Ostertagia ostertagi

Last updated

Ostertagia ostertagi
Scientific classification OOjs UI icon edit-ltr.svg
Domain: Eukaryota
Kingdom: Animalia
Phylum: Nematoda
Class: Chromadorea
Order: Rhabditida
Family: Trichostrongylidae
Genus: Ostertagia
Species:
O. ostertagi
Binomial name
Ostertagia ostertagi
(Stiles, 1892)

Ostertagia ostertagi, commonly known as the medium stomach worm or brown stomach worm, is a parasitic nematode (round worm) of cattle. O. ostertagi can also be found to a lesser extent in sheep, goats, wild ruminants, and horses. It causes ostertagiosis, which is potentially fatal in cattle. It is found worldwide and is economically important to cattle industries, particularly those found in temperate climates.

Contents

The abomasal nematode O. ostertagi is a clade V nematode of the order Strongylida , the family Trichostrongylidae and genus Ostertagia . [1] Ransom first described the genus Ostertagia in 1907, which currently contains approximately 15 species. All species of the genus Ostertagia infect domestic or wild ruminants. These species form a large and complex group, the taxonomy of which has not been fully elucidated.

Life cycle

O. ostertagi has a life cycle which consists of two stages: the free-living, pre-parasitic stage and the parasitic stage in the host (e.g. cattle). Eggs from mature females in the abomasum are passed in the faeces. These eggs hatch in the faeces to first-stage larvae (L1). The L1 larvae grow and moult to second-stage larvae (L2), which then moult to become the infective third-stage larvae (L3). The L3s retain the cuticle from the second stage (L2) as a protective sheath, and can survive for long periods within the faeces. The time taken to develop into infective larvae is dependent on favourable stimuli such as temperature (approximately 25–27 °C or 77–81 °F) and humidity. Typically, development takes 10 days to 2 weeks. [2]

The parasitic stage of the life cycle begins when warm moist conditions cause the L3 larvae to migrate onto herbage surrounding the fecal pat, which are ingested during grazing. In the host's rumen, the L3 larvae shed their protective sheath and pass into the abomasum, where they penetrate the gastric glands. After exsheathment and penetration into the gastric glands the L3 moult into L4 and subsequently to L5 larvae. The young adult worms then emerge from the gastric glands and continue their maturation on the mucosal surface of the abomasum. [3] Once fully mature, sexual reproduction begins and eggs are produced, thus completing the life cycle.

The normal prepatent period for O. ostertagi is 21 days. However, under certain circumstances, ingested L3 larvae can suspend their maturation and become dormant as inhibited L4 larvae inside the gastric glands. This arrested development is called hypobiosis , and can last for up to six or seven months. Studies suggest that the inhibition process in O. ostertagi depends on the weather conditions to which the infective L3 larvae are exposed on pasture, and the length of time that L3 larvae spend on pasture. In temperate regions of the northern hemisphere, hypobiosis occurs in autumn and early winter, but in the southern hemisphere there is evidence that this phenomenon occurs in spring and early summer. [4] [5]

Morphology

O. ostertagi adults are slender reddish-brown worms. Adult males are 6–7 mm (0.24–0.28 in) long, adult females 8–11 mm (0.31–0.43 in) long, and the eggs 70–86 μm (0.0028–0.0034 in) long. Identification of adult medium stomach worms is based on the structure of the bursa, genital cone, and spicules in males and on the dimensions of the oesophageal valve and the configuration of the synlophe in males and females. [6] The cuticle in the anterior region is striated transversely whereas the rest of the body is unstriated and bears around 36 longitudinal ridges. [7] The Ostertaginae are characterized by a reduced buccal capsule and square head, and well-developed copulatory bursa in the male. The genital cone ventrally bears two small slender papillae and dorsally bears two long slender papillae surrounded by an accessory bursal membrane. The lateral rays of the copulatory bursa are in a pattern of 2-1-2 or 2-2-1 pattern. The key to morphologically identifying O. ostertagi males is a prominent proconus and the remainder of the genital cone is not prominent. The spicules are of equal length and shape, tapering towards the distal end. [8] The key to morphologically identifying O. ostertagi females is the lateral synlophe with one pair of ridges ending next to the lateral ridge between cervical papilla and the posterior end of the oesophagus. The cervical papillae are prominent and thorn-like. A large number of surface cuticular ridges (synlophe) are perpendicular to the surface. [9] [10]

The infective L3 larvae of O. ostertagi can also be identified morphologically. The L3 will have an external sheath. The larva head is rounded and can be distinguished from Cooperia spp. as it lacks the two refractive bodies in the head that is seen in this species. The tail of the larvae within the sheath is rounded and the body contains 16 intestinal cells. The external sheath of the O. ostertagi larvae also has a much blunter tip then that of Copperia spp. or Haemonchus placei . O. ostertagi can also be distinguished from the L3 larvae of Trichostrongylus spp. as it has a much longer sheath tail extension. [11]

