2011 07 microbiology skin diseases1
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STAPHYLOCCOCUS
Gram (+) cocci in grape like cluster Facultative anaerobe Some are capsulated Non-motile Non-sporeforming
CLASSIFICATION OF STAPHYLOCOCCUS
1. S. aureus 4 biotypes (A-D)
o Biotype A mostcommonly found in
humans
Involved :a.) in superficial (local)
infection
b.)deep (systemic)diseases
c.) toxigenic diseases2. S. epidermidis
Nosocomial bacteremia Endocarditis associated with
valvular prosthesis
Intravenous catheter infection Peritonitis in patients
undergoing COPD
Ventricular shunt infections
Antigenic Structures of Staphyloccocus
Capsule Slime layer Protein A Peptidoglycan-techoic acid complex
Virulence Factors of Staphylococcus
Capsuleo Produced by some S. aureus
strains
o antiphagocytic Slime layer
o Produced by S. epidermidiso Involved in adherence,
persistence on foreign body
Protein Ao Surface protein; covalently
bound to peptidoglycan
o Regularly present in humanstrains of S. aureus; not found
in coagulase (-) staph
o Binds non-specifically with Fcportion of IgG
Prevents Fc-mediatedopsonization
Induces complementactivation
Used in antigendetection (co-
agglutination)
Polysaccharide A (ribitol techoic acid)o Peptidoglycan-techoic acid
complex
A. Peptidoglycan Provides rigid exoskeleton Has interpeptide bridge
connecting oligoglycine peptides
S. aureus L-lysine-glycine 5-6
S. epidermidis L-lysine-glycine 3-5 L-serine
Subject: MicrobiologyTopic: Bacteria Associated w/ skin Infections 1Lecturer: Dr. Eleanor PadlaDate of Lecture: July 5, 2011Transcriptionists: Blue Bolt, Aquamarine,
BrokenEditor: Blue BlinkPages: 8
SY
2011-2012
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S. saprophyticus LLysine-glycine 5-6 L-
serine
B. Techoic Acid Water soluble polymers of ribitol
glycerol P04
o Ribitol techoic acid(polysaccharide A)
Cell wall techoicacid
Found in S. aureus Antiphagocytic
o Glycerol techoic acid Cell membranes
techoic acid
Found in S.epidermidis andsaprophyticus
Extracellular enzymeso Hyaluronidase
Hydrolyzes hyaluronicacid in connective
tissues
o Lipase Splits fats and oils
o Staphylokinase (fibrinolysin) Dissolves fibrin clots
o Coagulase (free) Lays down fibrin barrier
during abscess
formation
Toxinso Leucocidin
Consists of 2 proteincomponents (F=fast; S =
slow)
Destroyspolymorphonuclear
leucocytes
o Hemolytic toxins
4 major types (alpha,beta, gamma, epsilon)
Damage red cellmembrane
Produce hemolyticzones on BAP
Alpha toxinso Forms
transmembrane
pores
o Has lethal,dermonecrotic and
leucocidal activities
o Formed by majorityof human strains of
S. aureus
o Not formed bycoagulase (-) staph
o Exfoliative toxins Proteins Produces intraepidermal
splitting of tissues and
necrosis seen in SSS;blisters in bullous
impetigo
Associated with S. aureusphage group II
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2 types ETA
Gene on
Chromosome
ETBGene on plasmid
Heat-
labile;stable in
EDTA
o Pyrogenic exotoxins Family of secreted
proteins
Act as superantigens1. Entorotoxins
a. Seven antigenictypes (A, B, C1,
C2, D, E F)
b. Enterotoxin Aand D food
posining
c. Enterotoxin B necrotizing
enterocolitis
2. Toxic Shock SyndromeToxin-1 (TSST-1)
a. Synonymouswith Enterotoxin
F
PATHOGENICITY
A. Habitat S. aureus
i. Anterior nares, skin,nasopharynx, perineum
S. epidermidisi. Skin, mucous
membrane, anterior
nares
S. saprophyticusi. Mucosa of GUT, skin
B. Transmission S. aureusi. Spread to normally
sterile sites by
traumatic
ii. Person-to-personspread (e.g. in
nosocomial setting)
S. epidermidisi. Spread to normally
sterile sites as a result
of implantation of
medical devices
ii. Person-to-personspread (e.g in
nosocomial setting)
C. Diseases caused byS. aureus
1. Superficial (local) infection
Impetigoo Honey colored scabs (on
arms, legs, face)
o 90% is caused by S. aureus,10% by GAS
o Bullous is caused staph whilenon bullous can be caused by
staph or strep
o More common in schoolchildren; occur in warm, humid
environments (coz u see
bacteria likes warm, most
areas)
o Highly contagious; spread bydirect contact with lesions or
with nasal carriers
