Toxic shock syndrome is an acute condition caused by bacterial infection with symptoms such as hypotension, fever, a sunburn-like rash, and end-organ dysfunction.
It was traditionally related with the use of high-absorbency tampons in menstruating women and was eventually discontinued.
Since then, it has been increasingly crucial to examine non-menstrual occurrences.
Epidemiology
The prevalence of menstrual and non-menstrual causes in the United States is estimated to be between 0.8 and 3.4 per 100,000 women. The prevalence is more significant in the winter and more common in developing nations.
Infants and the elderly are especially at risk for invasive Group A Strep infection; however, between one-fifth and one-third of cases occur in individuals with no underlying risk factors. The most prevalent source for contracting a severe infection is the skin.
Anatomy
Pathophysiology
It is a toxin-mediated disorder induced by toxin-generating Staphylococcus aureus or streptococci. These superantigens skip the regular T-cell activation route, producing an excess of cytokines and inflammatory cells.
This results in the symptoms of rash, fever, end-organ failure, and hypotension owing to capillary leak. Other toxins produced by Strep pyogenes (GAS) contribute to streptococcal toxic shock syndrome and necrotizing fasciitis.
Etiology
TSS is usually caused by a toxigenic strain of Group A Strep and Staphylococcus aureus. The disease appears most frequently during menstruation despite the cessation of high-absorbency tampons.
On the other hand, TSS can appear in non-menstrual contexts such as soft tissue infections, burns, post-surgical infections, and retained foreign bodies such as dialysis catheters and nasal packing.
A localized infection like an abscess usually causes staphylococcal TSS, but streptococcal TSS can be caused by necrotizing fasciitis, cellulitis, or bacteremia.
Genetics
Prognostic Factors
Streptococcal TSS has a case fatality rate of more than 50%, especially with delayed diagnosis, but non-streptococcal TSS has a case fatality rate of less than 3%.
Small research conducted in France discovered that non-menstrual toxic shock syndrome had a higher fatality rate (22%) than menstrual toxic shock syndrome (0%).
This was, however, a smaller case study of 55 individuals.
Clinical History
Physical Examination
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Hormone Therapy
Immunotherapy
Hyperthermia
Photodynamic Therapy
Stem Cell Transplant
Targeted Therapy
Palliative Care
Medication
Future Trends
Media Gallary
References
https://www.ncbi.nlm.nih.gov/books/NBK459345/
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Toxic shock syndrome is an acute condition caused by bacterial infection with symptoms such as hypotension, fever, a sunburn-like rash, and end-organ dysfunction.
It was traditionally related with the use of high-absorbency tampons in menstruating women and was eventually discontinued.
Since then, it has been increasingly crucial to examine non-menstrual occurrences.
The prevalence of menstrual and non-menstrual causes in the United States is estimated to be between 0.8 and 3.4 per 100,000 women. The prevalence is more significant in the winter and more common in developing nations.
Infants and the elderly are especially at risk for invasive Group A Strep infection; however, between one-fifth and one-third of cases occur in individuals with no underlying risk factors. The most prevalent source for contracting a severe infection is the skin.
It is a toxin-mediated disorder induced by toxin-generating Staphylococcus aureus or streptococci. These superantigens skip the regular T-cell activation route, producing an excess of cytokines and inflammatory cells.
This results in the symptoms of rash, fever, end-organ failure, and hypotension owing to capillary leak. Other toxins produced by Strep pyogenes (GAS) contribute to streptococcal toxic shock syndrome and necrotizing fasciitis.
TSS is usually caused by a toxigenic strain of Group A Strep and Staphylococcus aureus. The disease appears most frequently during menstruation despite the cessation of high-absorbency tampons.
On the other hand, TSS can appear in non-menstrual contexts such as soft tissue infections, burns, post-surgical infections, and retained foreign bodies such as dialysis catheters and nasal packing.
A localized infection like an abscess usually causes staphylococcal TSS, but streptococcal TSS can be caused by necrotizing fasciitis, cellulitis, or bacteremia.
Streptococcal TSS has a case fatality rate of more than 50%, especially with delayed diagnosis, but non-streptococcal TSS has a case fatality rate of less than 3%.
Small research conducted in France discovered that non-menstrual toxic shock syndrome had a higher fatality rate (22%) than menstrual toxic shock syndrome (0%).
This was, however, a smaller case study of 55 individuals.
https://www.ncbi.nlm.nih.gov/books/NBK459345/
medtigo
Toxic shock syndrome
Updated :
October 6, 2022
Toxic shock syndrome is an acute condition caused by bacterial infection with symptoms such as hypotension, fever, a sunburn-like rash, and end-organ dysfunction.
It was traditionally related with the use of high-absorbency tampons in menstruating women and was eventually discontinued.
Since then, it has been increasingly crucial to examine non-menstrual occurrences.
The prevalence of menstrual and non-menstrual causes in the United States is estimated to be between 0.8 and 3.4 per 100,000 women. The prevalence is more significant in the winter and more common in developing nations.
Infants and the elderly are especially at risk for invasive Group A Strep infection; however, between one-fifth and one-third of cases occur in individuals with no underlying risk factors. The most prevalent source for contracting a severe infection is the skin.
It is a toxin-mediated disorder induced by toxin-generating Staphylococcus aureus or streptococci. These superantigens skip the regular T-cell activation route, producing an excess of cytokines and inflammatory cells.
This results in the symptoms of rash, fever, end-organ failure, and hypotension owing to capillary leak. Other toxins produced by Strep pyogenes (GAS) contribute to streptococcal toxic shock syndrome and necrotizing fasciitis.
TSS is usually caused by a toxigenic strain of Group A Strep and Staphylococcus aureus. The disease appears most frequently during menstruation despite the cessation of high-absorbency tampons.
On the other hand, TSS can appear in non-menstrual contexts such as soft tissue infections, burns, post-surgical infections, and retained foreign bodies such as dialysis catheters and nasal packing.
A localized infection like an abscess usually causes staphylococcal TSS, but streptococcal TSS can be caused by necrotizing fasciitis, cellulitis, or bacteremia.
Streptococcal TSS has a case fatality rate of more than 50%, especially with delayed diagnosis, but non-streptococcal TSS has a case fatality rate of less than 3%.
Small research conducted in France discovered that non-menstrual toxic shock syndrome had a higher fatality rate (22%) than menstrual toxic shock syndrome (0%).
This was, however, a smaller case study of 55 individuals.
https://www.ncbi.nlm.nih.gov/books/NBK459345/
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