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67 Cards in this Set

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S. aureus
Pyogenic, aerobic GPC in nonmotile clusters, simple media. Catalase+, coagulase+.
Virulence: toxins, cell envelope constituents
Toxin diseases: food poisoning, TSS, scalded skin syndrome.
Invasive diseases: meningitis, wound infxn, septic arthritis, osteomyelitis, endocarditis, pneumonia.
Notes: naturally resistent to regular penicillin. Use dicloxacillin unless MRSA.
Pulse Field Gel Electrophoresis (PFGE)
Chromosomal analysis technique to do "DNA fingerprinting" to rapidly identify source of nosocomial outbreaks.
S. aureus cell envelope virulence factors
1.) capsule: antiphagocytic
2.) adhesin: MSCRAMM allow adherence to host proteins
3.) Teichoic/lipoteichoic acids: trigger cytokines, act as adhesins
4.) peptidoglycan: (+) cytokines, inflammation
5.) Protein A: (-)Abs; binds to Fc.
S. aureus toxin virulence factors
1.) coagulase: clots block PMNs
2.) catalase: destroys PMN hydrogen peroxide
3.) Staphylokinase: cleaves defensin peptides of neutrophils
4.) proteases/lipases: invasion
5.) Haemolysin: lyse RBCs, pore-forming
6.)Panton-Valentine leukocidin
7.) exfoliatin: scalded skin syndrome
8.) TSST-1: superantigen
9.) Enterotoxins: food poisoning.
Small Colony Variants (SCVs) of S. aureus
S. aureus that grow as tiny colonies due to defect in ETC. Renders organisms resistent to aminoglycosides.
Staphylococcal Scalded Skin Syndrome (SSSS)
Pts: neonates, infants
Sxs: skin desquamation
Agent: exfoliantin toxin of S. aureus.
Staphylococcal Food Poisoning
Agent: S. aureus enterotoxin (small, heat-stable, superantigen)
Incubation: 4-8hrs
Sxs: nausea, vomitting, diarrhoea, dehyration. Self-limiting in 6-12hrs.
Staphylococcus Toxic Shock Syndrome (STSS)
Menstrual/non-menstrual forms.
Agent: S. aureus TSST-1, also enterotoxin in non-menstrual.
Sxs: hypotension, fever, diarrhoea, desquamation of hands, multi-system organ failure.
Coagulase Negative Staphylococci (CoNS)
S. epidermidis (nosocomial)and S. saprophyticus (comm. UTIs)
Virulence: biofilms on foreign devices.
Sxs: typically subtle, slow, indolent.
Mycobacteria tuberculosis
Facultative intracellular, aerobic slender AFB, slow growth (2-4wks culture).
Dx: >10,000 organisms/ml in sputum.
Virulence: cord factor (parallel growth, (-) neutrophil migration), sulphur-containing gylcolipids [sulfatides] ((-) lysosome fusion, survival inside macs), Wax D (exaggerated DHS response immunopathy).
Tx: INH, rifampin, pyrazinamide.
Miliary TB
System TB infxn that occurs in immunocompromised where there is anergy (no DHS). Course is rapid and fatal.
PPD (tuberculoprotein)
elicits DHS in pts exposed to TB. Erythaema and induration >15mm after 48hrs is positive.
Reactivation (2° TB)
Most common clinical form in US. Onset may be years after 1° exposure. Reactivation due to aging, immunosuppression. 10% lifetime risk for PPD+ people.
BCG Vaccine
TB vaccine from attenuated M. bovis. Efficacy varies, but generally enhances CMI. Effective only in children.
M. avium complex (MAC)
Non-TB mycobacteria usually associated with AIDS, harbinger of death (T cells exhausted). Reservoirs are birds.
Sxs: chronic wasting illness. Disseminates.
M. marinum
Non-TB mycobacteria found in aquatic environments. Causese severe skin uclers ("swimming pool granulmoa") in limbs. Invasive disease in immunocompromised.
Mycobacteria Leprae
AFB, cannot be cultured, obligate intracellular parasite, armadillo.
Diseases: lepromatus, tuberculoid leprosy.
