staphylococci facultative, non-sporulating, non-motile, gram positive cocci cell division 3 planes...
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Staphylococci
• Facultative, non-sporulating, non-motile, Gram positive cocci
• Cell Division 3 planes– Daughter cells don’t fully separate form
clusters
• Greek nouns– Staphyle – “ a bunch of grapes– Coccus – “grain or berry”
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Staphylococci
27 species Three Important Species• Staphylococcus aureus
– Important human pathogen
• Staphylococcus epidermidis– Normal skin flora, disease under special
circumstances
• Staphylococcus saprophyticus– UTI’s in young females
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S. aureus S. epidermidis S. saprophyticus
Catalase positive positive positive
Coagulase positive negative negative
Novobiocin negative negative positive
Resistance
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STAPHYLOCOCCI - Cell Wall
1) Peptidoglycan – main component of the cell wall• Hydrated, semi-rigid polymer of two sugar derivatives:
• N-Acteylglucosamine & N-Acetylmuramic acid
• 90% of cell wall may contain peptidoglycan • Less in Gram negative organism
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STAPHYLOCOCCI - Cell Wall
2) Teichoic Acid• Polymer of glycerol or ribitol joined by phosphate groups• Covalently linked to muramic acid of peptidoglycan• Links various layers of the peptidoglycan mesh together.
2 classes of teichoic acidsLipoteichoic acid
– Embedded in the peptidoglycan layer – Linked to the cytoplasmic membrane
Wall teichoic acid – Linked to only the peptidoglycan layer
Teichoic acid is responsible for the antigenic determinant of the organism
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STAPHYLOCOCCI - Cell Wall3) Protein A
– Bind the Fc component of antibodies
4) Coagulase
– Bound and soluble forms– Activates the coagulation cascade
• Fibrin meshwork abscess formation
5) Capsule – Variable
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S. aureus - Epidemiology• Reservoir – Humans
• Asymptomatic Carriage Sites:– Nares– Rectum– Perineum– Pharynx
• Skin Colonization - Brief, Repeated • Transmission - Person to Person
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S. aureus Carriage RatesPopulation Carriage Rate (%)
General Population 25 Hemodialysis 75
Diabetic on insulin 50
Patients receiving 50allergy shots
Intravenous Drug Users 40
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Staphylococcal Infections - Risk Factors
• Skin Disease – Increased colonization
• Trauma – Expose binding sites
• Viral Respiratory Tract Infection (Influenza) – Expose binding sites– Decreased clearance
• Foreign Body• Liver disease• Neoplasia
• Diabetes• Renal Failure• Leukocyte &
Immunoglobulin Defects • Elevated Serum IgE
Levels • Narcotics Addiction• Broad Spectrum
Antibiotic Therapy
In general Healthy people don’t get serious Staph infections
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Patterns of Disease - S. aureus
1) Invasion with Tissue Destruction
2) Toxin Mediated – Toxic Shock Syndrome– Scalded Skin Syndrome– Staphylococcal Food Poisoning
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S. aureus - Invasive Infections
A Two Step Process:
1. Binding (adherence) to host tissues
2. Invasion
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Staphylococcal Virulence Factors - Adherence
1) Nasal Mucosa – Teichoic Acid
2) Traumatized Skin and Foreign Surfaces Breech in normal barrier of mucosa or skin Unmasked host
proteins that S. aureus has specific receptors• Fibronectin • Fibrinogen• Laminin • Type IV collagen
3) Endothelial Cell S. aureus has a unique affinity for the vascular tree
• Attach to Fibronectin, Laminin and Endothelium Itself
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Staphylococcal Virulence Factors - Invasion
A. Tissue Degrading Enzymes1) Hyaluronidase
Hydrolyzes hyaluronic acid in connective tissue matrix
2) LipaseBreak down lipids in matrix
3) DNase4) Hemolysins and Leukocidins
Family of membrane damaging toxins Dissolve RBCs, WBCs and tissue cells
5) CoagulaseCauses plasma to clot– Promotes abscess formation (wall)– Fibrin deposition around bacteria may protect from phagocytosis
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Staphylococcal Virulence Factors - Invasion