Molecular biology

The genome size estimate for O. ostertagi is ~58 MB, based on T. circumcincta (Ostertagia circumcincta), whose genome is 58.6 MB and on H. contortus at 52 MB, based on flow cytometry. [12] There are 7,006 identified expressed sequenced tags (ESTs), representing 2,564 genes. [13]

Disease

Clinical ostertagiosis normally occurs in first grazing season calves but can affect mature animals. [14] Subclinical infection results in reduced weight gain and growth rate, reduced reproductive efficiency and reduced milk production. [15] The primary clinical symptom of fulminant bovine ostertagiosis is watery diarrhoea and is usually accompanied by reduced appetite. [16] Infected animals are characterised by dull, rough coats and hindquarters soiled with faeces as a result of the profuse diarrhoea. Cattle are frequently co-infected with many gastrointestinal nematodes including species of the following genera: Ostertagia, Haemonchus, Bunostomum, Oesophagostomum, Trichuris, Trichostrongylus, Cooperia, and Nematodirus . The clinical signs between these species of nematodes are difficult to distinguish from each other, and are often referred to as a syndrome called parasitic gastroenteritis. [17] Clinical ostertagiosis can be observed under two sets of circumstances referred to as type I and type II disease.

Type I disease

Type I disease occurs in young cattle grazing on pastures for their first time during the period of high pasture contamination. [18] [19] This syndrome usually occurs in the summer and fall months in the Northern hemisphere and during the winter and spring months in the Southern hemisphere. [20] Infective larvae are ingested daily by the young stock on pasture. The pathological and clinical signs are due to the direct development of large numbers of L3 larvae to adult worms over a relatively short period of time (approximately 3 weeks) in young animals with an immune system naïve to Ostertagia infections. [21] The young adult worms then break out of the gastric glands, causing substantial damage to the abomasal wall. Mild cases result in reduced growth or production and severe cases can result in fulminating disease characterized by profuse watery diarrhoea, rapid weight loss, submandibular oedema ("bottle jaw"), anemia and death. [22] [23]

Type II disease

Type II disease can occur in yearlings and older cattle. [24] It is the result of arrested L4s resuming their development to immature adults and leaving the gastric glands. [25] [26] This can occur weeks or months after being ingested as L3s and is a consequence of favourable environmental conditions. [27] The larvae will then resume maturation gradually or in bursts. The clinical signs are identical to type I disease and the severity depends on the magnitude of the eruptions. [28] In the Northern hemisphere type II disease is often seen in the early spring, and in the fall in the Southern hemisphere. [29]

Pathology

Worms can readily be seen and identified in the abomasum, and small petechiae (blood spots) may be visible where the worms have been feeding. The most characteristic lesions of Ostertagia infections are multiple small, white, raised 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 fundus region but may cover the entire abomasal mucosa. In severe cases, edema may extend over the abomasum and into the small intestine and omentum. [30]

When examined histologically, abomasal gastric glands contain larvae in varying stages of development, which results in hyperplasia and distention of the glands, and flattening of the glandular epithelium. Affected glands lack differentiated acid-producing parietal and pepsinogen producing chief cells. Type I and type II disease is often differentiated by the presence of increased numbers of globule leucocytes, eosinophils and focal aggregates of lymphoplasmocytic cells in animals with type II disease. [31]

Pathophysiology

Consequences of the damage done to the gastric gland by O. ostertagi include:

  1. Pepsinogen is not activated to its active form, pepsin, due to decreased acid production caused by the loss of parietal cell function, resulting in an increase in abomasal pH. [32]
  2. Due to increased abomasal pH, proteins are not denatured and digested. Dietary energy and protein, which would otherwise be used for growth, must be used to replace these proteins. Weight loss is the result. [33]
  3. Also due to the increased abomasal pH, there is an increase in the number of bacteria in the abomasum, which can contribute to the diarrhoea seen in clinical cases. [34] [35]
  4. Movement of serum proteins, particularly albumin from the circulating blood into the abomasal lumen due to compromised intracellular junctions occur. The increased albumin decreases fluid absorption by the gut, causing diarrhoea. The loss of albumin also causes body fluids to collect in lower parts of the body such as under the jaw (bottle jaw) or in the abdomen (ascites).
  5. The increased abomasal pH also stimulates the production of gastrin and thus hypergastrinemia, which is closely associated with the inappetence. This parasite-associated drop in intake has been shown to be largely responsible for impaired weight gain.

