Dengue is an arthropod-borne (arbovirus) flavivirus infectioncharacterized by an acute febrile illness with severebone pain, rash and lymphadenopathy.

The vectors areAedes mosquitoes. The dengue virus is a 50 nm RNAcontainingflavivirus. Four serotypes are recognized, andthese can be differentiated in a range of regular serologicaltests. The serotypes are closely related antigenically, but cross-protection between serotypes is lacking. Thedengue shock syndrome and haemorrhagic fever happen inpatients, especially children, experiencing a second infectionwith a diverse Dengue serotype. Distribution and incidence Over the last 3 decades epidemics of dengue haveoccurred in all continents in the tropics, Africa, Asia, theAmericas and the Pacific, such that it is nowthe commonest mosquito-borne infection, and 50% of theworlds population live in endemic areas. With the spreadof dengue there has been a corresponding spread in theincidence of dengue haemorrhagic fever (DHF) whichuntil the 1970s was confined to southeast Asia. The reasonsfor this spread are incompletely understood, but includethe improve in travel worldwide distributing the serotypesto new areas, decline in mosquito control so that Aedesaegypti has proliferated, and the rise of densely populatedperiurban slums with no sanitary facilities except thosethat encourage the proliferation of A. aegypti. Transmission and epidemiology The most common vector is Aedes aegypti, a day-bitingmosquito that breeds in tiny collections of water in tincans, auto tyres etc. peridomestically, but other species havemore limited roles in transmission. Eight to 11 days afteringesting dengue virus in a human blood meal the mosquitois infective it remains infective for the rest of its life.Peak biting times are the 2hour periods following dawn andbefore dusk.Both sexes and all age groups are susceptible to dengueprovided they have not been infected just before with thatserotype. Dengue haemorrhagic fever has been predominantlya illness of kids, but with spread to new areas second infections, and hence DHF, are occurring in olderage groups. Pathology and pathogenesis After inoculation the virus replicates in nearby lymph nodecells. Viraemia follows and reticuloendothelial cells in skinand other tissues grow to be infected. Local inflammatorychanges happen around tiny vessels in the skin. Denguehaemorrhagic fever occurs in kids who have previouslybeen exposed to infection with a diverse serotype of thevirus, or who have acquired antibody passively from theirmother. Immune enhancement causes much more cells tobecome far more heavily infected by means of immune complexbinding to Fc receptors. Cytotoxic Tcell memory isactivated, causing enhanced clearance of virus but alsoresulting in excess cytokine release, with tissue-damagingconsequences: increased vascular permeability, causinghypovolaemia and coagulation defects owing to the releaseof cytokines with procoagulant properties.Clinical featuresThe incubation period is about 7 days prior to the onset ofhigh fever, headache, eye pains, backache and chills. Limbpain is often severe in dengue and this gives rise to itscommon name, breakbone fever. A blanching erythematousmacular rash may appear on the third or fourth dayof the illness. Lymphadenopathy could be present.Encephalopathy, cardiomyopathy and liver damage alsooccur. Leukopenia is usual in the peripheral blood.In dengue haemorrhagic fever the patient is far more ill, andblood pressure falls as a result of transudation of fluid fromthe vascular compartment. This fluid can accumulate in theabdominal cavity or in the pleural spaces. Monitoringblood pressure, haematocrit and platelet count in additionto urine output and conscious level give warning of itsonset. There might be spontaneous bleeding into the skinand at other sites. The loss of circulating blood volumecauses shock, with low blood pressure, rapid pulse, restlessnessand abdominal discomfort (the dengue shock syndrome),which can have a mortality of 50% if untreated. Diagnosis Virus can be isolated from blood employing Aedes or mammaliancell lines. Virus can also be identified in blood usingthe polymerase chain reaction, and IgM antibody or arising antibody titre in paired sera obtained 10-14 daysapart are serological indicators of the diagnosis, althoughthe

serological response may possibly not be so clear-cut in areaswhere populations are exposed to other flaviviruses. Management Patients with uncomplicated dengue need supportivemeasures, such as attention to nutrition and hydration andrelief of discomfort. Paracetamol, not aspirin, should be utilised forpain relief and as an antipyretic. Intensive management ofsevere dengue haemorrhagic fever can decrease the mortalityfrom 10% to 1% without highly sophisticated facilities.Intravascular volume is restored with Ringers lactate,giving a volume equal to daily requirements plus five% ofbody weight, and monitoring pulse, blood pressure andrespiration to steer clear of overload. Plasma protein fraction anddextran 40 could also be given to replace colloid losses.Haematocrit ought to be monitored to assess progress.The need for fluid replacement might last only 1-2 days. Nospecific antiviral treatment is helpful.ControlLive attenuated vaccines are under development. It isimportant that they include all four serotypes of the virusto steer clear of the risk of dengue haemorrhagic fever. Vectorcontrol comprises the removal of mosquito breeding web sites,which are often collections of water in tins, tyres, tubs andwater storage vessels around houses, and larviciding.

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