Dengue is a mosquito-borne disease which is currently an expanding global health problem. The disease is caused by four closely related viruses, the dengue virus. There are no specific dengue therapeutics and prevention is currently limited to vector control measures. Development of an effective tetravalent dengue vaccine would therefore represent a major advance in the control of the disease and is considered a high public health priority. While a licensed dengue vaccine is not yet available, the scope and intensity of dengue vaccine development has increased dramatically in the last decade. The uniqueness of the dengue viruses and the spectrum of disease resulting from infection have made dengue vaccine development difficult. Several vaccine candidates are currently being evaluated in clinical studies. The candidate currently at the most advanced clinical development stage, a live-attenuated tetravalent vaccine based on chimeric yellow fever dengue virus, has progressed to phase III efficacy studies. Several other live-attenuated vaccines, as well as subunit, DNA and purified inactivated vaccine candidates, are at earlier stages of clinical development. Additional technological approaches, such as virus-vectored and virus-like particle-based vaccines, are under evaluation in preclinical studies.
Dengue virus infection (DVI)/dengue hemorrhagic fever (DHF) is a common febrile illness with a variety of severities. The mortality rate is high in dengue shock syndrome (DSS), caused by circulatory failure due to plasma leakage resulting in multi-organ failure. However, acute kidney injury (AKI) is rarely reported. In areas of endemic DVI, the prevalence of AKI due to DVI has been reported to be as high as 6.0 % in children with AKI, and 0.9 % in children with DVI who were admitted to a hospital. The mechanism of AKI in DVI is not clear. It may result from (a) direct injury as in other infectious diseases, (b) an indirect mechanism such as via the immune system, since DHF is an immunological disease, or (c) hypotensive DSS, leading in turn to reduced renal blood supply and renal failure. The mortality rates of DF/DHF, DSS and DHF/DSS-related AKI are <1 %, 12-44 %, and >60 %, respectively. Kidney involvement is not actually that rare, but is under-recognized and often only reported when microscopic hematuria, proteinuria, electrolyte imbalance, or even AKI is found. The prevalence of proteinuria and hematuria has been reported as high as 70-80 % in DVI. A correct diagnosis depends on basic investigations of kidney function such as urinalysis, serum creatinine and electrolytes. Although DVI-related renal involvement is treated supportively, it is still important to make an early diagnosis to prevent AKI and its complications, and if AKI does occur, dialysis may be required. Fortunately, in patients who recover, kidney function usually completely recovers as well.
Pertussis is a highly infectious respiratory disease caused by Bordetella pertussis. Infants and young children are particularly at risk of severe and life-threatening disease. Infectious older individuals may transmit Bordetella pertussis to unprotected infants. Pertussis control measures have even failed in some countries with high pertussis vaccination coverage rates, leading to increased incidence rates. In 2014, this caused the World Health Organization to declare pertussis resurgent in some countries and led to recommendations regarding pertussis surveillance and national immunization programs. Despite the resurgence of pertussis, epidemiology of the disease in Southeast Asia has received little attention. In this narrative review, we describe pertussis surveillance systems, control measures, epidemiologic trends, and region-specific pertussis research in Southeast Asia. We also make recommendations for the intensification of pertussis surveillance and research in the region.
Among 47 children admitted to the Chulalongkorn Medical School Hospital for neurotoxic snake bite, the attackers were identified in 15; the cobra (Naja naja) was the snake involved in all cases. Clinical manifestations in all 47 children appeared to follow a similar pattern. Drowsiness heralded the systemic effects in most of the patients. The characteristic systemic signs were those resulting from the neuromuscular effects of the venom and included ptosis, frothy saliva, slurred speech, respiratory failure, and paralysis of the skeletal muscles. These episodes occurred within 8 hours in 94% of the cases, and at the latest 19 hours following the bite. In some cases unconsciousness accompanied respiratory failure. Necrosis in the region of the bite, the prominent local sign, developed in 40% of the cases at the end of the 1st week after the bite. Infusion of specific antivenom was an effective therapeutic measure for the neuromuscular changes. Respiratory assistance was mandatory in cases of respiratory failure. Edrophonium chloride demonstrated a supportive role as a countermeasure against the neuromuscular effects.
The mechanism of shock in patients with dengue hemorrhagic fever (DHF) has not yet been fully understood. In this study, we investigated the possibility of splanchnic venous pooling as a contributor for circulatory dysfunction in these patients. Ultrasonographic studies of portal vein and inferior vena cava were done in 45 patients with serologically or PCR-confirmed diagnosis of dengue virus infection. The size of portal vein and inferior vena cava, mean blood flow velocity in the right portal vein, and modified portal vein congestion index were compared between patients with dengue fever (DF, n = 20), DHF without shock (n = 14), and dengue shock syndrome (DSS, n = 11) during the toxic stage, convalescent stage, and at follow-up. The portal vein was significantly more dilated in patients with shock (DSS) than DHF without shock and than DF during the toxic and convalescent stages (P < 0.05), but not at follow-up. The change in the size of inferior vena cava followed the opposite trend (not statistically significant). Portal vein blood flow velocity was lower and congestion index was higher in shock cases (DSS) than DHF without shock and than DF at toxic and convalescent stages (P < 0.01). The differences disappeared at follow-up. Hepatosplanchnic venous pooling and/or dysfunction occur and correlate with the severity of circulatory derangement and shock in patients with DHF. The cause(s) and significance of hepatosplanchnic circulatory dysfunction in DHF and possibly other viral hepatic diseases deserve further study.
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