3- Bacteriology | staphylococcal toxic shock syndrome | pathology| clinical presentation| diagnosis
508 بار بازدید -
4 سال پیش
-
Reviews covers topics in the
Reviews covers topics in the United States Medical Licensing Exam (USMLE) Step 2CK examination.
we discuss the Pathology Clinical Presentation Diagnosis & Management of Toxic Shock Syndrome.
Lectures can be used by medical students to supplement their lecture materials.
Toxic shock syndrome (TSS) is a condition caused by bacterial toxins. Symptoms may include fever rash skin peeling and low blood pressure.
TSS is caused by bacteria of either the Streptococcus pyogenes or Staphylococcus aureus type. Streptococcal toxic shock syndrome (STSS) is sometimes referred to as toxic shock-like syndrome (TSLS). The underlying mechanism involves the production of superantigens during an invasive streptococcus infection or a localized staphylococcus infection. Risk factors for the staphylococcal type include the use of very absorbent tampons and skin lesions in young children. Diagnosis is typically based on symptoms.
Treatment includes antibiotics incision and drainage of any abscesses and possibly intravenous immunoglobulin. 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. Some recommend delaying surgical debridement. The overall risk of death in streptococcal disease is about 50% while in staphylococcal disease it is around 5%. Death may occur within 2 days.
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 via signs and symptoms including 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 phase 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-like rash.
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[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 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.
The gene encoding toxic shock syndrome toxin is carried by a mobile genetic element of S. aureus in the SaPI family of pathogenicity islands.
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. 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.
we discuss the Pathology Clinical Presentation Diagnosis & Management of Toxic Shock Syndrome.
Lectures can be used by medical students to supplement their lecture materials.
Toxic shock syndrome (TSS) is a condition caused by bacterial toxins. Symptoms may include fever rash skin peeling and low blood pressure.
TSS is caused by bacteria of either the Streptococcus pyogenes or Staphylococcus aureus type. Streptococcal toxic shock syndrome (STSS) is sometimes referred to as toxic shock-like syndrome (TSLS). The underlying mechanism involves the production of superantigens during an invasive streptococcus infection or a localized staphylococcus infection. Risk factors for the staphylococcal type include the use of very absorbent tampons and skin lesions in young children. Diagnosis is typically based on symptoms.
Treatment includes antibiotics incision and drainage of any abscesses and possibly intravenous immunoglobulin. 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. Some recommend delaying surgical debridement. The overall risk of death in streptococcal disease is about 50% while in staphylococcal disease it is around 5%. Death may occur within 2 days.
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 via signs and symptoms including 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 phase 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-like rash.
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[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 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.
The gene encoding toxic shock syndrome toxin is carried by a mobile genetic element of S. aureus in the SaPI family of pathogenicity islands.
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. 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.
4 سال پیش
در تاریخ 1399/06/08 منتشر شده
است.
508
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