Proposed guidelines for malaria antigen testing.
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Biomedical subjects
Publications and source records attributed to J A Frean.
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Acanthamoeba species can cause a chronic, progressive ulcerative keratitis of the eye which is not responsive to the usual antimicrobial therapy and is frequently mistaken for stromal herpes keratitis. An unusual case of coinfection with Acanthamoeba polyphaga and Pseudomonas aeruginosa as causes of corneal keratitis in a contact lens wearer from Gauteng, South Africa, is reported. These two pathogens have previously been assumed to be selectively exclusive. Cysts of the isolated acanthameba tolerated an incubation temperature of 40 degrees C, indicating a pathogenic species. This case highlights the importance of culture methods in the diagnosis of corneal infection and the choice of treatment regimen. The patient's history of careless contact lens-disinfecting habits emphasizes the need to adhere strictly to recommended methods of contact lens care.
A particular polymorphism in the cg2 gene has previously been linked to chloroquine resistance in reference isolates of Plasmodium falciparum. To assess the association of this polymorphism with chloroquine resistance in field specimens of P. falciparum, we analyzed the omega repeat region of the cg2 gene in 47 isolates of P. falciparum collected in the Ingwavuma District of northern KwaZulu-Natal, South Africa. Polymerase chain reaction (PCR) primers, which were designed to amplify the region of DNA surrounding the omega repeat, were used to obtain omega repeat PCR products from the field isolates. The PCR product for each isolate varied in length, depending on the number of cg2 omega repeats for that isolate. We found that several in vivo and in vitro chloroquine-resistant isolates of P. falciparum did not have the expected 16 omega repeats. These results suggest that the link between the cg2 polymorphism and chloroquine resistance identified previously may not apply in all malarious areas.
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A limited repertoire of antimicrobial agents is currently in use for the treatment of plague. We investigated the in vitro activities of some newer antimicrobial agents against Yersinia pestis. Among the injectable agents tested, cefotaxime was the most active, and among the oral agents, both levofloxacin and ofloxacin were highly active, with MICs at which 90% of isolates are inhibited of < 0.03 microgram/ml. the susceptibilities to the ketolide RU004 and the penem faropenem warrant attention. The enhanced activities of quinolones against Y. pestis suggest that these agents should be further investigated for the treatment of human plague in the future.
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An outbreak of fatal septicaemia caused by Serratia odorifera biotype 1 involved infants at several hospitals; the common vehicle of infection was contaminated parenteral nutrition fluid. The transfusate had been made up in a flexible film isolator system. The implicated organism was recovered from surfaces inside the isolator, despite routine decontamination procedures having been carried out shortly before. Our investigation into the origin of contamination revealed several shortcomings in the infusate compounding process. We noted deficiencies in cleaning and decontamination procedures, and in storage and sterility testing policies, but the origin and mechanism of the contamination were unclear. Withdrawal of parenteral nutrition products and revision of decontamination procedures terminated the outbreak. The efficacy of peracetic acid treatment of flexible film isolators, given the circumstances of this outbreak, may need further investigation. Regular training and assessment of admixture technicians is important.
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A ten year old boy developed lymphocutaneous sporotrichosis following a wild rodent bite. The infection was successfully treated with potassium iodide. Sporotrichosis in humans has followed bites, pecks and stings inflicted by a variety of animals, birds and insects. Many species of animals are susceptible to infection by Sporothrix schenkii, but transmission from infected animals to man is uncommon.
Twenty cases of blastomycosis have been confirmed in the RSA, 9 of which are presented for the first time. Patients came from all four provinces and the mean age was 40 years. Six cases were diagnosed between 1985 and 1987. Differences between strains of Blastomyces dermatitidis isolated in the RSA and in North America include morphological and cultural characteristics, mycelial-yeast conversion, antigenic structure, and compatibility in cross-mating experiments. The diagnosis of this disease can be made by direct examination of unstained specimens, by histological examination or by culture of the organism. Culture should be attempted in all cases for confirmation of microscopic findings.
The known African cases of blastomycosis to 1987 are presented, including thirteen previously undescribed cases. This brings to 81 the total number of cases known to have occurred in Africa. The question of whether the disease in Africa is the same in all respects as that in North America is addressed; the age and sex distributions of patients are similar. Minor differences in the clinical features relate particularly to the type of skin lesion, the more frequent bone involvement and the less frequent central nervous system involvement in the African patient. Little is known about the epidemiology of blastomycosis in Africa; one noteworthy feature is the apparent absence of the disease in dogs. Isolates of Blastomyces dermatitidis from the two continents, although closely related, differ in some respects.
Hepatitis E virus (HEV) causes sporadic and epidemic acute viral hepatitis in many developing countries. In Africa, hepatitis E has been documented by virus detection (reverse transcriptase polymerase chain reaction, RT-PCR) in Egypt, Chad, Algeria, Morocco and Tunisia. Cases of presumptive hepatitis E also have been documented by detection of antibody to HEV in the Sudan, Kenya, Ethiopia, Somalia, Djibouti and South Africa. Recently, we reported the recovery of 9 isolates of HEV from feces collected during an outbreak of jaundice in Namibia. These specimens were stored frozen for many years at the South African Institute for Medical Research awaiting new methods to determine the etiology of jaundice. HEV genomic sequences were detected by antigen-capture RT-PCR with primers that amplified 2 independent regions of the HEV genome (ORF-2 and ORF-3). To further characterize the HEV 83-Namibia isolates, we determined the nucleotide (nt) sequence of the 3' end of the capsid gene (296 of 1, 980 nt in ORF-2) and ORF-3 for 1 isolate. The capsid gene sequence shared 86% identity with the prototype Burma strain and up to 96% identity with other African strains at the (nt) level, and 99% identity with Burma or other Africa strains at the amino acid level. A 188 (nt) fragment amplified from ORF-3 was also highly homologous to other HEV but was too short for meaningful comparison. Phylogenetic analysis indicated that HEV 83-Namibia is closely related to other African isolates, and differs from Burmese, Mexican and Chinese HEV. These data link the HEV causing the 1983 Namibia outbreak to more recent HEV transmission in northern and sub-Saharan Africa, suggesting this subgenotype of HEV is firmly established throughout the continent.
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