• Except for Staph. aureus, all other
staphylococci are coagulase negative.
• They are salt tolerant and often hemolytic.
• Staph. lugdunensis can gives a positive
slide-coagulase test (bound coagulase) but
a negative tube-coagulase test (free
coagulase). DNAse negative. Commensal .
Can cause osteomyelitis, septicaemia, and
• Final Identification requires biotype analysis.
Staphylococci are Gram-positive cocci 1 µm in diameter.
They form clumps/clusters.
► S. aureus colonizes the nasal passage and axillae.
► S. epidermidis is a common human skin
► S. saprophiticus is a commensal of female
► Other species of staphylococci are infrequent
human commensals. Some are commensals of
► Gram positive cocci
► Morphologically striking clusters, due to division in
3 successive planes
- grape-like clusters (Greek: grape = staphylos)
► Facultative anaerobes
- grow better aerobically
- some better in presence of CO2
► Golden pigment
- produced by many strains (Latin: gold = aureus)
- especially with extended incubation
► S. aureus very resistant to drying, certain
disinfectants (HgCl2, phenol), salt (7.5 - 10.%),
Three Important Species
- usually coagulase negative, disease in
compromised hosts only
- minor abscesses
- postoperative endocarditis
- community acquired urinary tract
infections in females
► S. aureus
- coagulase positive
* skin infections (impetigo), boils, styes
- serious disease possible
* deep abscesses, wound infections,
* purulent arthritis, pneumonia, meningitis,
* exfoliative skin disease
* infection of spermatic cord stump following
* cattle: mastitis, favored by automatic milking
- also causes intoxications / food posioning
Golden Yellow growth of Staph. aureus with
Gram stain under the microscope.
TOXINS & ENZYMES
►(a) a-toxin (b) ß-toxin
(c) d-toxin (d) g-toxin
►Superantigens: enterotoxins and toxic
shock syndrome toxins
►Epidermolytic (exfoliative) toxin (ET)
This toxin causes the scalded skin syndrome in
neonates, with widespread blistering and loss of the
Other Extra cellular Proteins:
Many strains of S aureus express a
plasminogen activator called Staphylokinase.
As with coagulase there is no evidence that
staphylokinase is a virulence factor, although
it seems reasonable to imagine that localized
fibrinolysis might aid in bacterial spreading.
► S aureus expresses many potential virulence
(1) Surface proteins that promote colonization of
(2) Factors that probably inhibit phagocytosis
(capsule, immunoglobulin binding protein A).
(3) Toxins that damage host tissues and cause
disease symptoms. Coagulase-negative
staphylococci are normally less virulent and
express fewer virulence factors.
S. epidermidis readily colonizes implanted
A) Abscess/Furuncle: (``Phoora``)
Localized, begins when organism enters hair
follicle. Organism spreads to surrounding
tissues. Tiny lesion becomes larger and
swollen, inflamed. The localized lesion walled
off by deposition of fibrin by the tissue, walling
off is to prevent the Staph. infection from
going further. There is a lot of pus (organism
is Pyogenic). The main Pyogenic organisms are
Lancing: Allows drainage
to "get rid of the
This gets rid of the
material present so that
antibiotics can work.
(Antibiotics cannot diffuse
through non-living tissue.)
... Drainage does get rid of
some of the organisms,
but more importantly gets
rid of the fluid in which
they reside. After lancing,
the abscess is treated
topically with penicillin,
orally with penicillin, or
some other suitable
S. aureus gains access to the blood. This
may result from a cutaneous infection,
contamination during surgery, or from the
organism (S.a. is a skin resident) entering
via a scratch on the skin. Blood poisoning
is a chronic septicemia usually caused by
C. Impetigo: Occurs in neonates (impetigo of
the newborn) and in addition there are many
cases in older children.
In newborns: The organism overgrows the skin
rapidly, owing to the lack of other resident
bacteria. The organism may then enter the
dermis through an abrasion or a hair follicle.
Causes clustered lesions anywhere on the
body, which crust over, then break open. The
disease is spread further by scratching and
rubbing against sheets. Prevented in nurseries
by using lotions containing hexachlorophene.
Treat with penicillin.
In children: Similar, but not as aggressive spreading in older children
because the resident skin bacteria are well established. Is
considered contagious, spread easily by children wrestling and
fighting. Occurs mostly on face.
►D) Staphylococcal Scalded Skin Syndrome
Usually in neonates, when a strain of S.a. which
excretes exfoliatin (a pathogenic factor) invades the
skin. Rapid invasion of the skin occurs in neonates
because competing bacteria have not yet become
* The skin becomes reddened
and sloughs off rapidly, causing
causing drastic fluid loss.
* May be fatal.
* Treat with penicillin.
E) Minor Skin Infections:
►Pimples-localized and minor. Infection of
single hair follicle.
►Sty--minor Staph. skin infection.
►Follicle involved is the
“Acne and pimples are
► F) Toxic Shock Syndrome (TSST-1):
Super-absorbent types of tampon or wound
packing material can harbor Staph. aureus and
Low Mg availability to Staph. aureus triggers production
of TSST-1. Labile B/P, increase nausea, fever, rash,
finger tips peel and swell. May be fatal.
