Staphylococcus

Question 1

Staphylococcus aureus - species

Answer 1

• Genus Staphylococcus
• Gram + clusters
• aerobic
• coagulase +
• growth on mannitol salt agar
• fibronectin-binding proteins (FnBPs) on peptidoglycan cell wall

-Protein A

Question 2

Staphylococcus aureus - Protein A

Answer 2

The peptidoglycan of the cell wall is overlaid with surface proteins. These include fibronectin-binding proteins (FnBPs) and one called protein A which binds to the Fc portion of IgG molecules and is able to stimulate cytokines, and B cells.

Question 3

Staphylococcus aureus Exotoxins

Answer 3

•Alpha-toxin

• Protein secreted by almost all S. aureus strains but not by CoNS.
• Pore-forming by direct insertion into the lipid bilayer to form transmembrane pores.
• Action is similar to streptolysin O, complement, and the effector proteins of cytotoxic T lymphocytes.
• Another pore-forming toxin is a leukocidin (PV leukocidin) which lyses neutrophils. It is typically present in a minority of clinical isolates (<10%).
• Exfoliatin

-Causes intercellular splitting of the epidermis between the strratum spinosum and stratum granulosum by disruption of intercellular junctions.

Question 4

Staphylococcus aureus Staphylococcal Superantigen Toxins (StaphSAgs)

Answer 4

•systemic

Staphylococcal Enterotoxins

• Stimulate gastrointestinal symptoms (primarily vomiting) in humans and animals
• Once formed, these toxins are stable, retaining activity even after boiling or exposure to gastric and jejunal enzymes.
• In addition to superantigen-mediated actions, act directly on neural receptors in the upper gastrointestinal tract, leading to stimulation of the vomiting center in the brain.

•Toxic Shock Syndrome Toxin (TSST)

• Major cause of staphylococcal toxic shock syndrome •
• In addition to superantigen action has direct toxic effects on endothelial cells leading to capillary leakage, hypotension, and shock.

Question 5

Staphylococcus aureus Epidemiology

Answer 5

• The most common human habitat is the anterior nares.
• 30% carry the organism and rates among hospital personnel and patients may be much higher.
• Most S. aureus infections are auto-infections due to strains a carrier has shed from their anterior nares.
• Hospital outbreaks are caused by a virulent strain originally carried by the patient or a healthcare worker.

Question 6

Staphylococcus aureus and Food Poisoning

Answer 6

• Food becomes contaminated with an enterotoxin-producing strain of S. aureus (StaphSAg mediated) by a preparer who is a nasal carrier or has a staphylococcal lesion.
• If food is inadequately refrigerated the staphylococcal multiply and produce enterotoxin in the food.
• Because of the heat resistance of the toxin, its toxicity persists even if the food is cooked before eating.

Question 7

Staphylococcus aureus Primary Infection

Answer 7

• S. aureus is generally of low infectivity unless trauma, foreign matter, or other local conditions provide access for initiation of infection.
• The initial stages are mediated by the FnBPs, which bind to the glycoprotein fibronectin on epithelial cell surfaces.
• Protein A may aid in the initial stages by binding IgG
• This allows S. aureus to persist and to produce alpha-toxin and other cytolysins which injure the cell.
• The inflammatory cells, fibrin, and other tissue components form a wall which becomes the characteristic boil.
• In the skin, spontaneous resolution of the boil by granulation and fibrosis is the rule.
• In the lung, kidney, bone, and other organs the process may continue including spread to the bloodstream and distant organs.

Question 8

The initial stages are mediated by the [], which bind to the glycoprotein fibronectin on epithelial cell surfaces. [] may aid in the initial stages by binding IgG.

Answer 8

The initial stages are mediated by the FnBPs, which bind to the glycoprotein fibronectin on epithelial cell surfaces. Protein A may aid in the initial stages by binding IgG

Question 9

Initial attachment to fibronectin is mediated by fibronectin-binding proteins (FnBP), and the major injury is caused by the pore-forming [].

Answer 9

Initial attachment to fibronectin is mediated by fibronectin-binding proteins (FnBP), and the major injury is caused by the pore-forming α-toxin.

Question 10

What if the strain of S. aureus also produces exfoliatin?

Answer 10

• If the strain of S. aureus causing any of the effects described above also produces one or more of the exotoxins those actions will be added to those of the primary infection. The primary infection serves as a site for absorption of the toxin and need not be extensive or even clinically noticeable for the toxin action to take place.
• Exfoliatin toxin-producing strains cause blister-like separation of the epidermis.

