Epidemic Acute Nephritis With Reappearance of Type-49 Streptococcus

Anthony, Bascom F.; Kaplan, EdwardL.; Chapman, Stephen; Quie, P. G.; Wannamaker, Lewis W.

doi:10.1016/s0140-6736(67)92230-1

Cited by 52 publications

(26 citation statements)

References 5 publications

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“…Serotype M49 GAS has been widely reported as a causative strain of pyoderma-associated APSGN and has been responsible for previous outbreaks. 20,33,34 Emm 70 and emm 85 GAS have not been previously reported to be associated with APSGN. It is possible that unlike the outbreak in 2005, which appears to be related to one type of GAS, there may have been multiple types responsible for the outbreak in 2000.…”

Section: Discussionmentioning

confidence: 85%

Acute Post-Streptococcal Glomerulonephritis in the Northern Territory of Australia: A Review of 16 Years Data and Comparison with the Literature

Marshall¹,

Cheng²,

Markey³

et al. 2011

The American Society of Tropical Medicine and Hygiene

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Data relating to acute post-streptococcal glomerulonephritis (APSGN) from the notifiable diseases surveillance system in the Northern Territory of Australia was extracted and analyzed. Isolates of Streptococcus pyogenes from confirmed cases were emm sequence typed. From 1991 to July 2008, there were 415 confirmed cases and 23 probable cases of APSGN notified. Four hundred fifteen (94.7%) of these were Indigenous Australians and 428 (97.7%) were people living in remote or very remote locations. The median age of cases was 7 years (range 0–54). The incidence of confirmed cases was 12.5/100,000 person-years, with an incidence in Indigenous Australian children younger than 15 years of age of 94.3 cases/100,000 person-years. The overall rate ratio of confirmed cases in Indigenous Australians to non-Indigenous Australians was 53.6 (95% confidence interval 32.6–94.8). Outbreaks of disease across multiple communities occurred in 1995 (N = 68), 2000 (N = 55), and 2005 (N = 87 [confirmed cases]). Various emm types of S. pyogenes were isolated from cases of APSGN including some types not previously recognized to be nephritogenic. The widespread outbreak in 2005 was caused by emm55.0 S. pyogenes. Acute post-streptococcal glomerulonephritis continues to occur in remote Indigenous communities in Australia at rates comparable to or higher than those estimated in developing countries. Improvements in preventative and outbreak control strategies are needed.

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Section: Discussionmentioning

confidence: 85%

Acute Post-Streptococcal Glomerulonephritis in the Northern Territory of Australia: A Review of 16 Years Data and Comparison with the Literature

Marshall¹,

Cheng²,

Markey³

et al. 2011

The American Society of Tropical Medicine and Hygiene

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“…Insects were collected and processed intact in a similar manner. All other cultures were processed and beta-hemolytic streptococci classified serologically* as previously described (Anthony et al 1967b). Sub-cultures of three individual colonies were made from each primary plate and were identified serologically.…”

Section: Methodsmentioning

confidence: 99%

The role of normal skin in the spread of streptococcal pyoderma

Dudding

Chapman

et al. 1970

J. Hyg.

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SUMMARYThe primary body site of acquisition of group A streptococci was examined prospectively in a population with endemic streptococcal pyoderma. Weekly cultures were obtained during the skin infection season from apparently normal upper respiratory and cutaneous sites (and from skin lesions when present) in 44 children and adults living on the Red Lake Indian Reservation.During the 9-week period of the study 705 of a total of 2305 cultures were positive for group A streptococci. The percentage of positive cultures from the various sites were: throat (20 %); nose (24 %); wrist (32 %); ankle (35 %); back (22 %); and skin lesions (81 %). Group A streptococci were also isolated from fingernail dirt, clothing and bedding as well as from a few household pets and insects.Analysis of serial cultures obtained from the same individuals at weekly intervals suggested that the strains isolated from skin lesions first appeared on normal skin in the 2 weeks preceding the lesion. Spread to the nose and throat followed skin acquisition and/or skin lesions.The high prevalence of group A streptococci on normal skin in the absence as well as the presence of pyoderma, and their appearance on normal skin before recovery from either skin lesions or the upper respiratory tract are consistent with the view that skin acquisition was a primary predisposing factor to pyoderma. Since the literature indicates that group A streptococci are rarely part of the normal skin flora, these findings raise the possibility of unique biological properties of these and perhaps other pyoderma strains, as distinct from other group A streptococci.

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“…Soon after Maxted left Minneapolis, a large epidemic of acute glomerulonephritis was reported among American Indian children in the Red Lake Reservation in Northern Minnesota. Impetigo was rife among the children and was caused by group A streptococci that were untypable with existing M antisera, but were agglutinated by T14 antiserum [10]. Workers at the Center for Disease Control, Atlanta eventually succeeded in preparing an M antiserum from one of these strains from Red Lake, which was later numbered M49 [11].…”

Section: Impetigo and Nephritismentioning

confidence: 99%

Winston R. Maxted and the type specificity of group A streptococci

2001

Journal of Medical Microbiology

179

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Epidemic Acute Nephritis With Reappearance of Type-49 Streptococcus

Cited by 52 publications

References 5 publications

Acute Post-Streptococcal Glomerulonephritis in the Northern Territory of Australia: A Review of 16 Years Data and Comparison with the Literature

Acute Post-Streptococcal Glomerulonephritis in the Northern Territory of Australia: A Review of 16 Years Data and Comparison with the Literature

The role of normal skin in the spread of streptococcal pyoderma

Winston R. Maxted and the type specificity of group A streptococci

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