We present evidence that the El Niño phenomenon intensifies the annual cycle of malaria cases for Plasmodium vivax and Plasmodium falciparum in endemic areas of Colombia as a consequence of concomitant anomalies in the normal annual cycle of temperature and precipitation. We used simultaneous analyses of both variables at both timescales, as well as correlation and power spectral analyses of detailed spatial (municipal) and temporal (monthly) records. During "normal years," endemic malaria in rural Colombia exhibits a clear-cut "normal" annual cycle, which is tightly associated with prevalent climatic conditions, mainly mean temperature, precipitation, dew point, and river discharges. During historical El Niño events (interannual time scale), the timing of malaria outbreaks does not change from the annual cycle, but the number of cases intensifies. Such anomalies are associated with a consistent pattern of hydrological and climatic anomalies: increase in mean temperature, decrease in precipitation, increase in dew point, and decrease in river discharges, all of which favor malaria transmission. Such coupling explains why the effect appears stronger and more persistent during the second half of El Niño's year (0), and during the first half of the year (+1). We illustrate this finding with data for diverse localities in Buenaventura (on the Pacific coast) and Caucasia (along the Cauca river floodplain), but conclusions have been found valid for multiple localities throughout endemic regions of Colombia. The identified coupling between annual and interannual timescales in the climate-malaria system shed new light toward understanding the exact linkages between environmental, entomological, and epidemiological factors conductive to malaria outbreaks, and also imposes the coupling of those timescales in public health intervention programs.
The increase of malaria transmission in the Pacific Coast of Colombia during the occurrence of El Niño warm event has been found not to be linked to increases in the density of the vector Anopheles albimanus, but to other temperature-sensitive variables such as longevity, duration of the gonotrophic cycle or the sporogonic period of Plasmodium. The present study estimated the effects of temperature on duration of the gonotrophic cycle and on maturation of the ovaries of An. albimanus. Blood fed adult mosquitoes were exposed to temperatures of 24, 27, and 30 degrees C, held individually in oviposition cages and assessed at 12 h intervals. At 24, 27, and 30 degrees C the mean development time of the oocytes was 91.2 h (95% C.I.: 86.5-96), 66.2 h (61.5-70.8), and 73.1 h (64-82.3), respectively. The mean duration of the gonotrophic cycle for these three temperatures was 88.4 h (81.88-94.9), 75 h (71.4-78.7), and 69.1 h (64.6-73.6) respectively. These findings indicate that both parameters in An. albimanus are reduced when temperatures rose from 24 to 30 degrees C, in a nonlinear manner. According to these results the increase in malaria transmission during El Niño in Colombia could be associated with a shortening of the gonotrophic cycle in malaria vectors, which could enhance the frequency of man-vector contact, affecting the incidence of the disease.
Background: Malaria has recently re-emerged as a public health burden in Colombia. Although the problem seems to be climate-driven, there remain significant gaps of knowledge in the understanding of the complexity of malaria transmission, which have motivated attempts to develop a comprehensive model.
The natural habitat of Paracoccidioides brasiliensis remains undefined but the repeated demonstration of infection by this fungus in the nine-banded armadillo Dasypus novemcinctus has opened interesting research avenues. We report here the isolation of this fungus from the spleen of a naked-tailed armadillo Cabassous centralis (Miller 1899) captured in a coffee farm localized in the Colombian endemic area for paracoccidioidomycosis. This particular isolate was identified by its dimorphism and also by comparison of the PbGP43 gene and ribosomal internal transcribed spacer regions (ITS) with recognized P brasiliensis strains. This finding extends the range of naturally acquired infections in mammals of the family Dasypodidae and confirms the existence of this human pathogen in areas where human paracoccidioidomycosis is known to occur.
