Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
67 Cards in this Set
- Front
- Back
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+).
|
|
Streptococci
|
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. |
|
Enterococci
|
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. |
|
Actinomyces
|
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. |
|
Anthrax
|
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.
|