06 Gram Positive Organisms Flashcards
Catalase test
Bubble = positive = Staphylococcus
No bubble = neg = Streptococcus
Coagulase
Clotting = positive = S. aureus
No clotting = negative = S. saprophyticus / S. epidermidis
Susceptibility test
Disk diffusion test (Kirby-Bauer method)
S. saprophyticus = novobiocin resistant
Mannitol test
High salt content
Growth and yellow in color = positive = S. aureus
No growth and no yellow color = neg = not S. aureus
Staph culture
grey-yellow = hemolytic in media = S. aureus grey-white= non-hemolytic in media = S. epidermidis grey = non-hemolytic in media = S. saprophyticus
Antigenic structures (Staph)
Peptidoglycan: IL1 -> complement system, PMN, neutrophil
Teichoic acid: antigenic but nonvirulent
Capsules: inhibits phagocytosis; conjugate vaccines (capsule + carrier protein)
(MSCRAMM) Protein A: adhesin to Fc of IgG, decreases opsonization and phagocytosis
(MSCRAMM) Clumping factor: adhesin fo coagulase -> fibrinogen and platelets; aggregates bacteria
Coagulase: bind with prothrombin -> fibrin on bacterial cell wall; hides bacteria
Enzymes (Staph)
- Catalase: H2O2 -> H2O + O2
- Coagulase: clotting
- Hyaluronidase: spreading factor, degrades ECM/CT
- Staphylokinase: forms plasmin -> fibrinolysis -> bacteria can enter
- Beta lactamase: antibiotic resistance
- Proteinases and Lipases
- Hemolysin (alpha, beta, delta, gamma)
- PVL + gamma hemolysin: lyse WBC; seen in MRSA; bacteriophage mediated
- Exfoliative toxin: dissolves mucopolysaccharide in skin; toxin a (heat stable), toxin b (heat labile)
- TSST1: binds with MHC II, TSS
- Enterotoxin: resistant to gut enzymes, heat stable, pathogenicity islands in bacteriophages
Pathogenesis (Staph)
Fomites
Normal microbiota
Food poisoning
Furuncle
Clinical manifestations (Staph)
- Skin and soft tissue
- Direct Organ Dissemination (hematogenous spread)
- Toxin release (food poisoning, TSS, SSSS [neonates], blood and catheter infections)
Classification (Strep)
- Hemolysis patterns (B = complete lysis, yellow; a = partial/incomplete lysis, dark and green; Gamma = no lysis)
- Specific antigens: A (S. pyogenes) B (S. agalactiae),D (Enterococcus), no group (S. pneumoniae/S. viridans)
- Capsular polysaccharides
- Biochemical tests (bile esculin, sodium hippurate, CAMP factor production, susceptibility to chemical reagents)
Bile-esculin test
For group D strep
Black = pos = Enterococcus
No black = neg = Viridans
Sodium Hippurate test
for group B (S. agalactiae)
precipitation/purple = pos = S. agalactiae
no precipitation/purple = neg = group a/b
Group A Strep antigenic structure
M protein: prevents phagocytosis, inhibits complement activation, mediates bacterial attachment, can cross react with connective cardiac tissue -> rheumatic heart disease
Group a strep toxins and enzymes
- Streptokinase: escape blood clots. treats pulmonary emboli and coronary artery thrombosis
- Deoxyribonuclease (streptodornase): positive antibody after infection
- Streptococcal pyrogenic exotoxins: scarlet fever, STSS
- Hemolysins: streptolysin s (not antigenic) O (antigenic)
Local invasion/exotoxin release of strep
erysipela (superficial) cellulitis (deep) necrotizing fasciitis (Strep w M protein, cannot be phagocytosed) puerperal fever (after fever) bacteremia (bacteria in blood)/sepsis
Local infections of strep
strep sore throat (red tonsils)
streptococcal pyoderma
Systemic invasion of strep
Strep Shock Syndrome (soft tissue infection -> bacteremia, M type 1 and 3, pyrogenic toxin a and b) Scarlet Fever (pharyngitis, pyrogenic toxin a-c)
Post streptococcal diseases
Acute glomerulonephritis Rheumatic fever (M protein vs heart tissue = deformed valves and aschoff bodies)
Morphology (Bacilus)
Saprophytic
B anthracis: - hemolysis, nonmotile
