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== Treatment ==
== Treatment ==
The severity of this disease frequently warrants hospitalization. Admission to the [[intensive care unit]] is often necessary for supportive care (for aggressive fluid management, ventilation, renal replacement therapy and inotropic support), particularly in the case of [[multiple organ failure]].<ref name="Zimbelman">{{cite journal|journal=Ped Infect Dis J|volume=18|issue=12|page=1096&ndash;1100|title=Improved outcome of clindamycin compared with beta-lactam antibiotic treatment for invasive Streptococcus pyogenes infection|author=Zimbelman J, Palmer A, Todd J|url=http://www.pidj.org/pt/re/pidj/abstract.00006454-199912000-00014.htm;jsessionid=JZ2WwJhpv8J4dh2nDJWTywCFB4Lyy8L6Xw61G1hMCl2jYXBhQGp2!-2118404334!181195629!8091!-1}}</ref> The source of infection should be removed or drained if possible: abscesses and collections should be drained. Anyone wearing a tampon at the onset of symptoms should remove it immediately. Outcomes are poorer in patients who do not have the source of infection removed.<ref name="Zimbelman"/>
The severity of this disease frequently warrants hospitalization. Admission to the [[intensive care unit]] is often necessary for supportive care (for aggressive fluid management, ventilation, renal replacement therapy and [[inotropic]] support), particularly in the case of [[multiple organ failure]].<ref name="Zimbelman">{{cite journal|journal=Ped Infect Dis J|volume=18|issue=12|page=1096&ndash;1100|title=Improved outcome of clindamycin compared with beta-lactam antibiotic treatment for invasive Streptococcus pyogenes infection|author=Zimbelman J, Palmer A, Todd J|url=http://www.pidj.org/pt/re/pidj/abstract.00006454-199912000-00014.htm;jsessionid=JZ2WwJhpv8J4dh2nDJWTywCFB4Lyy8L6Xw61G1hMCl2jYXBhQGp2!-2118404334!181195629!8091!-1}}</ref> The source of infection should be removed or drained if possible: abscesses and collections should be drained. Anyone wearing a tampon at the onset of symptoms should remove it immediately. Outcomes are poorer in patients who do not have the source of infection removed.<ref name="Zimbelman"/>


Antibiotic treatment should cover both ''S.&nbsp;pyogenes'' and ''S.&nbsp;aureus''. This may include a combination of [[cephalosporin]]s, [[penicillin]]s or [[vancomycin]]. The addition of [[clindamycin]]<ref>{{cite journal|title=Clindamycin-induced suppression of toxic-shock syndrome-associated exotoxin production|author=Schlievert PM, Kelly JA|journal=J Infect Dis|volume=149|issue=3|page=471|year=1984|pmid=6715902}}</ref> or [[gentamicin]]<ref>{{cite journal|journal=Antimicrob Agents Chemother|date=1 August 1997|pages=1682&ndash;1685|volume=41|issue=8|title=Combination of flucloxacillin and gentamicin inhibits toxic shock syndrome toxin 1 production by Staphylococcus aureus in both logarithmic and stationary phases of growth|author=van Langevelde P, van Dissel JT, Meurs CJ, Renz J, Groeneveld PH|url=http://aac.asm.org/cgi/content/abstract/41/8/1682|pmid=9257741|pmc=163985}}</ref> reduces toxin production and mortality.
Antibiotic treatment should cover both ''S.&nbsp;pyogenes'' and ''S.&nbsp;aureus''. This may include a combination of [[cephalosporin]]s, [[penicillin]]s or [[vancomycin]]. The addition of [[clindamycin]]<ref>{{cite journal|title=Clindamycin-induced suppression of toxic-shock syndrome-associated exotoxin production|author=Schlievert PM, Kelly JA|journal=J Infect Dis|volume=149|issue=3|page=471|year=1984|pmid=6715902}}</ref> or [[gentamicin]]<ref>{{cite journal|journal=Antimicrob Agents Chemother|date=1 August 1997|pages=1682&ndash;1685|volume=41|issue=8|title=Combination of flucloxacillin and gentamicin inhibits toxic shock syndrome toxin 1 production by Staphylococcus aureus in both logarithmic and stationary phases of growth|author=van Langevelde P, van Dissel JT, Meurs CJ, Renz J, Groeneveld PH|url=http://aac.asm.org/cgi/content/abstract/41/8/1682|pmid=9257741|pmc=163985}}</ref> reduces toxin production and mortality.

