STAPHYLOCOCCI

Definition: Gram +ve cocci

arranged in clusters.
All Catalase test +ve #
[ streptococci] .
All Oxidase negative #
[Neisseria]
2
Gram positive cocci in clusters
staphylococci
MSA NA BA
White colonies 1
Pigmented golden
COLONIALyellow
MORPHOLOGY
Pigmented colonies of staph
on NA
 2
Complete ( β )
HEAMOLYSIS
Hemolytic staphylococci on
BA
Hemolytic staphylococci on BA
Ferment mannitol 3 Don’t Ferment
FERMENTATION
) yellow color ( mannitol (red
color )
 Staphylococci on mannitol salt agar
pathogenic (F+) non pathogenic(F-)
Staphylococci on mannitol salt agar
pathogenic (F+)
Oxidase 4 Catalase
ve- BIOCHEMICAL ve+
REACTION
 Differential Characteristics

Catalase
2H2O2  O2 + 2H2O
Streptococci vs. Staphylococci
Catalase POS

Staphylococcus
Catalase NEG
 Differential
Characteristics
Coagulase

Fibrinogen   Fibrin S. aureus

 Staphylococcus
aureus

Coagulase POS

Coagulase NEG
COAGULASE TEST
 Staphylococci

Coagulase +ve Coagulase –ve

(pathogenic) (non-pathogenic)

Staph.
Staph. aureus Staph. epidermidis
saprophyticus
Difference between pathogenic and non pathogenic

Pathogenic Non-pathogenic
1- coagulase +ve 1- Coagulase –ve.

Culture media 2- Pigmented golden yellow on NA 2- White colonies.

3- Haemolysis on BA. 3- No hemolysis on BA

4- Ferment mannitol on MSA . 4- Don not ferment
mannitol.

Biochemical Coagulase +ve Coagulase –ve

reactions of Mannitol fermentation +ve Mannitol fermentation –ve
staphylococci

1-Novobiocin sensitive.
* S. epidermidis.

2-Nov. resistant
* S. saprophyticus.
Novobiocin test
Staph epidermidis ---S Staph saprophytics ---R
Antigenic structure

Staph. aureus has several cell wall components and antigens:

1- Peptidoglycan polymer.

2- Telchoic acids that mediate adherence of the organism to

mucosal cells.
3- Protein A: 90% of staph. aureus posses this antigen. It is
antiphagocytic. Protein A binds IgG molecule non-specifically
through Fc portion leaving specific Fab sites free to combine
with specific antigen. When suspension of such sensitized
staphylococci is treated with homologous (test) antigen, the
antigen combines with free Fab sites of IgG attached to staph
cells leading to visible clumping of staphylococci within two
minutes. It is known as “coagglutination”.
 Antigenic structure
4- Clumping factor: which binds to
fibrinogen yielding aggregation of the
bacteria.
5- Capsular polysaccharide: A few strains of
staph. aureus are encapsulated and tend to
be more virulent that non capsulated
strains.
6- Surface receptors: for specific bacterial
phages, permit phage typing for
epidemiological purposes.
Toxins and Enzymes produced by Staph. aureus

Toxins : Enzymes :
 Hemolysin  Coagulase enzyme

 Leucocidin  Staphylokinase

 Toxic shock syndrome  Hyaluronidase

toxin-1 (TSST-1)  B- lactamase

 Exfoliative toxin (penicillinase )

 Enterotoxin  DNAase
25
Diseases produced by Staph. aureus

 Pyogenic infection (enzymes)

Disseminated
Focal

 Toxin mediated:
 Food poisoning .
 Toxic shock syndrome .
 Scalded skin syndrome.
 Staphylococcal Disease
Range from localized to systemic
Localized cutaneous infections – invade skin
through wounds, follicles, or glands
folliculitis – superficial inflammation of hair follicle;
usually resolved with no complications but can
progress
furuncle – boil; inflammation of hair follicle or
sebaceous gland progresses into abscess or pustule
carbuncle – larger and deeper lesion created by
aggregation and interconnection of a cluster of
furuncles
impetigo – bubble-like swellings that can break and
peel away; most common in newborns
27
28
Nonbullous Lesions of Impetigo

Figure 21.4
 Staphylococcal Disease
Systemic infections
osteomyelitis – infection is established in
the metaphysis; abscess forms
bacteremia - primary origin is bacteria
from another infected site or medical
devices; endocarditis possible

30
31
Bacterial Endocarditis

Figure 23.4
 Staphylococcal Disease
Toxigenic disease
food intoxication – ingestion of heat stable
enterotoxins; gastrointestinal distress
staphylococcal scalded skin syndrome –
toxin induces bright red flush, blisters, then
desquamation of the epidermis
 toxic shock syndrome – toxemia leading
to shock and organ failure

33
Lesions of Skin Syndrome

Figure 21.5
35
Staphylococcal Food Poisoning

Pathogen Staphylococcus aureus

Symptoms Nausea, vomiting, and
diarrhea

Intoxication/Infection Intoxication
Enterotoxin
(superantigen)
Diagnosis Phage typing
Treatment None
Events in Staphylococcal Food
Poisoning

Figure 25.6
 Carriers of Staph. aureus
Importance in hospital infection:
· Carriage of staph. by medical personnel→hospital
infection (nosocomial infection of patients) or food
poisoning.
 Carriage in :
 Nose.
§ Hands.
 Tracing the source of infection =
(epidemiological study of the isolated
strains)phage typing.
 Detection of carriers  nasal or skin
swabblood agar. staph (identification).
40
Phage typing
Phage Typing

Figure 10.13
 Methicillin-resistant Staph.aureus (MRSA)

 Resistant to all beta lactam antibiotics.

 resistant to other drugs (aminoglycosides).
  sensitive to vancomycin.
 Other Staphylococci
Coagulase-negative staphylococcus;
frequently involved in nosocomial and
opportunistic infections
S. epidermidis – lives on skin and mucous
membranes; endocarditis, bacteremia, UTI
S. saprophyticus – infrequently lives on
skin, intestine, vagina; UTI

45
Coagulase-Negative Staphylococci

Staphylococcus epidermidis

S. saprophyticus
Novobiocin test
Staph epidermidis ---S Staph saprophytics ---R
 Staph. saprophytics:
urinary tract infections in
young females
Staphylococcal Biofilms

Figure 21.3