Dengue haemorrhagic fever in Burma.

Although sporadic from 1965 to 1969, a major outbreak of dengue haemorrhagic fever (DHF) occurred for the first time in Rangoon in 1970. Since then the disease has occurred every year in Rangoon and is now observed to be expanding to other urban areas in the country. The clinical diagnosis of DHF was confused by concurrent outbreaks of influenza A in 1971 and influenza A and B in 1972. A laboratory study of 3,447 clinically diagnosed haemorrhagic fever cases showed that 1643 cases (47.8%) were due to dengue and chikungunya, 296 (8.6%) to influenza A, 85(2.5%) to influenza B, 12(0.3%) to measles and 1411(40.8%) were of unknown aetiology during the 5 year period 1970-1974. Ae. aegypti mosquitoes are widely distributed in the country up to and including 900 meters above sea level but breeding is not found above that altitude. The absolute larval population which is highest in July as well as landing rate correlated with the peak incidence of DHF cases.     

Dengue haemorrhagic fever: questions of pathogenesis

The year under review has seen a remarkable proliferation of papers on dengue. Four prospective studies have been carried out across the dengue belt, many groups have been pushing at the question of pathogenesis of dengue haemorrhagic fever, and a breakthrough has been achieved in the development of a mouse model for human dengue haemorrhagic fever.     

Dengue haemorrhagic fever with unusual manifestations

A retrospective study on 18 cases of DHF presented with jaundice and neurological signs which were considered unusual manifestation of DHF reveals that the causes or contributing factors are multifactorial. Most commonly found associated conditions were prolonged shock with metabolic acidosis and severe DIC that lead to hypoxia/ischaemia and resulted in both hepatic and brain dysfunction. Gross haemorrhage in the brain was noted in 6 of the 10 fatal cases while brain oedema was noted in 3 cases. Electrolyte disturbance such as hyponatremia could be another cause of brain oedema. It is certain from this study that there is no pathological evidence of encephalitis. Hepatic dysfunction found in associated with jaundice and encephalopathy is possibly caused by toxic substances, drugs and/or associated with underlying liver conditions. Reye's or Reye's-like syndrome was postulated in one case.     

Dengue fever with neurologic expression. Three cases in adults]

Dengue fever, unlike most other arboviral diseases, does not usually cause encephalitis. However, neurologic symptoms with poor prognosis have been regularly reported, mostly in Asian children affected by the severe dengue hemorrhagic fever/dengue shock syndrome, and attributed to a non specific, anoxic or metabolic encephalopathy. Recently, first isolations of dengue viruses from CSF or brain tissue, have renewed this concept. We report 3 dengue fever cases with neurologic manifestations and favorable outcome. Occurrence in adult age, during classic (benign) dengue fever (2 cases), and neurologic sequellae (1 case) were the three outstanding features. We point out the proteiform expression of these neurologic changes and their low incidence rate (< 3% in our series of adult dengue fever). Although their pathogenesis is poorly understood, different mechanisms are suggested: encephalopathy (case n. 1), acute specific encephalitis (questionable in case n(o) 2), or post-infective encephalitis (case n(o) 3).     

Dengue haemorrhagic fever in Thailand, 1987

In 1987, situation of DHF in Thailand was the worst for the past 30 years. There were 152,840 cases and 785 deaths from the preliminary report. The incidence was highest ever reported. Outbreak begun early in January and reached its peak in July. All 73 provinces were affected except six provinces which had incidence of less than 60 per 100,000 population. The highest attack rates were in school children, especially 5-9 year olds. Virus isolation in a north-eastern province recovered Den-3 and Den-2 more common than other serotypes. Although a large outbreak in 1987 is unlikely to happen in 1988 but with the endemic areas all over the country there is a potential for small outbreaks to occur. The Ministry of Public Health needs new approaches and increased resources to control this disease.     

