Lec 5 - STAPHYLOCOCCI

Staphylococcus
Properties
 GM + ve cocci
 Cocci arranged in clusters
( Grape like)
 Catalase + ve
 Relatively heat resistant.
 ( catalase degrades H2O2 into
O2 & H2O)
 Catalase is an important
virulence factor because H2O2
is microbicidal & its degradation
limits the ability of neutrophils
 All staphylococci produce
catalase, catalase degrades
H202 into 02 and H20. H202
degradation limits the ability of
neutrophils to kill
 Coagulase, by clotting plasma,
serves to wall off the infected

site, thereby retarding the
migration of neutrophils into
the site. It is only produced by
S. aureus.
Medically important
staphylococcus
Staphylococcus aureus
characterstics
 GM + ve cocci ( clusters )
 Reservoir :Normal flora on nasal mucosa (30%)
& skin
 Colonize skin because of ability to grow at high
salt and lipid concentration.
 β-hemolytic
 Catalase + ve ; Coagulase + ve
 ferments mannitol
 Important secondary pathogen from
patients recovering from influenza and
parainfluenza infection.
 Produce carotenoid pigment that
impart a golden colour to its colonies
 More than 90% of S. aures strain
contain plasmid that encode beta
lactamase the enzyme degrade many
but not all penicillins
 Some strain of S. aures are resistant to
the beta lactamase resistant
penicillin(ex- methicillin). These strain
are kown as methicillin resistant S.
aures (MRSA).
 S. aures causes disease by producing toxins and by
inducing pyogenic inflamation
 Importance toxin produced by S.aures are
 1) enterotoxin- food poisoning heat stable.
Superantigens (stimulate proliferation of T cells and
release of cytokines), stimulate release of
inflammatory mediators in mast cells, increasing fluid
loss, nausea and vomiting
 2) toxic shock syndrome toxin(TSST1)– cause toxic
shock ex tampon-tsst produced locally and enter into
bld stream causing toxemia. Toxic shock occurs in
people who do not have antibody against TSST. Fever,
rash, hypotension, peeling of kin and dysfunction of
several systems.
 3)exfoliatin. – causes scalded skin (SSS) life
threatening dx affecting majorly neonates.-
epidermolytic, leading to separation of the epidermis
Coagulase
 Is an enzyme that causes plasma
to clot by activating prothrombin
to form thrombin . Thrombin
then catalyzes the activation of
fibrinogen to form the fibrin
clot .
 Clumping factor: known as
bound coagulase. It binds fibrin

and helps the organism form
 The toxins produced by S. aureus
are known as superantigens because
of their novel way of interacting with
T-lymphocyte and macrophages. This
interaction causes release of
cytokines IL-1 and IFN-gamma that
mediate TSS.
Transmission
 Spread via the hands &
sneezing
 Lungs of cystic fibrosis
patients
 Food associated with food
poisoning
( Ham or canned meats ,
custard pastries & potato
VIRULENCE FACTOR
 Protein A binds to Fc portion of IgG.
Which is the complement binding
site of the antibody thereby
incapacitates the body function of Ig
inhibits complement fixation and
phagocytosis and opzonisation.
 Beta lactamase a powerful enzyme
that hydrolyses the penicillins.
Hence high resistance to penicillin
and cephalosporin.
Protein A inhibits
phagocytosis
PHAGOCYTE
Fc receptor
Protein A
immunoglobulin
BACTERIUM
Predisposing factors
 Surgery or any break in skin ,
 surgical packing or sutures or any
foreign body ( eg – tampons );
ventilators
 Severe neutropenia (<500/uL)
 IV drug abuse ( IV drug abusers in
general have more S. aureus on
skin than S. epidermis )
 Chronic granulomatous disease
( CGD )
Staphylococcal Aureus
diseases
Diagnosis
 Microscopy useful for pyogenic
infections but not blood infections
or toxin-mediated infections
 Staphylococci grow rapidly when

cultured on nonselective media
 Selective media (e.g., mannitol-

salt agar) can be used to recover S.
aureus in contaminated specimens
Treatment, Prevention, and Control
 Treatment is symptomatic for patients
with food poisoning (although the source
of infection should be identified so that
appropriate preventive procedures can be
enacted)
 Proper cleansing of wounds and use of

disinfectant help prevent infections
 Thorough hand washing and covering of

exposed skin helps medical personnel
prevent infection or spread to other
patients
treatment
 Most S. aures produce beta lactamase-
can be treated with beta lactamase
resistant penicillin(cloxacillin,
vancomycin)
 Combination of beta lactamase sensitive
penicillin( amoxicillin) and beta
lactamase inhibitor(clavulanic acid) is
also useful.
 About 20% of S. aures are methicillin
resistant(MRSA)- treatment with
The treatment of toxic shock syndrome involves
correction of the shock using:-
-Fluids
-Administration of a -lactamase resistant