Immune response and host defence

Gastrointestinal nematodes may elicit a variety of host immune responses depending on the initial immune status of the host, parasite species, and environmental conditions. The body has several physical defense mechanisms against parasites including the continual sloughing of the gut epithelium to prevent parasite attachment. However, once an infection has occurred, the host's immune system attempts to limit the damage caused by the worm. Apart from the importance of the extrinsic factors of weather, climate and grazing management, the immune status of cattle is perhaps the most significant of all host factors influencing infection with O. ostertagi. Unlike other common gastrointestinal nematodes of cattle, who are subject to a quick host immune response after relatively short periods of exposure and immune system memory, a protective host immune response against O. ostertagi requires far longer periods of exposure and is not always permanent. The failure to respond quickly to Ostertagia may be a result of the suggested immunosuppression or impairment of antibody and cellular responses. [36] O. ostertagi has been shown to induce cytokines and T-cells in the adaptive immune response in cattle, and recent advances have been made to produce suitable vaccines targeting adult stage Ostertagia. [37] [38] [39] The major limitations to reducing parasitic load using vaccines is the complex and dynamic host-parasite interaction that is unique to each species of host and parasite, which is often influenced by several environmental factors. [40]

Diagnosis

The presence of O. ostertagi within a host may be inferred by several methods. Faecal worm egg counts (FECs) in particular (preferably with speciation by way of larval culture and differentiation), and total worm counts are the tests most commonly employed in the diagnosis of helminth infections in ruminants. The direct counting of nematode eggs in feces is the method of choice for yearling animals, whereas in adult animals it may yield high variability due to a cow's immunity and low egg output. [41] Other biochemical methods have been developed to help more accurately diagnose O. ostertagi parasitism. These include the determination of specific anti-parasite antibodies in milk. [42] [43] Enzyme-linked immunosorbent assays (ELISAs) have been used as a diagnostic tool to quantify the impact of gastrointestinal nematodes in dairy cattle by measuring antibodies in milk. Higher levels of antibodies measured by ELISA methods, referred to as optical density ratios (ODRs), are associated with decreased milk production in dairy cattle. [44] Similar results have been established in the dairy industry between increased ODR and negative effects on health, body weight and reproductive measures [45] Blood pepsinogen concentration, which increases with abomasal mucosa injury has also been used to diagnose ostertagiosis. [46] [47] The analysis of sera for increased plasma pepsinogen levels is a useful diagnostic aid. Generally, increased levels of pepsinogen activity (tyrosine levels >3 IU) are associated with clinical abomasal parasitism. [48]

Treatment and control strategies

There are several classes of anthelmintic drugs used to control gastrointestinal nematodes in livestock. The most common in the cattle industry are macrocyclic lactones, which include ivermectin and eprinomectin, benzimidazoles, and imidazothiazoles are also used to a lesser extent. Due to routine, blanket herd treatment, there is widespread resistance to anthelmintic drugs in warm climates in sheep, and increasing evidence of resistance in cattle in temperate climates. [49] [50] As a consequence, livestock industries will have to adapt husbandry practices to manage internal parasites. This may include a variety of combinations of pasture rotations, flexible stocking rates, and genetic selection. Several new control methods are also being researched including vaccines, nematode-trapping fungi, and tannins in feed. [51] [52] [53]

Drench resistance

Given the importance of effective parasite control, there is heightened concern over reduced anthelmintic efficacy. There is a broad range of current literature reporting developing resistance of O. ostertagi to all major classes of anthelmintic worldwide including the United States, New Zealand, Brazil, Argentina, and the UK. [54] [55] [56] As recently as January 2016, O. ostertagi anthelmintic resistance was reported to all three major drug classes on 20 dairy farms in Southern Australia [57] The two most widely accepted anthelmintic resistance diagnosis methods for O. ostertagi are in vivo methods: the fecal egg count reduction test (FECRT) and the controlled efficacy test (CET). The World Association for the Advancement of Veterinary Parasitology (WAAVP) has provided guidelines on the detection of anthelmintic resistance. [58]

Related Research Articles

<span class="mw-page-title-main">Fasciolosis</span> Parasitic worm infection

Fasciolosis is a parasitic worm infection caused by the common liver fluke Fasciola hepatica as well as by Fasciola gigantica. The disease is a plant-borne trematode zoonosis, and is classified as a neglected tropical disease (NTD). It affects humans, but its main host is ruminants such as cattle and sheep. The disease progresses through four distinct phases; an initial incubation phase of between a few days up to three months with little or no symptoms; an invasive or acute phase which may manifest with: fever, malaise, abdominal pain, gastrointestinal symptoms, urticaria, anemia, jaundice, and respiratory symptoms. The disease later progresses to a latent phase with less symptoms and ultimately into a chronic or obstructive phase months to years later. In the chronic state the disease causes inflammation of the bile ducts, gall bladder and may cause gall stones as well as fibrosis. While chronic inflammation is connected to increased cancer rates, it is unclear whether fasciolosis is associated with increased cancer risk.

<span class="mw-page-title-main">Hookworm infection</span> Disease caused by intestinal parasites

Hookworm infection is an infection by a type of intestinal parasite known as a hookworm. Initially, itching and a rash may occur at the site of infection. Those only affected by a few worms may show no symptoms. Those infected by many worms may experience abdominal pain, diarrhea, weight loss, and tiredness. The mental and physical development of children may be affected. Anemia may result.

