Biomedical subjects
Publications and source records attributed to M Isaäcson.
A non-agglutinable Vibrio cholerae strain isolated from the blood of a child with kwashiorkor and fever was shown to have the potential to invade as well as to produce a toxin resembling cholera toxin.
A description is given of an outbreak of human plague in Lesotho in 1968 which was preceded by, and merged with, a typhoid epidemic. This circumstance was responsible for a diagnosis of typhoid fever being made in the earliest plague cases, especially as the clinical presentation was similar to that of the typhoid patients. Consequently, the plague epidemic ran its natural course and with the onset of winter the pneumonic form appeared. Serological follow-up studies of recovered patients were carried out up to 4 years after the outbreak.
The first recognised outbreak of Marburg virus disease in Africa, and the first since the original epidemic in West Germany and Yugoslavia in 1967, occurred in South Africa in February 1975. The primary case was in a young Australian man , who was admitted to the Johannesburg Hospital after having toured Rhodesia. Two secondary cases occurred, one being in the first patient's travelling companion, and the other in a nurse. Features of the illness included high fever, myalgia, vomiting and diarrhoea, hepatitis, a characteristic maculopapular rash, leucopenia, thrombocytopenia, and a bleeding tendency. The first patient died on the seventh day from haemorrhage resulting from a combination of disseminated intravascular coagulation and hepatic failure. The other two patients were given vigorous supportive treatment and prophylactic heparin and recovered after an acute phase lasting about seven days. During this period on developed pancreatitis, the serum amylase remaining raised until the 32nd day after the onset of the illness. The other developed unilateral uveitis after having been asymptomatic for two months. This persisted for several weeks and Marburg virus was cultured from the anterior chamber of the eye.
The recent invasion of southern Africa by cholera stimulated the establishment of a regional cholera reference laboratory and surveillance centre. This article describes its activities in general and details the methods employed in the isolation of Vibrio cholerae from sewage, water, seafoods, patients, and carriers. Importance is also attached to the isolation of NAG (non-agglutinable) V. cholerae and V. parahaemolyticus from certain categories of specimens. In recognition of the importance of regional co-operation in combating the problem of cholera, the collaboration of other countries on the subcontinent was invited, and the response is encouraging.
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.
The only non-human host of Lassa virus so far identified is the multimammate mouse, Praomys (Mastomys) natalensis, but its precise role in the natural Lassa fever cycle remains to be determined. This species is also an important link in the plague cycle in southern Africa and is one of the commonest rodents of Africa. It is a prolific breeder and can be kept and bred easily in captivity. It is thus an excellent laboratory animal, although it needs to be handled with care because it is aggressive towards man and bites readily. The current status of knowledge of its taxonomy, ecology, distribution, and role as a disease vector is reviewed, but attention is drawn to the possibly disastrous consequences of attempting to eradicate a vector species before the natural cycle of the disease and the ecology of the vector are fully understood.
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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.
Many factors, such as temperature, pH, organic nutrients, types of water storage containers, etc., determine the survival of Vibrio cholerae in water. Since the survival of V. cholerae O1 has been shown to be much longer in metal drums used as household water storage containers than in clay pots and plastic drums, the present study was designed to explore the possible role played by insoluble iron on the survival of V. cholerae O1 in water. The possibility of iron acting as particulate matter for the organisms to adhere to was also examined by using inert glass beads in water. Survival of V. cholerae O1 in dechlorinated tap water, with and without inert glass beads, ranged from < 24 h to 10 d. The number of surviving bacteria was, however, very low. In the presence of impure ferric oxide (Fe2O3), survival in tap water ranged from 4 to 12 d and the numbers of surviving bacteria were very high. Iron was thought to play an important role in the survival of V. cholerae O1 in water. Differences between the numbers of bacteria and the length of survival in surface water and in sediment were unremarkable. The El Tor and classical biotypes gave similar results.
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Many physicochemical factors affect the survival of Vibrio cholerae in the aquatic environment. An attempt was made to study the combined effect of pH and iron on the survival of V. cholerae in water in a laboratory environment. None of the 6 strains of V. cholerae used survived at pH 5.0; survival of all strains increased with increasing pH. The effect of ferric oxide on survival was significant for V. cholerae O1 only, not for non O1 strains. The longest survival of V. cholerae non O1 was 82 d, of El Tor V. cholerae 68 d, and of classical V. cholerae 56 d.
In 1992, a large outbreak of bloody diarrhea caused by Escherichia coli O157 infections occurred in southern Africa. In Swaziland, 40,912 physician visits for diarrhea in persons ages >5 years were reported during October through November 1992. This was a sevenfold increase over the same period during 1990-91. The attack rate was 42% among 778 residents we surveyed. Female gender and consuming beef and untreated water were significant risks for illness. E. coli O157:NM was recovered from seven affected foci in Swaziland and South Africa; 27 of 31 patient and environmental isolates had indistinguishable pulsed-field gel electrophoresis patterns. Compared with previous years, a fivefold increase in cattle deaths occurred in October 1992. The first heavy rains fell that same month (36 mm), following 3 months of drought. Drought, carriage of E. coli O157 by cattle, and heavy rains with contamination of surface water appear to be important factors contributing to this outbreak.
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