The use of a geographical information system (GIS) to evaluate the distribution of tuberculosis in a high-incidence community

CITATION: Beyers, N. et al. 1996. The use of a geographical information system (GIS) to evaluate the distribution of tuberculosis in a high-incidence community. South African Medical Journal, 86(1):40-44.The original publication is available at http://www.samj.org.zaObjective. To determine the geographical distribution of tuberculosis in the two Western Cape suburbs with the highest reported incidence of tuberculosis. Design. Descriptive illustrative study. Setting. Two adjacent Western Cape suburbs covering 2.42 km2 with a population of 34 294 and a reported tuberculosis incidence of > 1 000/100 000. Subjects. All patients notified as having tuberculosis over a 10-year period (1985-1994). Interventions. None. Outcome measure. The geographical distribution of the cases was determined using a geographical information system (GIS) and the National Population Census (1991). Results. One thousand eight hundred and thirty-five of the 5 345 dwelling units (34.3%) housed at least 1 case of tuberculosis during the past decade and in 483 houses 3 or more cases occurred. These cases were distributed unevenly through the community, with the tuberculosis incidence per enumerator subdistrict (ESD) varying from 78 to 3 150/100 000 population. Conclusion. In a small area with a high incidence of tuberculosis, the cases are spread unevenly through the community and there are certain houses where tuberculosis occurs repeatedly. This information should be used to direct health services to concentrate on certain high-risk areas.Publisher’s versio

Book Reviews

Book Review 1Book Title: Modern Coloproctology: Surgical Grand Rounds from St Mark's HospitalBook Authors: Robin Phillips & John Northover (Eds.)pp. 195. illustrated. London: Edward Arnold. 1993. ISBN 0-340-55258-1Book Review 2Book Title: Diagnostic Molecular Pathology: A Practical Approach. Vol. I & IIBook Authors: C.S. Herringron & J.O'D. McGee (Eds.)Pp. Vol. I xviii + 270; Vol. II xvi + 217. Cape Town: Oxford University Press. 1992. ISBN Vol. I 0-19-963236-7, Vol. II 0-19-963238-3.Book Review 3Book Title: Training Therapy: Prophylaxis and RehabilitationBook Authors: Rolf Gustavsen & Renate Streeck2nd revised ed. Pp. viii + 230. Illustrated. Stuttgart: George Thieme Verlag. 1993. ISBN 3-13-672502-6.Book Review 4Book Title: Handbook of Bereavement: Theory, Research and InterventionBook Authors: Margaret S. Stroebe, Wolfgang Stroebe & Robert O. Hansson (Eds.)Pp. xii + 546. Cambridge: Cambridge University Press. 1993. ISBN 0-521-39315-9 hardback, ISBN 0-52144853-0 paperback.Book Review 5Book Title: Atlas of Gynecologic PathologyBook Authors: J. Donald Woodruff, Teresita L. Angruaco & Tim H. Pannley (Eds.)pp.321. New York: Raven Press. 1993. ISBN 0-7817-0056-6.Book Review 6Book Title: Our Planet, Our Health: Report of the WHO Commission on Health and EnvironmentBook Author: World Health OrganisationPp. 282. Geneva. 1992. ISBN 92-4-156148-3.Book Review 7Book Title: Neonatal Tetanus Elimination Field Guide. Technical Paper No 35Book Author: Pan American Health OrganisationPp. v +37. Washington: Pan American Health Organisation. 1993. ISBN 92-75-13035-3

N-Terminal E-Cadherin Peptides Act as Decoy Receptors for Listeria monocytogenes

The observation that E-cadherin is the principal epithelial receptor for the bacterial pathogen Listeria monocytogenes led us to investigate whether N-terminal fragments of E-cadherin containing the L. monocytogenes binding domain could inhibit entry of the bacteria into cultured epithelial cells. Here we demonstrate that a conditioned medium from a gastric cancer cell line (Kato III) that carries a truncating CDH-1 mutation 3′ of the L. monocytogenes binding domain can inhibit the uptake of the bacteria into Caco-2 cells. The inhibitory activity of the Kato III conditioned medium could be mimicked by incubation of the bacteria with a recombinant 26-kDa N-terminal E-cadherin peptide prior to infection. Furthermore, these data suggest that cleavage of the 80-kDa extracellular domain of E-cadherin from the cell surface may provide an innate form of pathogen defense by acting as a decoy receptor for L. monocytogenes