<i>Haemonchus contortus</i> Species of roundworm

Haemonchus contortus, also known as the barber's pole worm, is a very common parasite and one of the most pathogenic nematodes of ruminants. Adult worms attach to abomasal mucosa and feed on the blood. This parasite is responsible for anemia, oedema, and death of infected sheep and goats, mainly during summer in warm, humid climates.

<i>Ascaridia galli</i> Species of roundworm

Ascaridia galli is a parasitic roundworm belonging to the phylum Nematoda. Nematodes of the genus Ascaridia are essentially intestinal parasites of birds. A. galli is the most prevalent and pathogenic species, especially in domestic fowl, Gallus domesticus. It causes ascaridiasis, a disease of poultry due to heavy worm infection, particularly in chickens and turkeys. It inhabits the small intestine, and can be occasionally seen in commercial eggs.

<span class="mw-page-title-main">Moxidectin</span> Chemical compound

Moxidectin is an anthelmintic drug used in animals to prevent or control parasitic worms (helminths), such as heartworm and intestinal worms, in dogs, cats, horses, cattle and sheep. Moxidectin kills some of the most common internal and external parasites by selectively binding to a parasite's glutamate-gated chloride ion channels. These channels are vital to the function of invertebrate nerve and muscle cells; when moxidectin binds to the channels, it disrupts neurotransmission, resulting in paralysis and death of the parasite.

<i>Dictyocaulus</i> Genus of nematode parasites of the bronchial tree of horses, sheep, goats, deer, and cattle

Dictyocaulus is a genus of nematode parasites of the bronchial tree of horses, sheep, goats, deer, and cattle. Dictyocaulus arnfieldi is the lungworm of horses, and Dictyocaulus viviparus is the lungworm affecting ruminants.

<i>Heligmosomoides polygyrus</i> Species of roundworm

Heligmosomoides polygyrus, previously named Nematospiroides dubius, is a naturally occurring intestinal roundworm of rodents. It belongs to the family Trychostrongylidae, and male and female worms are morphologically distinguishable. The parasite has a direct lifecycle, with its larval form being the infective stage. H. polygyrus has the ability to establish chronic infections in rodents and alter host immune responses. This nematode is widely used as a gastrointestinal parasitic model in immunological, pharmacological, and toxicological studies.

Mammomonogamus is a genus of parasitic nematodes of the family Syngamidae that parasitise the respiratory tracts of cattle, sheep, goats, deer, cats, orangutans, and elephants. The nematodes can also infect humans and cause the disease called mammomonogamiasis. Several known species fall under the genus Mammomonogamus, but the most common species found to infest humans is M. laryngeus. Infection in humans is very rare, with only about 100 reported cases worldwide, and is assumed to be largely accidental. Cases have been reported from the Caribbean, China, Korea, Thailand, and Philippines.

In population ecology, density-dependent processes occur when population growth rates are regulated by the density of a population. This article will focus on density dependence in the context of macroparasite life cycles.

<i>Toxocara canis</i> Species of roundworm

Toxocara canis is a worldwide-distributed helminth parasite that primarily infects dogs and other canids, but can also infect other animals including humans. The name is derived from the Greek word "toxon," meaning bow or quiver, and the Latin word "caro," meaning flesh. T. canis live in the small intestine of the definitive host. This parasite is very common in puppies and somewhat less common in adult dogs. In adult dogs, infection is usually asymptomatic but may be characterized by diarrhea. By contrast, untreated infection with Toxocara canis can be fatal in puppies, causing diarrhea, vomiting, pneumonia, enlarged abdomen, flatulence, poor growth rate, and other complications.

Capillaria plica is a parasitic nematode which is most often found in the urinary bladder, and occasionally in the kidneys, of dogs and foxes. It has also been found in the domestic cat, and various wild mammals. Its presence usually produces no clinical symptoms, but in some cases, it leads to hematuria, cystitis, or difficulty in urination.

<span class="mw-page-title-main">Thelaziasis</span> Medical condition

Thelaziasis is the term for infestation with parasitic nematodes of the genus Thelazia. The adults of all Thelazia species discovered so far inhabit the eyes and associated tissues of various mammal and bird hosts, including humans. Thelazia nematodes are often referred to as "eyeworms".

<i>Trichostrongylus</i> Genus of roundworms

Trichostrongylus species are nematodes, which are ubiquitous among herbivores worldwide, including cattle, sheep, donkeys, goats, deer, and rabbits. At least 10 Trichostrongylus species have been associated with human infections. Infections occur via ingestion of infective larvae from contaminated vegetables or water. Epidemiological studies indicate a worldwide distribution of Trichostrongylus infections in humans, with the highest prevalence rates observed in individuals from regions with poor sanitary conditions, in rural areas, or who are farmers / herders. Human infections are most prevalent in the Middle East and Asia, with a worldwide estimated prevalence of 5.5 million people.

