The fact that the host immune system appears to have difficulty controlling the malarial infection is probably the reason why so many aberrant responses have been described. The host overreacts, causing an immunologically inappropriate response which has no effect on the parasite, but may have immunopathological consequences of various degrees of severity.
The hypergammaglobulinaemia observed in malaria is the result of a polyclonal stimulation which leads to the production of a variety of auto-antibodies. The polyclonal stimulation of B-lymphocytes is a direct consequence of the mitogenic effect of molecules released by malaria parasites; the precise nature of the mitogens is not yet known.
As in many parasitic infections, various forms of immusuppression also occur in malaria. The response to primary vaccination with a wide range of antigens is suppressed by acute malaria (e.g. the response to meningococcal polysaccharide vaccine) and malaria infection may increase the risk to other infections (e.g. Salmonella septicaemia or respiratory tract infections). It has been suggested that this may explain the 'hidden mortality' due to malaria.
Specific forms of immunosuppression will be addressed:
There is a contribution of immunopathology in the pathogenesis of many aspects of malaria, including anaemia, thrombocytopaenia, cerebral malaria, malaria in pregnancy, which are described in the relevant sections.
Two immunopathological syndromes associated with malaria are of particular interest: