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Streptococcal infection remains almost the sole cause of the clinical syndrome of acute glomerulonephritis in African children. Evidence for this is in elevated levels of antistreptolysin "O" (ASO) titre in 93% of 28 patients and growth of Group Abeta haemolytic streptococci from the skin and throat in 32%. Spread of infection from the skin, where lesions were present in all patients, to the throat would account for positive cultures at both sites and the frequent and vigorous antistreptolysin "O" responses. Clinical recovery occurred in most within seven days and in all within 60 days of admission. IgG and IgA, but not IgM, were increased in patients; C4 was normal in the majority and low in seven out of 24 (29%), C3 was diminished in 26 out of 28 (93%) and the mean level of C3 PA was lower than in controls. Total haemolytic complement paralleled C3 values; C3 breakdown products were not detected in any patient. Renal biopsies in seven out of 28 patients showed typical histological changes of diffuse exudative proliferative glomerulonephritis on light microscopy and fibrinogen and C3 on immunofluorescent staining. These findings suggest that events leading to glomerular damage in acute post-streptococcal nephritis in African children involve activation of both classical and alternative pathways of complement proteins and also confirm the well recognized and predictable nature of the disease, irrespective of geographical distribution.

Vaginal swabs were taken from 60 Black women attending a family planning clinic and from 60 attending a special clinic for sexually transmitted diseases. Using selective media, the isolation rate for group B streptococci was 26,7% in the former group and 40,0% in the latter. The isolation rates of other streptococcal serogroups are also given. All group B streptococci isolated were uniformly sensitive to penicillin but resistant to gentamicin. Clinical details of 7 patients with group B streptococcal septicaemia are also given.

A 50-year-old man with recurrent life-threatening sepsis and a cutaneous condition resembling pyoderma gangrenosum, was found to have a defect of neutrophil phagocytic function. Phagocytosis could be enhanced by corticosteroids, both in vitro in a dose-dependent manner, and in vivo, when it was accompanied by rapid clinical improvement. Studies with steroid hormones and immuno-stimulatory drugs are described.

A live attenuated Yersinia pestis vaccine designated EV76-51f, which had previously been shown to be pathogenic in vervet monkeys but not in guinea pigs, was tested in the multimammate mouse Praomys (Mastomys) natalensis. Doses of 10(6) viable organisms inoculated subcutaneously as either a lyophilized suspension or an agar-grown culture resulted in vaccination fatalities in Praomys but not in white mice. Hemagglutinating antibodies to the fraction 1 antigen were not stimulated by doses lower than 10(4) viable organisms. Agar-grown cultures of the vaccine gave better protection against a virulent Y. pestis challenge than did a lyophilized suspension. All Praomys vaccinated with a dose of 10(6) agar-grown EV76-51f protected against a virulent challenge, whereas even doses up to 10(8) lyophilized bacilli failed to give complete protection. The pathogenicity of a live attenuated plague vaccine derived from the Y. pestis EV76 vaccine strain can be detected in Praomys (Mastomys) natalensis, a rodent species highly susceptible to plague. This animal species may therefore be valuable for the testing of live attenuated plague vaccines before they are tested in costly nonhuman primates.

Twenty-eight Black children with complicated measles were investigated for their capacity to produce antibodies when stimulated with TAB antigen. Their measles antibody titres were also measured. Antibody production to TAB was defective, especially the "H" antibody. Production of measles antibody was sometimes delayed in its appearance but subsequently reached normal levels.

Renal transplant recipients at Tygerberg Hospital were investigated to determine the importance of Epstein-Barr virus (EBV) as a pathogen in these patients. All 106 patients investigated were shown to have EBV antibodies before transplantation and most had serological evidence of reactivation of the infection after transplantation. A mild clinical illness was present in a few patients concomitant with EBV reactivation, which may suggest that this virus has a role in the morbidity of some renal transplant recipients. Lymphoblastoid cell lines were established from 11 renal transplant recipients; 5 of these cell lines were shown to be virus producers and 1 is thought to have unique properties.

The role of anaerobes in the pathogenesis of infections was investigated. Anaerobes were isolated from 0,25% of blood cultures and from 15,8% of other specimens tested; in 15,1% of cases where anaerobes were isolated, no aerobes were found. The strains most commonly encountered were Bacteroides fragilis, B. melaninogenicus, Peptostreptococcus anaerobius and Clostridium perfringens. Sensitivity tests in vitro showed all organisms to be sensitive to clindamycin, metronidazole and chloramphenicol, while a large proportion were resistant to penicillin G and smaller numbers were resistant to tetracycline.

In five children with measles who subsequently died and in one with measles in whom chronic bronchopneumonia developed (group A), immunosuppression was more pronounced during the acute rash (i.e., 3-20 days before death) than in six children with measles who recovered (group B). The absolute total lymphocyte-count (T and B cells) was significantly lower in group A. Mean serum-C3 was also lower in group A than in group B. There were no significant differences between the two groups for other complement factors or for serum-immunoglobulins. The mean phytohaemagglutinin stimulation index (S.I.) for lymphocytes from patients in group A resembled that in group B, although the S.I. in both groups was significantly lower than that in healthy controls. S.I.S were lowest in two patients who died. Counts of total white cells, neutrophils, null cells, and those with both B and T cell markers were not significantly different in groups A and B. The total lymphocyte-count (mean 2117 +/- S.E.M. 375 cells/mm3) in a further nineteen patients with measles who had died, studied retrospectively, was significantly lower than that (4487 +/- 540 cells/mm3) in twenty-seven patients with measles who recovered.

Three cases of meningitis and two of septicaemia were caused by pneumococci resistant to the penicillins/cephalosporins and chloramphenicol. No beta-lactamase was demonstrated in any of the organisms. All three patients with meningitis died, but the patients with septicaemia recovered after being given appropriate antibiotic therapy.

Immune responses in 24 children with acute measles (AM) were compared with those in 20 children who had chronic pulmonary complications (CPMC) following measles. The immuno-suppressive effects of acute measles were extensive: total white cells were reduced and this reduction was accounted for entirely by lymphopenia which was equally expressed among the major lymphocyte sub-populations studied; the function of 'T' cells, assessed by radio-isotope incorporation into phytohaemagglutin (PHA) transformed lymphocytes and delayed skin hypersensitivity (DHR) to dinitrochlorobenzene (DNCB), was depressed. Serum IgA was reduced in AM patients. In contrast there was a relative sparing of the measured indices of immunity in patients with chronic post-measles chest disease, with the major defect being an impaired DHR to DNCB. There were minor alterations of complement components in both groups of patients.

Serum levels of complement components C3, C4 and factor B were measured in twenty-five patients with Staphylococcus aureus bacteraemia. The levels of C3 were depressed in nine patients, five of whom also had low C4 levels, indicating activation of complement via the classical pathway. Two patients with low C3 levels also had low factor B levels, one of these being in association with a low C4 level, which indicates activation of both the classical and alternative pathways, the latter being via the C3b feedback cycle. The protein A content of the S. aureus cultures, as shown by the indirect haemagglutination titre, was high in nine patients with C3 hypocomplementaemia. There was some correlation between the presence of a high protein A content of the S. aureus culture and a low serum C3 level in the patient. Some clinical evidence of immune complex disease was found in three patients. Complement activation in S. aureus bacteraemia is most likely due to complex formation resulting from the interaction between the Fc portion of IgG and staphylococcal protein A. These complexes may also result in clinical symptoms of immune complex disease.

A postmortem bacteriological study of Black children in a respiratory intensive care unit showed that Pseudomonas aeruginosa was the most common opportunistic pathogen and that it usually complicated a viral infection. In a parallel study of non-debilitated patients in general hospital wards Klebsiella aerogenes and Escherichia coli were the most frequently isolated organisms. Counter-immuno-electrophoresis was used for the identification of Pseudomonas-precipitating antibody in serum and tracheal secretions, and also of Pseudomonas antigen in the latter.

Yersinia pestis fraction l passive haemagglutination studies on human sera obtained randomly during a plague epidemic showed a 10-fold increase in occurrence of antibodies compared with the results obtained on sera from the same population 11 months earlier during a quiescent phase. The pre-epidemic population antibody rate was lower than that in a comparable population tested simultaneously in another endemic region, where a recrudescence of plague was not experienced during the following year. The human plague epidemic was preceded and accompanied by a rodent die-off. A serological survey of the small mammals 2 years prior to the human survey also showed that Y. pestis was present in the environment. Otomys unisulcatus was indicated as being an important rodent in the plague cycle in the area.

