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source of outbreaks.
Grows acrobically a yellow or gold
colonies on blood agar catalase-positive (this
differentiates them from the catalase-negative
streptococci). Pathogenicity
Other test used to differentiate the A variety of enzymes and toxins are produced
more virulent S.aureus from the less pathogenic by Staphylococcus aureus, although no one
S.epidermidis include the following. strain produces the whole range listed Table
11.2. The two mostb important are coagulase
Coagulase test . S. aureus coagulates and enterotoxin. Coagulase is the best correlate
dilute human serum or rabbit plasma (i.e. it is of pathogenicity. Some of the diseases caused
coagulase-positive), whereas S. epidermidis by S. aureus are:
does not (coagulase-negative). This test could
be done either in a test tube (the tube test), Superficial infection: common agent of
wich requires overnight incubation, or on a slide boils, carbuncles, pustules, abscesses,
( the slide test), wich is a rapid test. conjunctivitis and wound infections;
rarely causes oral infections; may cause
Ptotein A-latex agglutination test. angular cheilitis (together with the
Protein A, synthesized by almost all stains of yeast Candida) at the angles of mouth
S.aureus, has a special affinity to the Fc Food-posioning (vomiting and diarrhea)
fragment of immunoglobulin G (IgG). Hence caused by enterotoxins
when latex particles coated with IgG (and
fibrinogen) are mixed with an emulsified Table 11.2 Toxxin and
suspension of S.aureus on a glass slide, vivible enzymes produced by
Staphylococcus aureus
agglutination of the latex particles occurs; no
Toxin/enzymes Activity
such reaction is seen with S. epidermidis Toxins
Cytotoxins (, , , )
Other tests. These include the
Leucocidin
phosphatase test, DNAase test and mannitol
fermentation test (most strains of S. aureus
form acid from mannitol, while few S.
epidermidis do so) Toxic shock syndrome, also caused bya
an enteroxin
Deep infection: osteomyelitis,
Typing of Staphylococcus aureus endocarditis, septicaemia, pneumonia
Typing is important to determine the source of Predisposing factors for infection are minor and
an outbreak of infection. This was commonly major breaks in the skin, foreign bodies such a
done by the pattern of suspectibility to a set of sutures, low neurotrophil levels and injecting
more than 20 bacteriophages phagestyping drug abuse.
and sero typing. These methods are currenty
Treatment and prevention 'tolerance, where the organism is
inhibited but not killed by the
The vast majority (>80%) of strains are resistant
antibiotic(i.e. there is a large difference
to -lactam drugs, and some to a number of
between minimum inhibitory
antibiotics. The latter phenomenon
concentration and minimum
(multiresistance) is common, particularly in
bactericidal concentration), leading to
strains isolated from hospitals; these cause
prolonged course of infections (e.g.
hospital (nosocomial) infection. Penicilin
staphylococcal infactive endocarditis)
resistance is due to the production of -
lactamase encoded by plasmids. The enzyme Staphylococcus epidermidis
destroys the efficacy of antibiotics with a -
lactam ring (i.e. the penicillin group drugs). Habitat and tranmision
Antibiotics actives against This species found on the skin surface, and is
Staphylococcus aureus include penicillin for spread by contact
sensitive isolates, flucloxacillin (stable againts -
lactamase), erythromycin, fusidle acid (udeful
for skin infections ), cephalosporins and Cluture and identification
vancomycin.
Grows as white colonies on blood agar, hence
Cleanliness, hand-washing and aseptic the earlier name S albus; catalase-positive;
management of lesions reduce the spread of catalase negative; biochemically characterized
staphylococci. by commercially available kits (e.g. APIStaph).