Revision as of 22:40, 20 May 2011

Toxic shock syndrome
SpecialtyInfectious diseases Edit this on Wikidata

Toxic shock syndrome (TSS) is a potentially fatal illness caused by a bacterial toxin. Different bacterial toxins may cause toxic shock syndrome, depending on the situation. The causative bacteria include Staphylococcus aureus and Streptococcus pyogenes. Streptococcal TSS is sometimes referred to as toxic shock-like syndrome (TSLS) or streptococcal toxic shock syndrome (STSS).

Signs and symptoms

Symptoms of toxic shock syndrome vary depending on the underlying cause. TSS resulting from infection with the bacterium Staphylococcus aureus typically manifests in otherwise healthy individuals with high fever, accompanied by low blood pressure, malaise and confusion, which can rapidly progress to stupor, coma, and multiple organ failure. The characteristic rash, often seen early in the course of illness, resembles a sunburn, and can involve any region of the body, including the lips, mouth, eyes, palms and soles. In patients who survive the initial onslaught of the infection, the rash desquamates, or peels off, after 10–14 days.

In contrast, TSS caused by the bacterium Streptococcus pyogenes, or TSLS, typically presents in people with pre-existing skin infections with the bacteria. These individuals often experience severe pain at the site of the skin infection, followed by rapid progression of symptoms as described above for TSS. In contrast to TSS caused by Staphylococcus, streptococcal TSS less often involves a sunburn rash.

In either case, diagnosis is based strictly upon CDC criteria modified in 1981 after the initial surge in tampon-associated infections.[1]:

  1. Body temperature > 38.9 °C (102.02 °F)
  2. Systolic blood pressure < 90 mmHg
  3. Diffuse rash, intense erythroderma, blanching with subsequent desquamation, especially of the palms and soles
  4. Involvement of three or more organ systems:

Pathophysiology

In both TSS (caused by S. aureus) and TSLS (caused by S. pyogenes), disease progression stems from a superantigen toxin that allows the nonspecific binding of MHC II with T cell receptors, resulting in polyclonal T cell activation. In typical T cell recognition, an antigen is taken up by an antigen-presenting cell, processed, expressed on the cell surface in complex with class II major histocompatibility complex (MHC) in a groove formed by the alpha and beta chains of class II MHC, and recognized by an antigen-specific T cell receptor. By contrast, superantigens do not require processing by antigen-presenting cells but instead interact directly with the invariant region of the class II MHC molecule. In patients with TSS, up to 20% of the body's T cells can be activated at one time. This polyclonal T-cell population causes a cytokine storm, followed by a multisystem disease. The toxin in S. aureus infections is TSS Toxin-1, or TSST-1. The TSST-1 is secreted as a single polypeptide chain.

Treatment

The severity of this disease frequently warrants hospitalization. Admission to the intensive care unit is often necessary for supportive care (for aggressive fluid management, ventilation, renal replacement therapy and inotropic support), particularly in the case of multiple organ failure.[2] The source of infection should be removed or drained if possible: abscesses and collections should be drained. Anyone wearing a tampon at the onset of symptoms should remove it immediately. Outcomes are poorer in patients who do not have the source of infection removed.[2]

Antibiotic treatment should cover both S. pyogenes and S. aureus. This may include a combination of cephalosporins, penicillins or vancomycin. The addition of clindamycin[3] or gentamicin[4] reduces toxin production and mortality.

