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Clinical Microbiology Reviews, October 2008, p. 594-605, Vol. 21, No. 4
0893-8512/08/$08.00+0     doi:10.1128/CMR.00020-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Emergence and Disappearance of a Virulent Clone of Haemophilus influenzae Biogroup aegyptius, Cause of Brazilian Purpuric Fever

Lee H. Harrison,1* Vera Simonsen,2 and Eliseu A. Waldman3

Infectious Diseases Epidemiology Research Unit, University of Pittsburgh Graduate School of Public Health and School of Medicine, Pittsburgh, Pennsylvania,1 Seção de Bacteriologia, Instituto Adolfo Lutz, São Paulo, Brazil,2 Faculdade de Saúde Pública, Universidade de São Paulo, São Paulo, Brazil3

Summary: In 1984, children presented to the emergency department of a hospital in the small town of Promissão, São Paulo State, Brazil, with an acute febrile illness that rapidly progressed to death. Local clinicians and public health officials recognized that these children had an unusual illness, which led to outbreak investigations conducted by Brazilian health officials in collaboration with the U.S. Centers for Disease Control and Prevention. The studies that followed are an excellent example of the coordinated and parallel studies that are used to investigate outbreaks of a new disease, which became known as Brazilian purpuric fever (BPF). In the first outbreak investigation, a case-control study confirmed an association between BPF and antecedent conjunctivitis but the etiology of the disease could not be determined. In a subsequent outbreak, children with BPF were found to have bacteremia caused by Haemophilus influenzae biogroup aegyptius (H. aegyptius), an organism previously known mainly to cause self-limited purulent conjunctivitis. Molecular characterization of blood and other isolates demonstrated the clonal nature of the H. aegyptius strains that caused BPF, which were genetically distant from the diverse strains that cause only conjunctivitis. This led to an intense effort to identify the factors causing the unusual invasiveness of the BPF clone, which has yet to definitively identify the virulence factor or factors involved. After a series of outbreaks and sporadic cases through 1993, no additional cases of BPF have been reported.

* Corresponding author. Mailing address: Infectious Diseases Epidemiology Research Unit, 521 Parran Hall, 130 Desoto Street, University of Pittsburgh, Pittsburgh, PA 15261. Phone: (412) 624-3137. Fax: (412) 624-2256. E-mail: lharriso{at}edc.pitt.edu

Clinical Microbiology Reviews, October 2008, p. 594-605, Vol. 21, No. 4
0893-8512/08/$08.00+0     doi:10.1128/CMR.00020-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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