only few reports on resistance of Bunostomum worms to most used anthelmintics (benzimidazoles, ivermectin, levamisole, etc) in sheep, goats and cattle. It seems that it is not such a serious problem as with other gastrointestinal roundworms (e.g. Cooperia spp, Haemonchus spp, Ostertagia spp, Trichostrongylus spp, etc.).
This means that if an anthelmintic fails to achieve the expected efficacy against Bunostomum worms, there is a certain risk that it is due to resistance to anthelmintics, particularly in sheep, goats and cattle. However, it is well known that many cases of product failure are due to incorrect use of a product, or to the use of an unsuited product, not to resistance.