Prognosis

With proper treatment, patients usually recover in two to three weeks. The condition can, however, be fatal within hours.

Epidemiology

Staphylococcal toxic shock syndrome is rare and the number of reported cases has declined significantly since the 1980s. Patrick Schlievert, who published a study on it in 2004, determined incidence at 3 to 4 out of 100,000 tampon users per year; the information supplied by manufacturers of sanitary products such as Tampax and Stayfree puts it at 1 to 17 of every 100,000 menstruating people per year.[5][6] The CDC has stopped tracking TSS. However, there was a rise in reported cases in the early 2000s: eight deaths from the syndrome in California in 2002 after three successive years of four deaths per year, and Schlievert's study found cases in part of Minnesota more than tripled from 2000 to 2003.[5] Schlievert considers earlier onset of menstruation to be a cause of the rise; others, such as Philip M. Tierno and Bruce A. Hanna, blame new high-absorbency tampons introduced in 1999 and manufacturers discontinuing warnings not to leave tampons in overnight.[5]

History

Initial description

The term toxic shock syndrome was first used in 1978 by a Denver pediatrician, Dr. James K. Todd, to describe the staphylococcal illness in three boys and four girls aged 8–17 years.[7] Even though S. aureus was isolated from mucosal sites in the patients, bacteria could not be isolated from the blood, cerebrospinal fluid, or urine, raising suspicion that a toxin was involved. The authors of the study noted reports of similar staphylococcal illnesses had appeared occasionally as far back as 1927, but the authors at the time failed to consider the possibility of a connection between toxic shock syndrome and tampon use, as three of the girls who were menstruating when the illness developed were using tampons. Many cases of TSS occurred after tampons were left in the person using them.[8]

Rely tampons

File:Rely Tampons Front.jpg
Package of Rely tampons

Following a controversial period of test marketing in Rochester, New York and Fort Wayne, Indiana,[9] in August 1978, Procter and Gamble introduced superabsorbent Rely tampons to the United States market[10] in response to women's demands for tampons that could contain an entire menstrual flow without leaking or replacement.[11] Rely used carboxymethylcellulose (CMC) and compressed beads of polyester for absorption. This tampon design could absorb nearly 20 times its own weight in fluid.[12] Further, the tampon would "blossom" into a cup shape in the vagina to hold menstrual fluids without leakage.

In January 1980, epidemiologists in Wisconsin and Minnesota reported the appearance of TSS, mostly in those menstruating, to the CDC.[13] S. aureus was successfully cultured from most of the subjects. A CDC task force investigated the epidemic as the number of reported cases rose throughout the summer of 1980, accompanied by widespread publicity. In September 1980, the CDC reported users of Rely were at increased risk for developing TSS.[14]

On 22 September 1980, Procter and Gamble recalled Rely[15] following release of the CDC report. As part of the voluntary recall, Procter and Gamble entered into a consent agreement with the FDA "providing for a program for notification to consumers and retrieval of the product from the market."[16] However, it was clear to other investigators that Rely was not the only culprit. Other regions of the United States saw increases in menstrual TSS before Rely was introduced.[17] It was shown later that higher absorbency of tampons was associated with an increased risk for TSS, regardless of the chemical composition or the brand of the tampon. The sole exception was Rely, for which the risk for TSS was still higher when corrected for its absorbency.[18] The ability of carboxymethylcellulose to filter the S. aureus toxin that causes TSS may account for the increased risk associated with Rely.[12]

By the end of 1980, the number of TSS cases reported to the CDC began to decline. The reduced incidence was attributed not only to the removal of Rely from the market, but also to reduced use of all tampon brands. According to the Boston Women's Health Book Collective, 942 women were diagnosed with tampon-related TSS in the US from March 1980 to March 1981, 40 of whom died.