B cereus: + hemolysis, motile, food poisoning
B subtilis: contaminant
B anthracis virulence factors
Capsule: virulence, antiphagocytic
Toxin: PA (protective antigen), LF (lethal factor), EF (edema factor), PA+LF (lethal toxin causing necrosis and death), PA+EF
B anthracis clinical pathology
Papules with necrotic ulcer, edema, eschar formation, inflammation Cutaneous anthrax (spores on skin), inhalation (bioterrorism), gastric
Types of B cereus
Emetic (nausea, vomiting, occasional diarrhea, found in sporulates of rise)
Diarrheal (no vomiting)
Eye infection
Localized infections
Clostridium morphology
Saprophytic
C botulinum
C tetani
C perfringes
Spore forming species
Bacillus (anthracis, cereus, subtilis)
Clostridium (botulinum, tetani, perfringes, difficile)
C botulinum characteristics
Causes flaccid paralysis
Spores are resistant to heat, decreased in high pH
Toxin: light chain lyses SNARE proteins + heavy chain
Types of botulism
Adult: eat neurotoxin
Infant/child: eat spores and it germinates in the gut
C tetani characteristics
Found in soil and feces
Flagellar antigen
Tetanospasmin (neurotoxin): spastic paralysis, non invasive, A and B units
C tetani clinical findings
Difficulty swallowing Vocal cord spasm Opisthotonos (back arching) Risus sardonicus (sardonic smile) Trismus (lockjaw)
C tetani prevention
Active immunization (toxoid antigen -> antibodies)
Prophylaxis with antitoxin
Wound care
Penicillin
C perfringes toxin
Clostridium perfringes enterotoxin Intense diarrhea Incubation period: 7-30 h Hypersecretion in small intestines Self-limiting Test: stormy fermentation (coagulates the milk)
C perfringes invasive toxin
a toxin: lecithinase (skin lecithin, platelet aggregation makes anaerobic environment)
C perfringes pathology
Gas gangrene (clostridial myonecrosis)
COH ferments and produces gas -> cackling sounds -> distention of tissues -> compromised blood supply
Crepitation (cracking skin from gas)
C difficile characteristics
Antibiotic associated diarrhea Psudomembranous colitis (type a = enterotoxin = watery and bloody diarrhea; type b = cytotoxin = plaques and micro-abscesses in intestine)
Non-spore forming species
Corynebacterium diptheriae
Listeria monocytogenes
C diptheriae characteristics
Metachromic granules (beaded appearance) Potassium tellurite growth (black) Loeffler media (white) Invasive Toxic (toxigenicity found in bacteriophage)
Diptheria
Bull neck (swollen lymphs from lymphatic edema)
Toxin produces necrotic epithelium
Psudeomembrane and bacteria grows inside nectrotic tissue
L monocytogenes morphology
Facultative anaerobe with short rods Tumbling motility Can survive in low temp, pH, and high salt Catale + Esculin +
L monocytogenes virulence factors
Intracellular organism = cell-mediated immunity
Antigenic structure: O somatic antigen / H flagellar antigen
Factors: Adhesin proteins (Ami, fbp a, flagellin proteins), surface proteins (for entrance; internalin a/b, actin a), listerolysin O, iron, filopodia
L monocytogenes pathophysio
adhesion (adhesin proteins) -> surface proteins for entering -> pH decreases inside vacuole due to listeriolysin O -> filopods+actin propel to another cell
B anthracis pathophysio
PA binds to surface receptors -> LF+EF enter cell -> EF = edema, LF = death
C botulinum pathophysio
Botulinum toxin goes to gut -> absorbed to blood -> goes to neuron -> light chain of toxin lyses SNARE SNAP protein -> no release of neurotransmitter -> flaccid paralysis
L monocytogenes clinical findings
Gastroenteritis
Granulomatous infanseptica (neonatal sepsis, pustular lesions, granuloma in organs, death on delivery)
Listeria meningoencephalitis
Actinomycetes characteristics
Aerobic
Chains with branches
Long cell wall with mycolic acid
