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Corynebacterium Diphtheriae Diphtheria Rod Gram + Aerobic Catalase Positive No No Tellurite agar Human carriers on skin or nasopharynx
-tox phage; regulated by DtxR FeDtxR bd to tox gene FeRNAP bd to tox gene AB subunit exotoxin B: bd glycoptn R, heparin-bding EGF, on ep surface (NAD+EF2ADP-ribosyl-EF2) A: ADP-ribosylase (irreversibly block ptn syn)
Clostridium Tetani Tetanus Rod Gram + Strict Anaerobe (very sensitive to O2) Yes Yes Water, normal human flora (GI), spores in soil
Tetanospasmin AB subunit exotoxin B: bd gangliosides on CNS n.n. A: Zn-dependent metalloprotease Toxinendocytosisactivation by acidification of endosome cleaves synaptobrevins (ess for nt rel)block rel of inhibitory nt Spastic paralysis
Clostridium Botulinum Botulism Very long rod Gram + Strict anaerobe (extremely sensitive to O2) Yes
Transmission Pathogenesis
Diagnosis Treatment
Bacteria Disease
Staphylococcus Aureus Invasive: abscesses, wound infections, pneumonia Toxigenic: scalded skin syndrome, toxic shock syndrome, food poisoning
Cell Structure Differential Staining Oxygen Requirements Motility Misc. Reservoir Virulence Factor Toxin
Cocci in clusters Gram + Facultative anaerobes Catalase positive No -hemolytic, high salt media, form golden colonies Human anterior nasopharynx, skin, normal microbiota, thrive in high salt environment
Surface Ags: capsule (prevent phago/chemotaxis by PMN), slime layer (bioflims), ptn A (prevent opsonization), peptidoglycan (act. alt C), Teichoic acid (bd fibronectin, act. C), MSCRAMM Toxins: -hemolysin: pore-forming -toxin: sphinogomyelinase C, hydrolyze mem P.lipids -toxin: dermonecrotic toxin, acts as surfactant P-V leukocidin & -toxin: pore-forming, damage PMN/m Super Ag Toxins: Toxic shock syndrome toxin (TSST-1, system toxicity), Enterotoxins: heat-resist, resist gastric enzymes, food pois Spreading factors & enzymes: coagulase, catalase, staphylokinase/ fibrinolysin, hyaluronidase, penicillinase, DNase, proteases, lipases,etc *AgrD controls expression of RNAIII which act/represses translation and transcription
Streptococcus Pyogenes Toxin mediated Delayed immunologic reaction Toxic-Shock like Rheumatic Fever, Syndrome, Scarlet Glomerulonephritis fever, Necrotizing fasciitis Cocci in chains Gram +
Strictly fermenatative (no respiration) Catalase negative Bacitricin-sensitive, -hemolytic (complete lysis of RBC), Lancefield groupings (cell wall carbohydrate Ag: not capsule) Human nasopharynx, (normal flora)
Surface Ags: hyaluronic acid capsule (mucoid-antiphag), lipoteichoic acid (bd fibronectin, attachment to pharayngeal cells), M ptn (adh, anti-phag, degrade C C3b, bd IgM), M-like ptns (bd IgM, IgG, 2-microglobulin), Ptn F, G (bd fibronectin) Toxins: Streptolysin O- O2 labile: pore-forming , lyse WBC, RBC, immunogenic Streptolysin S-serum soluble: O2 stable, non-immunogenic Pyogenic exotoxins, SPE: superAg Extracellular enzymes: streptokinase A & B (lyse blood clots), hyaluronidase (degrades capsule), C5a peptidase (degrade C), DNAses (degrade free DNA, viscosity in pus)
Transmission Pathogenesis
*Toxic Shock Syndrome: no bacteremia; toxin released fever, rash, hypotension, desquamation, diarrhea, vonmiting, sore throat, m. pain, purura fulminans *Scalded Skin Syndrome: large blisters, fluid-filled, complete desquamation of epithelium, no scarring Food poisoning: no ingestion of organisms necessary; rapid onset of vomiting, diarrhea, nausea Others: osteomyelitis, septic arthritis, endocarditis, pneumonia, empyema (pneumonia complication)