Question 11

What if the strain of S. aureus also produces Toxic Shock Syndrome Toxin?

Answer 11

• If the strain of S. aureus causing any of the effects described above also produces one or more of the exotoxins those actions will be added to those of the primary infection. The primary infection serves as a site for absorption of the toxin and need not be extensive or even clinically noticeable for the toxin action to take place.
• In staphylococcal toxic shock syndrome (TSS) the StaphSAg is produced during the course of infection at any of multiple sites. Menstruation-associated TSS requires a combination of improbable events.
• Less than 5% of women carry S. aureus in their vaginal flora, and only some of these (~10%) produce TSST-1.
• Menstruation and high-absorbency tampon usage provide growth conditions that enhance the production of TSST-1.
• Toxin absorbed from the vagina can then circulate to produce superantigen-mediated TSS.

-SS. ayreus itself usuallly not in blood

• fever, diarrhea, shock, renal failure
• Some cases of TSS (non menstrual) are associated with StaphSAgs other than TSST-1.

Question 12

S. aureus Clinical Manifestations in Primary Infection - Furuncle or Boil

Answer 12

• Furuncle or Boil
• A superficial skin infection that develops in a hair follicle, sebaceous gland, or sweat gland.
• Infection can spread from a furuncle with the development of one or more abscesses in adjacent subcutaneous tissues.
• May result in bloodstream invasion

Question 13

S. aureus Clinical Manifestations in Primary Infection - Impetigo

Answer 13

• Most often a secondary invader in group A streptococcal pustular impetigo
• Can produce the skin pustules of impetigo on its own. Strains that produce exfoliatin cause bullous impetigo, characterized by blisters

Question 14

S. aureus Clinical Manifestations in Primary Infection - Deep Lesions

Answer 14

• S. aureus can cause a wide variety of infections of deep tissues, by bacteremic spread from a skin lesion that may be unnoticed. These include infections of bones, joints, deep organs, and soft tissues including surgical wounds.
• Most of cases of acute osteomyelitis are caused by S. aureus.

Question 15

S. aureus Treatment

Answer 15

• S. aureus can cause a wide variety of infections of deep tissues, by bacteremic spread from a skin lesion that may be unnoticed. These include infections of bones, joints, deep organs, and soft tissues including surgical wounds. • Most of cases of acute osteomyelitis are caused by S. aureus.
• Penicillin G is still effective for susceptible strains but no longer used due to the high frequency of penicillinase-mediated resistance
• Penicillinase-resistant penicillins (methicillin, dicloxacillin) and first generation cephalosporins are commonly used.
• For methicillin-resistant (MRSA) strains vancomycin and daptomycin are used for deep seated infections.

-Clindamycin and doxycycline are alternatives for superficial infections.

Question 16

S. aureus Resistance

Answer 16

• 80 to 90 percent of isolates are now penicillin resistant.
• Penicillinase acts by opening the beta lactam ring rendering the drug unable to bind with its target.
• Alterations in the peptidoglycan transpeptidases (altered target mechanism) is the basis for MRSA
• New MRSA clones circulating in the USA may be more virulent due to a high prevalence of the PV leukocidin

Question 17

Alterations in the [] (altered target mechanism) is the basis for MRSA.

Answer 17

Alterations in the peptidoglycan transpeptidases (altered target mechanism) is the basis for MRSA

Question 18

Staphylococcus epidermidis - species

Answer 18

• Staphylococcus Genus
• Gram + clusters
• aerobic
• catalase +
• coagulase -
• novobiocin susceptible (as are all other CoNS except S. saprophyticus)

Question 19

Staphylococcus epidermidis

Answer 19

• S. epidermidis and a number of other species of CoNS are normal commensals of the skin, anterior nares, and ear canals of humans. With the increasing use of implanted catheters and prosthetic devices, they have emerged as important agents of hospital-acquired infections. Immunosuppressed or neutropenic patients have been particularly affected.
• Organisms may contaminate prosthetic devices from their skin habitat
• Some strains produce a viscous extracellular polysaccharide slime (biofilm) which mediates adhesion to plastic and serves as a mechanical barrier to antimicrobial agents and host defense mechanisms

Question 20

Staphylococcus saprophyticus - species

Answer 20

• Staphylococcus Genus
• Gram + clusters
• catalse +
• coagulase -
• S. saprophyticus colonizes the GI tract and is a significant cause of urinary tract infection particularly among sexually active women
• resistant to novobiacin