Folliculitiso Follicular-based pustule (in
areas of irritation)
o Can occur through shaving,scratching, or with an injury to
the skin
o Most commonly superficial(affecting upper part of hair
follicle; or deep (affecting the
whole hair follicle)
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FURUNCLES (boils)o Starts as hard, tender red
nodule surrounding a hair
follicle -> abscess -> pus
discharged from center ->
resolve
o Arise in hair- bearing areaswhere there is friction,
occlusion, perspiration
o Lesions may be isolated , ormultiple
CARBUNCLESo Start as smooth, dome-
shaped, acutely tender,
painful lesion -> develop
into swollen, painful area
discharging pus from
several sites (individual
boils clustered together)
o Often occur at the nape ofthe neck, the back or thighs
o Deeper, more severe,develop and heal more
slowly
2. Deep (Systemic) Diseases
Acute osteomyelitis Acute endocartitis Pneumonia
3. Toxigenic Diseases Staphylococcal scaled skin
syndrome
Staphylococcal foodpoisoning
Toxic shock syndromeSTAPHYLOCOCCAL SCALDED SKIN
SYNDROME (SSSS / RITTERS DISEASE)
Stripping of superficiallayers of the skin from the
underlying tissue
Mostly frequently involvesinfants and children < 5
years
Majority caused by S.aureus phage group II
(mostly commonly, type
71)
LABORATORY DIAGNOSIS
1. GRAM STAIN Gram (+) cocci in
clusters
0.5- 1.5 micrometer Gram-variable within
neutrophils, in
resolving lesions, in the
presence of antibiotics;
in old cultures
2. CULTURE Grows well on unenriched
media
Grows in 7.5% - 10% NaCl;in 40% bile
Media : BAP, selectivemedia (MSA, PEA)
Figure 1. Media: Mannitol
Salt Agar
Figure 2. Colonies on blood Agar Plate
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Form smooth, raisedcolonies; mucoid if
capsulate
Colonial pigment variableo s. aureus golden
yellow to white
o s. saprophyticuswhite to pale grey
o s. epidermis white
Hemolytic reactionvariable
o S. aureus- usuallybeta-hemolytic
o S. epidermis and s.saprophyticus
usually non-hemolytic
3. DIFFERENTIAL TESTSA. Catalase Test
Staphylococci (+) Streptococci (-)
B. Coagulase Test Slide Test (bound
coagulase / clumping
factor)
Produced exclusively byS. aureus forming free
coagulase
Tube Test (freecoagulase)
Clotting of citratedplasma in the presence of
coagulase reacting factor(CFR)
For suspected S. aureusthat fail to produce
bound coagulase
4. Susceptibility
Aids in choice ofsystemic drugs
Epidemiologic tool5. Serology (antigen detection)Phage Typing
For epidemiologic tracing ofinfection
Depends on differingsusceptibilities to lysis by
phages
Control and Prevention:
Suppurative Infections:o Cleanliness, hygiene,
and meticulous
handwashing
o Aseptic management oflesions
o Isolation of personswith open lesions
o Suppression/cure ofnasal carriage
STREPTOCOCCI
General Properties:
Gram (+) cocci in chains Facultative anaerobe Some are encapsulated Some are flagellated Non-sporeforming
Classification:
A. Hemolytic Patterns Alpha hemolytic
Incomplete hemolysis
Greening reaction
Beta hemolyticComplete hemolysis
Enhanced by AnO2 conditions
Gamma hemolyticNo hemolysis
B. Lancefield System Based on group-specific CHO antigen
(C-CHO)
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Amino sugar determines serologicspecificity
GAS = rhamnose-N-acetylglucosamine
GBS = rhamnose-glucosamine GDS = glycerol teichoic acid
Streptococci groups: A-H, K-V Human pathogens belong to Grps
A to G
Group A
- possess Lancefield group Bantigen
- synonymous with S. pyogenesGroup B
- possess Lancefield group Bantigen
- Synonymous with S. agalactiaeGroup D
- possess Lancefield group Dantigen
- includes Enterococcus spp.Viridans streptococci
- lacks group-specific cell wallantigen
- referred to as oralstreptococci
Streptococcus pneumonia
- lacks group-specific cell wallantigen
- referred to as pneumococcus-
Figure 3. Lancefield Test
C. Biochemical Reactions For untypable species Used to speciateviridans streptococci
Figure 4. Biochemical reaction
Clinical Diseases
Group A streptococci (GAS)
Pharyngitis (sore throat/tonsillitis) Impetigo (pyoderma) Erysipelas Cellulitis Necrotizing fascilitis Scarlet fever Puerperal fever (childbed fever) TSSL (toxic shock syndrome-like) Acute bacterial endocarditis
