Staphylococcus part 1

Staphylococcus


Introduction
The staphylococci are gram-positive spherical cells, usually arranged in grape-like irregular clusters. They grow readily on many types of media and are active metabolically, fermenting carbohydrates and producing pigments that vary from white to deep yellow. Some are members of the normal flora of the skin and mucous membranes of humans; others cause suppuration, abscess formation, a variety of pyogenic infections, and even fatal septicemia. The pathogenic staphylococci often hemolyze blood, coagulate plasma, and produce a variety of extracellular enzymes and toxins. The most common type of food poisoning is caused by a heat-stable staphylococcal enterotoxin. Staphylococci rapidly develop resistance to many antimicrobial agents and present difficult therapeutic problems.
The genus Staphylococcus has at least 35 species. The three main species of clinical importance are Staphylococcus aureus, Staphylococcus epidermidis, and Staphylococcus saprophyticus. Staphylococcus aureus is coagulase-positive, which differentiates it from the other species. S aureus is a major pathogen for humans. Almost every person will have some type of S aureus infection during a lifetime, ranging in severity from food poisoning or minor skin infections to severe life-threatening infections. The coagulase-negative staphylococci are normal human flora and sometimes cause infection, often associated with implanted appliances and devices, especially in very young, old, and immunocompromised patients. Approximately 75% of these infections caused by coagulase-negative staphylococci are due to S epidermidis; infections due to Staphylococcus lugdunensis, Staphylococcus warneri, Staphylococcus hominis, and other species are less common. S saprophyticus is a relatively common cause of urinary tract infections in young women. Other species are important in veterinary medicine.


Morphology & Identification
Typical Organisms
Staphylococci are spherical cells about 1 m in diameter arranged in irregular clusters. Single cocci, pairs, tetrads, and chains are also seen in liquid cultures. Young cocci stain strongly gram-positive; Staphylococci are nonmotile and do not form spores. Under the influence of drugs like penicillin, staphylococci are lysed.
Micrococcus species often resemble staphylococci. They are found free-living in the environment and form regular packets of four or eight cocci. Their colonies can be yellow, red, or orange.
Culture
Staphylococci grow readily on most bacteriologic media under aerobic or microaerophilic conditions. They grow most rapidly at 37 °C but form pigment best at room temperature (20–25 °C). Colonies on solid media are round, smooth, raised, and glistening. S aureus usually forms gray to deep golden yellow colonies. S epidermidis colonies usually are gray to white on primary isolation; many colonies develop pigment only upon prolonged incubation. No pigment is produced anaerobically or in broth.
Growth Characteristics
The staphylococci produce catalase, which differentiates them from the streptococci. Staphylococci slowly ferment many carbohydrates, producing lactic acid but not gas. Proteolytic activity varies greatly from one strain to another. Pathogenic staphylococci produce many extracellular substances, which are discussed below.
Staphylococci are relatively resistant to drying, heat (they withstand 50 °C for 30 minutes), and 9% sodium chloride but are readily inhibited by certain chemicals, eg, 3% hexachlorophene.
Staphylococci are variably sensitive to many antimicrobial drugs. Resistance falls into several classes:
1. B-Lactamase production is common, is under plasmid control, and makes the organisms resistant to many penicillins (penicillin G, ampicillin, ticarcillin, piperacillin, and similar drugs). The plasmids are transmitted by transduction and perhaps also by conjugation.
2. Resistance to nafcillin (and to methicillin and oxacillin) .
3. In the United States, S aureus is considered to be susceptible to vancomycin if the minimum inhibitory concentration (MIC) is 2 g/mL. The mechanism of resistance is associated with increased cell wall synthesis.
4. Plasmid-mediated resistance to tetracyclines, erythromycins, aminoglycosides, and other drugs is frequent in staphylococci.
5. "Tolerance" implies that staphylococci are inhibited by a drug but not killed by it, there is great difference between minimal inhibitory and minimal lethal concentrations of an antimicrobial drug. Patients with endocarditis caused by a tolerant S aureus may have a prolonged clinical course compared with patients who have endocarditis caused by a fully susceptible S aureus. Tolerance can at times be attributed to lack of activation of autolytic enzymes in the cell wall.


Antigenic Structure
Staphylococci contain antigenic polysaccharides and proteins as well as other substances important in cell wall structure. Peptidoglycan, a polysaccharide polymer containing linked subunits, provides the rigid exoskeleton of the cell wall. Peptidoglycan is destroyed by strong acid or exposure to lysozyme. It is important in the pathogenesis of infection: It elicits production of interleukin-1 (endogenous pyrogen) and opsonic antibodies by monocytes, and it can be a chemoattractant for polymorphonuclear leukocytes, have endotoxin-like activity, and activate complement.
Teichoic acids, which are polymers of glycerol or ribitol phosphate, are linked to the peptidoglycan and can be antigenic. Antiteichoic acid antibodies detectable by gel diffusion may be found in patients with active endocarditis due to S aureus.
Protein A is a cell wall component of many S aureus strains that binds to the Fc portion of IgG molecules except IgG3. The Fab portion of IgG bound to protein A is free to combine with a specific antigen. Protein A has become an important reagent in immunology and diagnostic laboratory technology; Some S aureus strains have capsules, which inhibit phagocytosis by polymorphonuclear leukocytes unless specific antibodies are present. Most strains of S aureus have coagulase, or clumping factor, on the cell wall surface; coagulase binds nonenzymatically to fibrinogen, yielding aggregation of the bacteria.