BackgroundMounting reports on severe Plasmodium vivax malaria from across the globe have raised concerns among the scientific community. However, the risk of P. vivax resulting in complicated malaria and mortality is not as firmly established as it is with Plasmodium falciparum. This study was conducted to determine the severity proportion and factors associated with severity in cases of vivax and falciparum malaria.MethodsAdult patients microscopically diagnosed to have P. vivax/P. falciparum infections from the year 2007-2011 were evaluated based on their hospital records. Severe malaria was defined as per the World Health Organization’s guidelines. Comparison was made across species and binary logistic regression was used to determine risk factors of severity.ResultsOf 922 malaria cases included in the study, P. vivax was the largest (63.4%, 95% confidence interval (CI) 60.3-66.5%) infecting species, followed by P. falciparum (34.4%, 95% CI 31.3-37.5%) and their mixed infection (2.2%, 95% CI 1.3-3.2%). Severity in P. vivax and P. falciparum was noted to be 16.9% (95% CI 13.9-19.9%) and 36.3% (95% CI 31.0-41.6%) respectively. Plasmodium falciparum had significantly higher odds [adjusted odds ratio (95% CI), 2.80 (2.04-3.83)] of severe malaria than P. vivax. Rising respiratory rate [1.29 (1.15-1.46)], falling systolic blood pressure [0.96 (0.93-0.99)], leucocytosis [12.87 (1.43-115.93)] and haematuria [59.36 (13.51-260.81)] were the independent predictors of severity in P. vivax. Increasing parasite index [2.97 (1.11-7.98)] alone was the independent predictor of severity in P. falciparum. Mortality in vivax and falciparum malaria was 0.34% (95% CI -0.13-0.81%) and 2.21% (95% CI 0.59-3.83%), respectively. Except hyperparasitaemia and shock, other complications were associated (P < 0.05) with mortality in falciparum malaria. Pulmonary oedema/acute respiratory distress syndrome was associated (P = 0.003) with mortality in vivax malaria. Retrospective design of this study possesses inherent limitations.ConclusionsPlasmodium vivax does cause severe malaria and mortality in substantial proportion but results in much lesser amalgamations of multi-organ involvements than P. falciparum. Pulmonary oedema/acute respiratory distress syndrome in P. vivax infection could lead to mortality and therefore should be diagnosed and treated promptly. Mounting complications and its broadening spectrum in ‘not so benign’ P. vivax warrants global vigilance for any probable impositions.Electronic supplementary materialThe online version of this article (doi:10.1186/1475-2875-13-304) contains supplementary material, which is available to authorized users.

BackgroundOf late there have been accounts of therapeutic failure and chloroquine resistance in Plasmodium vivax malaria especially from Southeast Asian regions. The present study was conducted to assess the therapeutic efficacy of chloroquine–primaquine (CQ–PQ) combined regimen in a cohort of uncomplicated P. vivax mono-infection.MethodsA tertiary care hospital-based prospective study was conducted among adult cohort with mono-infection P. vivax malaria as per the World Health Organization’s protocol of in vivo assessment of anti-malarial therapeutic efficacy. Participants were treated with CQ 25 mg/kg body weight divided over 3 days and PQ 0.25 mg/kg body weight daily for 2 weeks.ResultsOf a total of 125 participants recruited, 122 (97.6%) completed day 28 follow up, three (2.4%) participants were lost to follow-up. Eight patients (6.4%) were ascertained to have mixed P. vivax and Plasmodium falciparum infection by nested polymerase chain reaction test. The majority of subjects (56.8%, 71/125) became aparasitaemic on day 2 followed by 35.2% (44/125) on day 3, and 8% (10/125) on day 7, and remained so thereafter. Overall only one therapeutic failure (0.8%, 1/125) occurred on day 3 due to persistence of fever and parasitaemia.ConclusionsCQ–PQ combined regimen remains outstandingly effective for uncomplicated P. vivax malaria and should be retained as treatment of choice in the study region. One case of treatment failure indicates possible resistance which warrants constant vigilance and periodic surveillance.

Two distinct and potentially deceitful cases of neurologic melioidosis are reported. Case 1: A 39-year-old alcoholic and uncontrolled diabetic male presented with cough, fever, and left focal seizures with secondary generalization. An magnetic resonance imaging (MRI) brain scan revealed a small peripherally enhancing subdural collection along the interhemispheric fissure suggestive of minimal subdural empyema. Blood culture grew Burkholderia pseudomallei. Patient was diagnosed with disseminated bacteraemic melioidosis with subdural empyema. He was successfully treated with ceftazidime-cotrimoxazoledoxycycline. Case 2: A 45-year-old male presented with left lower limb weakness, difficulty in passing urine and stool, and back pain radiating to lower limbs. Neurological examination revealed flaccid left lower limb with absent deep tendon reflexes and plantar reflex. Spinal MRI showed T2 hyperintensity from D9 to L1 suggestive of demyelination. Patient was treated with high dose methylprednisolone. By day 3 of steroid treatment, lower limb weakness progressed. Subsequent MRI showed extensive cord hyperintensity on T2 weighted sequence extending from C5 to conus medullaris consistent with demyelination. Cerebrospinal fluid (CSF) culture grew B. pseudomallei, and the patient was given meropenem-cotrimoxazole. After three weeks of parenteral treatment, the lower limbs remained paralyzed. Patient was discharged on oral cotrimoxazole-doxycycline. Conclusions: Melioidosis should be considered as a differential in focal suppurative central nervous system (CNS) lesions, meningoencephalitis, or encephalomyelitis in endemic areas. CNS infections must be ruled out prior to steroid administration. The role of corticosteroids in demyelinating CNS melioidosis has been refuted. This is a rare documentation of effect of unintentional corticosteroid treatment in melioidosis.