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.
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Images
illustrating the pathogenesis of Strongylus vulgaris infections in horses
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| 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. |
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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.