B. Anti-Phagocytic Factors
1) Catalase• Made by all Staph (not Streptococcus)• Leukocytes use oxidative mechanism to kill bacteria
– Inactivates Hydrogen Peroxide H2O + O2
2) Protein A• Binds the Fc component of IgG• Inhibits opsonization by antibody
3) Capsule• Stearic Hindrance• Variable
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Anterior Nares
Skin Trauma Localized
Colonization Infection
BacteremiaMetastatic
Foci
Lungs
Endocarditis Liver/Spleen
CNS
Kidneys
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Furuncle
• Often starts as infection of hair follicle Folliculitis
• Firm, tender red nodule Painful
• Fluctuant with time Drain spontaneously
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Carbuncle
Larger than furuncle• Extends into
subcutaneous fat• Interconnected• Firm, inelastic skin
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Impetigo• Superficial infection of
skin• Usually
– S. aureus – Streptococcus pyogenes
• Children• Hot Weather• Minor Trauma• Initially vesicles
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Impetigo
• Later: Crusted with yellow dark brown material
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Erysipelas
• Strep pyogenes or S. aureus
• Sharp, raised borders
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Cellulitis• Acute, spreading
Infection• Involves both skin and
subcutaneous tissues• Prior trauma to skin• Warm and
erethematous
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Mitral Valve Endocarditis
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Endocardits
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Patterns of Disease - S. aureus
1) Invasion with Tissue Destruction
2) Toxin Mediated – Toxic Shock Syndrome– Scalded Skin Syndrome– Staphylococcal Food Poisoning
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TOXIC SHOCK SYNDROME
1978 - Todd and coworkers reported a group of children:• Acute Febrile Illness • Subsequent Development of Hypotension and Shock.• Noted association with S. aureus phage group I• Named the illness "Toxic Shock Syndrome“
1980 - Illness had been identified in 941 patients in the USA
1990 - More than 3,300 cases have been reported• 95% in women• 90% occurred during menstruation in women who
were using tampons1989 - 61 cases of TSS reported
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Toxic Shock Syndrome - Epidemiology
1. Menstrual• Colonization of the
Vagina and Cervix with TSST-1 producing strains of S. aureus– Tampon Associated
• Risk proportional to the absorbancy of Tampon
– Not tampon associated
2. Non-menstrual• Post-surgical• Influenza associated• Contraceptive device
associated– Diaphragm– Sponge
• Postpartum
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Pyrogenic Toxin
• Family of Proteins secreted by– S. aureus– Strep pyogenes
• Share biologic properties and Amino Acid Sequences– Molecular wgt: 20,000 30,000 daltons
• Include– TSST-1– Staphylococcal Enterotoxins A, B,C– Pyrogenic Exotoxin A & B– Streptococcal Scarlet Fever Toxins A, B,C
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TSST – A Superantigen
• Able to activate large number of Tcells– Up to 20% at one time
Massive Cytokine Release
• Interacts directly with invariable region of Class II MHC molecule
• Activated T Cells Release– IL-1: pyrogen, muscle
proteolysis– IL-2– TNF: inhibit PMN function– IFN-
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Physicochemical Factors that Promote TSST-1 Production
1) Protein (or amino acid) containing environment
2) Temperature 37oC - 40oC
3) Ph range 6.5 - 8
4) Presence of Oxygen
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Toxic Shock Syndrome - Clinical Manifestations
1. High Fever (>39.9oC)2. Scarlatiniform Eruption3. Hypotension and Shock4. Desquamation during
convalescence
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Manifestations of Specific Organ Involvement
• Mucous Membranes: hyperemia • Gastrointestinal Tract: vomiting and diarrhea • Muscle: severe myalgias • Central Nervous System: disorientation • Kidney: azotemia, pyuria urinary tract
infection• Liver: elevation of serum bilirubin and SGOT• Blood: Thrombocytopenia
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Toxic Shock Syndrome -Diagnosis
• Isolation of toxin producing S. aureus from a patient with a compatible clinical illness.