Tx: Dapsone, rifampin.
Lepromatus Leprosy
Sxs: extensive skin lesions. No CMI or DHS (Lepromin skin test-), severe disfigurement, massive # bacilli in macs, systemic infxn common.
Tuberculoid Leprosy
Milder form of leprosy limited to skin, nerve lesions with few bacilli. Intact CMI (thus Lepromin skin test+).
GNC growing in chains. Catalase-, fastidious.
Disease causing serogroups: A, B, C, D, G.
Group A Strep (S. pyogenes)
β-haemolysis, bacitracin sensitive.
Virulence: envelope and extracellular.
Diseases: suppurative infxns; acute rheumatic fever, glomerulonephritis, pharyngitis, pyoderma (impetigo).
Tx: usu. penicillin sensitive
Cell envelope virulence factors of Group A strep
1.) capsule (resistenc to phagocytosis)
2.) M protein (resistence to phagocytosis)
3.) protein F (adherence to epithelial cells)
4.) lipoteichoic acid (adherence to pharyngeal epithelial, activates alt. complement path.)
Extracellular virulence factors of Group A strep
1.) aggressins: hyaluronidase, streptokinase, DNAses: dissolving of clots, helps spread.
2.) Haemolysins: streptolysin O lyses RBCs, platelets, PMNs by pore formation.
3.) C5a peptidase: cleaves C5a.
4.) pyrogenic exotoxins/SPEs: superantigens (STSS, necrotising fascilitis, Scarlet Fever).
Streptococcal Pharyngitis
Agent: S. pyogenes
Pts: children 5-15yo
Sxs: sore throat, fever, chills, malaise.
Complication: scarlet fever (rash+fever), acute rheumatic fever, acute post-strep glomerulonephritis.
Dx: throat culture.
Tx: penicillins
Streptococcl Pyoderma (impetigo)
Agent: S. pyogenes
Pts: 2-5yo, tropical/subtropical.
Sx: supf. skin infxn., purulent lesions of lower extremities/face. Can progress to glomerulonephritis.
Invasive Streptococcal Infxn
1.) erysipelas (suf. cutaneous w. lymphatic involvement)
2.) strep. cellulitis
3.) necrotising fascilitis
4.) strep toxic shock syndrome. (mortality 50%)
5.) bacteraemia
Acute Rheumatic Fever
Non-suppurative post-streptococcal sequalae, typically following pharyngitis.
Dx: elevated ASO
Sxs: polyarthritis, carditis, heart lesions (Aschoff bodies).
Path: M protein of strep shares epitopes with human heart protein. Recurrence common.
Acute Glomerulonephritis
Non-suppurative post-streptococcal sequalae, typically following pharyngitis or skin infxn.
Path: soluble immune complexes on glomerular BM; activates complement, renal tissue injury. Rarely recurrs.
Group B Streptococcus (S. agalactiae)
β-haemolytic. Asymptomatically colonises gential/lower GI tract.
Virulence: capsule defeats alt. pathway. Peptidase inactivates C5a.
Disease: meningitis in neonates.
Dx.: culture of blood, CSF, Lancefield group antigen.
Tx: penicillin prophylactically for pregnant women.
Formerly group D strep. Grows on harsh conditions, 40% bile salts. Part of normal GI flora.
Pts.: those on antimicrobial chemotherapy.
Disease: 2nd/3rd most common nosocomial infxn, UTIs, endocarditis.
Notes: multidrug resistent, including vancomycin
S. bovis
Non-enterococcal grp D strep. Hardy.
Disease: endocarditis, bacteraemias. Links to colon cancer.
Notes: susceptible to penicillin.
Viridans streptococci
α-haemolytic non-enterococcal group D streptococci. Normal oral flora.
Disease: dental caries; grow on tooth surface biofilm, produce lactic acid from sugars. Infective endocarditis.
S. pneumoniae
Gram+ diplococci or short chains. α-haemolytic, catalase-, optochin susceptible.
Virulence: capsule, pneumolysin (toxic for pulmn. endothelial cells), adhesins.
Diseases: pneumonia, meningitis, sinusitis, otitis media.
