Introduction to Parasitology

Infection and disease

The terms infection and disease are not synonymous. While an animal must be infected with a parasite to produce disease it does not necessarily follow that all infected animals will show clinical signs of disease.

When susceptible animals are infected with viruses, bacteria and protozoa, the host's lack of immunity usually results in clinically obvious disease. The outcome of these infections will depend on an interaction of factors including the virulence of the organism and how rapidly and successfully the host can mount an effective immune response.

Protozoa are unique among the parasites in that they multiply rapidly in their hosts such that they may overwhelm them. This is particularly true of susceptible animals such as the young or older animals whose immune system has been compromised in some way. For  example in congenital infections with Toxoplasma and Neospora, the disease is usually more severe because the fetus lacks a fully developed immune system and the outcome is likely to be fetal death. In cats receiving kidney transplants their immune system will be compromised because they are being treated with immunosuppresive drugs like corticosteroids. These cats are at high risk for being overwhelmed by acute Toxoplasmosis, an infection that has lain dormant in these transplant recipients and kept in check by cell mediated immunity. Suppression of cmi by immunosuppressive drugs allows these dormant organisms to begin mutiplying again producing acute infections that may be severe enough to overwhelm transplant recipients causing their death.

This example illustrates another possible outcome to parasitic diseases  namely that the immune response allows a host to successfully overcome acute clinical disease but the infection is either not totally cleared or the animal remains susceptible to low level infections. In both cases,  the animal may harbor chronic subclinical infections throughout its life. Subsequent events during its lifetime may compromise the immune response and allow these chronic infections to flare up as potentially life-threatening acute diseases or make the anima, once more, susceptible to a new infection with a parasite.

Parturition and lactation are events that, in some cases, appear to make animals more susceptible to parasite infections probably resulting from  compromise of the immune response. For example, it is well established that parturient and lactating ewes are more susceptible to infections with Haemonchus contortus and post- partum dairy cattle are more susceptible to coccidial infections.

Nematodes are more complicated than protozoa partly because they do not multiply inside their hosts. One nematode egg can only produce one infective larvae that develops into one adult worm. Therefore the development of clinical disease in hosts infected with nematodes depends almost entirely on the actual number of larvae infecting a susceptible host. I other words, the  outcome of nematode infections is generally more dependent on the parasite burden and that is, in turn, directly related to the infecting dose. Generally speaking there is a direct correlation between the number of infecting larvae and the severity of any disease produced; a small number of infective larvae will produce minor pathological changes and generally no obvious clinical disease. It will often take many larvae (thousands or even tens of thousands) to incite pathological changes severe enough to produce serious clinical signs. For example, a foal infected with 100 Parascaris equorum will show either no clinical signs or at worst some coughing and minor nasal discharge. Conversely, a foal infected with 5,000
P. equorum will show severe clinical signs and may succumb to the infection.

However, like all general rules there are often exceptions. Within the nematodes there  are some whose anatomical locations, in a host, are such that even a small number of nematodes will incite pathological changes that can have devastating consequences for a host.

One example is Strongylus vulgaris in horses. Migration of even a few larvae in the mesenteric arterial tree can produce pathological changes (thrombi and emboli) severe enough to block blood supply to significant portions of the large intestine. The outcome is often acute colic that may be fatal. These changes are  shown in the images below.

Images illustrating the pathogenesis of Strongylus vulgaris infections in horses

The celiac axis and its branches and the cranial mesenteric artery and its branches showing thrombosis and thickening of arterial walls due to Strongylus vulgaris larval migrations. Image courtesy of Dr. Owen Slocombe and Merial Inc. Necrosis of the cecum and ventral colon of a horse resulting from ischemis and infarctions due to lesions produced by migrating larvae of Strongylus vulgaris.
Image courtesy of Dr. Harold Drudge and Hoechst-Roussel
The dorsal aorta of a horse showing fibrin tracks due to migrations of Strongylus vulgaris larvae beyond the root of the cranial mesenteric artery.
Image courtesy of Merial Inc.

Arteriographic picture of the abdomen of a foal 30 days after infection with 50 third stage larvae of Strongylus vulgaris.
Image courtesy of Dr Jay Georgi. The mesenteric artery and its branches show minor changes

Arteriographic picture of the abdomen of a foal 60 days after infection with 50 third stage larvae of Strongylus vulgaris.
Image courtesy of Dr Jay Georgi. The mesenteric artery and its branches show extensive changes.
Arteriographic picture of the abdomen of a foal 60 days after infection with 50 third stage larvae of Strongylus vulgaris and treatment at 30 days with a larvicidal anthelmintic. The mesenteric artery is essentially normal.
Image courtesy of Dr Jay Georgi


A second exception is Dirofilaria immitis (the heartworm) in cats. Infections with even one or two adult heartworms may cause severe pathophysiological changes and life-threatening disease.



Parasites and Parasitic Diseases of Domestic Animals
Dr. Colin Johnstone (principal author)
Copyright 1998 University of Pennsylvania
This page was last modified on January 24, 2000