<span class="mw-page-title-main">Anthelmintic</span> Antiparasitic drugs that expel parasitic worms (helminths) from the body

Anthelmintics or antihelminthics are a group of antiparasitic drugs that expel parasitic worms (helminths) and other internal parasites from the body by either stunning or killing them and without causing significant damage to the host. They may also be called vermifuges or vermicides. Anthelmintics are used to treat people who are infected by helminths, a condition called helminthiasis. These drugs are also used to treat infected animals.

<span class="mw-page-title-main">Oxfendazole</span> Chemical compound

Oxfendazole is a broad spectrum benzimidazole anthelmintic. Its main use is for protecting livestock against roundworm, strongyles and pinworms. Oxfendazole is the sulfoxide metabolite of fenbendazole.

<i>Teladorsagia circumcincta</i> Species of roundworm

Teladorsagia circumcincta is a nematode that is one of the most important parasites of sheep and goats. It was previously known as Ostertagia circumcincta and is colloquially known as the brown stomach worm. It is common in cool, temperate areas, such as south-eastern and south-western Australia and the United Kingdom. There is considerable variation among lambs and kids in susceptibility to infection. Much of the variation is genetic and influences the immune response. The parasite induces a type I hypersensitivity response which is responsible for the relative protein deficiency which is characteristic of severely infected animals. There are mechanistic mathematical models which can predict the course of infection. There are a variety of ways to control the infection and a combination of control measures is likely to provide the most effective and sustainable control.

<i>Cooperia oncophora</i> Species of roundworm

Cooperia oncophora is one of the most common intestinal parasitic nematodes in cattle in temperate regions. Infections with C. oncophora may result in mild clinical symptoms, but can lead to weight loss and damage of the small intestine, especially when co-infections with other nematodes such as O. ostertagi occur. Infections are usually treated with broad-spectrum anthelmintics such as benzimidazole, but resistance to these drugs has developed in the last decades and is now very common. C. oncophora has a direct life cycle. Infective larvae are ingested by the host. The larvae grow to adults, which reproduce in the small intestines. Eggs are shed onto the pasture with the faeces, which leads to new infections. Co-infections with other gastro-intestinal nematodes such as O. ostertagi and H. contortus are common.

<i>Cooperia</i> (nematode) Genus of roundworms

Cooperia is a genus of nematode from the Cooperiidae family that is one of the most common intestinal parasitic nematodes in cattle in temperate regions. Infections with Cooperia may result in mild clinical symptoms, but can lead to weight loss and damage of the small intestine, especially when co-infections with other nematodes such as Ostertagia ostertagi occur. Infections are usually treated with broad-spectrum anthelmintics such as benzimidazole, but resistance to these drugs has developed in the last decades and is now very common. Cooperia has a direct life cycle. Infective larvae are ingested by the host. The larvae grow to adults, which reproduce in the small intestines. Eggs are shed onto the pasture with the faeces, which leads to new infections. Co-infections with other gastro-intestinal nematodes such as O. ostertagi and Haemonchus contortus are common.

<span class="mw-page-title-main">Cat worm infections</span> Worm infections in cats

Cat worm infections, the infection of cats (Felidae) with parasitic worms, occur frequently. Most worm species occur worldwide in both domestic and other cats, but there are regional, species and lifestyle differences in the frequency of infestation. According to the classification of the corresponding parasites in the zoological system, infections can be divided into those caused by nematode and flatworms - in the case of the latter, mainly cestoda and trematoda - while other strains are of no veterinary significance. While threadworms usually do not require an intermediate host for their reproduction, the development cycle of flatworms always proceeds via alternate hosts.

<span class="mw-page-title-main">Nematode infection in dogs</span> Threadworm infections of dogs are frequent

Nematode infection in dogs - the infection of dogs with parasitic nemamotodes - are, along with tapeworm infections and infections with protozoa, frequent parasitoses in veterinary practice. Nematodes, as so-called endoparasites, colonize various internal organs - most of them the digestive tract - and the skin. To date, about 30 different species of nematode have been identified in domestic dogs; they are essentially also found in wild dog species. However, the majority of them often cause no or only minor symptoms of disease in adult animals. The infection therefore does not necessarily have to manifest itself in a worm disease (helminthosis). For most nematodes, an infection can be detected by examining the feces for eggs or larvae. Roundworm infection in dogs and the hookworm in dogs is of particular health significance in Central Europe, as they can also be transmitted to humans (zoonosis). Regular deworming can significantly reduce the frequency of infection and thus the risk of infection for humans and dogs.