Penicillin is treatment.
► G) Staphylococcal Food Poisoning:
Factor is enterotoxin F. It grows in certain foods.
(Cream filled and starchy.) e.g. Potato salads.
Organism gets in easily by handling potatoes and eggs.
It is a food toxicity, not infectious disease. It lasts 24
hours and the incubation period is two hours. There is
► G) Staphylococcal Food Poisoning:
Factor is enterotoxin F. It grows in
certain foods. (Cream filled and
Potato salad-organism gets in easily
by handling potatoes and eggs. It is
a food toxicity, not infectious
disease. It lasts 24 hours and the
incubation period is two hours.
There is no treatment.
► H. Osteomyelitis:
Staph. aureus gains
access to bone and
colonizes surface and
Becomes chronic. Can
be surgically removed
but surgery damages
bone tissue. Treatment
► I. Pyelonephritis:
Staph. aureus infection
of the kidneys.
Be mindful that most
cases of Pyelonephritis
are caused by
organism causes this
ascends from bladder
infection (cystitis) or
Identification of Staphylococci
in the Clinical laboratory
In addition to the several lab tests
(Catalase, glucose fermentation,
coagulase, etc.) in lab for identification
of G+ cocci, there are a few useful
media used in isolation and
identification of Staphylococcus:
►The catalase test is important in
distinguishing streptococci (catalase-
negative) from staphylococci which
are catalase positive.
►The test is performed by flooding an
agar slant or broth culture with several
drops of 3% hydrogen peroxide.
Catalase-positive cultures bubble at
►The test should not be done on blood
agar because blood itself will produce
► Blood Agar: Routinely used also differentiates
between S. aureus and epidermitis, colonies > 1
mm in diameter
► Mannitol-Salt Agar:MSA agar is useful in selectively
isolating Staphylococcus species from clinical
specimens, as well as skin, etc. It contains 7.5%
NaCl to inhibit all bacteria except Staph.
► DNAase Agar: This medium contains DNA. Colonies
of Staph. aureus produce DNAase, and the area
around the colonies clears, while the other species
don't produce this enzyme and no clearing occurs.
► Phage Typing: Used to identify different strains of
Staph. aureus. Often used to trace source of a
Staph. aureus strain which has caused a rash of
infections in particular O.R.
►Multiple antibiotic resistance is
increasingly common in S aureus and
►Methicillin resistance is indicative of
multiple resistance. Methicillin-resistant
►(MRSA) causes outbreaks in hospitals
and can be epidemic.
Resistance of Staphylococci to
►Hospital strains of S aureus are often
resistant to many different antibiotics.
Indeed strains resistant to all clinically
useful drugs, apart from the glycopeptides
vancomycin and teicoplanin, have been
described. The term MRSA refers to
methicillin resistance and most methicillin-
resistant strains are also multiply resistant
to other antibiotics.
► Prevention & Control.
1. Hand washing.
2. Universal Infection control methods .
►Patients and staff carrying epidemic strains,
particularly MRSA, should be isolated. Patients
may be given disinfectant baths or treated with
a topical antibiotic to eradicate carriage of
►Infection control programs are used in most
Staphylococcus aureus (MRSA)
aureus (MRSA) is a bacterium responsible
for several difficult-to-treat infections in
►MRSA is any strain of Staphylococcus aureus
that has developed resistance to beta-
lactam antibiotics, which include the
penicillins (methicillin, dicloxacillin, nafcillin,
oxacillin, etc.) and the cephalosporins.
►mecA gene is
►Troublesome in hospitals and nursing
►Patients with open wounds, invasive
devices, and weakened immune systems
are at greater risk of infection than the
►Treatment of MRSA:
• Vancomycin , teicoplanin are glycopeptide
antibiotics used to treat MRSA infections.
• Linezolid is now considered drug of choice.
Staphylococcus aureus (VISA)
daptomycin, and tigecycline are used to
treat severe infections that do not respond
to glycopeptides such as vancomycin.
Panton Valentine Leucocidin
Panton-Valentine leukocidin (PVL) is a cytotoxin - one of
the β-pore-forming toxins.
The presence of PVL is associated with increased virulence
of certain strains (isolates) of Staphylococcus aureus.
Present in the majority of community-associated
Methicillin-resistant Staphylococcus aureus (CA-MRSA)
Cause of necrotic lesions involving the skin or mucosa,
including necrotic hemorrhagic pneumonia.
PVL creates pores in the membranes of infected cells. PVL
is produced from the genetic material of a bacteriophage
that infects Staphylococcus aureus, making it more
The methicillin-resistance gene (mecA) can be passed from one bacterial cell to another as a transposable
element (a piece of DNA that inserts itself into the bacterial chromosome). The pvl gene is normally
present in the genome of the S. aureus bacteriophage and encodes a toxin known as the PVL protein.
Upon infection, the phage can insert its DNA into the bacterial chromosome transforming a non-toxic
bacterial cell into a bacterium capable of producing the PVL toxin. The mecA gene can be acquired by
both CA-MRSA and HA-MRSA. The pvl gene, on the other hand, is found normally in CA-MRSA but not in