Staphylococcus aureus

Staphylococcus aureus organisms are pyogenic, nonmotile, Gram-positive cocci that form
grapelike clusters. These bacteria cause a myriad of skin lesions (boils, carbuncles, impetigo,
and scalded skin) and also cause osteomyelitis, pneumonia, endocarditis, food poisoning,
and toxic shock syndrome (TSS).

Staphylococcus aureus organisms are pyogenic, nonmotile, Gram-positive cocci that form
grapelike clusters. These bacteria cause a myriad of skin lesions (boils, carbuncles, impetigo,
and scalded skin) and also cause osteomyelitis, pneumonia, endocarditis, food poisoning,
and toxic shock syndrome.

organ infections are described in other chapters. Staphylococcus epidermidis, a species that
is related to S. aureus, causes opportunistic infections in catheterized patients, patients with
prosthetic cardiac valves, and drug addicts. Staphylococcus saprophyticus is a common
cause of urinary tract infections in young women.

Pathogenesis. S. aureus and other virulent staphylococci possess a multitude of virulence

factors, which include surface proteins involved in adherence, secreted enzymes that
degrade proteins, and secreted toxins that damage host cells. Staphylococci are
distinguished by their large number of plasmids, which encode proteins involved in
antibiotic resistance and other virulence factors.

S. aureus expresses surface receptors for fibrinogen (called clumping factor), fibronectin,
and vitronectin, and uses these molecules as a bridge to bind to host endothelial cells.

Staphylococci infecting prosthetic valves and catheters have a polysaccharide capsule that
allows them to attach to the artificial materials and to resist host cell phagocytosis. The
lipase of S. aureus degrades lipids on the skin surface, and its expression is correlated with
the ability of the bacteria to produce skin abscesses. Staphylococci also have protein A on
their surface, which binds the Fc portion of immunoglobulins.

S. aureus produces multiple membrane-damaging (hemolytic) toxins, including -toxin,

which is a pore-forming protein that intercalates into the plasma membrane of host cells
and depolarizes them;76 -toxin, a sphingomyelinase; and -toxin, which is a detergent-like
peptide. Staphylococcal -toxin and leukocidin lyse erythrocytes and phagocytic cells,
respectively.

The exfoliative toxins produced by S. aureus are serine proteases that split the skin by
cleaving the protein desmoglein 1, which is part of the desmosomes that hold epidermal
cells tightly together.29 This can cause the superficial epidermis to split away from the
deeper skin, making the patient vulnerable to secondary infections.

Exfoliation can occur at the site of staphylococcal skin infection (bullous impetigo) or can be
widespread, when secreted toxin from a localized infection causes disseminated loss of the
superficial epidermis (staphylococcal scalded-skin syndrome).
Superantigens produced by S. aureus cause food poisoning and, of more concern, toxic
shock syndrome (TSS). TSS came to public attention because of its association with the use
of hyperabsorbent tampons, which became colonized with S. aureus during use. It is now
clear that TSS can be caused by growth of S. aureus at many sites, most commonly the
vagina and infected surgical sites.

TSS is characterized by hypotension (shock), renal failure, coagulopathy, liver disease,

respiratory distress, a generalized erythematous rash, and soft tissue necrosis at the site of
infection. If not promptly treated, TSS can be fatal. TSS can also be caused by Streptococcus
pyogenes.

Superantigens bind to conserved portions of MHC molecules and to relatively conserved

portions of TCR chains. In this manner, superantigens may stimulate up to 20% of T
lymphocytes.

The stimulation of so many T lymphocytes leads to massive T-lymphocyte proliferation and

cytokine release. The high levels of cytokines can lead to capillary leak and shock and may
cause vomiting by affecting the nervous system in the gut or the central nervous system.

Morphology

Whether the lesion is located in the skin, lungs, bones, or heart valves, S. aureus causes
pyogenic inflammation that is distinctive for its local destructiveness.

Excluding impetigo, which is a staphylococcal or streptococcal infection restricted to the

superficial epidermis, staphylococcal skin infections are centered around the hair follicles. A
furuncle, or boil, is a focal suppurative inflammation of the skin and subcutaneous tissue,
either solitary or multiple or recurrent in successive crops. Furuncles are most frequent in
moist, hairy areas, such as the face, axillae, groin, legs, and submammary folds.

Beginning in a single hair follicle, a boil develops into a growing and deepening abscess that
eventually "comes to a head" by thinning and rupturing the overlying skin. A carbuncle is
associated with deeper suppuration that spreads laterally beneath the deep subcutaneous
fascia and then burrows superficially to erupt in multiple adjacent skin sinuses.

Carbuncles typically appear beneath the skin of the upper back and posterior neck, where
fascial planes favor their spread.

Chronic abscess formation of apocrine gland regions, most frequently of the axilla, is known
as hidradenitis suppurativa. Those of the nail bed (paronychia) or on the palmar side of the
fingertips (felons) are exquisitely painful. They may follow trauma or embedded splinters
and, if deep enough, destroy the bone of the terminal phalanx or detach the fingernail.