Tx: penicillin, cephalosporins, vancomycin if resistent.
7-valent protein conjugate pneumococcal vaccine
Vaccine against S. pneumoniae; improvement over original 25-valent due to ↑'d immunogenicity due to conjugation with toxoid. Good in children.
Nocardia asteroides complex
Gram+ filamentous aerobic. Weakly AFB.
Disease: Norcardiosis
Habitat: soil
Sxs: abscesses; pulmonary (w. dissemination) or cutaneous infxn.
Dx: stain w. acid fast or silver stain. Readily cultured; white chalky colonies in 2-3wks.
Nocardia pulmonary infxn
Agent: usu. N. asteroides. Pathology: disseminiates to skin, brain in immunocompromised, esp. those with ↓PMNs
Nocardia 1° cutaneous infxn
Agents: N. brasiliensis, N. otitidiscaviarum.
Pathology: subcutaneous abscess, rarely disseminates. Usu. in immunocompromised.
Gram+, fungus-like pleomorphic anaerobes w. branching filaments.
Disease: actinomycosis; dental plaque.
Sxs: chronic production of suppurative abscesses or granulomas. Usu. cervicofacial, thoracic, abdominal.
Path: organisms found within firm yellow sulfur granules. Almost always a mixed infxn.
Corynebacterium diphtheriae
GPR, nonmotile, pleomorphic. Nonuniform staining due to metachromatic granules. Grows with tellurite.
Reservoir: humans; P2P via aerosols or skin exudate. Noninvasive; organism stays at site of innoculation.
Virulence: diphtheria toxin. Tox- strains cause minor localised infxns.
Dx: culture w. tellurite-containing medium. Screen for tox gene with PCR.
Tx: equine antitoxin, vaccinatino w. DPT series toxoid.
Respiratory Diphtheria (tonsillopharyngeal)
Agent: C. diphtheriae
Onset: sudden
Sx: malaise, sore throat, exudative pharyngitis, low-grade fever. Pseudomembrane adheres to resp. tissue.
Complications: Obstruction of airway by pseduomem., myocarditis, polyneuritis.
Cutaneous Diphtheria
Agent: C. diphtheria
Onset: chronic
Sx: non-healing ulcer covered by pseudomembrane. Tox- more common.
Diphtheria Toxin
Classic A/B toxin. ADP-ribosylation of EF-2. Toxin enters via RME. Tox gene carried by lysogenic phage, production maximal in low iron.
Listeria Monocytogenes
Small GPR, facultative anaerobe, β-haemolytic, catalase+, fac. intracellular
Vector: contaminated foodstuffs, grows at low temp. Congenital transmission as well. Peaks in warm months.
Diseases: invasive syndromes; meningitis, sepsis, stillbirth.
Virulence: listeriolysin O (to break out of phagosome), actin propulsion.
Pregnancy-Associated Listeriosis
Agent: L. monocytogenes
Mother often asymptomatic.
Early Onset Disease: transplacental transmission. Sepsis, resp. distress, skin lesions, disseminated abscesses.
Late Onset disease: acquired passing thru birth canal. Meningitis more likely.
dipicolinic acid
Compound from spore-forming bacteria used to complex with Ca2+ to confer heat-resistence to spores.
Clostridium botulinum
Large anaerobic GPB.
Diseases: food poisoning, wound botulism, infant botulism
Virulence: botulinum toxin
Botulinum Food Poisoning
Agent: C. botulinum toxin
Type A, B: Meats
Type E: fish
Sx: dizziness, mm weakness, double-vision, difficulty swallowing, breathing, flaccid paralysis.
Tx: ventilator, circulatory support. Equine trivalent antiserum.
Dx: detection of toxin or organism.
Wound botulism
Rare disease.
Sx: same as botulinum food poisoning.
Assoc.: cocaine snorting and "skin popping" of black tar heroin.
Infant botulism
"Floppy Infant Syndrome".
Pt: <1 yo; honey?
Path: ingested spores able to proliferate due to incomplete GI normal flora of youngling.
Tx: usu. self-limiting. Supportive care given.
Botulinum Toxin
A, B, E serotypes; not heat-resistent, inactivated by cooking).
