Clindamycin treatment of chronic pharyngeal carriage of group A streptococci

Tanz, Robert R.; Poncher, John R.; Corydon, Kathleen; Kabat, Kathleen; Yogev, Ram; Shulman, Stanford T.

doi:10.1016/s0022-3476(05)81052-2

Cited by 77 publications

(31 citation statements)

References 22 publications

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“…Streptococcus pyo genes reemerged as the causative agent of seri ous invasive infections, particularly necrotiz ing fasciitis and a toxic shock-like syndrome [1][2][3][4][5][6][7], In addition, there occurred a significant increase in the incidence of rheumatic fever [7][8][9], Furthermore, resistance of S. pyogenes to erythromycin, traditionally the alternative antibiotic for penicillin-allergic patients [10], increased sharply in certain geographic areas, but not in other regions [11][12][13][14][15][16][17][18][19][20], Sporadic resistance of S. pyogenes to clindamycin, con sidered to be more effective than penicillin [21][22][23] or rifampin [23,24] for the treatment of experimental myositis or for eradication of the group A streptococcal carrier state, was encountered as well [13. 25-27]; however, in other areas, S. pyogenes still was fully suscep tible to clindamycin [28,29], Currently, 5. pyogenes is considered uniformly susceptible to penicillin G and V, amoxicillin, and cepha losporins, such as cefuroxime and cefixime [24,26,27,[29][30][31].…”

Section: Introductionmentioning

confidence: 99%

Comparative Susceptibility of Clinical Group A, B, C, F, and G β-Hemolytic Streptococcal Isolates to 24 Antimicrobial Drugs

Traub

Leonhard²

1997

Chemotherapy

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A total of 312 clinical β-hemolytic streptococcal isolates (Streptococcus pyogenes, group A = 63; Streptococcus agalactiae, group B = 145; group C = 50; group F = 27; group G = 27) were examined for susceptibility to 23 and 24 antimicrobial drugs with the Bauer-Kirby agar disk diffusion and the agar dilution method, respectively. Sheep blood Mueller-Hinton agar served as the reference medium. Wilkins-Chalgren agar supported optimal growth of group A and B, but not of all group C, F, and G streptococci. The group A streptococci were susceptible to all β-lactam antibiotics, clindamycin, chloramphenicol, rifampin, teicoplanin, and vancomycin, but resistant to cotrimoxazole, fusidic acid, and, except for 2 strains, to fosfomycin. Resistance (R)/intermediate susceptibility (I) rates (R/I%) to ciprofloxacin (0/2%), ofloxacin (1/2%), erythromycin (1.6 / 0%), and clarithromycin (0/1%) were low. Higher resistance rates were noted with tetracyclines (doxycycline 23.8/15.9%; tetracycline 39.7/3.2%). Among the group B streptococcal isolates, one strain was resistant against oxacillin and of intermediate susceptibility to penicillin G and cefoxitin. All isolates were susceptible to teicoplanin and rifampin. Conversely, all group B isolates were resistant to cotrimoxazole and fusidic acid; 69% and 51 % of these isolates were susceptible to fosfomycin and rifampin, respectively. R/I rates of the group B streptococcal isolates were low for ciprofloxacin and ofloxacin (0/0.7%), clindamycin (0.7/0%), erythromycin (1.4/ 3.5%), clarithromycin (1.4/0%), and chloramphenicol (0.7/0%). Resistance to tetracyclines was significant (doxycycline: 72.4/2.1%; tetracycline: 74.5/1.4%). Among the non-A, non-B β-hemolytic streptococci, 2 group C strains were resistant to oxacillin and showed intermediate susceptibility to penicillin G. All isolates were susceptible to third and fourth-generation cephalosporins, imipenem, chloramphenicol, rifampin, teicoplanin, and vancomycin. R/I rates to the other antimicrobial drugs were: ciprofloxacin (3.9/1.9%), ofloxacin (2.9/1.9%), clindamycin (2.9/1%), erythromycin (5.8/0%), clarithromycin (3.8/2.9%), and cotrimoxazole (16.4/3.9%). Resistance against tetracyclines was more frequent (doxycycline: 18.3/2.9%; tetracycline: 20.2/6.7%). On the basis of various minor discrepancies between MIC and disk diffusion test results, it is proposed that the current NCCLS inhibition zone (diameter, mm) criteria indicative of intermediate susceptibility of β-hemolytic streptococci be changed for the following antimicrobial drugs: ampicillin: 22-27 mm (only for group A and B β-hemolytic streptococci); ciprofloxacin: 16-18 mm; clindamycin: 15-18 mm; doxycycline: 17-19 mm; tetracycline: 17-19 mm, and erythromycin: 14-19 mm.

