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.
Parasitoses of the digestive tract
Roundworm infection Two species of roundworms occur in dogs: Toxocara canis and Toxascaris leonina.
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.
Peroral infection (infection via the mouth) occurs through ingestion of eggs from the environment or larvae from collective hosts. The worm eggs are not infectious in the outside world until about two weeks after excretion in the feces. During this time, the second larval stage (larva L2) develops within the egg case, which - like larvae from collective hosts - is released during digestion in the small intestine of the new host. These larvae pierce the intestinal wall and enter the liver via the portal vein, where development to larva L3 takes place. Via the bloodstream, this migrates to the lungs, where it is coughed up and swallowed again. Only now do the larvae molt into adult worms. During their body migration, the larvae can also reach other organs, especially the skeletal muscles, where they cause tissue destruction. However, they often form persistent stages (stages in which the larvae persist in the tissue) in the tissue, which are important for the other two routes of infection. In transplacental infection (infection via the placenta), persistent larvae L3 migrate from the uterus through the placenta and infect the unborn pups while they are still in the womb. Galactogenic infection (infection via the mother's milk) of puppies occurs by excretion of roundworm larvae persisting in the mammary gland via the mother's milk during the suckling period.
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.
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. In Austria, T. canis was found to have a prevalence of 5.7%, while T. leonina had a prevalence of 0.6%. 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. Domestic dogs in Belgium showed a mean prevalence of T. canis of 4.4%, those from larger kennels of up to 31%. In domestic dogs in Serbia, T. canis was detectable in 30% of the animals, in herding and hunting dogs in Greece in 12.8% and T. leonina in 0.7% of animals. In Canada, T. canis was found to have a prevalence of 3.9%, and in the northeastern U.S., 12.6%. In Australia, T. canis was detected in 38% of domestic dogs, and in animals within the first year of life, as many as 73%. In Brazil, T. canis could be detected in about 9% of domestic dogs, in Thailand in 7.4%. In Nigeria, T. canis was observed in a prevalence of 9%, T. leonina only in one of 0.6%, in Gabon 58.5% of domestic dogs were infected with T. canis. In wolves living in the temperate climate zone, however, T. leonina is the most common intestinal nematode (prevalence 74%). Studies on red foxes in southern England showed a prevalence of 56% (T. canis) and 1.5% (T. leonina), in Denmark 59% and 0.6%, respectively. 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. 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.
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