lead to scarlet fever (12 days after pharyngitis) Toxic shock-like syndrome: pyogenic exotoxin, SpeA (bacteria are systemic)
Rheumatic Fever: infl of heart, joints, bld vessels, chronic progressive damage Glomerulonephritis Accumulation of immune complexes in kidneys, acute infl, blood, ptn in urine, edema, hypertension
Diagnosis Treatment
Easily cultured, yellow on MSA, no lasting immunity Penicillin resistant, Vancomycin (only useful one)
Easily cultured Penicillin is drug of choice! Add aminoglycoside if serious, vancomycin if penicillin allergy (no affect on glomerulonephritis)
Bacteria Disease
Cell Structure Differential Staining Oxygen Requirements Endospore Formation Motility Misc. Reservoir Virulence Factor Toxin
Streptococcus Pneumoniae Pneumonia (also Sinusitis, Otitis Media, Meningitis, Bacteremia) Cocci Gram + Facultative anaerobe Catalase negative
Legionella Pneumophila Legionnaires Disease Pontiac Fever Rod Gram Obligate Aerobe Catalase positive Facultative intracellular parasite Motile (flagella) Metabolize amino acids for energy, heatresistant, Cl- resistant Fresh water streams & lakes
Pili (type IV class, adh to m), outer membrane ptn (MOMP, bd C3b), m invasion protentiator (MIP), LPS, DOT (defect organelle trafficking ptnsinh maturation of phagosome/m), Icm (intracellular multiplication ptn, Type IV sec Dot), Degradative enzymes: phospholipase, extracel protease, Type II *can survive in m
Mycobacterium Tuberculosis Tuberculosis (also Leprosy, M. avium complex) Rod Acid fast (Gram + like) Strict Aerobe No Facultative intracellular pathogen Cell Wall: Very high lipid, mycolic acids, arabinogalactan, lipoarabinomannan (LAM) Humans
Cord factor: trehalose dimycolate (toxic, inh PMN migration), Wax D: immunostimulatory Lipoarabinomannan: (T cell prolif, prevent m act), Tuberculin: delayed hypersensitivity -produce NO extotoxins/endotoxins Ability to survive in m: bd C3b on muptakeinh ox burstsulfatidesinh phag-lysosome fusionfuse w/other vesicles
No Lancefield Ag, optochin sensitive -hemolytic Upper respiratory tract (normal flora)
Pneumolysin: not secreted, shed by autolysis, pore-forming, slow ciliary beating, act. C, inh resp burst. Polysac capsule: anti-phag, immunogenic, required for virulence Neuramindase, sIgA protease, H2O2, surface ptns (MSCRAMM), peptidoglycan, teichoic acid, phosphorylcholine
Transmission Pathogenesis
Aerosols, no person-to-person, no asymptomatic carriage Coiling phagocytosisuptake into mmultiplylyse/spread to others Legionnaires Disease: severe, progressive, toxic pneumonia: necrotizing, myalgia, headache, fever, dry coughshock, respiratory failure Pontiac Fever: non-progressive, selflimiting, fever, chills, headache, myalgia
Aerosol ID very low (< CFU) Hypersensitivitytissue destruction and necrosis (heightened immune response: cell mediated immunitymIL-12, IL-1, TNF; TH1recruit m; CD8) resistant to humoral immunity *chronic fever, weight loss, night sweats, productive cough w/ blood sputum, extensive tissue damage to lung Ghon Complex: influx of m (cheesy-like)
Diagnosis
Treatment
PPD skin text: measure DTH reaction to Tuberculin Culture sputum, acid-fast rods 1st line: isoniazids, ethambutol, rifampin 2nd line: ethionamid, streptomycin, etc
Bacteria Disease Cell Structure Differential Staining Oxygen Requirements Endospore Formation Motility Reservoir Misc. Virulence Factor Toxin Transmission Pathogenesis
