Staphylococcus

• less than 30 species recognized today; found on the skin and mucous membrane of warm-blooded animals, including man.

• Characteristics: gram+ cocci in grape-like clusters; facultative anaerobes; catalase positive; can withstand high salt concentrations (7.5 -10 %), extremes in pH, drying, and relatively high temperature (60 °C for 60 mins)

• S. aureus is by far most important human pathogen of group.

• Virulence factors (enzymes and toxins that allow cells to invade tissues and cause disease):

  • Coagulase – cause the coagulation of blood plasma to put a layer of fibrin around cells. Which may protect the cells from phagocytosis in body. Not just produced by S. aureus, also produced by S. intermedius (a pathogen in dogs).

  • Staphylokinase – activates a blood plasma protein (plasminogen) to protease (plasmin) that digests fibrin in clots.

  • Hyaluronidase – digests hyaluronic acid that binds together connective tissue to allow invasion of tissues.

  • Nucleases – digest DNA and RNA.

  • Lipase – allows staphylococci to colonize oily skin surfaces.

  • Penicillinase – destroy penicillins.

  • Hemolysisns – lyse RBCs.

  • Leukocidin – lyses WBCs.

  • Enterotoxins – damage intestinal epitherial cells causing water and electrolyte loss (secretorydiarrhea).

  • Exfoliative toxin – cause loss of epidermal layer of skin.

  • Protein A – a cell wall-associated protein that binds antibody molecules (IgG) nonspecifically and incapacitates them.

  • TSS (toxic shock syndrome) toxin – some strains produce a potent toxin that enters blood and causes fever, rash, vomiting, liver damage, renal failure, etc. Organism can be growing in nasal passages in men, women or children, but this is usually due to a vaginal infection in women.They have found that the use of ultra-absorbent tampons, which absorb large amounts of Magnesium irons, leads to heavy colonization by S. aureus and therefore puts women at risk for this disease.

• Type of disease:

  • Cutaneous infections –associated with skin, hair or nails. Infections of hair follicles, sweat glands, and/or sebaceous glands may lead to boils (furuncles) if follicle or gland abscesses. Clusters of furuncles (larger, deeper boils) are called carbuncles. Superficial skin infections (staphylococcal impetigo) may result in scalded skin syndrome due to production of exfoliative toxin.

  • Systemic infections – staphylococci can infect more tissues that any other organism. Infection spreads from skin infections to other sites. First get a bacteremia and then can spread to bebone (osteomyelitis), the lining of the heart (endocarditis), joints, lungs (pneumonia – rare but 50 % fatal), CNS (meningitis), or virtually any internal organ.

  • Food poisoning – organisms common on skin and in nasal passages so can easily contaminate foods such as custards, pies, cream-filled pastries, potato salad, ham and processed meats etc. Organism resistant to salt, pH extremes, heat, drying, radiation so must refrigerate foods quickly to prevent growth. Some strains produce potent enterotoxins (act on intestinal tract tocause cramping, diarrhea, nausea, committing) that is heat resistant – takes > 100 °C for 30 minutes to inactivate, so reheating food probably will not deactivate toxin. Takes about 106 cells/gm to produce enough toxin to cause symptoms. Symptoms appear within 2 – 6 h and last 24 h

• Immunizations – none available at present but there has been a recent breakthrough that may lead to one.

• Chemotherapy – most now resistant to penicillin ( 95%) due to penicillinase production; methicillin, which is resistant to penicillinases in general, was at one time the drug of choice but MRSA (methicillin-resistant S. aureus) now a major problem. Vancomycin now the only one that seems to work most of the time.

• Other pathogenic staphylococci – coagulase negative staphylococci also can less frequently cause disease in humans, including S. epidermidis, S. capitis, S. hominis, and S. saprophyticus.They can cause infections like those caused by S. aureus and also can cause urinary tract infections (UTIs). These are usually opportunistic pathogens that are introduced by breaks in the skin (as in surgical procedures), especially in immunocompromised individuals (so are common causes of nosocomial infections).

Streptococcus

• Characteristics: gram-positive cocci in chains of two or more (in liquid cultures): facultative anaerobes; catalase negative (have peroxidase to inactivate H2O2); commonly separated based on serological differences in cell wall carbohydrates and on type of lysis of red blood cells. Beta-hemolytic streptococci cause complete lysis of RBCs; alpha-hemolytic strep cause an incomplete lysis with a greenish zone on plates containing RBCs.

