Toxic shock syndrome

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Toxic shock syndrome ( TSS ) is a condition caused by bacterial toxins. Symptoms may include fever, rash, exfoliation, and low blood pressure. There may also be symptoms associated with a specific underlying infection such as mastitis, osteomyelitis, necrotising fasciitis, or pneumonia.

TSS is caused by bacteria of the streptococcus pyogenes type or Staphylococcus aureus . Streptococcal toxic shock syndrome (STSS) is sometimes referred to as toxic shock-like syndrome (TSLS). The underlying mechanism involves the production of superantigens during invasive streptococcal infections or local staphylococcus infections. Risk factors for staphylococcal types include the use of highly absorbing tampons and skin lesions in children. Diagnosis is usually based on symptoms.

Treatments include antibiotics, incisions and drainage of any abscess, and possibly intravenous immunoglobulin. The need for rapid removal of infected tissue via surgery in those with streptococcal causes, while generally recommended, is less supported by evidence. Some suggest to delay surgical debridement. The overall risk of death in streptococcal disease is about 50% while in staphylococcal disease about 5%. Death can occur within 2 days.

In the United States TSS streptococcus occurs at about 3 per 100,000 per year while staphylococcal TSS occurs at about 0.5 per 100,000 per year. This condition is more common in developing countries. This was first described in 1927. Due to its highly absorbing tampon relationship, these products were removed from sales.

Video Toxic shock syndrome

Signs and symptoms

Symptoms of toxic shock syndrome vary depending on the underlying cause. TSS resulting from infection with bacteria Staphylococcus aureus usually manifests in healthy individuals through signs and symptoms including high fever, accompanied by low blood pressure, malaise and confusion, which can rapidly develop into stupor, coma, and multiple organ failure. A typical rash, often seen early in the course of the illness, resembles a sunburn, and can involve every area of ​​the body including the lips, mouth, eyes, palms and soles of the feet. In patients who survive in the initial phase of infection, the rash is decreased, or loose, after 10-14 days.

In contrast, TSS caused by bacteria Streptococcus pyogenes , or TSLS, usually appears in people with pre-existing skin infections with bacteria. These people often experience severe pain at the site of skin infections, followed by the rapid development of symptoms as described above for TSS. In contrast to TSS caused by Staphylococcus , streptococcal TSS less frequently involves rashes such as sunlight.

Maps Toxic shock syndrome

Pathophysiology

In both TSS (caused by S. aureus ) and TSLS (due to S. pyogenes ), the development of the disease comes from superantigen toxin which allows the identification of MHC II nonspecifically with cell receptors T, resulting in a polyclonal T cell activation. In the identification of typical T-cells, antigens were taken by antigen-presenting cells, processed, expressed in cell surfaces in complexes with class II major histocompatibility complex (MHC) in the grooves formed by the alpha and beta chains of class II. MHC, and is recognized by specialized antigen-specific receptors.

In contrast, superantigens do not require processing by cells presenting antigens but interact directly with the invariant region of the class II MHC molecule. In patients with TSS, up to 20% of the T-cells of the body can be activated at one time. These polyclonal T cell populations cause cytokine storms, followed by multisystem disease. Toxins in S. aureus Infection is TSS Toxin-1, or TSST-1. TSST-1 is secreted as a single polypeptide chain.

The gene encoding toxic shock syndrome toxin is carried by a moving genetic element of S. aureus in the family pathogenic of the island of SaPI.

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Diagnosis

For staphylococcal toxic shock syndrome, the diagnosis is based on CDC criteria established in 2011, as follows:

1. Body temperature & gt; 38.9 Â ° C (102.02 Â ° F)
2. systolic blood pressure & lt; 90 mmHg
3. Diffuse macular erythrocroses
4. Desquamation (especially the palms and soles of the feet) 1-2 weeks after onset
5. Involvement of three or more organ systems:
   • Gastrointestinal (vomiting, diarrhea)
   • Muscular: severe myalgia or creatine phosphokinase level at least twice the normal upper limit for the laboratory
   • Mucosal mucous membranes (vagina, mouth, conjunctiva)
   • Kidney failure (serum creatinine & gt; 2 times normal)
   • Liver inflammation (bilirubin, AST, or ALT & gt; 2 times normal)
   • Low platelet count (platelet count & lt; 100.000/mm ³ )
   • Involvement of the central nervous system (confusion without focal neurological findings)
6. Negative results from:
   • Blood, throat, and CSF cultures for other bacteria (other than S. aureus )
   • The negative serology for Rickettsia , leptospirosis, and measles
   infections

Cases are classified as confirmed or possibly based on:

• Confirmed: The six criteria above are met (unless the patient dies before desquamation can occur)
• Possible: Five of the above six criteria are met

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Treatment

The severity of this disease often ensures hospitalization. Admission to the intensive care unit is often necessary for supportive care (for aggressive fluid management, ventilation, renal replacement therapy and inotropic support), especially in the case of multiple organ failure. Sources of infection should be removed or dried if possible: abscesses and collections should be dried. Anyone taking tampons at the onset of symptoms should immediately remove them. The worse outcome in patients with no source of infection is removed.

