Dengue is caused by a flavivirus and is found mainly in Asia and Africa, although it has been reported from the USA as well. Four different antigenic varieties of the dengue virus are recognized and all are transmitted by the daytime-biting A. aegypti. Humans are infective during the first 3 days of the illness (viraemic stage). Mosquitoes become infective about 2 weeks after feeding on an infected individual, and remain so for the rest of their lives. The disease is usually endemic, but epidemics have been recorded. Immunity after the illness is partial.


The incubation period varies from 5 to 6 days. Two clinical forms are recognized.
CLASSIC DENGUE FEVER is characterized by the abrupt onset of fever, malaise, headache, retrobulbar pain which worsens on eye movements, conjunctival suffusion and severe backache, which is a prominent symptom. Lymphadenopathy  petechiae on the soft palate and skin rashes may also occur. The rash is transient and morbilliform. It appears on the limbs and then spreads to involve the trunk. Desquamation occurs subsequently. Cough is uncommon. The fever subsides after 3-4 days, the temperature returns to normal for a couple of days, and then the fever returns, together with the features already mentioned, but milder. This biphasic or saddleback pattern is considered characteristic. Severe fatigue, a feeling of being unwell and depression are common for several weeks after the fever has subsided.
DENGUE HAEMORRHAGIC FEVER is a severe form of dengue fever and is believed to be the result of two or more sequential infections with different dengue serotypes. It is a disease of children and has been described almost exclusively in South East Asia. The disease has a mild start, often with symptoms of an upper respiratory tract infection. This is then followed by the abrupt onset of shock and haemorrhage into the skin and ear, epistaxis, haematemesis and melaena known as the dengue shock syndrome. Serum complement levels are depressed and there is laboratory evidence of a consumptive coagulopathy.


Isolation of the dengue virus by tissue culture in sera obtained during the first few days of illness is diagnostic. Demonstration of rising antibody titres by neutralization (most specific), haemagglutination inhibition or complement- fixing antibodies in sequential serum samples is evidence of dengue virus infection.


Treatment is symptomatic.

Rift Valley fever

Rift Valley fever is primarily an acute febrile illness of livestock-sheep, goats and camels. It is found in southern and eastern Africa. The vector in East Africa is Culex pipiens and in southern Africa, Aedes cabal/us. Following an incubation period of 3-6 days, the patient has an acute febrile illness that is difficult to distinguish clinically from other viral fevers. The temperature pattern is usually biphasic. The initial febrile illness lasts 2-4 days and is followed by a remission and a second febrile episode. Complications are indicative of severe infection and include retinopathy, meningo-encephalitis, haemorrhagic manifestations and hepatic necrosis. Mortality approaches 50% in severe forms of the illness. Treatment is symptomatic Japanese encephalitis Japanese encephalitis is a mosquito-borne encephalitis caused by a flavivirus. It has been reported most frequently from the rice-growing countries of South East Asia and the Far East. Culex tritaeniorhynchus is the most important vector and feeds mainly on pigs as well as birds such as herons and sparrows. Humans are accidental hosts. As with other viral infections, the clinical manifestations are variable. The onset is heralded by severe rigors. Fever, headache and malaise last from 1 to 6 days. Weight loss is prominent. In the acute encephalitic stage the fever is high (38-41°C), neck rigidity occurs and neurological signs such as altered consciousness, hemiparesis and convulsions develop. Mental deterioration occurs over a period of 3-4 days and culminates in coma. Mortality varies from 7 to 40% and is higher in children. Residual neurological defects such as deafness, emotional lability and hemiparesis occur in about 70% of patients who have had eNS involvement. Convalescence is prolonged. Antibody detection in serum and CSF by IgM capture ELISA is a useful rapid diagnostic test. An inactivated mouse brain vaccine is effective and available. Treatment is symptomatic.


Bunyaviruses belong to a large family of more than 200 viruses, most of which are arthropod-borne. Congo-Crimean haemorrhagic fever This is found mainly in Asia and Africa. The primary hosts  are cattle and hare and the vectors are the Hyalomma ticks. Following an incubation period of 3-6 days there is an influenza-like illness with fever and haemorrhagic manifestations. The mortality is 10-50%.


Hantaviruses are enzootic viruses of wild rodents which are spread by aerosolized excreta and not by insect vectors. The disease was first recognized in 1951 in United Nations soldiers in Korea. The most severe form of this  infection is Korean haemorrhagic fever (or haemorrhagic fever with renal syndrome HFRS). This condition has a mortality of 5-10% and is characterized by fever, shock and haemorrhage followed by an oliguric phase. Milder forms of the disease are associated with related viruses e.g. Puumala virus, and may present as Nephropathia epidemica, an acute fever with renal involvement. This has been recognized for many years in Scandinavia (and recently in other European countries in people who have been in contact with bank voles). In the United States, a new Hantavirus (transmitted by the deer mouse) causes the acute respiratory distress syndromes (ARDS). Diagnosis is made by an ELISA technique.


Three types of influenza virus are recognized-A, Band C. The influenza A virus is a spherical or filamentous enveloped virus. Haemagglutinin, a surface glycopeptide, aids attachment of the virus to the wall of susceptible host cells at specific receptor sites. Cell penetration, probably by pinocytosis, and release of replicated viruses from the cell surface is effected by budding through the cell membrane or by the action of viral neuraminidase. INFLUENZA A is generally responsible for pandemicsand epidemics.
INFLUENZA B often causes smaller or localized and  milder outbreaks, e.g. in camps or schools.
INFLUENZA C rarely produces disease in humans. Antigenic shift (major antigenic change within an influenza A subtype) usually heralds the onset of a pandemic. This results from genetic recombination of the virus with an animal virus. Antigenic drift (minor changes in influenza A and B viruses) results from point mutations leading to amino acid changes in haemagglutinin and neuraminidase. Sporadic cases of influenza and outbreaks among groups of people living in a confined environment are frequent. The incidence increases during the winter months, when crowding is common. Spread is mainly by droplet infection but fomites and direct contact have alsobeen implicated.
The clinical features, diagnosis, treatment and prophylaxis of influenza.


These are a heterogeneous group of enveloped viruses of varying size that are responsible for parainfluenza, mumps, measles and other respiratory infections.

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