IntroductionDrug-related hepatotoxicity is a common medical problem with implications for health systems. It constitutes a cause of acute liver failure and, in many cases, is responsible for the rejection of new pharmacological agents during efficacy and safety studies. Risk factors, as well as pathogenesis of drug-induced liver injury, are poorly understood. The diagnosis of drug-induced liver injury is challenging; it is difficult to define the cause of drug hepatotoxicity due to the heterogeneity of the clinical presentation and the absence of established criteria for accurate and reproducible identification of drug-associated liver toxicity.Case presentationWe report the case of a 25-year-old Hispanic woman admitted to our Clinical Hepatology Unit with symptoms of acute hepatitis of unknown etiology. She was diagnosed with albendazole-induced granulomatous hepatitis after ruling out other possible causes, based on laboratory studies, liver biopsy, medical history, detailed drug history, and spontaneous improvement of her liver biochemical profile after medication withdrawal. This diagnosis was supported by the Council for International Organizations of Medical Sciences-Roussel Uclaf Causality Assessment Method, which showed a likely correlation between hepatocellular damage and drug toxicity as the etiology.ConclusionsOur patient’s suspected diagnosis was albendazole-induced granulomatous hepatitis with confirmatory histologic pattern. This case deserves particular attention due to the wide use of albendazole in our country (Colombia) and the prevalent medical issue of drug-related hepatotoxicity.
Background and AimDrug‐induced autoimmune hepatitis (DIAIH) is an adverse effect associated with several drugs that usually occurs acutely, with variable latency, and it may potentially be mortal. There are a few reports and studies about DIAIH.MethodsThis was an analytical study of a retrospective cohort of patients, discriminated according to idiopathic or drug‐induced etiology, followed up for a 7‐year period until 31 December 2016.ResultsA total of 190 patients were selected for the analysis, 12 (6.3%) with DIAIH. The two main drugs related to DIAIH were nitrofurantoin, n = 8 (67%), and NSAID, n = 2 (17%), constituting 84% of the cases. There were no significant differences in seropositivity between AIH with DIAIH in antinuclear antibodies (ANA) and anti‐smooth muscle antibodies (ASMA) antibodies, with 82.6% versus 82.6% and 34% versus 16%, respectively. The fibrosis stages were similar, except for the F4 stage, in a greater proportion in AIH. None of the patients with DIAIH had cirrhosis or developed it during follow‐up, but it was present in 42.1% of the AIH cases at diagnosis (P = 0.003). Biochemical remission with management was higher in DIAIH but not significant (91.7% vs 80.9%, P = 0.35). The definitive interruption of immunosuppression was successfully performed in 25% of those with DIAIH without relapses but was only possible in 2.8% in AIH (P < 0.001) with 32 cases of relapses.ConclusionDIAIH constitutes a minor proportion of AIH. The clinical and histological characteristics may be similar; DIAIH patients have a greater chance of having treatment suspended with a low risk of relapse, progression to cirrhosis, or need for liver transplant.
We report a 19-year-old female with systemic lupus erythematosus and lupus nephritis who developed pulmonary hemorrhage (PH) refractory to conventional immunosuppressive treatment. She was initially treated with intravenous methylprednisolone and cyclophosphamide pulses. She required mechanical ventilation due to a lack of responsiveness and her disease was considered refractory to conventional treatment. Rituximab was administered and this was followed by clinical improvement in both PH and nephritis. Rituximab may be a useful therapeutic option for the treatment of refractory PH.
IntroductionBrown tumors are a rare focal manifestation of osteitis fibrosa cystica, which results from hyperparathyroidism. Chronic kidney failure may lead to secondary or tertiary hyperparathyroidism and thus to osteitis fibrosa cystica and brown tumors.Case presentationA 60-year-old man with a history of diabetes mellitus and chronic kidney failure presented with a 15-day history of dyspnea, cough, malaise and fever. Initially, there was little correlation between his history and his physical examination. Various pulmonary, cardiac and infectious etiologies were ruled out. A chest X-ray showed a costal mass that was further verified by tomography and gammagraphy. The mass was suspected of being neoplastic. After a failed biopsy, the mass was removed surgically and on histopathology was compatible with a giant-cell tumor versus a brown tumor caused by hyperparathyroidism. Laboratory tests showed elevated calcium, phosphate and parathyroid hormone concentrations. The patient was diagnosed with a brown tumor secondary to refractory hyperparathyroidism.ConclusionTending towards a diagnosis because it is more frequent or it implies more risk for the patient may delay the consideration of other diagnostic options that, although rare, fit well into the clinical context. The patient presented here was suspected to have an osseous neoplasia that would have had major implications for the patient. However, reassessment of the case led to the diagnosis of a brown tumor. Brown tumors should be an important diagnostic consideration in patients with chronic kidney failure who have secondary or tertiary hyperparathyroidism and an osseous mass.
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