"SSSS is caused by the release of two exotoxins (epidermolytic toxins A and B) from toxigenic strains of the bacteria (or a germ) Staphylococcus aureus. Desmosomes are the part of the skin cell responsible for adhering to the adjacent skin cell. The toxins bind to a molecule within the desmosome called Desmoglein 1 and break it up so the skin cells become unstuck," reports Staphylococcal scalded skin syndrome (2006).
SSSS can be detected by a fever, redness that has spread on the skin, and irritability. Fluid-filled blisters, which rupture easily, appear within 24-48 hours of the fever and widespread redness of the skin. After the blisters rupture, the skin looks like it has been scalded, or burned. Approximately 15-40% of healthy individuals are carriers of Staphylococcus aureus and as carriers, they carry the bacteria but no signs of the disease or symptoms are revealed. These carriers introduce the Staphylococcus aureus (without any sign of infection or disease) into the childcare facility. But these individuals, particularly infants, get SSSS from a localised staphylococcal infection, which is the producer of the two exotoxins (epidermolytic toxins A and B) and outbreaks can often be found occurring in facilities that provide childcare. The reason older
children and adults commonly do not get SSSS is because throughout a lifetime, immunities are built. In children younger than the age of five (especially infants), there is a lack of immunity built up that can defend against the toxin. Also, toxins are removed from the body via the kidneys due to the immature renal clearance system. These are the reasons why infants are more at risk. (Staphylococcal scalded skin syndrome, 2006).
Diagnosing SSSS can be as simple as looking at the appearance of the skin. Skin tissue can be examined with a microscope. The bacteria can be found by examining surface fluid or pus. Blood can be tested for the SSSS infection. (Staphylococcal Scalded Skin Syndrome, 2006.)
Pathophysiology has revealed a connection with other complications. For example, staphylococcus aureus causes the autoantibodies and bullous impetigo, a generalized form of SSS, which in turn causes pemphigus. Pemphigus was known to be unrelated to the other conditions. However, a study by Stanley and Amagai (2006) of the molecular pathophysiology of pemphigus revealed that the molecular pathophysiology contributes to the mechanism of the formation of blisters in bullous impetigo and the staphylococcal scalded-skin syndrome. Stanley and Amagai (2006) report the following:
Staphylococcal skin infections are among the most common skin diseases in children. Classic studies more than 30 years ago showed that the blisters in bullous impetigo and the scalded-skin syndrome are caused by exfoliative toxin released by staphylococcusSubsequently, it was discovered that two major serotypes of this toxin, A and B, cause bullous impetigo and the scalded-skin syndrome in cases of the scalded-skin syndrome, it circulates throughout the body, causing blisters at sites
Staphylococcal Scalded Skin Syndrome 4
distant from the infection.49 The risk of death from the