Non-suppurativeSequelae
acute rheumatic fever acute glomerulonephritis
Group B Streptococci (GBS)
bacteremia, pneumonia, meningitis innewborns
Group D Streptococci (GDS)
bacteremia, endocarditis, nosocomialinfections
Viridans Streptococci
dental plaque/carries subacute bacterial endocarditisStreptococcus Pneumoniae
lobar pneumonia meningitis otitis media
GROUP A STREPTOCOCCI
Group Characteristics:
possess the Lancefield group Aantigen
rhamnose-N-acetylglucosamine synonymous with S. pyogenes
Antigenic Structures:
capsule pili protein antigens (M,F,G,T proteins) C5a peptidase Group-specific polysaccharides (C-
CHO)
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Virulence Factors:
1. Capsule- composed of hyaluronic acid- not immunogenic- antiphagocytic
2. Lipoteichoic acid- component of pili- together with M protein,
mediates oral/pharyngeal, skin
epithelial attachment
3. M protein- major virulence factor of GAS- component of pili- anti-phagocytic (prevents
alternative
Cpathwayopsonization)
- dominant in binding toepidermis
- strongly immunogenic- >80 antigenic types
4. F protein- fibronectin-binding protein- together with M protein,
mediates nasopharyngeal
adherence
5. G protein- Fc receptor (prevents Fc-
mediated opsonization)
6. C5a peptidase- surface-bound endopeptidase- anti-polymorphonuclear
leucocyte chemoattractant
(cleaves C5a)
7. Serum opacity factor- an alpha-lipoproteinase- produce opalescence in horse
serum broth
- adjunct to M typing8. Pyrogenic exotoxins
- protein in nature- 4 antigenic types (A-D)EXOTOXIN A
Associated with rash inscaret fever; TSS-L
A superantigen Produced only by
lysogenized strains
Basis ofDick/ Schultz-Charlton tests
EXOTOXIN B
Responsible for tissuedestruction in necrotizing
fascilitis
9. Hemolysins- responsible for beta-hemolysis
on BAP
- cytotoxic- 2 distinct types of hemolysins
a. Streptolysin O- oxygen-labile- hemolytic in reduced form;
responsible for subsurface
hemolysis
- formstransmembrane pores- strongly immunogenic
b.
Streptolysin S- serum soluble, oxygen-stable- responsible for surface
hemolysis
- non-immunogenic10.Spreading factors
Hyaluronidase- splits hyaluronic acids in
connective tissue
Streptokinase(fibrinolysin)
- dissolves fibrin clots DNAse (streptodornase)
- depolymerizes viscous DNA inpus
- strongly immunogenicPathogenicity
A. Habitat Inhabits URT, skin of
humans
B. Transmission Persons to person by direct
contact with mucosa or
secretions
Fomites
C. Clinical Diseases Pharyngitis Impetigo (pyoderma)
- non-bullous Erypselas (St. Anthonys
fire)
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- peripherally spreading, hot,bright-red, edematous, well-
circumscribed, sharply
marginated lesions
- most often affects the face, legs;spreads thru the lymphatic
vessels
- common in infants, children,the elderly
- accompanied by severeconstitutional symptoms
Cellulitis Necrotizing fascilitis Scarlet fever Acute bacterial endocarditis Puerperal fever TSSL (toxic shock
syndrome-like)
Necrotizing fasciitis (flesh- eating
bacteria; streptococcal gangrene)
toxin-mediated, highlydestructive and potentially
lethal infection of soft tissued
(fatty tissues, fascia, muscles)
always follows traumaScarlet fever (scarlatina)
Scarlet-colored (boiled-lobster)body rashes (sandpaper-like);
fever; strawberry-like
appearance of tongue
Exotoxin mediated Evolves from tonsillar /
pharyngeal focus
Laboratory Diagnosis:
1. Gram stain
2. Culture Media BAP chocolate agar selective media (CAN, PEA) greyish white, transparent to
translucent matt or glossy
beta hemolytic
3. Identification4.Antigen Detection
Based on monoclonalantibodies which
react with C-CHO
(e.g. latexagglutination, co-
agglutination, ELISA)
5. Serology
Anti DNAse BDetermination
To demonstrateprevious or recent
streptococcal infection
Significant response inpatients with
pyoderma
Prevention and Control:
Early detection andantimicrobial therapy
DOC: penicillin treating carriers
End of transcription
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