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Delayed onset of systemic bacterial dissemination and subsequent death in mice injected intramuscularly with
M Saito1, H Kajiwara, T Ishikawa
1Department of Bacteriology, Faculty of Medical Sciences, Kyushu University, Fukuoka, Japan. msaito@bact.med.kyushu-u.ac.jp
Abstract:
Streptococcus pyogenes causes severe invasive diseases in humans, including necrotizing fasciitis, sepsis, and streptococcal toxic shock syndrome (STSS). We found that mice infected intramuscularly (i.m.) with S. pyogenes strains developed bacteremia and subsequent sudden death after at least 10 days of a convalescent period. Mostly, it occurred more than 21 days after muscle infection. We provisionally designate this phenomenon as "delayed death." Just after muscle infection, all the mice lost weight and activity, but recovered completely within 3 days. They had kept good activity and a fine coat of fur till one or two days before their death. Some of the dead mice were found to have soft-tissue necrosis. There was no correlation between the virulence leading to the delayed death and the severity of diseases from which strains were isolated. It was also found that the production of neither streptococcal pyrogenic exotoxin (SPE) A nor B correlated to the virulence leading to delayed death. The bacteria obtained from the organs of the mice with delayed death expressed capsule. We suggest that the mice with delayed onset of systemic bacterial dissemination and subsequent death after muscle infection with S. pyogenes are the animal models of STSS, because the pathophysiology is extremely similar to that of human STSS.
Insights
Streptococcus pyogenes can cause a delayed death in mice, mimicking human streptococcal toxic shock syndrome (STSS). This delayed mortality, occurring weeks after initial infection, suggests a novel animal model for studying STSS pathogenesis.
Area of Science:
- Microbiology
- Infectious Diseases
- Immunology
Background:
- Streptococcus pyogenes is a significant human pathogen responsible for severe invasive diseases.
- Existing models do not fully replicate the delayed onset of severe symptoms seen in some S. pyogenes infections.
Purpose of the Study:
- To investigate a novel phenomenon of delayed mortality in mice infected with S. pyogenes.
- To establish a potential animal model for streptococcal toxic shock syndrome (STSS).
Main Methods:
- Intramuscular infection of mice with various S. pyogenes strains.
- Observation of clinical signs, weight, activity, and survival over an extended period.
- Analysis of bacterial characteristics, including capsule expression and toxin production, in deceased animals.
Main Results:
- Mice developed bacteremia and delayed death, typically over 21 days post-infection, after an initial recovery period.
- Clinical presentation in deceased mice included soft-tissue necrosis, with no clear correlation to initial disease severity or specific exotoxin production (SPE A/B).
- Recovered bacteria from organs of deceased mice expressed capsules.
Conclusions:
- The observed delayed death phenomenon in mice presents a promising animal model for studying the pathophysiology of human STSS.
- Capsular expression by S. pyogenes may play a role in the delayed systemic dissemination and mortality.
- This model could facilitate research into the mechanisms underlying delayed-onset invasive streptococcal disease.