Antibiotic treatment should include both S. pyogenes and S. aureus. This may include a combination of cephalosporins, penicillins or vancomycin. The addition of clindamycin or gentamicin reduced the production and mortality of toxins.

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Prognosis

With proper care, people usually recover within two to three weeks. However, this condition can be fatal within hours.

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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 of him in 2004, determined incidents in three to four of the 100,000 tampon users per year; the information provided by manufacturers of sanitary products such as Tampax and Stayfree puts it in one to 17 out of every 100,000 men who menstruate each year.

Philip M. Tierno Jr., helped determine that the tampon was behind the TSS case in the early 1980s. Tierno blamed the introduction of high absorbent tampons in 1978. A study by Tierno also determined that all cotton tampons were less likely to produce conditions in which TSS could grow; this is done by using a direct comparison of 20 brands of tampons including conventional cotton/rayon tampons and 100% organic cotton tampons from Natracare. In fact, Dr. Tierno goes so far as to state, "The bottom line is you can get TSS with a synthetic tampon, but not with a cotton powder tampon."

Increase in reported cases occurred in the early 2000s: eight deaths from syndrome in California in 2002 after three consecutive years of four deaths per year, and Schlievert's study found cases in Minnesota increased threefold from 2000 to 2003. Schlievert considers earlier onset menstruation is the cause of the increase; others, such as Philip M. Tierno and Bruce A. Hanna, blamed the new high-absorption tampon introduced in 1999 and manufacturers stopped warning not to leave overnight tampons.

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History

Initial Description

The term "toxic shock syndrome" was first used in 1978 by a Denver pediatrician, James K. Todd, to describe staphylococcal disease in three boys and four women aged 8-17 years. Although S. aureus is isolated from the mucosal site in patients, bacteria can not be isolated from blood, cerebrospinal fluid, or urine, raising the suspicion that there are toxins involved. The authors of the study noted reports of similar staphylococcal disease occasionally reappeared in 1927, but the authors at the time failed to consider the possibility of an association between toxic shock syndrome and the use of tampons, as three of the girls who were menstruating when the disease developed with tampons. Many cases of TSS occur after the tampon is left on the person who uses it.

Rely on tampons

Following the controversial marketing tests in Rochester, New York and Fort Wayne, Indiana, in August 1978, Procter and Gamble introduced the Superabsorbent Rise tampon to the US market in response to a woman's demand for tampons that could contain all menstrual flow without leak or replacement.. Use carboxymethylcellulose (CMC) and polyester granules for absorption. The design of this tampon can absorb nearly 20 times its own weight in the liquid. Next, the tampon will "bloom" into a cup shape in the vagina to hold menstrual fluids without leaks.

In January 1980, epidemiologists in Wisconsin and Minnesota reported the emergence of TSS, mostly in those who were menstruating, to the CDC. S. aureus was successfully cultured from most subjects. The Toxic Shock Syndrome Task Force was created and investigated the epidemic as the number of reported cases increased during the summer of 1980. In September 1980, the CDC reported that Rely users were at increased risk for developing TSS.

On September 22, 1980, Procter and Gamble withdrew Rely after the release of the CDC report. As part of a voluntary withdrawal, Procter and Gamble entered into an agreement with the FDA "to provide a program for notification to consumers and the taking of products from the market". However, it is clear to other researchers that Rely is not the only culprit. Other regions in the United States saw an increase in menstrual TSS before Rely was introduced.

It was shown later that higher absorption of tampons was associated with an increased risk for TSS, regardless of chemical composition or tampon brand. The only exception is Rely, where the risk for TSS is still higher when corrected for absorption. The ability of carboxymethylcellulose to screen out S. aureus toxins that cause TSS can lead to an increased risk associated with Rely.

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Famous cases

• Clive Barker, fully recovered, has syndrome after visiting a dentist.
• Lana Coc-Kroft, fully recovered, has syndrome due to group A streptococcal infection.
• Jim Henson, d. 1990, contracted syndrome due to group A streptococcal infection and subsequently died of it.
• Nan C. Robertson, d. 2009, 1983 Pulitzer Prize-winning Writer Feature for a detailed medical account of his struggle with toxic shock syndrome, a cover story for The New York Times Magazine which at the time became the most syndicated article in Time history.
• Mike Von Erich, d. 1987, developed syndrome after shoulder surgery: he made a real recovery but suffered brain damage as a result of the condition, eventually committing suicide.
• Lauren Wasser recovered from the near-death experience of TSS and then debuted in New York Fashion week despite wearing prosthetic legs. He is now advocating the law to ask for more research on the safety of women's hygiene products.

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References

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External links

• Stevens DL (1995). "Streptococcus toxic shock syndrome: disease spectrum, pathogenesis, and new concepts in treatment". Emerging Infectious Diseases . 1 (3): 69-78. doi: 10.3201/eid0103.950301. PMCÃ, 2626872 . PMIDÃ, 8903167
• "Toxic Shock Syndrome (TSS): Fact". Soxic Shock Syndrome information service . tssis.com Ã,

Source of the article : Wikipedia