Hepatitis D virus (HDV) is the cause of an unusually severe form of liver disease with distinct histologic features (morula cell) that occurs throughout northern South America and certain other areas of the world. Clinical studies of HDV dLsease worldwide indicate that there is, in fact, a wide variation in pathogenesis, and the reasons for these differences are presently unknown. One possible explanation is that factors associated with the viral genotype are determinants of HDV pathogenesis. In this study, nucleic acid sequences were determined for three different northern South American HDV isolates which were obtained from individuals with severe disease or a family history of severe disease, in areas that are hyperendemic for this dise pattern. (HBV), which provides the coat protein for the HDV virion (1,2). Compared with infection with HBV alone, coinfection of HDV with HBV is associated with a higher rate of fulminant hepatitis in an acute infection; and superinfection with HDV ofindividuals with chronic HBV infection can lead to both acute and more progressive, chronic liver disease (3). The HDV genome is a 1.68-kb single-stranded circular RNA which is similar to the RNA genomes of unusual pathogens of higher plants (reviewed in ref. 4). HDV produces one known protein, the hepatitis D antigen (HDAg), which is encoded on the antigenomic strand (5) and has two forms (6) that differ in structure by 19 amino acids at the C terminus (5, 7). These two forms also differ functionally: the short form (HDAg-p24) is required for RNA replication (8); the long form (HDAg-p27) suppresses viral RNA replication (9, 10) and is required for packaging of the HDV genome with hepatitis B surface antigen (HBsAg) (11). HDAg-p27 arises via a specific RNA editing process that occurs during HDV replication (12) and that is dependent on a specific structure in the HDV RNA (13).Viral hepatitis due to HDV infection, type D hepatitis, is found worldwide, and the complete nucleic acid sequence has
Until we can better understand what constitutes health and illness in all adult populations, we risk repeated occurrences of unexplained symptoms among veterans after each war.
BackgroundPreviously thought to be rabies free, Bali experienced an outbreak of animal and human rabies cases in November 2008. We describe the epidemiological and clinical data of human rabies cases occurring in the first two years of the outbreak.MethodsWe analysed the patient records of all rabies cases from the Sanglah General Hospital in Denpasar, and district hospitals in Buleleng and Tabanan. A conventional reverse transcriptase polymerase chain reaction was developed to detect the rabies virus genome in saliva, corneal swabs, and ante- and post-mortem cerebrospinal fluid (CSF).ResultsThere were 104 human rabies cases in Bali during November 2008-November 2010. Patients' mean age was 36.6 years (range 3-84 years; SD 20.7), most were male (56.7%), and originated from rural districts. Almost all (92%) cases had a history of dog bite. Only 5.8% had their wounds treated and received an anti-rabies vaccine (ARV) after the bite incident. No patients received rabies immunoglobulin (RIG). The estimated time from dog bite to the onset of signs and symptoms was 110.4 days (range 12-720 days; SD 118.2). The mean length of medical care until death was 21.8 hours (range 1-220 hours; SD 32.6). Less than 50% of patients had prodromal symptoms. The most frequent prodromal symptom was pain or paraesthesia at the bite site (37.6%). The two most common central nervous system infection signs were agitation (89.2%) and confusion (83.3%). Signs of autonomic nervous system dysfunction included hydrophobia (93.1%), hypersalivation (88.2%), and dyspnea (74.4%). On admission, 22 of 102 patients (21.6%) showed paralytic manifestations, while the rest (78.4%) showed furious rabies manifestations. The case-fatality rate was 100%. The rabies virus genome was detected in 50 of 101 patients (49.5%) with the highest detection rate from post-mortem CSF samples.ConclusionsRabies is a major public health problem in Bali. Human fatalities occur because of a lack of knowledge regarding rabies risk, the poor management of dog bites, and the limited availability of RIG. Increasing public awareness of dog bite management, increasing the availability of ARV and RIG, and implementing an island-wide dog vaccination campaign will help prevent human rabies cases.
The only recommended treatment for mucosal leishmaniasis is ineffective in patients with severe disease. The acceptable toxicity of the regimen suggests that longer courses of therapy with antimony, or that trials with other antileishmanial agents alone or combined with antimony be evaluated as initial therapy for this disease.
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