Page 926 - Veterinary Immunology, 10th Edition
P. 926
Trypanosomiasis is not the only protozoan infection in which
VetBooks.ir variation of surface antigens occurs. It has also been recorded in
infections by Babesia bovis, the plasmodia, and the intestinal parasite
Giardia lamblia.
Since parasitic protozoa must evade the immune responses, it is
not surprising that they preferentially invade immunosuppressed
individuals. Organisms that are normally well controlled by the
immune response, such as Toxoplasma gondii or Cryptosporidium
bovis, can grow and produce severe disease in immunosuppressed
animals. For this reason, acute toxoplasmosis and cryptosporidiosis
commonly occur in humans immunosuppressed for transplantation
purposes or for cancer therapy and in AIDS patients.
Parasites often trigger a very robust T cell response.
Unfortunately this may fail to eliminate the pathogen that then
persists in the form of a chronic infection. Over time this can lead to
T cell exhaustion. The T cells may be functionally impaired or even
eliminated. These defects tend to follow a consistent pattern with an
initial inability to produce IL-2, followed by loss of cytotoxicity and
proliferative ability, followed by impaired TNF-α and IFN-γ
production. T cell exhaustion and loss of function occurs in chronic
protozoan diseases such as Toxoplasmosis and Leishmaniasis.
Adverse Consequences
The immune responses to protozoa may result in hypersensitivity
reactions. Type I hypersensitivity is a feature of trichomoniasis and
results in local irritation and inflammation in the genital tract. Type
II cytotoxic reactions are of significance in babesiosis and
trypanosomiasis, in which they contribute to the anemia. In
babesiosis, red cells express parasite antigens on their surfaces and
are thus recognized as foreign and eliminated by hemolysis and
phagocytosis. In trypanosomiasis, either fragments of disrupted
organisms or possibly preformed immune-complexes bind to red
cells and provoke their elimination, causing anemia. Immune
complex formation on circulating red cells is not the only problem
of this type in trypanosomiasis. Excessive immune complex
formation may lead to vasculitis and glomerulonephritis (type III
hypersensitivity; see Chapter 32). Immune-complex lesions are a
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