Type-Specific Streptococcal Antibodies in Pyodermal Nephritis

Bergner-Rabinowitz, S; Ofek, Itzhak; Davies, Michael A.; Rabinowitz, K.

doi:10.1093/infdis/124.5.488

Cited by 12 publications

(3 citation statements)

References 11 publications

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“…Serotypes 52 through 63 are relatively new designations for types isolated predominantly from impetigo infections leading to AGN. Many of the pyodermic strains among these serotypes grow in normal human blood, although convalescent sera from AGN patients are occasionally bactericidal (13,72,160), and therefore these streptococci are presumed to contain an M antigen. Titers of type-specific antibodies in patients recovered from AGN of pyodermic origin are rarely high; antistreptolysin 0 titers are frequently low and serological evidence of a recent streptococcal infection is found primarily in the elevated anti-deoxyribonuclease and anti-hyaluronidase titers (168).…”

Section: Antigens Streptococcal Infection and Epidemiologymentioning

confidence: 99%

M proteins of group A streptococci.

Fox¹

1974

Bacteriological Reviews

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Section: Antigens Streptococcal Infection and Epidemiologymentioning

confidence: 99%

M proteins of group A streptococci.

Fox¹

1974

Bacteriological Reviews

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“…Despite the frequency with which pyoderma, cellulitis, and erysipelas recur in individual patients, data on acquired protective immunity to skin and soft tissue infections are lacking. Although type-specific opsonic antibodies to M protein are detectable in patients with streptococcal pyoderma (5,10,20), the role of such antibodies in prevention of subsequent skin infection is unknown.…”

Section: Discussionmentioning

confidence: 99%

Murine model of recurrent group G streptococcal cellulitis: no evidence of protective immunity

Bisno

Gaviria

1997

Infect Immun

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Despite the well-known tendency of cellulitis due to beta-hemolytic streptococci to recur, little is known regarding the mechanisms of human immunity to this infection. We established cellulitis in mice by using a strain of group G streptococcus (1750) originally isolated from the bloodstream of a patient with acute cellulitis. This strain, which has been studied extensively in our laboratory, expresses M protein structurally and functionally analogous to that of group A streptococci, and we have cloned and sequenced the gene encoding this protein (emmMG1). Mice injected with 5 ؋ 10 7 CFU of strain 1750 developed nonlethal necrotic skin and soft tissue infections that healed spontaneously after 14 to 16 days. After healing, the mice were repetitively reinoculated three times with the same challenge dose of 1750. Lesion size did not decrease in severity, size, or time to healing after repetitive challenge. The maximum lesion size and tissue concentration of microorganisms increased between the first and fourth challenges. Pretreatment of 1750 cells with opsonic antisera to MG1 diminished neither the maximum lesion size nor the time course of evolution of the lesions. Thus, in the mouse model used here, there was no evidence of acquired protective immunity to experimentally induced cellulitis.

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“…The percentage of sera which were positive varied over time, and the opsonic power of many of the sera tested was weak. Bergner-Rabinowitz et al (4) found TSA in the majority of patients convalescing from glomerulonephritis due to M-type 55 streptococci. Antibodies were detectable in 2 to 4 months after the disease and waned gradually over the ensuing 1 to 3 months.…”

mentioning

confidence: 99%

Type-Specific Opsonic Antibodies in Streptococcal Pyoderma

Bisno

Nelson

1974

Infect Immun

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Prospective studies of streptococcal pyoderma were carried out among black children enrolled in Project Headstart centers in Holmes County, Miss. Sera collected from 28 of these children in early October were tested for opsonic antibodies to one of two prevalent skin strains of group A streptococci isolated from them on one or more occasions over the preceding 3 months. The two streptococcal strains (A and B) belong to M-types previously unrecognized. Ten subjects (36%) had antibody to their homologous serotypes detectable by the indirect bactericidal test: this included 6 of 10 subjects infected with strain B but only 4 of 18 infected with strain A (P < 0.05). Of 17 children who had strains A or B isolated from skin lesions only, 12% developed type-specific antibodies (TSA) against the infecting serotype. In contrast, 11 subjects had these strains isolated from throat cultures (either with or without associated pyoderma), and 72% had detectable TSA (P < 0.01). There was no demonstrable relationship between the development of antibodies to streptococcal extracellular products or to non-typespecific cellular antigens and the development of TSA. These results demonstrate that type-specific immune responses do occur following infection with pyoderma streptococci. The frequency with which such antibodies develop is variable and appears related to a number of factors, including the immunologic properties of the infecting strain and the site of bacterial colonization. Pharyngeal carriage may represent an important mechanism for development of acquired immunity to skin strains of group A streptococci.

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Type-Specific Streptococcal Antibodies in Pyodermal Nephritis

Cited by 12 publications

References 11 publications

M proteins of group A streptococci.

M proteins of group A streptococci.

Murine model of recurrent group G streptococcal cellulitis: no evidence of protective immunity

Type-Specific Opsonic Antibodies in Streptococcal Pyoderma

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