References

  1. ↑ Blaxter, M. L., De Ley, P., Garey, J. R., Liu, L. X., Scheldeman P., Vierstraete, A., Vanfleteren, J. R., Mackey, L. Y., Dorris, M., Frisse, L. M., Vida, J. T., and Thomas W. K. 1998. A molecular evolutionary framework for the phylum Nematoda. Nature 392: 71–75.
  2. ↑ Fox, M. T. 2014. Gastrointestinal Parasites of Cattle: Gastrointestinal Parasites of Ruminants: Merck Veterinary Manual. Merck Veterinary Manual. Retrieved from http://www.merckvetmanual.com/mvm/digestive_system/gastrointestinal_parasites_of_ruminants/gastrointestinal_parasites_of_cattle.html
  3. ↑ Fox, M. T. 1993. Pathophysiology of infection with Ostertagia ostertagi in cattle. Vet Parasitol 46: 143–158. doi : 10.1016/0304-4017(93)90055-r
  4. ↑ Couvillion, C. E., Siefker, C., and Evans, R. R. 1996. Epidemiological study of nematode infections in a grazing beef cow-calf herd in Mississippi. Vet Parasitol 64: 207–218. doi : 10.1016/0304-4017(95)00899-3
  5. ↑ Fernández, A. S., Fiel, C. A., and Steffan, P. E. 1999. Study on the inductive factors of hypobiosis of Ostertagia ostertagi in cattle. Vet Parasitol 81: 295–307. doi : 10.1016/S0304-4017(98)00252-0
  6. ↑ Lichtenfels JR, H. E. 1993. The systematics of nematodes that cause ostertagiasis in domestic and wild ruminants in North America: an update and a key to species. Vet Parasitol 46: 33–53.
  7. ↑ Taylor, M. A., Coop, R. L., and Wall, R. L. 2015. Veterinary Parasitology 4th Edition. Wiley-Blackwell ISBN   978-0-470-67162-7.
  8. ↑ Taylor, M. A., Coop, R. L., and Wall, R. L. 2015. Veterinary Parasitology 4th Edition. Wiley-Blackwell ISBN   978-0-470-67162-7.
  9. ↑ Lichtenfels JR, H. E. 1993. The systematics of nematodes that cause ostertagiasis in domestic and wild ruminants in North America: an update and a key to species. Vet Parasitol 46: 33–53.
  10. ↑ Lichtenfels, J. R., Hoberg, E. P., and Zarlenga, D. S. 1997. Systematics of gastrointestinal nematodes of domestic ruminants: advances between 1992 and 1995 and proposals for future research. Vet Parasitol 72: 225–245. doi : 10.1016/S0304-4017(97)00099-X.
  11. ↑ van Wyk, J. ., Cabaret, J., and Michael, L. . 2004. Morphological identification of nematode larvae of small ruminants and cattle simplified. Vet Parasitol 119: 277–306. doi : 10.1016/j.vetpar.2003.11.012
  12. ↑ Casser, R. B., Ranganathan, S., Baillie, D., Sternberg, P., Mitreva, M., Mardis, E., and Wilson, R. K. 2007. Whole genome sequences of nematodes of the order strongylida. Proposal. http://eprints.ugd.edu.mk/2898/. Accessed online March 22, 2016.
  13. ↑ Casser, R. B., Ranganathan, S., Baillie, D., Sternberg, P., Mitreva, M., Mardis, E., and Wilson, R. K. 2007. Whole genome sequences of nematodes of the order strongylida. Proposal. http://eprints.ugd.edu.mk/2898/. Accessed online March 22, 2016.
  14. ↑ Merial. 2001. Ostertagia ostertagi. Online Producer Publication: http://us.merial.com/producers/pdfs/Ostertagia_ostertagi.pdf Archived 2017-05-10 at the Wayback Machine . Accessed March 23, 2016.
  15. ↑ Gibbs, H. C. 1988. The epidemiology of bovine ostertagiasis in the north temperate regions of North America. Vet Parasitol 27: 39–47.
  16. ↑ Gibbs, H. C. 1988. The epidemiology of bovine ostertagiasis in the north temperate regions of North America. Vet Parasitol 27: 39–47.
  17. ↑ Boden, E., and Andrews, A. 2015. Black's Veterinary Dictionary Vol. 17. Bloomsbury. ISBN   140817572X
  18. ↑ Merial. 2016. Endoparasites – Ostertagia. Online Publication: http://www.merial.co.nz/Cattle/beef/disease_information/Pages/oster.aspx. Accessed March 23, 2016.
  19. ↑ Beck, M. A., Colwell, D. D., Goater, C. P., Kienzle, S. W. 2015. Where's the risk? Landscape epidemiology of gastrointestinal parasitism in Alberta beef cattle. Parasit Vectors 8: 434.
  20. ↑ Stromberg, B. E. 1997. Environmental factors influencing transmission. Vet Parasitiol 72: 247–264.
