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known. However, with the reports of thrombotic microangiopathy in
some cases, vivax-associated kidney disease ( Sinha et al., 2012 ; Saharan
et al., 2008 ; Sharma et al., 1993 ), these processes may contribute to
at least a proportion of vivax associated AKI, coma, anaemia and/or
thrombocytopenia.
11.1.7. Susceptibility to bacterial co-infection?
It remains to be determined whether, as with falciparum malaria ( Berkley
et al., 1999 ), the risk of bacteraemia is increased in vivax malaria. Plasmodium
falciparum is thought to increase the risk of concurrent bacteraemia through
multiple mechanisms, including impairment of granulocyte oxidative burst
through induction of hemoxygenase-1 ( Cunnington et al., 2012 ), impaired
phagocyte function through ingestion of haemozoin ( Schwarzer et al.,
2008 ) and quenching of monocyte nitric oxide ( Yeo et al., 2009 ). Similar
pathophysiological processes are plausible in vivax malaria but have not
been studied specifically with this species. However, impairment of neu-
trophil chemotaxis has been shown in P. vivax infection and hypothesised
to contribute to an increased risk of bacterial co-infection in vivax malaria
( Leoratti et al., 2012 ).
Whether or not P. vivax increases susceptibility to bacterial co-infection,
it is likely to exacerbate the consequences of bacterial co-infection. Plasmo-
dium falciparum is capable of priming the innate immune response due to
interferon-γ-induced enhancement of toll-like receptor expression and
function ( Franklin et al., 2009 ). This has been proposed to prime the host
to a greater systemic inflammatory response to bacterial and other TLR
agonists than would otherwise occur, e.g. during bacterial, viral and other
co-infections ( Franklin et al., 2009 ; Leoratti et al., 2012 ). While data in
P. vivax are awaited, given the greater inflammatory response in P. vivax than
P. falciparum , it is possible that marked priming of innate immune responses
in P. vivax infections may account for the relatively high proportion of
severe vivax reports occurring with septic shock and multiorgan dysfunc-
tion, particularly in endemic regions with a high prevalence of bacterial
co-infections. With such TLR priming, excessive sepsis-like responses to
circulating bacterial products may well occur with bacterial burdens less
than those detectable using routine blood culture systems, which, along
with widespread community availability of antibiotics, may be a plausible
explanation for septic-shock presentations in P. vivax despite a low rate of
reported blood culture-positivity.
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