Microbio: Staphylococcus/ Streptococcus

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Staph v. Strep

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Staph = catalase (+)
-->clusters of G(+) cocci

Strep = catalase (-)
-->strings of G(+) cocci
-->diplococci for pneumoniae

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C-carbohydrate

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-->Strep. Group A


-->determines group β-hemolytic
Strep
-Strep. pyogenes
-Strep. agalactiae

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β-hemolytic Strep. species

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1. S. pyogenes
2. S. agalactiae

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Strep. pyogenes Diseases

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-most common bacterial pharyngitis
-cellulitis, necrotizing faciitis

Streptococcus Toxic Shock Syndrome

Rheumatic Fever

Acute Glomerulonephritis

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Streptococcus Toxic Shock Syndrome

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Strep. Group A (S. pyogenes)

-->requires bacteremia (as opposed to staph TSS)
-->use Pyogenic Toxin A (superAg)

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Pyogenic Toxin A

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Group A Strep (S. pyogenes)

-->assoc. w/ Strep. TSS
-->superAg
-->bonds to non-specific portion of MHCII

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Rheumatic Fever

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Group A Strep.

-->common sequellae with cross-rxn of Ab (anti-heart, brain, joints)
-->Type II hypersensitivity
-->migratory arthritis, heart problems, facial/limb spasms

PREVENT: early treatment of GAS infections with penicillin

NOT ASSOCIATED WITH SKIN INFECTIONS

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Acute Glomerulonephritis

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-->associated sequellae with GAS skin infections

-->Type III Hypersensitivity: Ag-Ab complexes damage kidneys
-->hypertension, smoky urine, edema

PENICILLIN WILL NOT DECREASE INCIDENCE

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Hyaluronidase

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GAS/ Strep. pyogenes

-->spreading factor: breaks down hyaluronic acid in epithelium

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Exotoxin B

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GAS/ Strep. pyogenes

-->PROTEASE

-->assoc. w/ flesh-eating Strep (necrotizing faciitis)

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M-protein

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GAS

-->group-determining protein

-->binds to keratinocytes in human skin
-->mediates internalization
-->anti-phagocytic (binds Factor H)

-->80 serotypes--> some assoc. w/ increased sequallae

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M-Protein Anti-Phagocytic Action

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GAS group-determining Ag

-->binds to Factor H

-->Factor I will not be able to cleave C3b (alternative complement cascade)

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Hyaluronic acid capsule

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GAS

-->not capable of generating humoral response (self-Ag)

-->most important anti-phagocytic factor for GAS

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Anti-Phagocytic Properties of GAS

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1. Hyaluronic acid capsule= most important

2. M-protein--> binds Factor H

3. C5a peptidase--> C5a chemotaxic for phagocytes

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F-Protein

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GAS

-->binds to fibronectin in PHARYNX epithelium

***ALSO binding factors***
-->M-protein= keratinocytes
-->Lipoteichoic Acid= epithelium

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Streptokinase

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(aka: Fibrinolysin)

-->degrades fibrin clots
-->used in heart attack patients to quickly remove blocks

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Erythrogenic Toxin

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GAS

-->responsible for Scarlet Fever
-->requires conversion of strain via phage
-->similar to TSS1 staph toxin; superAg

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Factors contributing to GAS β-hemolytic

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Strepolysin O= req. low O2, major Ab-response

Stretoplysin S= O2 stable

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Major Determinants for Strep. pyogenes

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Gram (+), catalase (-)

β-hemolytic--> Streptolysin O/S with C-carbohydrates

BACITRACIN SUSCEPTIBLE

(+) ASO test = confirmatory step

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ASO Test

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-->confirmatory for GAS

-->measure subsequent Ab anti-Streptolysin O
-->lack of RBC lysis = (+)

2 TODD UNIT CHANGE = significant

(Ab > 240 titer) is elevated

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Group B Strep Diseases

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-->neonatal meningitis, pneumonia

1. Early-Onset= birth canal exposure
2. Late-Onset= exogenous source, post. 3 wks.

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CAMP Test

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-->enhanced β-hemolysis with presence of Staph.

