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Acute respiratory infection (ARI) is the most common cause of illness and death in young children worldwide. Because of inadequate laboratory facilities and financial resources the etiological agents responsible for most cases in developing countries remain unknown, thus obviating appropriate management. Therefore, an ARI program was commenced at the Kenyatta National Hospital, Nairobi, Kenya in 1981 with the objectives of establishing the microbial causes, clinical presentations, and diagnoses of ARI in children under 5 years of age and of developing simple, rapid, and inexpensive diagnostic techniques. Viruses were demonstrated in 54% of the 822 children studied, but over half of the viruses identified were types not commonly associated elsewhere with the causation of severe ARI. Respiratory syncytial, parainfluenza, and adenoviruses occurred in the same age groups and during similar weather conditions as elsewhere. Measles virus occurred most frequently in those 7 to 9 months old. Herpes simplex, rhino-, and enteroviruses play causative roles in some cases of severe ARI in Kenyan children. A combination of immunofluorescent and cell culture techniques were shown to be essential for the detection of viruses.

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Laboratory studies were performed on 128 children clinically diagnosed as measles when seen at the Infectious Diseases Hospital, Kenyatta National Hospital (IDH), Nairobi (86 cases) and the Rural Health Training Centre, Maragua, Central Province (42 cases) between 9 July and 31 August 1984. A concurrent measles infection was confirmed in 95% of the children seen at IDH and in 85% of those seen at Maragua, with similar proportions of confirmations in children who had, and who had not, received measles vaccine. No differences in the number of sero-conversions nor in the absolute levels of acute or convalescent HI antibody titres could be detected between vaccinated and unvaccinated children. Analysis of the cases seen at Maragua indicates that about two thirds of the children who had received vaccine were protected. A pilot study of vaccinating children at 8 months and again at 12-13 months is suggested in an attempt to eradicate measles.

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PIP: Of 110 males selected for review with possible chancroid, 96 were clinically diagnosed as having chancroid, 7 as having herpetic lesions, and 7 as having syphilis. Of the 96 patients diagnosed clinically as chancroid, 76 (79.2%) were culture positive for H. ducreyi. 9 (9.4%) of these 96 patients yielded Herpes Simplex Virus (HSV). Both HSV and H. ducreyi were isolated from 5 of the patients, and from 4 of the patients HSV alone was isolated. 7 patients (6.4%) were clinically diagnosed as having herpetic ulcers. 5 of these grew HSV. Overall, 14 of the 110 patients (12.7%) yielded HSV. 1 patient, who presented with small vesicular lesions characteristic of HSV, yielded the virus on culture. The vesicles were initially negative for H. ducreyi, but 6 days later he had developed deep purulent ulcers in the same sites as the vesicular lesions and became culture positive for H. ducreyi snd HSV-negative. The possible association between HSV and chancroid is discussed in the light of these findings and comparisons made between the results of the present study and earlier findings made in Kenya and elsewhere, with suggestions being given as to the reasons for the apparent differences. The HSV isolation techniques used in this study may be less sensitive than those used in other studies, but it is highly unlikely that this possibility alone accounts for all of the observed differences. Patients with hepetic ulcers may be less likely to present early in the course of the disease, if at all, believing the infection to be minor and one that will heal on its own. It is also possible that HSV infection is less common in Kenya, either alone or as an initiator of chancroid, than in the US or Europe, becuase of a higher rate of childhood HSV infections in Kenya, which may confer a degree of immunity against genital HSV infection in this population. The lower prevalence of HSV in association with H. ducreyi reported may be at least partly the result of a much higher incidence in Kenya of chancroid which is not initiated by HSV. A higher incidence of HSV genital infection in Europe and America would also make it more likely that HSV would fortuitously be isolated more frequently from H. ducreyi positive lesions.^ieng

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A cell-free strain of malignant catarrhal fever virus which produced a readily recognizable cytopathic effect was obtained by serial passage of the virus in a rabbit kidney cell line. Plaque assay of the virus was more rapid and gave higher titres 11 days postinoculation than tube titration, but the latter advantage decreased with a longer incubation period. Plaques were clear with sharp edges and measured 0.5 to 2 mm in diameter after 15 days. A plaque neutralization test was developed and successfully employed for the titration of malignant catarrhal fever virus neutralizing activity in the sera and nasal secretions of blue wildebeest.