penicillin such as nafcillin
-Removal of the tampon or debridement of the

infected site as needed.
-Pooled serum globulins, which contain antibodies

against TSST, may be useful.
Staphylococcus epidermidis
• major component skin flora
• opportunistic infections
– less common than S.aureus
• nosocomial infections
– heart valves
S epidermidis is part of the normal
human flora on the skin and
mucous membranes but can cause
infections of intravenous catheters
and prosthetic implants, eg, heart
valves, vascular grafts, and joints. S
epidermidis is also a major cause of
sepsis in neonates and of peritonitis
in patients with renal failure who
are undergoing peritoneal dialysis
through an indwelling catheter.
Strains of S epidermidis that
produce a glycocalyx are more
likely to adhere to prosthetic
implant materials and therefore
are more likely to infect these
implants than strains that do not
produce a glycocalyx.
Identification
• Non-hemolytic
– sheep blood agar
• Does not ferment mannitol
• coagulase-negative
• sensitive to novobiocin
Staphylococcus saprophyticus
• non hemolytic
• urinary tract infections
• coagulase-negative
– not differentiated from S. epidermidis
• resistant to novobiocin
S saprophyticus causes urinary
tract infections, particularly in
sexually active young women.
Most women with this infection
have had sexual intercourse within
the previous 24 hours. This
organism is second to E coli as a
cause of community-acquired
urinary tract infections in young
women.
Antibiotic therapy
 90% or more of S aureus strains
are resistant to penicillin G.
 Most strains produce -
lactamase.
 Such organisms can be treated

with -lactamase-resistant
penicillins, eg, nafcillin,
methicillin or cloxacillin
Summary Figure (Identification Scheme)
Note: Strep. viridans
GRAM POSITIVE COCCI are alpha hemolytic and
negative for all the tests
below
Catalase
+
Staphylococcus (Clusters)
-
Streptococcus (pairs & chains)
Coagulase Hemolysis
+
S. aureus
-
S. epidermidis
(1) BETA: Bacitracin
+ S.pyogenes (group A)
ß hemolytic nonhemolytic (usually)

CAMP/Hippurate + S. agalactiae (group B)
S saprophyticus
mannitol mannitol (2) ALPHA: Optochin/Bile Solubility + S. pneumoniae
yellow
mannitol white
- Does not ferment mannitol
fermentation
- Non hemolytic (3) GAMMA: Bile Esculin + 6.5% NaCl + Group D*
Enterococcus
- S epidermidis is sensitive to novobiocin.
- S saprophyticus is resistant to
Bile Esculin + 6.5% NaCl
- Group D*
Non-Enterococcus
novobiocin.
(*can also be beta or alpha hemolytic)
You’re in the clinical laboratory looking at a Gram stain
when the laboratory technician comes up to you and
says, “I think your patient has Staph epi [short for
Staphylococcus epidermidis] bacteremia.” Which one
of the following sets of results did the tech find with
the organism recovered from the blood culture?
(A) Gram-positive cocci in chains, catalase-positive,
coagulase-positive
(B) Gram-positive cocci in chains, catalase-negative,
coagulase-negative
(C) Gram-positive cocci in clusters, catalase-positive,
coagulase-negative
(D) Gram-positive cocci in clusters, catalase-negative,
coagulase-positive
(E) Gram-positive diplococci, catalase-negative,
coagulase-positive
Superantigen production by
Staphylococcus aureus is involved in
the pathogenesis of which one of the
following diseases?
(A) Impetigo
(B) Osteomyelitis
(C) Scalded skin syndrome
(D) Septicemia
(E) Toxic shock syndrome
The main reason why methicillin-resistant
Staphylococcus aureus
(MRSA) strains are resistant to methicillin and
nafcillin is:
(A) they produce β-lactamase that degrades the
antibiotics.
(B) they have altered penicillin-binding proteins
that have reduced binding of the antibiotics.
(C) they have mutant porin proteins that
prevent the antibiotics
from entering the bacteria.
(D) they have plasmid-encoded export proteins
that remove the
drug from the bacteria.

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Staphylococcus

serves to wall off the infected

bound coagulase. It binds fibrin

 Staphylococci grow rapidly when

 Selective media (e.g., mannitol-

 Proper cleansing of wounds and use of

 Thorough hand washing and covering of

-Administration of a -lactamase resistant

-Removal of the tampon or debridement of the

-Pooled serum globulins, which contain antibodies

 Such organisms can be treated

ß hemolytic nonhemolytic (usually)

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