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PubMed · 2500819

[Meningococcal plasmids].

K G Khetsuriani·N L Gotsiridze·T K Mironova·T G Gabisoniia·N N Kostiukova
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Abstract

In Neisseria meningitidis strains isolated from patients with meningococcal infection and from carriers, the presence of plasmids has been detected by the modified method of H. C. Bernboim and J. Doly. The strains have been studied with respect to their pathogenicity and sensitivity to antibacterial substances. No correlation between the presence of plasmids and pathogenicity factors, such as antilysozyme activity, the presence of hyaluronidase and the positive reaction to Congo red, resistance to penicillin, serogroup and the sources of isolation, has been established.

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Carrier StateDrug Resistance, MicrobialHumansMeningitis, MeningococcalMicrobial Sensitivity TestsNeisseria meningitidisPlasmidsSerotypingJournal Article

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K G Khetsuriani, N L Gotsiridze, T K Mironova, T G Gabisoniia, N N Kostiukova. 1989. [Meningococcal plasmids].. https://pubmed.ncbi.nlm.nih.gov/2500819/

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PubMed2002

The clinical and molecular spectrum of galactosemia in patients from the Cape Town region of South Africa.

BACKGROUND: The objective of this study was to document the clinical, laboratory and genetic features of galactosemia in patients from the Cape Town metropolitan region. METHODS: Diagnoses were based on thin layer chromatography for galactosuria/galactosemia and assays of erythrocyte galactose-1-phosphate uridyltransferase (GALT) and galactokinase activities. Patients were screened for the common S135L and Q188R transferase gene mutations, using PCR-based assays. Screening for the S135L mutation in black newborns was used to estimate the carrier rate for galactosemia in black South Africans. RESULTS: A positive diagnosis of galactosemia was made in 17 patients between the years 1980 to 2001. All had very low or absent galactose-1-phosphate uridyltransferase (GALT) activity, and normal galactokinase levels. The mean age at diagnosis was 5.1 months (range 4 days to 6.5 months). A review of 9 patients showed that hepatomegaly (9/9), and splenomegaly, failure to thrive, developmental delay, bilateral cataracts (6/9) were the most frequent features at diagnosis. Six had conjugated hyperbilirubinemia. Four experienced invasive E. coli infection before diagnosis. Ten patients were submitted to DNA analysis. All 4 black patients and 2 of mixed extraction were homozygous for the S135L allele, while all 3 white patients were homozygous for the Q188R allele. The remaining patient of mixed extraction was heterozygous for the Q188R allele. The estimated carrier frequency of the S135L mutation in 725 healthy black newborns was 1/60. CONCLUSIONS: In the absence of newborn screening the delay in diagnosis is most often unacceptably long. Also, carrier frequency data predict a galactosemia incidence of approximately 1/14 400 for black newborns in the Cape Metropole, which is much higher than the current detection rate. It is thus likely that many patients go undetected.

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