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infection ( Price et al., 2009 ). In areas of chloroquine resistance, this is exac-
erbated further by delayed parasite clearance, and recrudescent and chronic
infections ( Price et al., 2007b ).
Impaired production of red cells is also likely to contribute to vivax-
related anaemia, particularly with chronic and repeated infections, but the
exact mechanisms are unclear. Cytokine-related dyserythropoiesis has been
demonstrated in P. vivax malaria in adults ( Wickramasinghe et al., 1989 ) but
not yet in children. Wickramasinghe et al. proposed that this might relate to
direct toxicity of P. vivax on erythroblasts or enhanced bone marrow phago-
cyte activity with associated release of locally cytotoxic molecules ( Wick-
ramasinghe and Abdalla, 2000 ). Erythroblasts can be infected and lysed by
P. vivax in vitro , and recent bone marrow studies have shown erythroblast
infection in vivo in adult P. vivax infection ( Ru et al., 2009 ). Bone marrow
hypoxia may contribute to impaired erythropoiesis in P. falciparum malaria
as a result of marrow sinusoid obstruction by cytoadherent schizonts ( Gan-
dapur et al., 1997 ; Chang and Stevenson, 2004 ). Sequestration of schizonts
in the marrow of patients with P. vivax infection has not been clearly dem-
onstrated and, therefore, hypoxia is unlikely to be an important mechanism
of impaired erythrocyte production in this disease. Impaired erythropoietin
production or response is also an important mechanism of anaemia in P.
falciparum malaria ( Vedovato et al., 1999 ; Burgmann et al., 1996 ; el Hassan
et al., 1997 ) but erythropoietin metabolism is yet to be studied in vivax
infection.
11.2.2. Acute lung injury
Even in uncomplicated vivax malaria, clinical pulmonary function testing
shows subclinical evidence of small airways obstruction, impaired ventilation
and reduced gas transfer at the alveolar-capillary membrane ( Anstey et al.,
2002 , 2007 ). Non-invasive imaging shows that these changes are associ-
ated with increased pulmonary phagocytic cell activity ( Anstey et al., 2002 ).
Autopsy findings in a fatal Indian case of ARDS from PCR-confirmed
P. vivax prior to antimalarial treatment showed heavy intravascular mono-
cytic infiltrates with diffuse endothelial and alveolar damage ( Valecha et al.,
2009 ). In contrast, in the Manaus autopsy series, mostly post-treatment, the
predominant interstitial inflammatory cells were neutrophils ( Lacerda et al.,
2012 ). While indirect in vivo gas transfer studies infer possible accumulation
of P. vivax -infected RBCs in the lung ( Anstey et al., 2007 ) and parasites
were seen in alveolar capillaries after peripheral blood clearance in one of
the Manaus autopsy cases of ALI ( Lacerda et al., 2012 ), the Indian severe
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