See also

References

  1. ^ Case Definitions for Public Health Surveillance
  2. ^ a b Zimbelman J, Palmer A, Todd J. "Improved outcome of clindamycin compared with beta-lactam antibiotic treatment for invasive Streptococcus pyogenes infection". Ped Infect Dis J. 18 (12): 1096–1100.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  3. ^ Schlievert PM, Kelly JA (1984). "Clindamycin-induced suppression of toxic-shock syndrome-associated exotoxin production". J Infect Dis. 149 (3): 471. PMID 6715902.
  4. ^ van Langevelde P, van Dissel JT, Meurs CJ, Renz J, Groeneveld PH (1 August 1997). "Combination of flucloxacillin and gentamicin inhibits toxic shock syndrome toxin 1 production by Staphylococcus aureus in both logarithmic and stationary phases of growth". Antimicrob Agents Chemother. 41 (8): 1682–1685. PMC 163985. PMID 9257741.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  5. ^ a b c Julie Sevrens Lyons/Knight Ridder Newspapers, "A New Generation Faces Toxic Shock Syndrome," The Seattle Times, January 25, 2005, http://seattletimes.nwsource.com/html/health/2002160362_healthtoxicshock26.html, accessed April 8, 2009, first published as "Lingering Risk," San Jose Mercury News, December 13, 2004
  6. ^ "Stayfree - FAQ About Toxic Shock Syndrome (TSS)". 2006. Retrieved 2006-10-13.
  7. ^ Todd J, Fishaut M, Kapral F, Welch T (1978). "Toxic-shock syndrome associated with phage-group-I staphylococci". Lancet. 2 (8100): 1116–1118. doi:10.1016/S0140-6736(78)92274-2. PMID 82681.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  8. ^ Todd J (1981). "Toxic shock syndrome--scientific uncertainty and the public media". Pediatrics. 67 (6): 921–923. PMID 7232057.
  9. ^ Finley, Harry. "Rely Tampon: It Even Absorbed the Worry!". Museum of Menstruation. Retrieved 2006-03-20.
  10. ^ Hanrahan S; Submission, Haworth Continuing Features (1994). "Historical review of menstrual toxic shock syndrome". Women Health. 21 (2–3): 141–65. doi:10.1300/J013v21n02_09. PMID 8073784.
  11. ^ Citrinbaum, Joanna (Oct. 14, 2003). "The question's absorbing: 'Are tampons little white lies?'". The Digital Collegian. Retrieved 2006-03-20. {{cite web}}: Check date values in: |year= (help)CS1 maint: year (link)
  12. ^ a b Vitale, Sidra (1997). "Toxic Shock Syndrome". Web by Women, for Women. Archived from the original on 2006-03-16. Retrieved 2006-03-20.
  13. ^ CDC 1980. "Toxic-shock syndrome--United States." MMWR 29(20):229-230.
  14. ^ CDC 1980. "Follow-up on toxic-shock syndrome." MMWR 29(37):441-445.
  15. ^ Hanrahan S; Submission, Haworth Continuing Features (1994). "Historical review of menstrual toxic shock syndrome". Women Health. 21 (2–3): 141–165. doi:10.1300/J013v21n02_09. PMID 8073784.
  16. ^ Kohen, Jamie (2001). "The History and Regulation of Menstrual Tampons". RTF document. Retrieved 2006-03-30. {{cite web}}: External link in |work= (help)
  17. ^ Petitti D, Reingold A, Chin J (1986). "The incidence of toxic shock syndrome in Northern California. 1972 through 1983". JAMA. 255 (3): 368–72. doi:10.1001/jama.255.3.368. PMID 3941516.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  18. ^ Berkley S, Hightower A, Broome C, Reingold A (1987). "The relationship of tampon characteristics to menstrual toxic shock syndrome". JAMA. 258 (7): 917–20. doi:10.1001/jama.258.7.917. PMID 3613021.{{cite journal}}: CS1 maint: multiple names: authors list (link)

For more information on Toxic Shock Syndrome - visit http://www.tssis.com/

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