-->confirmatory for GBS/ S. agalatiae

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Indicators for GBS

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-->Gram (+), catalase (-)

-->hydrolyses hippurate

-->β-hemolytic

-->resistant to bacitracin

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Bacitractin test for Strep:

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resistant = Group B/ S. agalactiae

susceptible= GAS/ Strep. pyogenes

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Main Immunologic Response to GBS

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-->Ab anti-capsule polysac.

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Strep. agalactiae toxins/ pathogenic factors

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-->NOT TOXINS

-->polysac. capsule= anti-phagocytic, main antigentic target for Ab

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Strep. pneumococci determinants

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-α-hemolytic
-may appear as diplococci
-bile soluble (amidase activity)
-susceptible to optochin

Quellung Test- commercially Ab to Ag swells the capsule

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Quellung Test

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-->confirmatory for Strep. pneumococci

-->use commercially available Ab anti-pneumococcus capsule
-->cause capsule to SWELL

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Pneumococci Diseases

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***risk factor= elderly, lacking SPLEEN***

-->Bacterial Pneumonia= rusty sputum

-->Otitis media: most common reason for antibiotic use in peds

-->Sinusitis

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Pneumococci Vaccine

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-->target for polysac. capsular sugars

-->conjugate with C. Dipth. toxin to trigger TC-dependant response

-->contains 23 most common sugars

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Treatment of Pneumococci pneumonia

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-->Penicillin will cause exacerbation of symptoms (due to immune response)

-->pair with Dexamethasone to modulate response

***neuotoxicity from dexamethasone BARELY outweighs risks of neuro effects of penicillin****

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Pneumococci Pathological Factors

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1. Pneumolysin--> activate Complement; hemolysin; forms pores, alters cilia movement; spreads infection

2. Capsular sugars-->allows for mucosal appearance; vaccine target

3. Amidase--> cleaves layers of peptidoglycan, solubility in bile sol.

4. C-Substance: increase inflammation, activate Alt. Complement via binding to CRP

5. IgA Protease

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Pneumolysin

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Pneumococci

-->forms pores in target cells
-->alters cilia movement
-->spreading factor
-->hemolysin
-->damages epithelium/endothelium of lungs
-->activates complement

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Bile soluble Strep

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Pneumococcus

-->ability due to AMIDASE acitivty

-->amidase= cleaves peptidoglycan layers; autolysis

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Strep Hippurate Hydrolysis

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GBS/ Strep. agalactiae

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Optochin tests on Strep

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susceptible= pneumococci

resistant= strep. viridans

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α-hemolytic strep

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S. pneumococci = optochin susceptible

S. viridans = optochin resistant

Enterococci= has variable hemolysis, define by ability to grow in NaCl and bile

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Strep. viridans

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α-hemolytic

optochin resistant

-->endocarditis = splinter-hemmorages in nail beds/ conjunctiva
-->brain ulcerations

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Nosocomial UTI

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Enterococcus (Group D/E)

-->variable hemolysis
-->ability to grow in high NaCl and bile
-->hydrolyze esculin

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Indicators for Enterococcus

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-->variable hemolysis
-->hydrolyze esculin (black precipate on MAC)

-->ability to grow in high NaCl and bile

-->MUST POSSES GROUP D Ag

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Enterococcus Treatment

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-->pair penicillin with aminoglycoside

-->antibiotic synergism: penicillin allows aminoglycoside to penetrate and kill cells

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Enterococcus Diseases

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-->nosocomial UTIs

-->bedsores, wounds
-->intra-abdominal infections

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Abcess

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a localized infection of pus with live/dead PMNs

walled off with fibrin capsule

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Folliculitis

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infected hair follicle

may progress to furuncles>carbuncles

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Impetigo

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(aka: Pyoderma)

epidermal infection with "pimple" forming yellow-crust

Staph aureus or GAS

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Fasciitis

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infection of the fasical plane

nerves, vessels are destroyed

SEPSIS and life-threatening--> fast spread

***do not confuse with cellulitis***

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Penicillin resistance in Staph. aureus

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-->beta-lactamase hydrolyzes penicillin's ring
-->gene carried on plasmid
-->S. epidermidis may be reservoir

**don't' confuse with mechanism for methicillin resistance = mecA gene**

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Methicillin resistance for S. aureus

