Toxic shock syndrome

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Toxic shock syndrome
PDB 1aw7 EBI.jpg
Toxic shock syndrome toxin-1 protein from staphylococcus
Specialty Infectious disease
Symptoms Fever, rash, skin peeling, low blood pressure [1]
Complications Shock, kidney failure [2]
Usual onsetRapid [1]
TypesStaphylococcal (menstrual and nonmenstrual), streptococcal [1]
Causes Streptococcus pyogenes , Staphylococcus aureus , others [1] [3]
Risk factors Very absorbent tampons, skin lesions in young children [1]
Diagnostic method Based on symptoms [1]
Differential diagnosis Septic shock, Kawasaki's disease, Stevens–Johnson syndrome, scarlet fever [4]
Treatment Antibiotics, incision and drainage of any abscesses, intravenous immunoglobulin [1]
Prognosis Risk of death: ~50% (streptococcal), ~5% (staphylococcal) [1]
Frequency3 per 100,000[ definition needed ] per year (developed world) [1]

Toxic shock syndrome (TSS) is a condition caused by bacterial toxins. [1] Symptoms may include fever, rash, skin peeling, and low blood pressure. [1] There may also be symptoms related to the specific underlying infection such as mastitis, osteomyelitis, necrotising fasciitis, or pneumonia. [1]

Contents

TSS is typically caused by bacteria of the Streptococcus pyogenes or Staphylococcus aureus type, though others may also be involved. [1] [3] Streptococcal toxic shock syndrome is sometimes referred to as toxic-shock-like syndrome (TSLS). [1] The underlying mechanism involves the production of superantigens during an invasive streptococcus infection or a localized staphylococcus infection. [1] Risk factors for the staphylococcal type include the use of very absorbent tampons, skin lesions in young children characterized by fever, low blood pressure, rash, vomiting and/or diarrhea, and multiorgan failure. [1] [5] [6] Diagnosis is typically based on symptoms. [1]

Treatment includes intravenous fluids, antibiotics, incision and drainage of any abscesses, and possibly intravenous immunoglobulin. [1] [7] The need for rapid removal of infected tissue via surgery in those with a streptococcal cause, while commonly recommended, is poorly supported by the evidence. [1] Some recommend delaying surgical debridement. [1] The overall risk of death is about 50% in streptococcal disease, and 5% in staphylococcal disease. [1] Death may occur within 2 days. [1]

In the United States, streptococcal TSS occurs in about 3 per 100,000[ definition needed ] per year, and staphylococcal TSS in about 0.5 per 100,000[ definition needed ] per year. [1] The condition is more common in the developing world. [1] It was first described in 1927. [1] Due to the association with very absorbent tampons, these products were removed from sale. [1]

Signs and symptoms

Symptoms of toxic shock syndrome (TSS) vary depending on the underlying cause. TSS resulting from infection with the bacterium Staphylococcus aureus typically manifests in otherwise healthy individuals via signs and symptoms including high fever, accompanied by low blood pressure, malaise and confusion, [3] 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 [3] (conversely, streptococcal TSS will rarely involve a sunburn-like rash), and can involve any region of the body including the lips, mouth, eyes, palms and soles of the feet. [3] In patients who survive, the rash desquamates (peels off) after 10–21 days. [3]

STSS 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.[ citation needed ]

Pathophysiology

In both TSS (caused by S. aureus) and TSLS (caused by S. pyogenes), disease progression stems from a superantigen toxin. The toxin in S. aureus infections is TSS Toxin-1, or TSST-1. The TSST-1 is secreted as a single polypeptide chain. The gene encoding toxic shock syndrome toxin is carried by a mobile genetic element of S. aureus in the SaPI family of pathogenicity islands. [8] The toxin causes the non-specific binding of MHC II, on professional antigen presenting cells, with T-cell receptors, on T cells.

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. This results in polyclonal T-cell activation. Superantigens do not require processing by antigen-presenting cells but instead, interact directly with the invariant region[ citation needed ] 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, [7] followed by a multisystem disease.