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Section: Introductionmentioning

confidence: 99%

Comparative Susceptibility of Clinical Group A, B, C, F, and G β-Hemolytic Streptococcal Isolates to 24 Antimicrobial Drugs

Traub

Leonhard²

1997

Chemotherapy

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“…Clindamycin's intrinsic resistance to the enzyme ␤-lactamase enabled it to eliminate BLPO such as S. aureus, pigmented Prevotella species, and Fusobacterium species. This feature explained its efficacy in the treatment of acute (15) and recurrent (2) GABHS pharyngotonsillitis and eradication of the carrier state (17). However, since there were no differences in the recovery rates of BLPO in this study of acutely inflamed tonsils, the increased activity of clindamycin over penicillin in this report cannot be explained by its enhanced activity against BLPO.…”

Section: Discussionmentioning

confidence: 53%

In vitro and in vivo effects of penicillin and clindamycin on expression of group A beta-hemolytic streptococcal capsule

Brook

Gober

Leyva

1995

Antimicrob Agents Chemother

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Encapsulation of group A beta-hemolytic streptococci (GABHS) is an important virulence factor. The changes that occur in the frequency of encapsulation of GABHS during pharyngotonsillitis, in 20 patients treated with penicillin and 20 treated with clindamycin, were investigated. The effects of subinhibitory concentrations of these agents were also evaluated in vitro. At day 4, 8 of 10 (80%) GABHS isolates recovered from children treated with penicillin were encapsulated, compared with 1 of 5 (20%) of those from children treated with clindamycin (P < 0.05). Two days following 10 days of therapy, GABHS was eliminated from 13 of the 20 (65%) children treated with penicillin and from all treated with clindamycin (P < 0.05). At that time, six of the seven GABHS isolates recovered in patients treated with penicillin were encapsulated. GABHS were not detected after 4 days of therapy in those treated with clindamycin. Incubation of GABHS isolates with one-half of the MIC of clindamycin reduced the frequency of encapsulation, compared with that after incubation with one-half of the MIC of penicillin (12.5 versus 67.5%). These data illustrate the superiority of clindamycin over penicillin in reducing the expression of a capsule by GABHS.The virulence of group A beta-hemolytic streptococci (GABHS) has been associated with two cell wall structures: the M protein and the hyaluronic acid capsule (6, 14). The virulence was assessed by resistance to phagocytosis (6,7,14) and induction of mortality in mice after intraperitoneal inoculation (18). Variation in the elaboration of M protein during the natural course of respiratory infections was observed (14). Compared with characteristics during the acute stages of the infection, about half of GABHS isolates gradually lost their ability to elaborate type-specific M-protein antigen and became susceptible to the antibacterial activity of the human blood during the convalescent and carrier stages. However, variations in the presence of capsule of GABHS and the effects of antimicrobial therapy on expression of a capsule were not evaluated during the different phases of pharyngotonsillitis in children.This study was performed to investigate the dynamics of expression of capsule by GABHS during pharyngotonsillitis in patients treated with penicillin or clindamycin. The in vitro effects of subinhibitory concentrations of these agents were also evaluated. MATERIALS AND METHODSPatients. Children who were seen for acute GABHS pharyngotonsillitis were considered for inclusion in the study. These children had symptoms of acute uncomplicated pharyngotonsillitis of 1 to 4 days' duration. They had sore throats, swollen and enlarged tonsils with or without exudate, tender cervical lymph glands, and temperatures above 38ЊC. More than 10 colonies of GABHS were isolated from their pharyngotonsillar cultures. None had received antimicrobial therapy for the past 6 weeks, and none had had an acute pharyngotonsillar inflammation in the past 3 months. Included in the analysis were the first 20 consecutive...

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“…In this outbreak, the specimen from the surgeon's hands was still positive for the pathogen two days after treatment. Previous studies focused mainly on the effectiveness of antibiotics in eradicating upper respiratory tract carriage of GAS [14][15][16][17][18]. There are few data on how long it takes to eradicate GAS from the skin lesions, anus, and vagina of asymptomatic colonized HCWs.…”

Section: Discussionmentioning

confidence: 99%

Outbreak of Infections Caused by Group AStreptococcusafter Modified Radical Mastectomy

Qing-Zeng

Yun-Bo²,

Liu³

et al. 2013

Surgical Infections

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Background: Eight infections occurred after modified radical mastectomies in a tertiary-care hospital. Group A streptococci (GAS) were isolated from three of the eight patients. Methods: To control the outbreak, an epidemiologic investigation was conducted, and healthcare workers were screened for pathogens. Strains isolated from healthcare workers were compared with patient strains by emm typing. Results: One surgeon attended one of the eight operations and observed the other seven. Streptococcus strains from the hands of this surgeon were identical to the patient strains. After the surgeon was suspended from duty and underwent eradication treatment, the outbreak was controlled. Conclusions: This outbreak of GAS infection is believed to have occurred by airborne transmission. Suspending patient care by healthcare workers who carry the causative GAS in a site(s) other than the respiratory tract for only the first 24 h they are receiving chemoprophylaxis may not be long enough. Sampling of the hands of healthcare workers during an investigation of nosocomial GAS infection is valuable.

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Clindamycin treatment of chronic pharyngeal carriage of group A streptococci

Cited by 77 publications

References 22 publications

Comparative Susceptibility of Clinical Group A, B, C, F, and G β-Hemolytic Streptococcal Isolates to 24 Antimicrobial Drugs

Comparative Susceptibility of Clinical Group A, B, C, F, and G β-Hemolytic Streptococcal Isolates to 24 Antimicrobial Drugs

In vitro and in vivo effects of penicillin and clindamycin on expression of group A beta-hemolytic streptococcal capsule

Outbreak of Infections Caused by Group AStreptococcusafter Modified Radical Mastectomy

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