Corkscrew motility Periplasmic flagella Human mucosal surfaces, strict pathogen Cant be cultured No known toxins (some hly-like genes), adhesins, hyaluronidase (anti-phag) Sexually
Primary Syphilitic chancre 10-90 days after infection, painless ulceration, elevated, neucrotic lymphadenopathy Secondary Metastatic stage 6 weeks after 1 Bacteria systemic Diffuse skin eruptions, widespread rash; CMI Asymptomatic for yearslatency Tertiary Bacteria hard to find, not infectious, granulomatous lesions (skin,bones,joints) Irreversible
Corkscrew motility Periplasmic flagella Deer, ticks, and rodents No person-to-person, linear genome, Fe abstinence, no LPS, TCAC, ETC None listed Ticks
Initial (Skin) Phase Erythema migrans (bulls eye), local infl, fatigue, chills, fever, headache, m./joint ache, swollen lymph nodes Second (Systemic) Phase Bacteria systemic, between endothelial cells, in joints, disseminated rash *skin, nervous system, heart, joints Chronic Phase Immunopathologic reactions, Autoimmunity, inh C, neurological manifestations, difficult to cure
Diagnosis Treatment
Bacteria Disease Cell Structure Differential Staining Oxygen Requirements Endospore Formation Motility Reservoir Misc. Virulence Factor Toxin
Neisseria Gonorrhoeae Gonorrhea (localized infection) Cocci Gram Oxidase positive Catalase positive Facultative intracellular pathogen
Neisseria Meningitis Meningitis Cocci Gram Oxidase positive Catalase positive Facultative intracellular pathogen
Gram type No peptidylglycan Can respire, has ETC Obligate Intracellular pathogen
Require CO2 for growth Strictly human mucosal ep surfaces Human upper respiratory tract
Pili (type IV class, adhesin, twitch motility, Ag variation), Outer membrane ptns: P I (Porin, adh, invasion, resist C, inh phag-lysosomal fusion), P II (Opa, phase/Ag variation, adh, invasion), P III (Rmp, block Ab), Fe-bding ptns, LOS: endotoxin, IgA1 proteases: cleave IgA/lysosomal ptns, Peptidoglycan: cytotoxic Fe-bding ptns, LOS: may be sialylated, IgA1 protease: cleave IgA and lysosomal ptns in cells Type IV Pili: adh, phase/Ag variation Outer membrane ptns: porins (adh/invasion), PII: adherence, phase/Ag variation, LOS: 1 toxin, damage ep/endo cells, infl response Not in GC: Capsule: polysac, -phag
Transmission Pathogenesis
Sex Men: epididymitis, prostatitis Women: vaginitis/cervicitis Lymphogranuloma venereum (LGV): chronic disease caused by L1, L2, L2a, L3 *Infl of draining lymph nodes, painful buboes Trachoma: can lead to blindness
Direct contact of mucosal surfaces Men: epididymitis, prostatitis Women: vaginitis/cervicitis Disseminated Gonococcal Infection: Tbp: acquire Fe in blood, LOS (can survive in PMNs), OMPs, piliGonococcal arthritis
Respiratory aerosols Meningitis: cross BBB, replicate in the meningesmassive infl resp in SAS Meningococcal septicemia: Nasopharynxsubmucosabloodstream meningococcemia frequently fatal bacteremia
Waterhouse-Friderichsen syndrome: Diagnosis Treatment Obtain infected ep cells, grow in cell, ELISA, PCR No vaccine, antibiotics: tetracycline, azithromycin, trichaisis (surgery) Gram stain purulent of exudates, antibiogram No vaccine, antibiotic resistance (esp to penicillin/tetracycline/cipro, tx with ceftriaxone, doxycycline, azithromycin
Vaccine-capsular polysaccharide subunit vaccine, multivalent ptn conjugate vaccine Antibiotics-penicillin, chloramphenicol
Bacteria Disease Cell Structure Differential Staining Oxygen Requirements Endospore Formation Motility Reservoir Misc. Virulence Factor Toxin