Risk factors

A few possible causes of toxic shock syndrome are: [9] [10]

Diagnosis

For staphylococcal toxic shock syndrome, the diagnosis is based upon CDC criteria defined in 2011, as follows: [5]

  1. Body temperature > 38.9 °C (102.0 °F)
  2. Systolic blood pressure < 90 mmHg
  3. Diffuse macular erythroderma
  4. Desquamation (especially of the palms and soles) 1–2 weeks after onset
  5. Involvement of three or more organ systems:
  6. Negative results of:

Cases are classified as confirmed or probable as follows:

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. [11] Treatment includes removal or draining of the source of infection—often a tampon—and draining of abscesses. Outcomes are poorer in patients who do not have the source of infection removed. [11]

Antibiotic treatment should cover both S. pyogenes and S. aureus. This may include a combination of cephalosporins, penicillins or vancomycin. The addition of clindamycin [12] or gentamicin [13] reduces toxin production and mortality.

In some cases doctors will prescribe other treatments such as blood pressure medications (to stabilize blood pressure if it is too low), dialysis, oxygen mask (to stabilize oxygen levels), and sometimes a ventilator. These will sometimes be used to help treat side effects of contracting TSS. [9]

Prognosis

With proper treatment, people usually recover in two to three weeks. The condition can, however, be fatal within hours. TSS has a mortality rate of 30%–70%. Children who are affected by TSS tend to recover easier than adults do. [14]

Complications

Prevention

During menstruation: [17]

For anyone: [18]

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 three to four out of 100,000 tampon users per year; the information supplied by manufacturers of sanitary products such as Tampax and Stayfree puts it at one to 17 of every 100,000 menstruating females per year. [19] [20]

TSS was considered a sporadic disease that occurred in immunocompromised people. It was not a more well-known disease until the 1980s, when high-absorbency tampons were in use by menstruating women. Due to the idea of the tampons having a high absorbency this led women to believe that they could leave a tampon in for several hours. Doing this allowed the bacteria to grow and infect women. This resulted in a spike of cases of TSS. [21]

Philip M. Tierno Jr. helped determine that tampons were behind TSS cases in the early 1980s. Tierno blames the introduction of higher-absorbency tampons in 1978. A study by Tierno also determined that all-cotton tampons were less likely to produce the conditions in which TSS can grow; this was done 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 as far to state, "The bottom line is that you can get TSS with synthetic tampons, but not with an all-cotton tampon." [22]

A rise in reported cases occurred 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. [19] 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. [19]

TSS is more common during the winter and spring and occurs most often in the young and old. [3]

Toxic shock syndrome is commonly known to be an issue for females who menstruate, although fifty percent of Toxic Shock Syndrome cases are unrelated to menstruation. TSS in these cases can be caused by skin wounds, surgical sites, nasal packing, and burns. [17]

History

Awareness poster from 1985 Toxic shock syndrome is so rare you might forget it can happen - (6946668685).jpg
Awareness poster from 1985

Initial description

The term "toxic shock syndrome" was first used in 1978 by a Denver pediatrician, James K. Todd, to describe the staphylococcal illness in three boys and four girls aged 8–17 years. [23] 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 after they should have been removed. [24]

Rely tampons

Following controversial test marketing in Rochester, New York, and Fort Wayne, Indiana, [25] in August 1978, Procter and Gamble introduced superabsorbent Rely tampons to the United States market [26] in response to women's demands for tampons that could contain an entire menstrual flow without leaking or replacement. [27] Rely used carboxymethylcellulose (CMC) and compressed beads of polyester for absorption. This tampon design could absorb nearly 20 times its own weight in fluid. [28] Further, the tampon would "blossom" into a cup shape in the vagina to hold menstrual fluids without leakage.[ citation needed ]

In January 1980, epidemiologists in Wisconsin and Minnesota reported the appearance of TSS, mostly in those menstruating, to the CDC. [29] S. aureus was successfully cultured from most of the subjects. The Toxic Shock Syndrome Task Force was created and investigated the epidemic as the number of reported cases rose throughout the summer of 1980. [30] In September 1980, CDC reported users of Rely were at increased risk for developing TSS. [31]

