Literature DB >> 8980208

An outbreak of invasive group A streptococcal disease associated with high carriage rates of the invasive clone among school-aged children.

F R Cockerill1, K L MacDonald, R L Thompson, F Roberson, P C Kohner, J Besser-Wiek, J M Manahan, J M Musser, P M Schlievert, J Talbot, B Frankfort, J M Steckelberg, W R Wilson, M T Osterholm.   

Abstract

OBJECTIVES: To determine if a common strain of group A streptococcus was responsible for an outbreak of invasive streptococcal disease in southeastern Minnesota and to determine whether this strain was prevalent among residents of this area during the outbreak who either had streptococcal pharyngitis or were asymptomatic streptococcal carriers.
DESIGN: Pharyngeal culture survey and case-contact evaluation.
SETTING: Three adjacent counties in southeastern Minnesota defined as the outbreak area. Outbreak period, January 1 through March 31, 1995. PATIENTS: Seven patients with invasive streptococcal infection, 1249 patients (adults and children) with sore throat who resided in the outbreak area, children from an elementary school located in 1 community where the majority of invasive cases occurred, and 896 students from 3 schools located in Minnesota counties outside the outbreak area. MEASUREMENTS: Pulsed-field gel electrophoresis (DNA fingerprinting) of group A streptococcal isolates obtained from patients with invasive disease, throat swabs of patients with sore throat, and throat swabs of asymptomatic school-aged children.
RESULTS: All patients with outbreak-associated invasive disease had group A streptococcal isolates that were indistinguishable by pulsed-field gel electrophoresis. Additional testing showed that these isolates carried significant virulence factors including pyrogenic exotoxin A and streptococcal superantigen. Five of these 7 patients with invasive disease had underlying medical conditions; 4 developed toxic shock syndrome and died (case fatality, 57%). The outbreak-associated group A streptococcal clone was found in 69 (26.5%) of the 260 patients with sore throat from whom group A streptococcus was isolated. The frequency of the outbreak clone among pharyngeal carriers from the 3 schools outside the outbreak area was significantly less (range, 0%-10%) than in children from the school in the outbreak area (78%; relative risk, 29; 95% confidence interval, 11.1-78.1; P<.001). Four of the 7 patients with outbreak-associated disease had contact with children who attended the school in the outbreak area.
CONCLUSIONS: A single clone of group A streptococcus was responsible for 7 cases of invasive streptococcal disease during an outbreak in Minnesota and for a significant number of pharyngitis cases that also occurred during the outbreak. Invasive disease occurred most frequently in persons with underlying medical conditions. This outbreak was also associated with increased carriage rates of the invasive streptococcal clone among community school-aged children. Cases of invasive group A streptococcal infection may therefore reflect the tip of the iceberg with regard to the burden of colonization of a specific invasive streptococcal clone in a community.

Entities:  

Mesh:

Substances:

Year:  1997        PMID: 8980208

Source DB:  PubMed          Journal:  JAMA        ISSN: 0098-7484            Impact factor:   56.272


  49 in total

1.  Pyrogenic toxin superantigen site specificity in toxic shock syndrome and food poisoning in animals.

Authors:  P M Schlievert; L M Jablonski; M Roggiani; I Sadler; S Callantine; D T Mitchell; D H Ohlendorf; G A Bohach
Journal:  Infect Immun       Date:  2000-06       Impact factor: 3.441

2.  Therapeutic Approaches to Streptococcal Toxic Shock Syndrome.

Authors: 
Journal:  Curr Infect Dis Rep       Date:  1999-08       Impact factor: 3.725

3.  Prevalence of group A streptococcal carriers in asymptomatic children and clonal relatedness among isolates in Malatya, Turkey.

Authors:  Riza Durmaz; Bengul Durmaz; Mehmet Bayraktar; Ibrahim Halil Ozerol; Mahmut Tayyar Kalcioglu; Elif Aktas; Zeynep Cizmeci
Journal:  J Clin Microbiol       Date:  2003-11       Impact factor: 5.948

4.  Directional gene movement from human-pathogenic to commensal-like streptococci.

Authors:  A Kalia; M C Enright; B G Spratt; D E Bessen
Journal:  Infect Immun       Date:  2001-08       Impact factor: 3.441

5.  Nonpolar inactivation of the hypervariable streptococcal inhibitor of complement gene (sic) in serotype M1 Streptococcus pyogenes significantly decreases mouse mucosal colonization.

Authors:  S Lukomski; N P Hoe; I Abdi; J Rurangirwa; P Kordari; M Liu; S J Dou; G G Adams; J M Musser
Journal:  Infect Immun       Date:  2000-02       Impact factor: 3.441

6.  Genetic characterization and virulence role of the RALP3/LSA locus upstream of the streptolysin s operon in invasive M1T1 Group A Streptococcus.

Authors:  Laura A Kwinn; Arya Khosravi; Ramy K Aziz; Anjuli M Timmer; Kelly S Doran; Malak Kotb; Victor Nizet
Journal:  J Bacteriol       Date:  2006-11-17       Impact factor: 3.490

7.  A nonpeptide integrin antagonist can inhibit epithelial cell ingestion of Streptococcus pyogenes by blocking formation of integrin alpha 5beta 1-fibronectin-M1 protein complexes.

Authors:  D Cue; S O Southern; P J Southern; J Prabhakar; W Lorelli; J M Smallheer; S A Mousa; P P Cleary
Journal:  Proc Natl Acad Sci U S A       Date:  2000-03-14       Impact factor: 11.205

8.  Mosaic prophages with horizontally acquired genes account for the emergence and diversification of the globally disseminated M1T1 clone of Streptococcus pyogenes.

Authors:  Ramy K Aziz; Robert A Edwards; William W Taylor; Donald E Low; Allison McGeer; Malak Kotb
Journal:  J Bacteriol       Date:  2005-05       Impact factor: 3.490

9.  A globally disseminated M1 subclone of group A streptococci differs from other subclones by 70 kilobases of prophage DNA and capacity for high-frequency intracellular invasion.

Authors:  P P Cleary; D LaPenta; R Vessela; H Lam; D Cue
Journal:  Infect Immun       Date:  1998-11       Impact factor: 3.441

10.  Active and passive intranasal immunizations with streptococcal surface protein C5a peptidase prevent infection of murine nasal mucosa-associated lymphoid tissue, a functional homologue of human tonsils.

Authors:  Hae-Sun Park; P Patrick Cleary
Journal:  Infect Immun       Date:  2005-12       Impact factor: 3.441

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.