Olias, Philipp; Meyer, Anne; Klopfleisch, Robert; Lierz, Michael; Kaspers, Bernd; Gruber, Achim D.
(11. February 2013):
Modulation of the host Th1 immune response in
pigeon protozoal encephalitis caused by
In: Veterinary Research, Vol. 44, No. 10
Pigeon protozoal encephalitis (PPE) is an emerging central-nervous disease of domestic pigeons (Columba livia f.
domestica) reported in Germany and the United States. It is caused by the apicomplexan parasite Sarcocystis
calchasi which is transmitted by Accipter hawks. In contrast to other members of the Apicomplexa such as
Toxoplasma and Plasmodium, the knowledge about the pathophysiology and host manipulation of Sarcocystis is
scarce and almost nothing is known about PPE. Here we show by mRNA expression profiling a significant
down-modulation of the interleukin (IL)-12/IL-18/interferon (IFN)-γ axis in the brains of experimentally infected
pigeons during the schizogonic phase of disease. Concomitantly, no cellular immune response was observed in
histopathology while immunohistochemistry and nested PCR detected S. calchasi. In contrast, in the late
central-nervous phase, IFN-γ and tumor necrosis factor (TNF) α-related cytokines were significantly up-modulated,
which correlated with a prominent MHC-II protein expression in areas of mononuclear cell infiltration and necrosis.
The mononuclear cell fraction was mainly composed of T-lymphocytes, fewer macrophages and B-lymphocytes.
Surprisingly, the severity and composition of the immune cell response appears unrelated to the infectious dose,
although the severity and onset of the central nervous signs clearly was dose-dependent. We identified no or only
very few tissue cysts by immunohistochemistry in pigeons with severe encephalitis of which one pigeon repeatedly
remained negative by PCR despite severe lesions. Taken together, these observations may suggest an immune
evasion strategy of S. calchasi during the early phase and a delayed-type hypersensitivity reaction as cause of the
extensive cerebral lesions during the late neurological phase of disease.