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Toxic shock syndrome (TSS) is a toxin-mediated acute life-threatening illness, usually
precipitated by infection with either Staphylococcus aureus or group A Streptococcus (GAS),
also called Streptococcus pyogenes. It is characterized by high fever, rash, hypotension,
multiorgan failure (involving at least 3 or more organ systems), and desquamation, typically of
the palms and soles, 1-2 weeks after the onset of acute illness. The clinical syndrome can also
include severe myalgia, vomiting, diarrhea, headache, and non focal neurologic abnormalities.
Toxic shock syndrome toxin 1(TSST-1), a prototype superantigen secreted by a Staphylococcus
aureus bacterium strain in susceptible hosts, acts on the vascular system by causing
inflammation, fever, and shock.This bacterium strain that produces the TSST-1's can be found
in any area of the body. TSST-1 is a bacterial exotoxin found in patients who have developed
toxic shock syndrome (TSS), which can be found in menstruating women or any man or child for
that matter.
GAS is an aerobic gram-positive organism that forms chains and is an important cause of soft
tissue infections. Diabetes, alcoholism, varicella infections, and surgical procedures all increase
the risk of severe GAS infections and hence may potentially increase the risk of GAS TSS.
Severe, invasive GAS infections can cause necrotizing fasciitis and spontaneous gangrenous
myositis. An increasing number of severe GAS infections associated with shock and organ
failure have been reported. These infections are termed streptococcal TSS.
Toxic shock syndrome toxin (TSST) 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.
Pathogensis:
M proteins: Filamentous proteins on the cell membrane with antiphagocytic properties.
More than 80 M types.
Solution
Toxic shock syndrome (TSS) is a toxin-mediated acute life-threatening illness, usually
precipitated by infection with either Staphylococcus aureus or group A Streptococcus (GAS),
also called Streptococcus pyogenes. It is characterized by high fever, rash, hypotension,
multiorgan failure (involving at least 3 or more organ systems), and desquamation, typically of
the palms and soles, 1-2 weeks after the onset of acute illness. The clinical syndrome can also
include severe myalgia, vomiting, diarrhea, headache, and non focal neurologic abnormalities.
Toxic shock syndrome toxin 1(TSST-1), a prototype superantigen secreted by a Staphylococcus
aureus bacterium strain in susceptible hosts, acts on the vascular system by causing
inflammation, fever, and shock.This bacterium strain that produces the TSST-1's can be found
in any area of the body. TSST-1 is a bacterial exotoxin found in patients who have developed
toxic shock syndrome (TSS), which can be found in menstruating women or any man or child for
that matter.
GAS is an aerobic gram-positive organism that forms chains and is an important cause of soft
tissue infections. Diabetes, alcoholism, varicella infections, and surgical procedures all increase
the risk of severe GAS infections and hence may potentially increase the risk of GAS TSS.
Severe, invasive GAS infections can cause necrotizing fasciitis and spontaneous gangrenous
myositis. An increasing number of severe GAS infections associated with shock and organ
failure have been reported. These infections are termed streptococcal TSS.
Toxic shock syndrome toxin (TSST) 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.
Pathogensis:
M proteins: Filamentous proteins on the cell membrane with antiphagocytic properties.
More than 80 M types.

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Toxic shock syndrome (TSS) is a toxin-mediated acute life-threatenin.pdf

  • 1. Toxic shock syndrome (TSS) is a toxin-mediated acute life-threatening illness, usually precipitated by infection with either Staphylococcus aureus or group A Streptococcus (GAS), also called Streptococcus pyogenes. It is characterized by high fever, rash, hypotension, multiorgan failure (involving at least 3 or more organ systems), and desquamation, typically of the palms and soles, 1-2 weeks after the onset of acute illness. The clinical syndrome can also include severe myalgia, vomiting, diarrhea, headache, and non focal neurologic abnormalities. Toxic shock syndrome toxin 1(TSST-1), a prototype superantigen secreted by a Staphylococcus aureus bacterium strain in susceptible hosts, acts on the vascular system by causing inflammation, fever, and shock.This bacterium strain that produces the TSST-1's can be found in any area of the body. TSST-1 is a bacterial exotoxin found in patients who have developed toxic shock syndrome (TSS), which can be found in menstruating women or any man or child for that matter. GAS is an aerobic gram-positive organism that forms chains and is an important cause of soft tissue infections. Diabetes, alcoholism, varicella infections, and surgical procedures all increase the risk of severe GAS infections and hence may potentially increase the risk of GAS TSS. Severe, invasive GAS infections can cause necrotizing fasciitis and spontaneous gangrenous myositis. An increasing number of severe GAS infections associated with shock and organ failure have been reported. These infections are termed streptococcal TSS. Toxic shock syndrome toxin (TSST) 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. Pathogensis: M proteins: Filamentous proteins on the cell membrane with antiphagocytic properties. More than 80 M types. Solution Toxic shock syndrome (TSS) is a toxin-mediated acute life-threatening illness, usually precipitated by infection with either Staphylococcus aureus or group A Streptococcus (GAS), also called Streptococcus pyogenes. It is characterized by high fever, rash, hypotension, multiorgan failure (involving at least 3 or more organ systems), and desquamation, typically of the palms and soles, 1-2 weeks after the onset of acute illness. The clinical syndrome can also include severe myalgia, vomiting, diarrhea, headache, and non focal neurologic abnormalities.
  • 2. Toxic shock syndrome toxin 1(TSST-1), a prototype superantigen secreted by a Staphylococcus aureus bacterium strain in susceptible hosts, acts on the vascular system by causing inflammation, fever, and shock.This bacterium strain that produces the TSST-1's can be found in any area of the body. TSST-1 is a bacterial exotoxin found in patients who have developed toxic shock syndrome (TSS), which can be found in menstruating women or any man or child for that matter. GAS is an aerobic gram-positive organism that forms chains and is an important cause of soft tissue infections. Diabetes, alcoholism, varicella infections, and surgical procedures all increase the risk of severe GAS infections and hence may potentially increase the risk of GAS TSS. Severe, invasive GAS infections can cause necrotizing fasciitis and spontaneous gangrenous myositis. An increasing number of severe GAS infections associated with shock and organ failure have been reported. These infections are termed streptococcal TSS. Toxic shock syndrome toxin (TSST) 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. Pathogensis: M proteins: Filamentous proteins on the cell membrane with antiphagocytic properties. More than 80 M types.