Background: In Europe, with few exceptions, there is a lack of systematic reporting for invasive infections by Streptococcus pyogenes (Group A Streptococcus, GAS), making the assessment of national and global disease burden very scattered. In Italy, except for scarlet fever, invasive GAS infection is not a notifiable disease. Material/methods: A nationwide enhanced laboratory-based surveillance on invasive infections by GAS and other beta-haemolytic streptococci (group G and C streptococci) was launched from January 2015 to June 2016. Cases were notified according to a common questionnaire. Invasive infection was defined as the isolation of the bacterium from a usually sterile site, from deep-body-site exudates, or from a nonsterile site in association with one of the following conditions: necrotizing fasciitis, clinically diagnosed pneumonia, or STSS. Species identification was confirmed by the Lancefield group and the API 20 Strep system. Susceptibility to penicillin, norfloxacin, rifampicin, vancomycin, tetracycline, erythromycin, clindamycin was assessed by the disc diffusion method. emm sequence typing was performed on all strains. The presence of the superantigen speA and speC genes in GAS, and tet, erm and mef resistance genes in all isolates was determined by PCR. Results: 104 notifications and 95 bacterial strains were received; 66 strains were identified as GAS, 26 as S. dysgalatiae subsp. equisimilis (SDSE) and three strains as S. equi subsp. zooepidemicus (SESZ). Most infections affected elderly (> 65 years old, 55.5% and 92% for GAS and SDSE, respectively). The majority of strains were isolated from blood (70.8% and 72% for GAS and SDSE, respectively) and skin and soft tissue infections were the prevalent clinical manifestations (57.1% for GAS; 54.2% for SDSE). The case fatality rate was 24.3% for GAS and 0% for SDSE. One out of two patients infected with SESZ died. Among GAS isolates, emm types 1, 28, and 5 were predominant. The spe genes strongly correlated to emm type. Low resistance rate to norfloxacin (4.5%), and erythromycin (6%) was recorded. Tetracycline resistance rate was of 22.7%. Among SDSE, the most abundant emm types were stG2078, stG480, and stG6. The resistance rate to tetracycline (26.9%) was comparable to that of GAS, while resistance rates to norfloxacin (19.2%) and erythromycin (15.4%) were higher. All three S. equi subsp. zooepidemicus strains were erythromycin susceptible and clindamycin resistant. Conclusions: By providing new data on the epidemiology of invasive infections caused by GAS and other beta-haemolytic streptococci, this work is a priming effort to fill the gap represented by the non-inclusion of invasive infections by beta-haemolytic streptococci among the currently networks of surveillance in Italy. Enhanced surveillances are the only means to assess the real time burden of such infections, their outcomes as well as to monitor the antibiotic resistance and virulence traits of circulating bacterial clones.

Invasive beta-haemolytic group A, C, and G streptococcal infections in Italy: a 2015-2016 survey

PETRELLI, Dezemona;VITALI, Luca Agostino
2017-01-01

Abstract

Background: In Europe, with few exceptions, there is a lack of systematic reporting for invasive infections by Streptococcus pyogenes (Group A Streptococcus, GAS), making the assessment of national and global disease burden very scattered. In Italy, except for scarlet fever, invasive GAS infection is not a notifiable disease. Material/methods: A nationwide enhanced laboratory-based surveillance on invasive infections by GAS and other beta-haemolytic streptococci (group G and C streptococci) was launched from January 2015 to June 2016. Cases were notified according to a common questionnaire. Invasive infection was defined as the isolation of the bacterium from a usually sterile site, from deep-body-site exudates, or from a nonsterile site in association with one of the following conditions: necrotizing fasciitis, clinically diagnosed pneumonia, or STSS. Species identification was confirmed by the Lancefield group and the API 20 Strep system. Susceptibility to penicillin, norfloxacin, rifampicin, vancomycin, tetracycline, erythromycin, clindamycin was assessed by the disc diffusion method. emm sequence typing was performed on all strains. The presence of the superantigen speA and speC genes in GAS, and tet, erm and mef resistance genes in all isolates was determined by PCR. Results: 104 notifications and 95 bacterial strains were received; 66 strains were identified as GAS, 26 as S. dysgalatiae subsp. equisimilis (SDSE) and three strains as S. equi subsp. zooepidemicus (SESZ). Most infections affected elderly (> 65 years old, 55.5% and 92% for GAS and SDSE, respectively). The majority of strains were isolated from blood (70.8% and 72% for GAS and SDSE, respectively) and skin and soft tissue infections were the prevalent clinical manifestations (57.1% for GAS; 54.2% for SDSE). The case fatality rate was 24.3% for GAS and 0% for SDSE. One out of two patients infected with SESZ died. Among GAS isolates, emm types 1, 28, and 5 were predominant. The spe genes strongly correlated to emm type. Low resistance rate to norfloxacin (4.5%), and erythromycin (6%) was recorded. Tetracycline resistance rate was of 22.7%. Among SDSE, the most abundant emm types were stG2078, stG480, and stG6. The resistance rate to tetracycline (26.9%) was comparable to that of GAS, while resistance rates to norfloxacin (19.2%) and erythromycin (15.4%) were higher. All three S. equi subsp. zooepidemicus strains were erythromycin susceptible and clindamycin resistant. Conclusions: By providing new data on the epidemiology of invasive infections caused by GAS and other beta-haemolytic streptococci, this work is a priming effort to fill the gap represented by the non-inclusion of invasive infections by beta-haemolytic streptococci among the currently networks of surveillance in Italy. Enhanced surveillances are the only means to assess the real time burden of such infections, their outcomes as well as to monitor the antibiotic resistance and virulence traits of circulating bacterial clones.
2017
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11581/396703
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