On 22 September 1980, Procter and Gamble recalled Rely [32] 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". [33] 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. [34]

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. [35] The ability of carboxymethylcellulose to filter the S. aureus toxin that causes TSS may account for the increased risk associated with Rely. [28]

Notable cases

Related Research Articles

<span class="mw-page-title-main">Group A streptococcal infection</span> Medical condition

Group A streptococcal infections are a number of infections with Streptococcus pyogenes, a group A streptococcus (GAS). S. pyogenes is a species of beta-hemolytic Gram-positive bacteria that is responsible for a wide range of infections that are mostly common and fairly mild. If the bacteria enter the bloodstream an infection can become severe and life-threatening, and is called an invasive GAS (iGAS).

<span class="mw-page-title-main">Scarlet fever</span> Infectious disease caused by Streptococcus pyogenes

Scarlet fever, also known as scarlatina, is an infectious disease caused by Streptococcus pyogenes, a Group A streptococcus (GAS). It most commonly affects children between five and 15 years of age. The signs and symptoms include a sore throat, fever, headache, swollen lymph nodes, and a characteristic rash. The face is flushed and the rash is red and blanching. It typically feels like sandpaper and the tongue may be red and bumpy. The rash occurs as a result of capillary damage by exotoxins produced by S.pyogenes. On darker-pigmented skin the rash may be hard to discern.

<span class="mw-page-title-main">Streptococcal pharyngitis</span> Medical condition

Streptococcal pharyngitis, also known as streptococcal sore throat, is pharyngitis caused by Streptococcus pyogenes, a gram-positive, group A streptococcus. Common symptoms include fever, sore throat, red tonsils, and enlarged lymph nodes in the front of the neck. A headache and nausea or vomiting may also occur. Some develop a sandpaper-like rash which is known as scarlet fever. Symptoms typically begin one to three days after exposure and last seven to ten days.

<i>Staphylococcus aureus</i> Species of Gram-positive bacterium

Staphylococcus aureus is a Gram-positive spherically shaped bacterium, a member of the Bacillota, and is a usual member of the microbiota of the body, frequently found in the upper respiratory tract and on the skin. It is often positive for catalase and nitrate reduction and is a facultative anaerobe that can grow without the need for oxygen. Although S. aureus usually acts as a commensal of the human microbiota, it can also become an opportunistic pathogen, being a common cause of skin infections including abscesses, respiratory infections such as sinusitis, and food poisoning. Pathogenic strains often promote infections by producing virulence factors such as potent protein toxins, and the expression of a cell-surface protein that binds and inactivates antibodies. S. aureus is one of the leading pathogens for deaths associated with antimicrobial resistance and the emergence of antibiotic-resistant strains, such as methicillin-resistant S. aureus (MRSA), is a worldwide problem in clinical medicine. Despite much research and development, no vaccine for S. aureus has been approved.

<span class="mw-page-title-main">Tampon</span> Feminine hygiene product to absorb menstrual flow by insertion into the vagina

A tampon is a menstrual product designed to absorb blood and vaginal secretions by insertion into the vagina during menstruation. Unlike a pad, it is placed internally, inside of the vaginal canal. Once inserted correctly, a tampon is held in place by the vagina and expands as it soaks up menstrual blood. However, in addition to menstrual blood, the tampon also absorbs the vagina's natural lubrication and bacteria, which can change the normal pH, increasing the risk of infections from the bacterium Staphylococcus aureus, which can lead to toxic shock syndrome (TSS). TSS is a rare but life-threatening infection that requires immediate medical attention.

<span class="mw-page-title-main">Necrotizing fasciitis</span> Infection that results in the death of the bodys soft tissue

Necrotizing fasciitis (NF), also known as flesh-eating disease, is a bacterial infection that results in the death of parts of the body's soft tissue. It is a severe disease of sudden onset that spreads rapidly. Symptoms usually include red or purple skin in the affected area, severe pain, fever, and vomiting. The most commonly affected areas are the limbs and perineum.

