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Virological investigations were carried out on 4 151 patients with respiratory disease hospitalized between May 1966 and April 1972. The groups examined were Black and White children and Black miners. Influenza viruses were more common among malnourished Black children and tended to cause more severe disease. This was also true of adenovirus and Herpesvirus hominis type 1 infections. Adenoviruses appear to be secondary invaders, frequently after a measles or influenza attack. A generalized epidemic of adenovirus type 7 occurred in 1967, the longest, coldest and most humid winter during the survey. The season of peak occurrence for respiratory syncytial (RS) virus is autumn, not winter as found elsewhere. The parainfluenza viruses differ from each other, types 1 and 2 being commoner in older children (12--48 months), mainly causing laryngotracheobronchitis (LTB), whereas type 3 is commoner in younger children (0--23 months), mainly causing pneumonia. The miners showed a preponderance of influenza A infections. The miners' origin from remote villages and high turnover rate create a situation where a given strain will persist at a moderate level for long periods, unlike in the general population where an outbreak lasts for only about 6--8 weeks. As opposed to other closed communities, adenovirus infections were rare. The reason for this is obscure.

The handling of potentially lethal and highly infective material in a routine clinical pathology laboratory and in a viral diagnostic unit is detailed. Extensive precautions were taken at each step of the receiving, processing and disposal cycle. Disposable protective clothing and apparatus were used whenever possible. Laboratory tests were limited to those essential for the clinical management and diagnosis. Technologists who handled infective material were limited to minimal numbers of experienced, non-pregnant, informed volunteers. They wore special protective clothing, including gloves, caps, gowns and masks. When possible, specimens were handled under special protective hoods. Potentially infective material was processed through automated apparatus, and care was taken to prevent contamination of its exterior. The effluent from the machines was collected into viricidal agents (glutaraldehyde, sodium hypochlorite). After processing, the machines were flushed extensively with viricidal solution. This procedure has caused no damage to the automated equipment and has been adopted as a routine laboratory safety measure. The protective procedures adopted were successful in that there was no outbreak of the viral infection among the associated laboratory workers.

In considering the diagnosis of a patient admitted to the Johannesburg Hospital, suffering from an illness characterized by high fever and complicated by a hemorrhagic state from which he died, a list of possible causes of his illness was drawn up. This list included the arthropodborne viral infections prevalent in southern Africa, namely, chikungunya fever, Sindbis fever, West Nile fever, yellow fever, and Rift Valley fever; viral infections associated with rodents, such as Lassa fever; the viral infection associated with monkeys, Marburg virus disease; the rickettsial infections; tick-bite fever (the variety of spotted fever of tick typhus occurring in southern Africa) and Q fever; the bacterial infections, especially the coccal infections, plague septicemia, and meningococcal, staphylococcal, and streptococcal septicemia; and the blood protozoal infections malaria and trypanosomiasis. In addition, rubella, Gasser's syndrome, Henoch-Schönlein purpura, and viperine snakebite were briefly described in this review. All of these conditions may be complicated by the development of a hemorrhagic state. The circulation of large numbers of infecting organisms, by they viruses, rickettsiae, bacteria, or protozoa, may initiate the coagulation cascade, the formation of fibrin and its deposition in the finer blood vessels, and the aggregation and entanglement of platelets resulting in marked thrombocytopenia and bleeding. This bleeding tendency is greatly aggravated when the infection specifically involves the parenchymal cells of the liver; such a condition results in defective formation of coagulation factors such as prothrombin. The proper care of patients in whom a hemorrhagic state has developed requires urgent and accurate diagnosis followed by immediate and appropriate treatment that will combat the infection and alleviate the hemorrhagic state and liver disorder. If the hemorrhagic state is due to one of the dangerous infectious fevers, adequate protection of the medical, nursing, and laboratory staff concerned is also vital.