Dengue haemorrhagic fever and Japanese B encephalitis in Indonesia

Dengue haemorrhagic fever (DHF) was first recognized in Indonesia in the cities of Jakarta and Surabaya in 1968, 15 years after its recognition in the Philippines. During the 1968 outbreak, a total of 58 clinical cases with 24 deaths were reported. The number of reported cases since then has increased sharply, with the highest number of cases recorded in the years 1973 (10,189 cases), 1983 (13,668 cases), and 1985 (13,588 cases). Outbreaks of the disease have spread to involve most of the major urban areas, as well as some of the rural areas. In 1985, the disease had spread to 26 of 27 Provinces and 160 of 300 regencies of municipalities. At present, the disease is endemic in many large cities and small towns. Interestingly, DHF has not been reported in some cities, even though dengue virus transmission rates in those cities are high. The epidemic pattern of DHF for the country as a whole has become irregular. Since 1982, the intensity and spread of DHF has created an increasing public health problem in Indonesia, particularly in Java where 60% of the total population of the country resides. Java contributed about 71% of all cases occurring in the country in 1982, 84% in 1983, and 91% in 1984. The peak monthly incidence of DHF was frequently reported during October through April, months which coincide with the rainy season. The morbidity rate for Indonesia, estimated from reported cases over five years (1981-1985), ranged between 3.39 to 8.65 per 100,000 population. The overall case fatality rate has steadily declined from 41.3% in 1968 to 3% in 1984.(ABSTRACT TRUNCATED AT 250 WORDS)     

Crimean-Congo haemorrhagic fever cases in Turkey

Crimean-Congo haemorrhagic fever (CCHF) is an arbovirus infection, which is transmitted through ticks or via blood and secretions. Until recently, human cases of CCHF were unknown in Turkey; however, several acute disease cases were reported in 2002. We report on the investigation of a cluster of suspected CCHF cases in the middle part of the Black Sea from May 2002 to October 2003. The medical charts that we reviewed were obtained from all local physicians and our field investigations. 'Suspected case' was defined with regard to time, place, and both clinical and laboratory characteristics. A total of 108 patients were defined as suspected case. Among them 36 patients were reached and blood samples taken for examination for CCHF by using ELISA and RT-PCR. According to the laboratory analysis, 80.6% (29/36) were acute cases and 8.3% (3/36) were past CCHF infections. The overall mortality rate was 5.6%. There was no nosocomial infection; however, there were 2 family clusters. Tick exposure was the most prevalent risk factor (74.2%). A multidisciplinary collaboration should be developed in order to understand the magnitude of the disease and also to keep it under control.     

Dengue fever: a review

INTRODUCTION: Transmitted by Aedes mosquitoes all over the inter-tropical area, Dengue fever is the leading arboviral disease in humans. It is also an emerging disease. CURRENT KNOWLEDGE AND KEY POINTS: Increasing morbidity-mortality, and geographical expansion are the drastic changes noted in the recent epidemiology of the disease. They are related to those occurring at the bio-climatic, socio-demographic and behavioural levels, which in turn may have led to enhanced viral circulation and virulence, and also vectorial resistance. The various clinical patterns (undifferentiated febrile episode of children, acute and algid classic form, the potentially fatal dengue hemorrhagic fever/dengue shock syndrome, and the atypical forms) are reviewed, as well as the diagnostic methods, and the pathogenesis (sequential infections, facilitating antibodies, capillary leakage). FUTURE PROSPECTS AND PROJECTS: Dengue fever is actually much more than a traveller's fever or an exotic curiosity. It presently threatens half the world's population, and remains a puzzling disease in many aspects, such as the virus-vector and host-virus relationships, and clinical expression variability. In this respect, dengue fever appears as a model of viral disease. The current molecular approach is expected to provide us with new insights into pathophysiology, more efficient tools for disease control, and also an efficient vaccine in the near future.     

Dengue fever/dengue haemorrhagic fever in Filipino children: clinical experience during the 1983-1984 epidemic

A total of 377 Filipino children out of a total of 5,427 admissions from October 31, 1983 to March 31, 1984 were found to have dengue fever/dengue haemorrhagic fever The present clinical presentation of these infections was basically similar to that in previous epidemics but hepatomegaly and pleural effusion were less frequent and cardiac involvement, more frequent. The discrepancies between the clinical syndromes and HI antibody responses were evident; thus, the values used for the interpretation of the antibody titers must be reassessed.