<span class="mw-page-title-main">Menstrual cup</span> Feminine hygiene device worn inside the vagina during menstruation

A menstrual cup is a menstrual hygiene device which is inserted into the vagina during menstruation. Its purpose is to collect menstrual fluid. Menstrual cups are usually made of flexible medical grade silicone, latex, or a thermoplastic isomer. They are shaped like a bell with a stem or a ring. The stem is used for insertion and removal, and the bell-shaped cup seals against the vaginal wall just below the cervix and collects menstrual fluid. This is unlike tampons and menstrual pads, which absorb the fluid instead.

<span class="mw-page-title-main">Feminine hygiene</span> Personal care products for menstruation, vaginal discharge etc.

Feminine hygiene products are personal care products used during menstruation, vaginal discharge, and other bodily functions related to the vulva and vagina. Products that are used during menstruation may also be called menstrual hygiene products, including menstrual pads, tampons, pantyliners, menstrual cups, menstrual sponges and period panties. Feminine hygiene products also include products meant to cleanse the vulva or vagina, such as douches, feminine wipes, and soap.

<span class="mw-page-title-main">Superantigen</span> Antigen which strongly activates the immune system

Superantigens (SAgs) are a class of antigens that result in excessive activation of the immune system. Specifically they cause non-specific activation of T-cells resulting in polyclonal T cell activation and massive cytokine release. Superantigens act by binding to the MHC proteins on antigen-presenting cells (APCs) and to the TCRs on their adjacent helper T-cells, bringing the signaling molecules together, and thus leading to the activation of the T-cells, regardless of the peptide displayed on the MHC molecule. SAgs are produced by some pathogenic viruses and bacteria most likely as a defense mechanism against the immune system. Compared to a normal antigen-induced T-cell response where 0.0001-0.001% of the body's T-cells are activated, these SAgs are capable of activating up to 20% of the body's T-cells. Furthermore, Anti-CD3 and Anti-CD28 antibodies (CD28-SuperMAB) have also shown to be highly potent superantigens.

<span class="mw-page-title-main">Enterotoxin</span> Toxin from a microorganism affecting the intestines

An enterotoxin is a protein exotoxin released by a microorganism that targets the intestines. They can be chromosomally or plasmid encoded. They are heat labile (>60⁰), of low molecular weight and water-soluble. Enterotoxins are frequently cytotoxic and kill cells by altering the apical membrane permeability of the mucosal (epithelial) cells of the intestinal wall. They are mostly pore-forming toxins, secreted by bacteria, that assemble to form pores in cell membranes. This causes the cells to die.

A complication in medicine, or medical complication, is an unfavorable result of a disease, health condition, or treatment. Complications may adversely affect the prognosis, or outcome, of a disease. Complications generally involve a worsening in the severity of the disease or the development of new signs, symptoms, or pathological changes that may become widespread throughout the body and affect other organ systems. Thus, complications may lead to the development of new diseases resulting from previously existing diseases. Complications may also arise as a result of various treatments.

Rely was a brand of superabsorbent tampons made by Procter & Gamble starting in 1975. The brand's advertising slogan was "It even absorbs the worry!", and claimed it could hold up longer than the leading tampon, because it was made differently. "Remember, They named it Rely" was the last line of most commercials.

<span class="mw-page-title-main">Toxic shock syndrome toxin-1</span>

Toxic shock syndrome toxin-1 (TSST-1) is a superantigen with a size of 22 kDa produced by 5 to 25% of Staphylococcus aureus isolates. It causes toxic shock syndrome (TSS) by stimulating the release of large amounts of interleukin-1, interleukin-2 and tumour necrosis factor. In general, the toxin is not produced by bacteria growing in the blood; rather, it is produced at the local site of an infection, and then enters the blood stream.

<span class="mw-page-title-main">Staphylococcal infection</span> Medical condition

A staphylococcal infection or staph infection is an infection caused by members of the Staphylococcus genus of bacteria.

