Biology Reference
In-Depth Information
of three doses of 30 mg primaquine per week. That resulted in relatively
poor efficacy (74% against
P. falciparum
; 90% against
P. vivax
): suggesting
that parasites developing for more than 48 h before exposure to prima-
quine seemed more likely to survive (
Baird et al., 1995b
). Daily dosing
proved more efficacious and equally well tolerated as weekly chloroquine
over 16 weeks, and in one trial, over 50 weeks of daily dosing (
Fryauff et al.,
1995
;
Baird et al., 2001
). These studies, conducted in endemic zones, could
only gauge efficacy against the primary attack. The possibility of relapses
could not be ruled out because of constant reinfection of subjects, but, at
least in concept, prevention of primary attack by killing very early devel-
opmental forms would also kill parasites attempting development to hyp-
nozoites. In 2012, primaquine is recommended by many authorities as safe
and effective for primary prophylaxis against vivax malaria, despite lack-
ing regulatory approval for this indication because of a lack of commercial
incentives to obtain such for a drug without patent protection.
5. DIAGNOSIS OF VIVAX MALARIA
5.1. Clinical Diagnosis
Clinical diagnosis of vivax malaria is difficult because signs and symptoms
are non-specific and impacted by endemicity and host immunity. Com-
mon symptoms include malaise, fever, chills, diaphoresis, headache, arthral-
gia, myalgia, cough, abdominal pain, nausea, vomiting, and diarrhoea, which
can also occur with many common systemic febrile illnesses such as men-
ingitis, pneumonia or gastroenteritis. Splenomegaly, anaemia, leukopenia
and thrombocytopenia are also common, but non-specific. Depending on
where infection is acquired, the differential diagnosis should also include
dengue fever, typhoid fever (particularly in south central Asia), infectious
mononucleosis, rickettsiosis, influenza, bacteremia and region-specific arbo-
viral infections (
Freedman et al., 2006
;
Wilson et al., 2007
). The periodicity
of fever, classically described as 48 h paroxysms, is a poor predictor of diag-
nosis since most patients, particularly non-immunes, present with asynchro-
nous erythrocytic schizogony with 24-h cycles of paroxysm.
A multitude of clinical algorithms have been evaluated for utilization
in resource-poor areas where microscopic diagnosis of malaria may be
limited. Such efforts are designed to reduce inappropriate prescription of
antimalarials for non-malarial illness, which contributes to emergence of
antimalarial resistance (
White and Olliaro, 1996
;
Gbotosho et al., 2009
).
