[The clinician and streptococcal infections].
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The recent unexplained increase in severe streptococcal diseases in the United States and Great Britain is compared to the 1825-1885 pandemic of fatal scarlet fever. Although scarlet fever may not be representative of all severe streptococcal disease, it was the only one reliably identified in the 19th century. The epidemiology of scarlet fever during the 19th century pandemic suggests the following features of the disease; cocirculation of both virulent and less-virulent streptococcal strains eliciting cross-immunity; circulation of hyperendemic prevalent strains in urban centers of developed nations, with periodic spillovers to rural areas and developing nations; and protection of infants from infection (but not from fatal disease once infection occurred) by the transfer of maternal antibodies via the placenta, breast milk, or both. The 19th century data suggest that efforts to prevent severe streptococcal diseases should begin with better characterization of the epidemiology of streptococcal disease, a task entailing identification of streptococcal virulence factors and measurement of their distribution among isolates from individuals with streptococcal diseases and in open populations.
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We sent a questionnaire to all members of the European Society for Paediatric Infectious Diseases and to all delegates of the European Association of Perinatal Medicine to determine existing policies for prevention of neonatal group B streptococcal (GBS) infection in Europe. The incidence of GBS colonization in pregnant women and of neonatal GBS infection varies. Policies for prevention of GBS infection are not well-developed.
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This article reviews the immunologic and microbiologic characteristics of the group B streptococcal organism, perinatal acquisition, clinical presentation, and therapy. A discussion of immunoglobulin transfusion therapy is included, and a case study is presented.
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Some 115 R- and 143 S-streptococcal strains were isolated from 258 pigs that had died or been killed for disease, between 1969 and 1973. They were cultured and biochemically tested for sensitivity to chemotherapeutics. All R- and S-strains were of normal sensitivity to penicillin and, with few exceptions, to chloramphenicol and oxytetracycline as well. Most of the strains caused primary Sc.-infection, such as septicaemia, leptomeningitis, endocarditis, and arthritis. R-Sc.-infections were contracted mainly by store pigs and animals in advenced age, while S-Sc.-infections affected mainly piglets.
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A term female infant developed late onset group B streptococcal disease on Day 12 of life. The source of the organism appeared to be expressed maternal breast milk in the absence of clinical mastitis. Asymptomatic excretion of group B Streptococcus in breast milk may be an underrecognized cause of neonatal infection.
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Groups A, B, C and G streptococci were cultured from 63 consecutive in-patients recruited between November 1987 and April 1988 and monitored until the end of July 1988. Chronic leg ulcers were present in 34 patients. Group G was found in 34 patients, 25 of whom had pyoderma and 3 had sepsis. Six of the patients had no signs of clinical infection, and treatment with antibiotics was therefore withheld. Recurrent phlegmon or erysipelas developed in 2 of 28 patients with clinical Group G infections. Erysipelas developed some 1-7 months later in 3 of the 6 patients who were not initially treated. No significant difference in severity or additional medical conditions was found between the patients with either Group G or Group A streptococci. In comparison, data on all streptococcal cultures at the Department indicated that Group G was isolated 2.6 times as often as Group A streptococci for the in-patients, compared with 1.1 for all patients seen. It is concluded that Group G streptococcal skin infections must be regarded with the same clinical vigilance as Group A infections.
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