Epidemiologie, mikrobiologie, imunologie : casopis Spolecnosti pro epidemiologii a mikrobiologii Ceske lekarske spolecnosti J.E. Purkyne · 2026
Non-menstrual toxic shock syndrome - cases reported to the National Reference Laboratory for Staphylococci, Centre for Epidemiology and Microbiology, National Institute of Public Health, 1983-2025.
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Bílý J, Kmječová H, Kseničová J, Petráš P
Аннотация
OBJECTIVE: To identify the virulence factors responsible for toxic shock syndrome in causative strains submitted by field laboratories throughout the Czech Republic.
METHODS: To detect the production of TSST-1 and staphylococcal enterotoxins, the micro-slide gel diffusion test was initially used and later followed by reverse passive latex agglutination. Currently, the polymerase chain reaction is the preferred tool for the detection of toxin genes as well as genes for other toxins of S. aureus strains: exfoliatins A, B, and D, Panton-Valentine leukocidin, and the mecA and mecC genes responsible for resistance to methicillin/cefoxitin and other beta-lactam antibiotics. A simple form was used to obtain information which confirmed the diagnosis of toxic shock syndrome (A48.3).
RESULTS: Over a 42-year period from 1983 to 2025, the toxinogenicity of the causative agent was confirmed in 174 cases of non-menstrual toxic shock syndrome. The TSST-1 toxin (either alone or in combination with enterotoxin) was produced by 60% of the strains studied. Only 40% of the strains were positive for a specific type of enterotoxin. Most strains were methicillin-sensitive, and seven strains (4.0%) were positive for the mecA gene. Genes for Panton-Valentine leukocidin were detected in a single strain. The most common type of staphylococcal infection leading to toxic shock syndrome was pyoderma. Other cases were associated with hospital acquired and post-traumatic wound infections. Of the entire cohort, the disease resulted in death of 38 patients, representing a high case fatality rate of 21.8%.
CONCLUSION: Toxic shock syndrome is a serious staphylococcal disease affecting multiple organs, which can be fatal in severe cases. Given the wide range of symptoms, establishing a clinical diagnosis can sometimes be difficult. It is crucial to recognize the staphylococcal toxin aetiology and initiate early appropriate treatment.
METHODS: To detect the production of TSST-1 and staphylococcal enterotoxins, the micro-slide gel diffusion test was initially used and later followed by reverse passive latex agglutination. Currently, the polymerase chain reaction is the preferred tool for the detection of toxin genes as well as genes for other toxins of S. aureus strains: exfoliatins A, B, and D, Panton-Valentine leukocidin, and the mecA and mecC genes responsible for resistance to methicillin/cefoxitin and other beta-lactam antibiotics. A simple form was used to obtain information which confirmed the diagnosis of toxic shock syndrome (A48.3).
RESULTS: Over a 42-year period from 1983 to 2025, the toxinogenicity of the causative agent was confirmed in 174 cases of non-menstrual toxic shock syndrome. The TSST-1 toxin (either alone or in combination with enterotoxin) was produced by 60% of the strains studied. Only 40% of the strains were positive for a specific type of enterotoxin. Most strains were methicillin-sensitive, and seven strains (4.0%) were positive for the mecA gene. Genes for Panton-Valentine leukocidin were detected in a single strain. The most common type of staphylococcal infection leading to toxic shock syndrome was pyoderma. Other cases were associated with hospital acquired and post-traumatic wound infections. Of the entire cohort, the disease resulted in death of 38 patients, representing a high case fatality rate of 21.8%.
CONCLUSION: Toxic shock syndrome is a serious staphylococcal disease affecting multiple organs, which can be fatal in severe cases. Given the wide range of symptoms, establishing a clinical diagnosis can sometimes be difficult. It is crucial to recognize the staphylococcal toxin aetiology and initiate early appropriate treatment.