Staphylococci (Lecture)

STAPHYLOCOCCI
Classification
• Family Staphylococcaceae
• Genus Staphylococcus
S. aureus
• Species S. saprophyticus
S. epidermidis
more
than 40
species
Introduction
• Staphylococci and streptococci constitute
the main group of medically important
gram positive bacteria
• There are also bacilli that are pathogenic
such as Anthrax and the Clostridia group.
These are also spore forming organisms
• There are also some other gram positive
rods such as Listeria, Lactobacillus,and
Cornybacterium diptheria
Staphylococci
• Staphylococci stain dark purple with the gram
stain.
• There are three medically important forms of
staphylococci
• Staphylococcus aureus – this causes many types
of infections, food poisoning,and toxic shock
• Staphylococcus epidermidis – this is a cause of
infections in indwelling catheters
• Staphylococcus saprophyticus that is an ongoing
cause of cystitis in women
INTRODUCTION
• Staphyloccocci - derived from Greek
“stapyle” (bunch of grapes)
• Gram positive cocci arranged in clusters
• Hardy organisms surviving many non
physiologic conditions
• Include a major human pathogen and
skin commensals
Staphylococci
• Found in the air and on surfaces
• Very resistant to drying and dehydration
• They produce Catalase which is one of their distinguishing
characteristics* this is an enzyme vital to the survival of
many aerobic bacteria
• The most virulent form of staphylococcus, SA also
secretes coagulase, that causes citrated plasma to clot.
These are referred to as coagulase positive
• There are other staph that do not have this ability and are
labeled coagulase negative
Grouping for Clinical
Purposes
• 1. Coagulase positive Staphylococci
– Staphylococcus aureus
• 2. Coagulase negative Staphylococci

– Staphylococcus epidermidis
– Staphylococcus saprophyticus
A. Staphylococcus aureus
• Major human pathogen
• Habitat - part of normal flora in some humans

and animals
• Source of organism - can be infected human

host, carrier, fomite or environment
Staphylococcus aureus
• Carried by 20-40 % of healthy individuals
in their mouths or on their skin
• It also found in their nasal mucosa
• Carriers can serve as a source of infections
as well as inanimate objects – these are
called fomites
Characteristics of
Staphylococcus
• Gram-positive cocci 0.5-1.5 m in diameter
occurring singly, in pairs or short chains, and
as irregular grape-like clusters (staphyle=a
bunch of grapes)
• Catalase positive
• Growth on sheep blood and chocolate agar but
not MacConkey or eosin methleye blue agar
• No growth requirement for CO2
Pathogenicity
• “Staph’ infections result when staphylococci
breach the body’s physical barriers
• Entry of only a few hundred bacteria can result
in disease
• Pathogenicity results from 3 features
– Structures that enable it to evade phagocytosis
– Production of enzymes
– Production of toxins
Structural Defenses Against
1.
Phagocytosis
Protein A coats the cell surface
– Interferes with humoral immune responses by
binding to class G antibodies
– Inhibits the complement cascade
2. Clumping Factor (Bound coagulase)
– Converts the soluble blood protein fibrinogen in
insoluble fibrin molecules that form blood clots
– Fibrin clots hide the bacteria from phagocytic cells
Structural Defenses Against
Phagocytosis
3. Synthesize loosely organized polysaccharide