H (binding) L (active) subunits inhibit ACh release by lysing SNAP.
Medical uses: strabismus, dysphonias, dystonias, facial wrinkles.
Clostridium Tetani
Anaerobic GPB. Colonises only devitalised tissue (low Eh)
Disease: Tetanus (lockjaw); spastic paralysis
Virulence: tetanus toxin
Tx: wound debridement, human antiserum, toxoid vaccine.
Tetanus Toxin
H (binding) L (metalloprotease) subunits bind to GM1 R in CNS, degrades SNAP. Blocks inhibitory ntm release, results in spastic paralysis.
Note: only 1 serotype, vs. 7 for botulinum toxin.
Clostridium perfringens
Anaerobic GPB, type A pathogenic.
Disease: histotoxic necrosis, gas gangrene, anaerobic cellulitis, generalised sepsis.
Virulence: aggressins, toxins (phospholipase C)
Gas Gangrene (histotoxic necrosis)
Low O2 tension in wound starts with anaerobic cellulits, but becomes gas gangrene when extends to healthy tissue.
Tx: surgical debridement, antibiotics, amputation, hyperbaric O2.
Dx: anaerobic culture.
Nontraumatic (spontaneous) histotoxic infection
Agents: C. perfringes, C. histolyticum, C. septicum.
Path: normal flora may cause infxn in pts. w. leukaema or other cancers. Radiation and chemotherapy may alter perm. barriers allowing translocation of the bacteria across GI lumen.
C. perfringes food poisoning
Path: opposite of C. botulinum or C. tetanus; vegetative cell is ingested (often w. meat), then sporulates in GI tract.
Virulence: spore-associated enterotoxin
Sx: brief (1-2d) enteritis; organism/toxin usu. flushed out.
Clostridium difficile
Normal flora in 5%; anaerobic GPB. 1ºly nosocomial, subsequent to antibiotic therapy (clindamycin)
Disease: pseudomembranous colitis.
Virulence: Toxin A (enterotoxin), Toxin B (cytotoxin)
Pseudomembranous colitis
Agent: C. difficile profileration after clindamycin Tx.
Path: Toxin A, B both monoglycosyl transferases causing haemorrhagic necrosis w. sig. mortality.
Tx: metronidazole, vancomycin. Restoration of normal flora essential.
Dc: culture from stool. ELISA.
Bacillus anthracis
Aerobic GPB, spore-forming (like anaerobic clostridia). Zoonitic organisms, no P2P. Only pathogenic bacteria whose spore surivives in soil.
Virulence; capsule, anthrax toxin.
Agent: B. anthracis
Tm: infected animals (agricultural), animal products (industrial).
Forms: cutaneous (thru broken skin), respiratory (wool-sorter's), visceral (rare; from contaminated meat).
Dx: Penicllin, ciprofloxacin, PA vaccine
Cutaneous Anthrax
Most common form of anthrax.
Sx: malignant uclers, blacked skin lesions. Often self-limiting, but may become systemic.
Path: spore germinates on skin, extends to lymphatics, disseminates. Toxaemia, death.
Respiratory Anthrax
Most severe form of anthrax with rapid course, sepsis, high mortality.
Path: spores germinate in alveoli and macs.
Sx: anthrax pneumonia
Visceral Anthrax
Rare form of anthrax from ingestion of contaminated meats.
Sx: mucosal ulceration, lymph node dissemination, toxaemia.
Anthrax Toxin
3 discrete protein components (all 3 needed for full toxicity):
Oedema Factor (EF): AC, ↑s cAMP.
Protective Antigen (PA)
Lethal Factor (LF): zinc metalloprotease; lyses macs to release cytokines (IL-2, TNF). Toxic shock ensues.
B. cereus
Disease: food poisonings, eye infxns after injury, severe infxns in immunocompromised.
Virulence: 2 types of enterotoxins.
Notes: resistent to penicllin (B. anthracis is not)
B. subtilis
Aerobic spore-forming GPC.
Disease: infxn in I.V. drug users
B. thuringensis
Not a human pathogen. Used for pest control; lethal to insect pest larvae.