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Toxic Shock Syndrome - Treatment
1) Treatment of Hypotension and Shock– Vigorous Fluid Replacement
2) Attention to the Site of S. aureus Colonization– Removal of Tampons– Drainage of Staphylococcal Abscess
3) Anti-Staphylococcal Antibiotic Therapy
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STAPHYLOCOCCAL SCALDED SKIN SYNDROME
• A Disease of Infants– Localized Infection with Diffuse Skin Rash
• S. aureus (Phage group II) recovered from:– Nose– Pustules– Eye – Umbilicus
• Exfoliative Toxin– Two Serologically and Biologically Distinct Proteins
• Exfoliatin A• Exfoliatin B
– Inter-Epithelial Splitting of Stratum Granulosum Layer
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Staphylococcal Scalded Skin Syndrome - Clinical Features
• Starts Abruptly– Perioral erythema – Sunburn like, tender rash spreads
over entire body
• Bullae Appear Rapidly – Nikolsky sign– Flaccid bullae slough off Denuded
areas
• Exfoliated Areas Eventually Dry– Flaky desquamation lasting 3-5 days
• Within 10 days After Onset Complete Recovery – New epidermis has replaced the
denuded areas
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Staphylococcal Food Poisoning• 20% of Outbreaks of Acute Food Poisoning • Toxigenic Strain of S. aureus growing in
contaminated food– Produces Enterotoxin B (Heat Stable)
• Person to Person Transmission– Responsible organism usually isolated from
person involved meal preparation • Commonly implicated foods
– Custard filled bakery good– Canned food– Potato salad – Ice cream
• Food appears normal in appearance, odor and taste
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Staphylococcal Food Poisoning - Clinical Features
• Incubation period 2-6 hours• Enterotoxin stimulates intestinal peristalsis and CNS
– Abrupt onset:• Salivation• Nausea and vomiting • Abdominal cramps • Watery diarrhea
• Afebrile• Self limited, symptoms disappear in 8 hours
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S. aureus Treatment
1941 – Penicillin available1945 – Penicillin resistance reported
– Plasmid mediated – 2o to beta-lactamase (penicillinase)
1960-64 Semi-synthetic pencillins produced– Methacillin, oxacillin, nafcillin
1961 Methacillin resistant S. aureus (MRSA) reported
– Resistant to all beta-lactam antibiotics
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Methacillin Resistant S. aureus (MRSA)
• 2 Penicillin binding proteins (PBPs) normally have enzymatic activity responsible for cross linking peptidoglycan wall
• MRSA have acquired a chromosomal gene MecA code for alternate PBP (“PBP 2a”)– Low affinity for beta lactam– Enzymatically active generate peptidoglycan
• Treatment Vancomycin (glycopeptide AB)
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Glycopeptide Resistant S. aureus
• First reported in 1997
• Increased production of cell wall precursors including PBP2a– “Soak up” antibiotic in thickened cell wall
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Staphylococcus epidermidis
• Normal Flora – Virtually all humans carry S. epidermidis on the
skin and in and around body orifices
• Hospital Acquired Infection– Contamination by S. epidermidis carried by the
patient most important event in infections associated
with foreign bodies
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S. epidermidis - Virulence Factors
Production of an exo-polysaccharide ("slime")
• Promotes adherence to plastic surfaces
• Increases resistance to phagocytosis
• Increases resistance to antimicrobial therapy
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S. epidermidis - Patterns of Infection
• Nosocomial Bacteremia -most common cause
• Endocarditis A. Native Valve
– Uncommon- 5% of cases
B. Prosthetic Valve– Single most common cause
(40% of cases)– Probably caused by
inoculation at the time of surgery
– Indolent course
• Intravenous Catheters-Single most common cause (50-75% of cases)
• Cerebrospinal Fluid Shunts
• Peritoneal Dialysis Catheter
• Vascular Grafts
• Prosthetic Joints
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Foreign Body - Mechanisms of Staphylococcal Persistence
1) Fibronectin and Fibrinogen Coating– Firm Anchor for
Staphylococci
2) Glycocalyx Production– Protects Bacteria
3) Dysfunctional Phagocyte Population– Incapable of Killing
Bacteria
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S. epidermidis Infection - Treatment
1. Antimicrobial Therapy
• Usually resistant to multiple antibiotics– Beta lactams– Erythromycin, Clindamycin, Tetracycline
• Require therapy with Vancomycin
2. Removal of Foreign Body
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Staphylococcus saprophyticus
• Colonizes the genitourinary mucosa of some young women
• Causes both upper and lower urinary tract disease– 95% of cases are in females 16-35 years old– Responsible for 20 of the UTI's in this age group
• Second only to E. coli
• Pathogen of young, sexually active females – 70% sexual intercourse within 24 hours preceding onset
of symptoms