slime layers (often called capsules)
– Inhibit chemotaxis of and phagocytosis by leukocytes
– Facilitates attachment of Staphylococcus to artificial
surfaces
Enzymes
1. Coagulase
– Triggers blood clotting
2. Hyaluronidase
– Breaks down hyaluronic acid, enabling the bacteria
to spread between cells
3. Staphylokinase
– Dissolves fibrin threads in blood clots, allowing
Staphylococcus aureus to free itself from clots
Enzymes (cont.)
4. Lipases
– Digest lipids, allowing staphylococcus to grow on
the skin’s surface and in cutaneous oil glands
5. -lactamase
– Breaks down penicillin
– Allows the bacteria to survive treatment with -
lactam antimicrobial drugs
Toxins
• Staphylococcus aureus produces different types
of toxins
1. Cytolytic toxins
– Disrupts the cytoplasmic membrane of a variety of
cells
– Leukocidin can lyse leukocytes specifically
Virulence Factors: Exotoxins
• Cytolytic (cytotoxins; cytolysins)
– Alpha toxin - hemolysin
• Reacts with RBCs
– Beta toxin
• Sphingomyelinase
– Gamma toxin
• Hemolytic activity
– Delta toxin
• Cytopathic for:
– RBCs
– Macrophages
– Lymphocytes
– Neutrophils
– Platelets
• Enterotoxic activity
– Leukocidin
Toxins (cont.)
2. Exfoliative toxins
• Causes the patient’s skin cells to separate from each other and slough off the body
3. Toxic-shock-syndrome toxin
– Causes toxic shock syndrome
4. Enterotoxins
– Stimulate the intestinal muscle contractions, nausea, and intense vomiting
associated with staphylococcal food poisoning
Virulence factors of Staphylococcus aureus
III.
Staphylococcal Diseases
• 3 categories
– Noninvasive Disease
• Food poisoning from the ingestion of enterotoxin-
contaminated food
– Cutaneous Disease
• Various skin conditions including scalded skin syndrome,
impetigo, folliculitis, and furuncles
Staphylococcal Diseases
– Systemic Disease
• Toxic shock syndrome-TSS toxin is absorbed into
the blood and causes shock
• Bacteremia-presence of bacteria in the blood
• Endocarditis-occurs when bacteria attack the lining
of the heart
• Pneumonia-inflammation of the lungs in which the
alveoli and bronchioles become filled with fluid
• Osteomyelitis-inflammation of the bone marrow and
the surrounding bone
Natural history of disease
• Many neonates, children, adults -
intermittently colonised by S. aureus
• Usual sites - skin, nasopharynx,
perineum
• Breach in mucosal barriers - can enter
underlying tissue
• Characteristic abscesses
• Disease due to toxin production
DISEASES
• Due to direct effect of • Toxin mediated
organism – Food poisoning
– Local lesions of – toxic shock
skin syndrome
– Deep abscesses – Scalded skin
– Systemic syndrome
infections
Factors predisposing to S.
aureus infections
• Host factors • Pathogen Factors
– Breach in skin – Catalase (counteracts
– Chemotaxis defects host defences)
– Opsonisation defects – Coagulase
– Neutrophil functional – Hyaluronidase
defects – Lipases (Imp. in
– Diabetes mellitus disseminating
infection)
– Presence of foreign
– B lactasamase(ass.
bodies
With antibiotic
resistance)
SKIN LESIONS
• Boils
• Styes
• Furuncles(infection of hair follicle)
• Carbancles (infection of several hair follicles)
• Wound infections(progressive appearance of
swelling and pain in a surgical wound after
about 2 days from the surgery)
• Impetigo(skin lesion with blisters that break
and become covered with crusting exudate)
DEEP ABSCESSSES
• Can be single or multiple
• Breast abscess can occur in 1-3% of
nursing mothers in puerperiem
• Can produce mild to severe disease
• Other sites - kidney, brain from septic
foci in blood
Systemic Infections
• 1. With obvious focus
– Osteomyelitis, septic arthritis
• 2. No obvious focus
• heart (infective endocarditis)
• Brain(brain abscesses)
• 3. Ass. With predisposing factors
– multiple abscesses, septicaemia(IV drug
users)
– Staphylococcal pneumonia (Post viral)
B. TOXIN MEDIATED
DISEASES
• 1. Staphylococcal food poisoning
– Due to production of entero toxins
– heat stable entero toxin acts on gut
– produces severe vomiting following a very
short incubation period
– Resolves on its own within about 24 hours
2. Toxic shock syndrome
• High fever, diarrhoea, shock and erythematous
skin rash which desquamate
• Mediated via ‘toxic shock syndrome toxin’
• 10% mortality rate
• Described in two groups of patients
– ass. With young women using tampones during
menstruation
– Described in young children and men
3. Scalded skin syndrome
• Disease of young children
• Mediated through minor Staphylococcal
infection by ‘epidermolytic toxin’
producing strains
• Mild erythema and blistering of skin
followed by shedding of sheets of
epidermis
• Children are otherwise healthy and most
eventually recover
Antibiotic sensitivity pattern
• Very variable and not predictable
• Very imp. In Pt. Management
• Mechanisms
– 1.B lactamase production - plasmid mediated
• Has made S. aureus resistant to penicillin group of
antibiotics - 90% of S. aureus (Gp A)
• B lactamase stable penicillins (cloxacillin, oxacillin,
methicillin) used
– 2. Alteration of penicillin binding proteins
• (Chromosomal mediated)
• Has made S. aureus resistant to B lactamase stable
penicillins
• 10-20% S. aureus Gp (B) GH Colombo/THP resistant to
all Penicillins and Cephalasporins)
• Vancomycin is the drug of choice
• Tested in lab using methicillin
• Referred to as methicillin resistant S. aureus
(MRSA)
• Emerging problem in the world
• In Sri Lanka prevalence varies from 20- 40% in
hospitals
• Drug of choice - vancomycin
• In Japan emergence of VIRSA(vancomycin
intermediate resistant S. aureus)
• No effective antibiotics discovered -We might
have to discover
DIAGNOSIS
• 1. In all pus forming lesions
– Gram stain and culture of pus
• 2. In all systemic infections
– Blood culture
• 3. In infections of other tissues
– Culture of relevant tissue or exudate

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STAPHYLOCOCCI

• 2. Coagulase negative Staphylococci

• Habitat - part of normal flora in some humans

• Source of organism - can be infected human

3. Synthesize loosely organized polysaccharide

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