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-->mecA gene codes for an altered Penicillin-Binding Protein (PBP)
-->allows resistance to all beta-lactam drugs

chormosomal

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Vancomycin resistance for S. aureus

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-->vanA gene codes for altered cell wall: D-alanine D-lactate (compare to D-alanine D-alanine)

-->vanA plasmid acquired from VR Enterococci

plasmid

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Chronic Granulomatous Disease

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-->def. of phagocytic cells ability to produce H2O2 and superoxide radicals

-->normally can use catalase (-) species radicals to destroy it
-->Staph is catalase (+) and won't leave phagocytes any radicals to use

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Differential Tests for Staph

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ALL CATALASE (+)

1. Coagulase Test
(+) = S. aureus
(-) = S. epidermidis / S. saphrophyticus

2. Novobiocin Test
resistant = saphrophyticus
susceptible = epidermidis

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Novobiocin Tests for Staph

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resistant = saphrophyticus

susceptible = epidermidis

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Cause of yellow S. aureus colonies

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Staphyloxanthin

inactivates superoxidases and other reactive oxygen species

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Indicators for S. Aureus

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Gram (+), clusters
catalase (+), coagulase (+)

-->beta-hemolytic
-->yellow colonies= staphyloxanthin
-->ferments mannitol

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Coagulase

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-->staph. aureus

activates prothrombin ---->thrombin

thrombin converts fibrinogen--->fibrin

**staph. aureus also has fibrinolysin-->clever little bug!***

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Protein A

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S. aureus

-->binds Fc region of IgG, prevents complement activation and phagocytosis

-->used in lab tests with RBCs for coagglutinate properties

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S. aureus Teichoic Acids

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polymers of ribitol phosphate

help adhere to mucosal cells

induce septic shock

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S. Aureus Polysac. Capsule

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-->11 serotypes, poor immunogen

-->types 5 and 8 cause 85% of infections

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Phage typing

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for S. aureus

-->specific receptors for phages allow epidemiologic typing

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S. aureus Peptidoglycan

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-->exotoxin-like properties

-->stimulate macrophages to secrete cytokines, induce shock

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Type of Staph/Strep NOT NORMAL FLORA

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Group A Strep / S. pyogenes

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Predispositions to S. aureus infections

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-->immunocompromised, especially POOR HUMORAL

-->high levels of colonization (family/ fomites)
-->diabetes
-->IV use

CHRONIC GRANULOMATOUS DISEASE

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Staph. Food Poisoning

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S. aureus

-->ENTEROTOXIN- stimulates release of cytokines in GI
-->IL-1 = macrophages
-->IL-2 = THC

-->lymphoid cells stimulate enteric nervous system to induce vomitting

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Enterotoxin

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S. aureus Food Poisoning

-->stimulates release of cytokines from macrophages (IL-1) and THC (IL-2)

-->lymphocytes induce ENS to cause vomitting

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Staph TSS

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-->does not require bacteremia

-->use TSST-1 superAg
-->release IL-1, IL-2, and TNF

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Exfoliatin

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common in S. aureus Scalded Skin Syndrome

-->protease cleaving desmoglein (cleaves desmosomes)

-->separation of epidermis at hte granular cell layer

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Alpha toxin

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S. aureus

-->kills leukocytes (along with PVL toxin)
-->maked necrosis of the skin and hemolysis
-->forms holes in cell membrane

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PV Leukocidin

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S. aureus

-->forms holes in leukocytes
-->2 sub-units

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Staph. epidermidis Infections

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-->biomaterials associated infections

-->grow on catheters, implants, etc
-->form biofilms
-->bacterial endocarditis

-->neonatal sepsis
-->CNS bacteriemia

ALMOST ALWAYS NOSOCOMIAL

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Kawasaki Syndrome

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Staph aureus

-->small/med. artey vasculitis
-->bilateral conjunctivitis, 5d. high fever, diffuse erythmatous maculopapular rash
-->desquamation, cervical lymphadenopathy

-->minoutbreaks in Japan, most under 5 yrs.

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Staph. saphrophyticus

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Almost always community acquired

-->UTI (also strep. enterococcus and e. coli)

-->novobiocin resistant