Campylobacter fetus was isolated from five recent cases of human vibriosis, of which two were adults and three were children. One adult presented with pericarditis and the other with recurrent pyrexia. Campylobacter fetus subsp. intestinalis which resembled cattle strains serologically, was isolated under CO2 or anaerobic conditions from blood cultures of these patients. Two of the three children had kwashiorkor and the third was only 8 days old. Isolates identified as Campylobacter fetus subsp. jejuni were cultured from blood of these patients, two of whom had diarrhoea. Three patients succumbed, despite adequate antibiotic therapy. The epidemiology of the disease is discussed and it is suggested that infection may have been from the patients' own flora.

A nosocomial outbreak of Crimean-Congo haemorrhagic fever occurred in Tygerberg Hospital near Cape Town in September 1984 when 7 medical personnel became ill after admission of an index patient. The disease was fatal in the index and 1 secondary case, and was confirmed in the index and 6 secondary cases by isolation of the virus. An antibody response was demonstrated in the remaining patient, thought to be a tertiary case, but the fact that the patient received immune plasma therapy raises doubts about the validity of the diagnosis. The index case had contact with ticks and horses but his infection could not be related to a specific incident.

This report describes a case of meningitis caused by a Lancefield group C streptococcus (Streptococcus dysgalactiae) in a 9-week-old infant. Bacteria of this group rarely cause serious infections in man. The organism was identified as a member of Lancefield group C by the acid extraction method and as S. dysgalactiae by biochemical tests. The patient's condition responded well to penicillin and tobramycin therapy, with no obvious neurologic sequelae.

A multicentre study to evaluate the activity of amoxycillin when combined with clavulanic acid against clinical bacterial isolates was performed in South Africa. Minimum inhibitory concentrations for amoxycillin alone and in combination with clavulanic acid were determined by agar dilution. The majority of amoxycillin-resistant Klebsiella and Escherichia coli strains became sensitive to amoxycillin in the presence of low concentrations of clavulanic acid. Beta-lactamase-producing strains of Staphylococcus aureus showed increased susceptibility to amoxycillin in the presence of clavulanic acid. Minimum bactericidal concentrations indicated that amoxycillin retains bactericidal activity in the presence of clavulanic acid. Enterobacter and Serratia species and Pseudomonas aeruginosa remained amoxycillin-resistant in the presence of clavulanic acid.

The clinical course of generalized Yersinia enterocolitica infection in 13 patients was observed. Two syndromes were apparent; seven patients had an acute septicemic picture, whereas the rest had a subacute localizing infection that usually produced hepatic or splenic abscesses. The latter form often resembled amebic hepatitis clinically, and five of the six patients died despite antibiotic treatment. The acute septicemic form of the disease resembled systemic salmonellosis, and most cases responded to therapy with the appropriate antibiotics.

A live attenuated Yersinia pestis (Pasteurella pestis) vaccine strain designated EV51f, which had been passaged through guinea pigs previously treated with ferrous sulfate, was shown to be pathogenic for African green vervet monkeys (Cercopithecus aethips pygerythrus), but not for guinea pigs. The bacilli multiplied in the monkeys, as shown by positive blood cultures, caused an elevation of white cell counts and rectal temperatures, and resulted in death of 26% (13/50) of animals. Postmortem findings of these animals were typical of bubonic-septicemic plague. This vaccine did not cause deaths in 50 guinea pigs even in doses up to 100 million viable bacilli inoculated subcutaneously. It is suggested that the virulence of an attenuated Y. pestis strain which does not produce pigment on a defined medium containing hemin, but possesses all other known virulence determinants, is dependent on the availability of iron in vivo. The serological response of the monkeys as determined by the hemagglutinating and mouse protective antibodies was high one month after vaccination and also in guinea pigs, as shown by virulent challenge. This antibody level declined in monkeys over a period of nearly 6 months, and a decline in immunity was confirmed by virulent challenge which resulted in the death of 30% of vaccinated monkeys. The level of immunity in monkeys did not appear to be related to the dose of vaccine.