  21. ↑ Merial. 2016. Endoparasites – Ostertagia. Online Publication: http://www.merial.co.nz/Cattle/beef/disease_information/Pages/oster.aspx. Accessed March 23, 2016.
  22. ↑ Merial. 2016. Endoparasites – Ostertagia. Online Publication: http://www.merial.co.nz/Cattle/beef/disease_information/Pages/oster.aspx. Accessed March 23, 2016.
  23. ↑ Myers, G. H., and Taylor, R. F. 1989. Ostertagiasis in cattle. J Vet Diagn Invest 1: 195–200. doi : 10.1177/104063878900100225
  24. ↑ Williams, J. C., Knox, J. W., and Loyacano, A. F. 1993. Epidemiology of Ostertagia ostertagi in weaner-yearling cattle. Vet Parasitol 46: 313–324.
  25. ↑ Merial. 2016. Endoparasites – Ostertagia. Online Publication: http://www.merial.co.nz/Cattle/beef/disease_information/Pages/oster.aspx. Accessed March 23, 2016.
  26. ↑ Eysker, M. 1993. The role of inhibited development in the epidemiology of Ostertagia infections. Vet Parasitol 46: 259–269.
  27. ↑ Eysker, M. 1993. The role of inhibited development in the epidemiology of Ostertagia infections. Vet Parasitol 46: 259–269.
  28. ↑ Merial. 2016. Endoparasites – Ostertagia. Online Publication: http://www.merial.co.nz/Cattle/beef/disease_information/Pages/oster.aspx. Accessed March 23, 2016.
  29. ↑ Myers, G. H., and Taylor, R. F. 1989. Ostertagiasis in cattle. J Vet Diagn Invest 1: 195–200. doi : 10.1177/104063878900100225
  30. ↑ Fox, M. T. (2014). Gastrointestinal Parasites of Cattle: Gastrointestinal Parasites of Ruminants: Merck Veterinary Manual. Merck Veterinary Manual. Retrieved from http://www.merckvetmanual.com/mvm/digestive_system/gastrointestinal_parasites_of_ruminants/gastrointestinal_parasites_of_cattle.html.
  31. ↑ Myers, G. H., and Taylor, R. F. 1989. Ostertagiasis in cattle. J Vet Diagn Invest 1: 195–200. doi : 10.1177/104063878900100225
  32. ↑ Fox, M. T. (1993). Pathophysiology of infection with Ostertagia-ostertagi in cattle. Vet Parasitol 46: 143–158. doi : 10.1016/0304-4017(93)90055-r
  33. ↑ Fox, M. T. (1993). Pathophysiology of infection with Ostertagia-ostertagi in cattle. Vet Parasitol 46: 143–158. doi : 10.1016/0304-4017(93)90055-r
  34. ↑ Fox, M. T. (1993). Pathophysiology of infection with Ostertagia-ostertagi in cattle. Vet Parasitol 46: 143–158. doi : 10.1016/0304-4017(93)90055-r
  35. ↑ Myers, G. H., and Taylor, R. F. 1989. Ostertagiasis in cattle. J Vet Diagn Invest 1: 195–200. doi : 10.1177/104063878900100225
  36. ↑ Claerebout, E., and Vercruysse, J. 2000. The immune response and the evaluation of acquired immunity against gastrointestinal nematodes in cattle: a review. Parasitol 120: S25–S42. doi : 10.1017/S0031182099005776
  37. ↑ Claerebout, E., Vercauteren, I., Geldhof, P., Olbrechts, A., Zarlenga, D. S., Goddeeris, B. M., & Vercruysse, J. 2005. Cytokine responses in immunized and non-immunized calves after Ostertagia ostertagi infection. Parasite Immunol 27: 325–331. doi : 10.1111/j.1365-3024.2005.00780.x
  38. ↑ Rinaldi, M., and Geldhof, P. 2012. Immunologically based control strategies for ostertagiosis in cattle: where do we stand? Parasite Immunol 34: 254–264. doi : 10.1111/j.1365-3024.2011.01313.x
  39. ↑ Vlaminck, J., Borloo, J., Vercruysse, J., Geldhof, P., and Claerebout, E. 2015. Vaccination of calves against Cooperia oncophora with a double-domain activation-associated secreted protein reduces parasite egg output and pasture contamination. Int J Parasitol 45: 209–213. doi : 10.1016/j.ijpara.2014.11.001
  40. ↑ Gasbarre, L. C., Leighton, E. A., and Sonstegard, T. 2001. Role of the bovine immune system and genome in resistance to gastrointestinal nematodes. Vet Parasitol 98: 51–64. doi : 10.1016/S0304-4017(01)00423-X
  41. ↑ Claerebout, E., and Vercruysse, J. 2000. The immune response and the evaluation of acquired immunity against gastrointestinal nematodes in cattle: a review. Parasitol 120: S25–S42. doi : 10.1017/S0031182099005776
  42. ↑ Charlier, J., Vercruysse, J., Smith, J., Vanderstichel, R., Stryhn, H., Claerebout, E., and Dohoo, I. 2010. Evaluation of anti-Ostertagia ostertagi antibodies in individual milk samples as decision parameter for selective anthelmintic treatment in dairy cows. Prev Vet Med 93:147–152. doi : 10.1016/j.prevetmed.2009.10.002
