Neurological complications in patients with Plasmodium vivax malaria from Karachi, Pakistan.

BACKGROUND: Malaria remains an endemic disease in Pakistan with an estimated healthcare burden of 1.6 million cases annually, with Plasmodium vivax accounting for 67% of reported cases. P. vivax is the most common species causing malaria outside of Africa, with approximately 13.8 million reported cases worldwide. METHOD: We report a series of P. vivax cases with cerebral involvement that presented at Aga Khan University Hospital, Karachi, Pakistan. RESULTS: The majority of the patients presented with high-grade fever accompanied by projectile vomiting and abnormal behaviour, seizures, shock and unconsciousness. Seven of 801 patients with P. vivax monoinfection presented or developed cerebral complications. P. vivax infections were diagnosed based on peripheral smears and rapid diagnostic testing. CONCLUSION: P. vivax infection can lead to severe complications, although not with the frequency of Plasmodium falciparum infection. Current cases highlight an increasing trend of cerebral complications caused by P. vivax.

Plasmodium vivax hospitalizations in a monoendemic malaria region: severe vivax malaria?

Severe malaria caused by Plasmodium vivax is no longer considered rare. To describe its clinical features, we performed a retrospective case control study in the subregion of Luciano Castillo Colonna, Piura, Peru, an area with nearly exclusive vivax malaria transmission. Severe cases and the subset of critically ill cases were compared with a random set of uncomplicated malaria cases (1:4). Between 2008 and 2009, 6,502 malaria cases were reported, including 106 hospitalized cases, 81 of which fit the World Health Organization definition for severe malaria. Of these 81 individuals, 28 individuals were critically ill (0.4%, 95% confidence interval = 0.2-0.6%) with severe anemia (57%), shock (25%), lung injury (21%), acute renal failure (14%), or cerebral malaria (11%). Two potentially malaria-related deaths occurred. Compared with uncomplicated cases, individuals critically ill were older (38 versus 26 years old, P < 0.001), but similar in other regards. Severe vivax malaria monoinfection with critical illness is more common than previously thought.

Algid malaria treated with early goal-directed therapy.

Severe malaria complicated by circulatory shock is known as algid malaria. Cases of severe imported malaria are seen increasingly frequently in emergency departments in the United States, Europe, and other locales. The optimal volume resuscitation strategy for patients with severe malaria is not well-defined. A 20-year-old woman, who immigrated 2 weeks ago from Niger, Africa, presented to the emergency department of an urban teaching hospital with fever, hypotension, and malaise. She was resuscitated with 5.5 L of normal saline solution and norepinephrine. Thin blood smear demonstrated Plasmodium falciparum with parasitemia of 10% to 15%. She had rapid reversal of circulatory shock, cleared her parasitemia in less than 48 hours with antimalarial therapy, and was discharged home on hospital day 6 in good condition. The optimal resuscitation strategy for algid malaria is unknown, and volume restriction has been advocated as a means to prevent life-threatening cerebral and pulmonary edema. Although not identical, the late inflammatory response in severe malaria leading to capillary permeability shares many similarities with the immunologic response in bacterial sepsis. Our case report discusses a patient with severe imported malaria complicated by shock, successfully managed with large-volume fluid resuscitation, hemodynamic optimization, early antimalarial agents, and broad-spectrum antibiotics. This report questions the strategy of cautious fluid resuscitation in algid malaria and suggests that case series comparing goal-directed resuscitation to historic controls along with prospective multicenter controlled trials should be conducted to determine the best fluid resuscitation strategy.

Three unusual presentations of plasmodium vivax malaria.

We present three cases of unusual and complicated malaria caused by Plasmodium vivax. Parenteral artemisinin derivatives or quinine should be used, irrespective of chloroquine sensitivity, for treatment of severe malaria.

P. vivax malaria complicated by shock and ARDS.

We report a case of Plasmodium vivax malaria complicated by shock and ARDS. The patient responded to oral chloroquine and primaquine and PCR was positive for P. vivax DNA and negative for P. falciparum DNA. P. vivax may cause severe complications and where the possibility of mixed infections exists, blood should be sent for PCR analysis so that mixed infections can reliably be excluded.

Trypanosoma cruzi sensitizes mice to fulminant SEB-induced shock: overrelease of inflammatory cytokines and independence of Chagas' disease or TCR Vbeta-usage.

Trypanosoma cruzi-infected mice display increased susceptibility to shock induced by injection of lipopolysaccharide (LPS), anti-CD3, or resulting from interleukin (IL)-10-defective response to the parasite itself, but the basis of such susceptibility remains unknown. Herein, we tested the susceptibility of mice inoculated with virulent and avirulent T. cruzi to staphylococcal enterotoxins (SE), potent inducers of inflammatory cytokine secretion. Mice infected with T. cruzi CL-strain or inoculated with the avirulent clone CL-14, a clone that does not induce disease or polyclonal lymphocyte activation, succumb suddenly to low doses of staphylococcal enterotoxin B (SEB), but not to staphylococcal enterotoxin A (SEA). High plasma levels of TNF, IFN-gamma, and liver transaminases alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were found in these mice, indicating lethal toxic shock. Sensitization to shock required inoculation of live avirulent trypomastigotes and a time interval before challenge with SEB. We found no prior skewing of T cell receptor (TCR) Vbeta-repertoire in CL-14-inoculated mice that could be responsible for sensitization. Splenocytes from CL-14-inoculated mice proliferated more under anti-Vbeta8 than anti-TCRbeta stimulation when compared with normal mice, but were suppressed to SEB stimulation. Both SEB and anti-Vbeta8 antibodies stimulated splenocytes from T. cruzi-inoculated mice to secrete higher levels of inflammatory cytokines than normal controls. Taken together, our results show that T. cruzi inoculation can sensitize mice to lethal SEB-induced shock even in the absence of tissue damage, polyclonal lymphocyte activation, or previously increased levels of inflammatory cytokines, and they suggest that altered reactivity of Vbeta8 lymphocytes may be involved in the phenomenon.