Staphylococcal lung infections (Fig. 8-19) have a polymorphonuclear infiltrate similar to that
of pneumococcus (see Fig. 8-7) but are much more destructive of lung tissues. S. aureus lung
infections usually occur in patients with predisposing conditions such as influenza or
hematogenous spread of infected thrombi.
Staphylococcal scalded skin syndrome (SSSS)

Staphylococcal scalded skin syndrome (SSSS), also called Ritter disease, is caused by the
exfoliative A and B toxins. It is an exfoliative dermatitis that most frequently occurs in
children with staphylococcal infections of the nasopharynx or skin. In staphylococcal scalded
skin syndrome, there is a sunburnlike rash that spreads over the entire body and forms
fragile bullae that lead to partial or total skin loss. The intraepithelial split in staphylococcal
scalded skin syndrome is in the granulosa layer, distinguishing it from toxic epidermal
necrolysis, or Lyells disease, which is secondary to drug hypersensitivity and causes splitting
at the epidermal-dermal junction.

Pathogenesis

S. aureus and other virulent staphylococci possess a multitude of virulence factors, which
include surface proteins involved in adherence, secreted enzymes that degrade proteins,
and secreted toxins that damage host cells. Staphylococci are distinguished by their large
number of plasmids, which encode proteins involved in antibiotic resistance and other
virulence factors.

S. aureus expresses surface receptors for fibrinogen (called clumping factor), fibronectin,
and vitronectin, and uses these molecules as a bridge to bind to host endothelial cells.

Staphylococci infecting prosthetic valves and catheters have a polysaccharide capsule that
allows them to attach to the artificial materials and to resist host cell phagocytosis.

The lipase of S. aureus degrades lipids on the skin surface, and its expression is correlated
with the ability of the bacteria to produce skin abscesses.

Staphylococci also have protein A on their surface, which binds the Fc portion of
immunoglobulins.

S. aureus produces multiple membrane-damaging (hemolytic) toxins, including -toxin,

which is a pore-forming protein that intercalates into the plasma membrane of host cells
and depolarizes them; -toxin, a sphingomyelinase; and -toxin, which is a detergent-like
peptide. Staphylococcal -toxin and leukocidin lyse erythrocytes and phagocytic cells,
respectively.

Cutaneous bullous lesions

The exfoliative toxins produced by S. aureus are serine proteases that split the skin by
cleaving the protein desmoglein-1 (DSG1), which is part of the desmosomes that hold
epidermal cells tightly together.

This can cause the superficial epidermis to split away from the deeper skin, making the
patient vulnerable to secondary infections.
Exfoliation can occur at the site of staphylococcal skin infection (bullous impetigo) or can be
widespread, when secreted toxin from a localized infection causes disseminated loss of the
superficial epidermis (staphylococcal scalded-skin syndrome or SSSS).

Superantigens

Superantigens produced by S. aureus cause food poisoning and, of more concern, toxic
shock syndrome (TSS). TSS came to public attention because of its association with the use
of hyperabsorbent tampons, which became colonized with S. aureus during use. It is now
clear that TSS can be caused by growth of S. aureus at many sites, most commonly the
vagina and infected surgical sites.

TSS is characterized by hypotension (shock), renal failure, coagulopathy, liver disease,

respiratory distress, a generalized erythematous rash, and soft tissue necrosis at the site of
infection. If not promptly treated, TSS can be fatal. TSS can also be caused by Streptococcus
pyogenes.

Superantigens bind to conserved portions of MHC molecules and to relatively conserved

portions of TCR chains. In this manner, superantigens may stimulate up to 20% of T
lymphocytes. The stimulation of so many T lymphocytes leads to massive T-lymphocyte
proliferation and cytokine release. The high levels of cytokines can lead to capillary leak and
shock and may cause vomiting by affecting the nervous system in the gut or the central
nervous system.

http://www.humpath.com/spip.php?article8808

Streptococcus

Group B strep may live harmlessly in the human body, which is called "colonization" or
"carriage." During colonization, the organism lives on surfaces and membranes but does not
invade tissues or organs. The most common site of colonization for group B strep is in the
bowels. Approximately 20%-40% of women are colonized with group B strep in the vagina or
cervix. Colonization is more common in people with diabetes and those who are sexually
active.

An infection occurs when the bacteria invade the bloodstream, tissues, or organs. Newborns
can become infected with group B strep as they pass through the birth canal if the mother
carries the organism in her vagina. These infections are early-onset since they appear within
the first week of life, often in the first hours after birth. In mothers colonized with group B
strep, approximately 1% of newborns will have early-onset infection. Since group B strep is
carried in the bowels, the organism may also be spread if a person does not wash their
hands properly after using the bathroom. Babies can also be infected this way, usually in the
home, causing late-onset infections, which occur when the baby is 1 week to 3 months old.