Shigella Dysenteriae Dysentery (Bloody Diarrhea) Rod Gram Facultative anaerobe Oxidase negative No Resistant to bile salts No, no flagella Human intestinal tract, contaminated water/food, strict pathogen Glucose fermenter, not lactose fermenter, does not produce H2S, Ag based on O-Ag
Ipa ptns: invasion plasmid organisms (A-D, adh, invasion, escape endocytic vesicle, Type III sec), IcsA, IcsB: intracellular spread on polymerized actin tails Shigatoxin: AB subunitdegrade 23S RNAblock ptn synthesisNa abs, excess fluid, cell death, necrosis of colonic ep, hemorrhagic colitis, neurocytotoxin
Enterobacteriaceae Salmonella Typhi Typhoid Fever Rod Gram Facultative anaerobe Oxidase negative No Resistant to bile salts Yes Human carriers, not part of the normal flora Glucose fermenter, Non-lactose fermenter, produces H2S, Ag based on O-Ag & H-Ag
LPS Invasins Inv-H: Type III sec, PAI I/SPI-1 Ability to survive in m: Type III sec, PAI II/SPI-2 Vi Ag: polysac capsule surrounds O Ag Complex regulatory cascade
Escherichia coli Watery, Cholera-like diarrhea Rod Gram Facultative anaerobe Oxidase negative No Resistant to bile salts EHEC: large intestine Glucose AND Lactose fermenter
Enterotoxigenic E. coli (ETEC) Heat-labile toxin (LT): LT-I, AB-subunit like Cholera toxin, LTII (animal disease); Heat-stable toxin (ST): STa (bd GCcGMPhyper-secretion of H2O), STb (animal dis, HCO3-, Colonizing factors (CF) Enteroinvasive E. coli (EIEC) Like Shigella but no shiga toxin, Ipas (invasion ptns) Enteropathogenic E. coli (EPEC) Bundle-forming pili (BFP): Type IV, local adh, on EPEC adh factor, microcolony formation (interbac interactions, twitch motility LEE Locus: Intimin (bd Tir), Tir (translocated intimin rec, on surf of host cell), Esp (EPEC sec ptns, Type III sec, trigger signals/actin rearrangement) Enterohemorrhagic E. coli (EHEC) Acid-resistant, LEE Locus (Intimin, Tir, Esp), Shiga-like Toxin: bd 28S rRNA, stimulate infl cytokine production Uropathogenic E. coli Adhesins: Type I pili (bd mannose-containing glycoptn rec, fim gene cluster); Pyelonephritis-associated pili Toxins: Hemolysin (HlyA, poreslyses), Cytotoxic necrotizing factor (CNF-1, change cytoskeleton)
SEC Capusle: polysac K Ag, poorly immunogenic, anti-phag, serum resistance, block C, Ab deposition Adhesins: Type I pili, S-fimbriae (bd fibronectin) Invasins: Ibe (invasion of brain endothelium), OmpA (pore forming)
Transmission
Pathogenesis
Diagnosis Treatment
Samenellosis (Gastroenteritis): spontaneously resolves in a couple of days Typhoid Fever: antibiotics, vaccine
Bugs in a Nut Shell: Hey, Im a bug and Im in a nutshell *We only need to know 17 TEST YOUR KNOWLEDGE: CAN YOU FILL IN THE REST OF THIS CHART? Bacteria Staining (only 6 G+ and 1 acid fast, the rest are G-) G+ G+ G+ GG+ G+ G+ GAF GGGGGGGGShape O2 Requirements Toxin Disease
1. Corynebacterium Diphtheriae 2. Clostridium Tetani 3. Clostridium botulinum 4. Vibrio Cholera 5. Staphylococcus aureus 6. Streptococcus pyogenes 7. Streptococcus pnemoniae 8. Legionella pnemoniae 9. Mycobacterium Tuberculosis 10. Treponema pallidum 11. Borrelia burgdorferi 12. Chlamydia trachomatis 13. Neisseria gonorrhoeae 14. Neisseria meningitis 15. Shigella dysenteriae 16. Salmonella typhi 17. Escherichia coli
Rod Rod Rod Rod Cocci Cocci Cocci Rod Rod Helical Helical Cocci Cocci Rod Rod Rod
Aerobe Anaerobe Anaerobe Facultative anaerobe Facultative anaerobe Anaerobe Facultative anaerobe Aerobe Aerobe