High impact information on Encephalitozoonosis

• Thus, it appeared that the relative susceptibility of C57BL/6 mice to encephalitozoonosis may be due to defective accessory cell function of splenic and peritoneal macrophages, depressed lymphoproliferation against spore fragments (possibly due to prostaglandin-mediated suppression) and a delay in LK production [1].
• Blood samples of animals with and without spontaneous encephalitozoonosis were evaluated, and compared for the presence of epinephrine (EPI), norepinephrine (NE), and dopamine (DA) [2].
• Infection with the intracellular microsporidium Encephalitozoon cuniculi can cause serious disease, encephalitozoonosis, in the blue fox (Alopex lagopus) [3].
• Lethal encephalitozoonosis in cyclophosphamide-treated rabbits [4].
• Hypergammaglobulinemic lpr mice with encephalitozoonosis did not develop more severe lesions than lpr mice without encephalitozoonosis nor was their death accelerated [5].

Chemical compound and disease context of Encephalitozoonosis

• Fox encephalitozoonosis: isolation of the agent from an outbreak in farmed blue foxes (Alopex lagopus) in Finland and some hitherto unreported pathologic lesions [6].

Gene context of Encephalitozoonosis

• The results suggested that the lpr gene does not influence susceptibility to murine encephalitozoonosis [5].

Analytical, diagnostic and therapeutic context of Encephalitozoonosis

• The results suggest that immunosuppression induced by cyclophosphamide can give rise to a lethal form of encephalitozoonosis [4].

References