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Single-step concentration of porcine enterovirus strain T80 by adsorption to the polyelectrolyte PE60 gave virus concentration factors of 35- to 88-fold in terms of plaque-forming units, with recovery rates of 22 to 75% of total virus present in the original virus suspension. Concentration by separation in an aqueous polymer two-phase system gave virus concentration factors of 56- to 105-fold and recovery rates of 37 to 107%. In the latter procedure, sodium dextran sulfate appeared to have no effect on plaque numbers, although plaques were sharper and clearer when this substance was incorporated in the overlay. The failure of sonication of virus concentrated by either procedure to increase plaque numbers indicated the absence of virus aggregates in the concentrates. T80 virus was not effectively concentrated by cobalt chloride or polyethylene glycol precipitation or by adsorption to either aluminium hydroxide or calcium hydrogen phosphate.

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The virus neutralizing substance in the gastrointestinal tract of swine vaccinated in different ways with porcine enterovirus strain T80 was characterized by tests for enhancement and absorption of virus neutralizing activity by class specific antiporcine Ig antisera. The gastrointestinal virus neutralizing activity of piglets which were vaccinated with live virus orally resided predominantly in the IgA class, although some activity was present also in the IgM and IgG classes. The serum virus neutralizing activity of this group was present in all three classes but primarily in the IgG class. The IgA in the serum of this group was presumably of gut origin. However, in piglets vaccinated with live virus intramuscularly, with formaldehyde-inactivated virus orally or intramuscularly or with ethylenimine-inactivated virus by both oral and subcutaneous routes, both serum and gastrointestinal virus neutralizing activity were attributable predominantly to antibodies of the IgG and IgM classes. None possessed serum IgA. There was evidence also for the presence of Ig fragments in some gastrointestinal extracts.

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Piglets vaccinated with a single oral dose of live porcine enterovirus strain T80 were protected to a highly significant degree against an oral challenge dose of 140 plaque forming units of T80 virus, in comparison with nonvaccinated controls, in terms of serum antibody response, titres and distribution of virus in the gastrointestinal tract contents and tissues and duration of virus excretion in the feces. Piglets vaccinated with multiple doses of adjuvanted, PE60-concentrated ethylenimine-inactivated virus administered both orally and subcutaneously showed only a slight degree of protection against the same challenge dose, despite the fact that they possessed high serum antibody titres at the time of challenge. Piglets vaccinated orally with live virus showed a degree of protection even against a challenge dose of 10(7.41) plaque forming units of T80 virus in terms of titres and distribution of virus in the gastrointestinal tract and duration of excretion of virus in the feces. Protection in the piglets dosed orally with live virus appeared to be attributable to the presence of relatively high levels of virus neutralizing antibody of the IgA class in the gastrointestinal tract.

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Neutralizing activity against porcine enterovirus strain T80 was demonstrated in the gastrointestinal contents of piglets given live T80 virus orally or parenterally, but little or no neutralizing activity was detected in the gastrointestinal contents of piglets given formaldehyde-inactivated virus by either route. The gastrointestinal neutralizing response was first detected 14 days after oral dosing, coincidentally with a fall in the titre and distribution of virus. The neutralizing response was highest at 23 days, and dropped markedly by 36 days, whereas no response was detected until 36 days in piglets which received live virus by the intramuscular route. Virus generally appeared earlier, was more widely distributed, and reached higher titres in the gastrointestinal tract of piglets which received live virus orally than in those which received the same preparation by the intramuscular route. The highest serum neutralizing response occurred in the piglets given live virus orally. The serum response in the piglets which received live virus intramuscularly appeared earlier and was biphasic. The serum response in the piglets receiving formaldehyde-inactivated virus appeared as early as the response to live virus given by the same route, but remained relatively low throughout the period of observation.

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