  43. ↑ Sanchez, J., Dohoo, I., Nodtvedt, A., Keefe, G., Markham, F., Leslie, K., DesCoteaux, L., and Campbell, J. 2002. A longitudinal study of gastrointestinal parasites in Canadian dairy farms: The value of an indirect Ostertagia ostertagi ELISA as a monitoring tool. Vet Parasitol 107: 209–226. doi : 10.1016/S0304-4017(02)00158-9
  44. ↑ Delafosse, A. 2013. The association between Ostertagia ostertagi antibodies in bulk tank milk samples and parameters linked to cattle reproduction and mortality. Vet Parasitol 197: 212–220. doi : 10.1016/j.vetpar.2013.05.023
  45. ↑ Delafosse, A. 2013. The association between Ostertagia ostertagi antibodies in bulk tank milk samples and parameters linked to cattle reproduction and mortality. Vet Parasitol 197: 212–220. doi : 10.1016/j.vetpar.2013.05.023
  46. ↑ Entrocasso, C., McKellar, Q., Parkins, J. J., Bairden, K., Armour, J., and Kloosterman, A. 1986. The sequential development of type I and type II ostertagiasis in young cattle with special reference to biochemical and serological changes. Vet Parasitol 21: 173–188. doi : 10.1016/0304-4017(86)90064-6
  47. ↑ Simpson, H. 2000. Pathophysiology of abomasal parasitism: Is the host or parasite responsible? Vet J 160: 177–191. doi : 10.1053/tvjl.2000.0491
  48. ↑ Vercruysse, J., Charlier, J., Dorny, P., and Claerebout, E. 2006. Diagnosis of helminth infections in cattle : World Buiatrics Congress.
  49. ↑ Areskog, M., Ljungström, B., and Höglund, J. 2013. Limited efficacy of pour-on anthelmintic treatment of cattle under Swedish field conditions. Int J Parasitol 3: 129–134. doi : 10.1016/j.ijpddr.2013.06.002
  50. ↑ Sutherland, I. A., and Leathwick, D. M. 2011. Anthelmintic resistance in nematode parasites of cattle: a global issue? Trend Parasitol 27: 176–181. doi : 10.1016/j.pt.2010.11.008
  51. ↑ Andersson, K.-M., Kumar, D., Bentzer, J., Friman, E., Ahrén, D., and Tunlid, A. 2014. Interspecific and host-related gene expression patterns in nematode-trapping fungi. BMC Genomics 15:968–981. doi : 10.1186/1471-2164-15-968
  52. ↑ Novobilský, A., Mueller-Harvey, I., and Thamsborg, S. M. 2011. Condensed tannins act against cattle nematodes. Vet Parasito 182: 213–220. doi : 10.1016/j.vetpar.2011.06.003
  53. ↑ Vlaminck, J., Borloo, J., Vercruysse, J., Geldhof, P., and Claerebout, E. 2015. Vaccination of calves against Cooperia oncophora with a double-domain activation-associated secreted protein reduces parasite egg output and pasture contamination. Int J Parasitol 45: 209–213. doi : 10.1016/j.ijpara.2014.11.001.
  54. ↑ Anziani, O. S., Suarez, V., Guglielmone, A. A., Warnke, O., Grande, H., and Coles, G. C. 2004. Resistance to benzimidazole and macrocyclic lactone anthelmintics in cattle nematodes in Argentina. Vet Parasitol 122: 303–306. doi : 10.1016/j.vetpar.2004.05.018
  55. ↑ Edmonds, M. D., Johnson, E. G., and Edmonds, J. D. 2010. Anthelmintic resistance of Ostertagia ostertagi and Cooperia oncophora to macrocyclic lactones in cattle from the western United States. Vet Parasitol 170: 224–229. doi : 10.1016/j.vetpar.2010.02.036.
  56. ↑ Waghorn, T., Leathwick, D., Rhodes, A., and Jackson, R. 2006. Prevalence of anthelmintic resistance on 62 beef cattle farms in the North Island of New Zealand. NZ Vet J 546: 278–282. doi : 10.1080/00480169.2006.36711.
  57. ↑ Bullen, S., Beggs, D., Mansell, P., Runciman, D., Malmo, J., Playford, M., and Pyman, M. 2016. Anthelmintic resistance in gastrointestinal nematodes of dairy cattle in the Macalister Irrigation District of Victoria. Aust Vet J 94: 35–41. doi : 10.1111/avj.12407
  58. ↑ De Graef, J., Claerebout, E., and Geldhof, P. 2013. Anthelmintic resistance of gastrointestinal cattle nematodes. Vlaams Diergeneeskundig Tijdschrift 82: 113–123.
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.