• S. pyogenes – most serious pathogen in group A on serotyping. (pyogenic means pus producing.) Found in throat, nasopharynx and sometimes on the skin of humans.

• Virulence factors:

  • Capsule – protects against phagocytosis and aide in attachment.

  • Surface polysaccharides. Including teichoic acids and lipoteichoic acids – protect cells from lysozyme and aid in adherence to epithelial cells

  • M protein – part of fimbriae, gives resistance to phagocytosis and aids in adherence.

  • Hemolysins (streptolysins) – damages RBCs, WBCs, liver, and heart muscle cells.

  • Erythrogenic (pyogenic) toxin – produces red rash and fever associated with scarlet fever (only produced by lysogenized strains).

  • Streptokinase – activates a blood plasma protein (plasminogen) to a protease (plasmin) that digests fibrin in clots.

  • Hyaluronidase – digests hyaluronic acid that binds together connective tissue to allow invasion of tissues.

  • Nucleases – digest DNA and RNA.

• Types of disease:

  • Cutaneous infections – streptococcal impetigo or pyoderma is a superficial skin infection while erysipelas is a deeper skin infection. A much deeper infection is called necrotizing fasciitis (“flesh-eating disease”) in which the organisms are very invasive, spreading deep into the connective tissue where enzymes and toxins destroy the skin and muscle layers beneath. In all cases, the organisms probably enter through a wound in the skin. Strep throat (streptococcalpharyngitis and tonsillitis) is the most common disease caused this organism, especially in children (most individuals build immunity as they get older). Causes swelling, redness, soreness often with pus nodules on the tonsils. If the strain causing the strep throat is lysogenized, it may produce an erythrogenic toxin that is spread throughout the body causing high fever and a red rash all over the body, called scarlantina or scarlet fever.

  • Systemic infections – septicemia (rare); pneumonia (rare); toxic shock (rare); puerperal or childbed fever, and infection of the uterus after childbirth that can be fatal if not controlled.

• Complications that can arise following S. pyogenes infections:

  • Rheumatic fever and acute glomerulonephritis – autoimmune diseases that are triggered by the similarity between the M protein on the surface of the streptococci and certain surface proteins in tissues of the heart, joints and kidneys. Antibodies against the streptococci attack these tissues and cause inflammation and damage. Damage to the joints causes a disabling arthritis. In the worst cases this autoimmune disease can lead to permanent damage to the heart valves or complete renal failure and death.

• Other pathogenic streptococci and related organisms:

  • S. agalactiae – usually only a problem if normal defenses weakened (part of our normal flora). Can cause wound and skin infections, neonatal infections, puerperal infections, and streptococcal endocarditis.

  • Enterococcus faecalis (and other related organisms) – old name was Streptococcus faecalis. Part of normal flora in large intestine. E. faecalis and related organisms can occasionally cause infections of the urinary tract, wounds, blood, appendix, and endocardium. Post-surgical infections with this organism are quite common.

  • Viridians group (means green, referring to alpha-hemolysis of RBCs) – mostly found in oral cavity. Can be introduced into tissue or blood by trauma such as dental procedures leading to bacteremia, meningitis, tooth abscesses, and endocarditis. Including S. mutans, S. sanguis, S.mitis, S. salivarius and others. S. mutans and S. sanguis also cause dental caries. Capsules → plaque → tartar. When these bacteria colonize teeth they (and other organisms that join them) ferment sugars → acids that erode tooth enamel.

  • S. pneumoniae (old name was Diplococcus pneumoniae or pneumococcus) – cause 60 – 70 % of all bacterial pneumonias. Must be encapsulated to be pathogenic (S strains have smooth colonies), which makes them resistant to phagocytosis. R (rough) strains are not virulent because phagocytic cells rapidly kill them. Often get disease after come down with other infection, especially flu. May be from endogenous flora in nasopharynx or from a carrier. IN children this organism is the major cause of otitis media (they have short eustachian tubes and organism can more easily get into their middle ear), which is probably the major cause of medical problems in young children.

• Immunizations – none available at present for group A. Clinical trials are underway for a vaccine for S. mutans (to prevent tooth decay). Do have effective vaccines available for S. pneumoniae that are used primarily for elderly and others at high-risk for pneumonia.

• Chemotherapy – in general, penicillins are the drug of choice. Drug-resistant strains are becoming more prevalent, which could be a major public health problem in the future.