<span class="mw-page-title-main">Bullous impetigo</span> Medical condition

Bullous impetigo is a bacterial skin infection caused by Staphylococcus aureus that results in the formation of large blisters called bullae, usually in areas with skin folds like the armpit, groin, between the fingers or toes, beneath the breast, and between the buttocks. It accounts for 30% of cases of impetigo, the other 70% being non-bullous impetigo.

Perianal cellulitis, also known as perianitis or perianal streptococcal dermatitis, is a bacterial infection affecting the lower layers of the skin (cellulitis) around the anus. It presents as bright redness in the skin and can be accompanied by pain, difficulty defecating, itching, and bleeding. This disease is considered a complicated skin and soft tissue infection (cSSTI) because of the involvement of the deeper soft tissues.

<span class="mw-page-title-main">Streptococcal pyrogenic exotoxin</span>

Streptococcal pyrogenic exotoxins also known as erythrogenic toxins, are exotoxins secreted by strains of the bacterial species Streptococcus pyogenes. SpeA and speC are superantigens, which induce inflammation by nonspecifically activating T cells and stimulating the production of inflammatory cytokines. SpeB, the most abundant streptococcal extracellular protein, is a cysteine protease. Pyrogenic exotoxins are implicated as the causative agent of scarlet fever and streptococcal toxic shock syndrome. There is no consensus on the exact number of pyrogenic exotoxins. Serotypes A-C are the most extensively studied and recognized by all sources, but others note up to thirteen distinct types, categorizing speF through speM as additional superantigens. Erythrogenic toxins are known to damage the plasma membranes of blood capillaries under the skin and produce a red skin rash. Past studies have shown that multiple variants of erythrogenic toxins may be produced, depending on the strain of S. pyogenes in question. Some strains may not produce a detectable toxin at all. Bacteriophage T12 infection of S. pyogenes enables the production of speA, and increases virulence.

<span class="mw-page-title-main">Enterotoxin type B</span> Enterotoxin produced by the bacteria Staphylococcus aureus

In the field of molecular biology, enterotoxin type B, also known as Staphylococcal enterotoxin B (SEB), is an enterotoxin produced by the gram-positive bacteria Staphylococcus aureus. It is a common cause of food poisoning, with severe diarrhea, nausea and intestinal cramping often starting within a few hours of ingestion. Being quite stable, the toxin may remain active even after the contaminating bacteria are killed. It can withstand boiling at 100 °C for a few minutes. Gastroenteritis occurs because SEB is a superantigen, causing the immune system to release a large amount of cytokines that lead to significant inflammation.

Bacteriophage T12 is a bacteriophage that infects Streptococcus pyogenes bacteria. It is a proposed species of the family Siphoviridae in the order Caudovirales also known as tailed viruses. It converts a harmless strain of bacteria into a virulent strain. It carries the speA gene which codes for erythrogenic toxin A. speA is also known as streptococcal pyogenic exotoxin A, scarlet fever toxin A, or even scarlatinal toxin. Note that the name of the gene "speA" is italicized; the name of the toxin "speA" is not italicized. Erythrogenic toxin A converts a harmless, non-virulent strain of Streptococcus pyogenes to a virulent strain through lysogeny, a life cycle which is characterized by the ability of the genome to become a part of the host cell and be stably maintained there for generations. Phages with a lysogenic life cycle are also called temperate phages. Bacteriophage T12, proposed member of family Siphoviridae including related speA-carrying bacteriophages, is also a prototypic phage for all the speA-carrying phages of Streptococcus pyogenes, meaning that its genome is the prototype for the genomes of all such phages of S. pyogenes. It is the main suspect as the cause of scarlet fever, an infectious disease that affects small children.

Sharra L. Vostral is a Professor of History and Science and Technology at the College of Liberal Arts at Purdue University. She has written two books about menstruation and history: Under Wraps: A History of Menstrual Hygiene Technology and Toxic Shock: A Social History.

References

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  44. ↑ "After Toxic Shock Syndrome Claimed Her Legs, Lauren Wasser Set About Reshaping The Fashion Industry". British Vogue . 7 August 2022. Retrieved 15 March 2023.
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