Veterinary Nematodes
Marthe Bernskoetter
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Before revised World Association for the Advancement of Veterinary Parasitology (WAAVP) guidelines on the detection of anthelmintic resistance can be produced, validation of modified and new methods is required in laboratories in different parts of the world. There is a great need for improved methods of detection of anthelmintic resistance particularly for the detection of macrocyclic lactone resistance and for the detection of resistant nematodes in cattle. Therefore, revised and new methods are provided here for the detection of anthelmintic resistance in nematodes of ruminants, horses and pigs as a basis for discussion and with the purpose that they are evaluated internationally to establish whether they could in the future be recommended by the WAAVP. The interpretation of the faecal egg count reduction test has been modified and suggestions given on its use with persistent anthelmintics and continuous release devices. An egg hatch test for benzimidazole (BZ) resistance is described. A microagar larval development test for the detection of benzimidazole and levamisole resistance provides third stage larvae for the identification of resistant worms. The sensitivity of these two tests can be increased by using discriminating doses rather than LD(50) values. Details are given of a PCR based test for the analysis of benzimidazole resistance in strongyles of sheep and goats, horses and cattle. Although promising for ruminant trichostrongyles, quantitative determination of gene frequency using real time PCR requires further development before PCR tests will be used in the field. Apart from faecal egg count reduction tests there are currently no satisfactory tests for macrocylic lactone resistance despite the great importance of this subject. Except for treatment and slaughter trials there are no validated tests for fasciolicide resistance or for the detection of resistance in cestodes.
Reports of drug resistance have been made in every livestock host and to every anthelmintic class. In some regions of world, the extremely high prevalence of multi-drug resistance (MDR) in nematodes of sheep and goats threatens the viability of small-ruminant industries. Resistance in nematodes of horses and cattle has not yet reached the levels seen in small ruminants, but evidence suggests that the problems of resistance, including MDR worms, are also increasing in these hosts. There is an urgent need to develop both novel non-chemical approaches for parasite control and molecular assays capable of detecting resistant worms.
Nematode infection in dogs - the infection (also infestation) of dogs with parasitic nemamotodes - are, along with tapeworm infections and infections with protozoa (giardiasis, neosporosis), frequent parasitoses in veterinary practice. Nematodes, as so-called endoparasites ("internal parasites"), 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.
T. canis is an 8 to 18 cm long nematode that parasitizes (lives as a parasite) in the small intestine. There, the adult females release approximately 85 μm large unfurrowed eggs, whose shell is thick and rough (golf ball-like) and which are released into the outside world via the feces. The period from infection to egg laying (prepatency) is three to six weeks, depending on the route of infection and the age of the dog. T. canis does not require an intermediate host for development, but infection of dogs can occur via collective hosts such as rodents and birds. In collective hosts (paratenic hosts), no complete development cycle of the parasites occurs, but infective stages can accumulate in them through multiple infections. In principle, three routes of infection are possible for T. canis: peroral infection and transplacental and galactogenic infection, which are much more common in puppies.
T. leonina is 6 to 10 cm long, the eggs are about 80 μm in size and thick-shelled. Unlike the eggs of T. canis, they have a smooth surface. Infection occurs perorally by ingestion of eggs from contaminated (polluted) food or via collective hosts such as rodents, birds, reptiles, or arthropods. The prepatency is 7 to 10 weeks.[2]
In a German study, T. canis was detected at a frequency (prevalence) of 22.4%, while T. leonina was detected in only 1.8% of domestic dogs.[3] In Austria, T. canis was found to have a prevalence of 5.7%, while T. leonina had a prevalence of 0.6%.[4] Both roundworms occur worldwide. A Czech study showed large differences in prevalence depending on living conditions: 6% of privately owned dogs in Prague, 6.5% of shelter dogs, and almost 14% of dogs from rural areas were infected with T. canis. In addition, an increase in prevalence has been shown in autumn.[5] Domestic dogs in Belgium showed a mean prevalence of T. canis of 4.4%, those from larger kennels of up to 31%.[6] In domestic dogs in Serbia, T. canis was detectable in 30% of the animals,[7] in herding and hunting dogs in Greece in 12.8% and T. leonina in 0.7% of animals.[8] In Canada, T. canis was found to have a prevalence of 3.9%,[9] and in the northeastern U.S., 12.6%.[10] In Australia, T. canis was detected in 38% of domestic dogs, and in animals within the first year of life, as many as 73%.[11] In Brazil, T. canis could be detected in about 9% of domestic dogs,[12] in Thailand in 7.4%.[13] In Nigeria, T. canis was observed in a prevalence of 9%, T. leonina only in one of 0.6%,[14] in Gabon 58.5% of domestic dogs were infected with T. canis.[15] In wolves living in the temperate climate zone, however, T. leonina is the most common intestinal nematode (prevalence 74%).[16] Studies on red foxes in southern England showed a prevalence of 56% (T. canis) and 1.5% (T. leonina),[17] in Denmark 59% and 0.6%, respectively.[18] Foxes thus represent a natural reservoir of the pathogen.
While infection with T. leonina only very rarely causes clinical manifestations such as diarrhea, the disease-causing (pathogenic) effect of T. canis is much stronger. In puppies, a reduced general condition, shaggy coat, retardation in growth, alternating diarrhea and constipation, a distended abdomen ("worm belly") and anemia occur. Complications of T. canis infection, some of which are fatal, include intestinal obstruction due to worm clusters, small intestinal rupture, pneumonia, liver inflammation, or neurological manifestations due to stray migratory larvae in the central nervous system.[2]
In the case of worms in vomit, the diagnosis can already be made without special examinations. A roundworm infection can be detected with relative certainty by microscopic detection of the eggs extracted from the feces by the flotation method, but only after the expiration of the prepatency period.[2]
Females of A. caninum release eggs about 6540 μm in size, which already have 4-10 furrowing stages at deposition. They are oval and thin-shelled and enter the outside world via feces. The prepatency is two to four weeks. The larvae released from the eggs can bore through the skin into a new host (percutaneous infection) or be ingested perorally - mostly via collective hosts such as rodents. As with T. canis, infection of puppies is also possible through the mother's milk (galactogenic infection). Larvae dormant in the mammary gland can be shed over a period of up to three suckling periods after a bitch has been infected once.[19]
The eggs of U. stenocephala are similar to those of A. caninum, but have a larger longitudinal axis of 8545 μm. Infection occurs exclusively by peroral ingestion of larvae via contaminated food or collective hosts.
In Germany, an infection frequency of 8.6% was determined,[3] in Austria of 0.1% for A. caninum and 0.2% for U. stenocephala.[4] A Czech study determined a prevalence of 0.4% each for both hookworms,[5] a Greek one of 2.8% together.[8] In studies of domestic dogs in Serbia[7] and Nigeria,[20] hookworms were detectable in a quarter of the domestic dogs examined, but U. stenocephala was detectable in only 0.4% of animals.[14] In Gabon, both hookworms were detectable in 35% of domestic dogs.[15] In Canada, A. caninum was detected in only 1.3% of domestic dogs,[9] but in the northeastern U.S. it was detected in 12%.[10] In fact, in a Brazilian study (37.8% of domestic dogs)[12] and a Thai study (58.1% of domestic dogs)[13] A. caninum was the most common nematode of all. In Australia, a prevalence of 26% was found for U. stenocephala.[11] In contrast, in wolves that inhabit tundras, U. stenocephala is the most common intestinal nematode (prevalence 45%).[16] In red foxes, this parasite is also very common, with a prevalence of 68%.[17][18]
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