These can be divided into the rubella virus and the arboviruses.
Rubella (‘German measles’) is caused by a spherical, enveloped fragile RNA virus that is easily killed by heat and ultraviolet light. While the disease can occur sporadically, epidemics are not uncommon. It has a worldwide distribution. Spread of the virus is via droplets; maximum infectivity occurs before and during the time the rash is present.
The incubation period varies from 14 to 21 days, averaging 18 days. The clinical features are largely determined by age, with symptoms being mild or absent in children under 5 years of age. The peak incidence of the disease is at 15 years.
During the prodrome the patient complains of malaise and fever. Mild conjunctivitis and lymphadenopathy may be present. The distribution of the lymphadenopathy is characteristic and involves the suboccipital, postauricular and posterior cervical groups of lymph nodes. Small petechial lesions on the soft palate (Forchheimer spots) are suggestive but not diagnostic. Splenomegaly may be present. The eruptive or exanthematous phase usually occurs within the first 7 days of the initial symptoms. The rash first appears on the forehead and then spreads to involve the trunk and the limbs. It is pinkish-red, macular and discrete, although some of these lesions may coalesce. It usually fades by the second day and rarely persists beyond the third day after its appearance.
Complications are rare; they include superadded pulmonary bacterial infection, arthralgia, haemorrhagic manifestations due to thrombocytopenia, encephalitis and the ongenital rubella syndrome. Rubella affects the fetuses of 15-30% of all women who contract the infection during the first trimester of pregnancy. The incidence of congenital abnormalities diminishes in the second trimester and no ill-effects result from infection in the third trimester. Congenital rubella syndrome is characterized by the presence of fetal cardiac malformations, especially patent ductus arteriosus and ventricular septal defect, eye lesions, especially cataracts, microcephaly, mental retardation and deafness. The expanded rubella syndrome consists of the manifestations of the congenital rubella syndrome plus hepatosplenomegaly, myocarditis, interstitial pneumonia and metaphyseal bone lesions.
The diagnosis may be suspected clinically but the laboratory diagnosis is essential to distinguish the illness from other virus infections (e.g. echovirus) and drug rashes. This is achieved by demonstrating a rising antibody titre(measured using the sensitive haemagglutination inhibition test) in two successive blood samples taken 14 days apart or by the detection of rubella-specific IgM. The virus can be cultured from throat swabs, urine and, in the case of intrauterine infection, the products of conception.
Treatment is symptomatic.
Prevention of rubella is important. Human immunoglobulin can decrease the symptoms of this already mild illness, but does not prevent the teratogenic effects. Severallive attenuated rubella vaccines have been used with great success in preventing this illness and these have been successfully combined with the measles and mumps vaccine. The side-effects of vaccination have been dramatically decreased by using vaccines prepared in human embryonic fibroblast cultures (RA 27/3 vaccine). Use of the vaccine is contraindicated during pregnancy or if there is a likelihood of pregnancy within 3 months of immuniz-ation. Inadvertent use of the vaccine during pregnancy has not, however, revealed a risk af teratogenicity. Arbovirus (arthropod-borne) infection Arboviruses are zoonotic viruses, with the possible exception of the O’nyong-nyong fever virus of which humans are the only known vertebrate hosts. They are transmitted through the bites of insects, especially mosquitoes and ticks. Over 385 viruses are classified as arboviruses. Culex, Aedes and Anopheles mosquitoes account for the transmission of the majority of these viruses. Although most arbovirus diseses are generally mild, epidemics are frequent and when these occur the mortality is high. In general, the incubation period is less than 10 days. The illness tends to be biphasic and, as in other viral fevers, pyrexia, conjunctival suffusion, a rash, retroorbital pain, myalgia and arthralgia are common. Lymphadenopathyis seen in dengue. Lifelong immunity to a particular virus is usual. In some of these viral fevers, haemorrhage is a feature , although its pathogenesis is speculative. Increased vascular permeability, capillary fragility and DIe have been implicated. Encephalitis due to cerebral invasion may be prominent in some fevers.
The 24 viruses of this group are all transmitted by mosquitoes; eight result in human disease. These viruses are globally distributed and tend to acquire their names from the location where they were first isolated (such as Ross River, Eastern Venezuelan, and Western encephalitis viruses) or by the local expression for a major symptom caused by the virus (such as chikungunya meaning ‘chronic bleeding’). Infection is characterized by fever, skin rash, arthralgia, myalgia and sometimes encephalitis.
There are 60 viruses in this group, some of which are transmitted by ticks and others by mosquitoes. Yellow fever Yellow fever, caused by a flavivirus, results in an illness of widely varying severity. It is a disease confined to Africa and South America between latitudes 15°N and 15°S of the equator. For poorly understood reasons, yellow fever has not been reported from Asia, despite the fact that climatic conditions are suitable and the vector, Aedes aegypti, is common. The infection is transmitted in the wild by A. africanus in Africa and the Haemagogus species in South and Central America. These mosquitoes are responsible for maintaining infection in monkeys, which form the sylvan reservoir. A. aegypti and the Haemagogus species are responsible for transmission of this disease from monkeys to humans in Africa and South and Central America, respectively. Once infected, a mosquito remains so for its whole life.
The incubation period varies from 3 to 6 days. When the infection is mild, the disease is indistinguishable from other viral fevers such as influenza or dengue. Classically, however, jaundice, proteinuria and haemorrhage occur. Three phases in the illness are recognized. Initially the patient presents with a high fever of acute onset, usually 39-40°C, which then returns to normal in 4-5 days. During this time, headache is prominent. Retrobulbar pain, myalgia, arthralgia, a flushed face and suffused conjunctivae are common. Epigastric discomfort and vomiting are present when the illness is severe. Relative bradycardia (Faget’s sign) is present from the second day of illness. The patient then makes an apparent recovery and feels well for several days. Following this ‘phase of calm’ the patient again develops increasing fever, deepening jaundice and hepatomegaly. Ecchymosis, bleeding from the gums, haematemesis and melaena may occur. Coma, which is usually a result of uraemia or haemorrhagic shock, occurs for a few hours preceding death. The mortality rate is up to 40% in severe cases.
The diagnosis is established by isolating the virus (when possible) from blood during the first 3 days of illness, by demonstrating increasing neutralizing antibody titres, or by finding the typical histological lesions on liver biopsy. These include mid-zone necrosis, fatty degeneration and intracellular hyaline necrosis (Councilman bodies).
Treatment is supportive. Bed rest, analgesics, and maintenance of fluid and electrolyte balance are important.
PREVENTION AND CONTROL
Yellow fever is an internationally notifiable disease. It is easily prevented using either the 17 d chick embryo vaccine, which is more popular, or the Dakar vaccine. Eradication of the breeding places of the vectors will help in decreasing the prevalence of the disease.