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Bacteria Disease Cell Structure Differential Staining Oxygen Requirements Endospore Formation Motility Misc.

Reservoir Virulence Factor/Toxin

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

Vibrio Cholerae Cholera Rod Gram Facultative Anaerobe

Prefer slightly alkaline conditions

Botox AB subunit exotoxin B: protective against acid A: Zn-protease Potent neurotoxin (similar to tetanus toxin) Blocks rel of Ach at NMJinhibits muscle contraction Flaccid paralysis

Yes (highly) O-Ag: O1/O139 cause cholera Contaminated water

Flagella, mucinase, Zot (get bet cells) Adhesins Cholera toxin/AB subunit exotoxin B: bind GM1 ganglioside A: ADP-ribosylatesinactivates GptnACcAMP hypersecretion of H2O/Cl-, blocked absorption of Na+ explosive hypermotility, copious watery diarrhea

Transmission Pathogenesis

Aerosol route, sometimes fomites

Infl Reponseinflux of PMN, killed by toxinneucrosis *anorexia, lethargy, enlarged cervical lymph nodes Pseudomembrane in throat (dead ep cells, bld, leukocytes, fribin) block respiration Systemic Toxemia myocarditis

Injection of spores into deep traumatic wound, low ID50

Toxin spreads thru nerve fibers or blood to CNS Spastic Paralysis: locked jaw (masseter), back and neck, abdominal, extremity m.m.

Food Not person-to-person

Flaccid Paralysis Foodbourne Botulism: double/blurred vision, drooping eyelids, slurred speech, difficulty swallowing, dry mouth, m. weakness, paraylysis, no fever Also wound and inhalation botulism possible

Must survive acidic pH of stomach, ID50~109 ; oral-fecal route

No inflammation Rica water stools of Cholera: mucus flecked, watery, no blood or fecal leukocytes

Diagnosis Treatment

Throat culture, difficult Antitoxin, antibiotics, vaccine

Clinical presentation Antitoxin (human tetanus immune globulin), sometimes antibiotics

Cant culture Antitoxin, most recover after supportive care

Symptoms, selective medium Replacement of fluids/electrolytes *improved sanitation

Bacteria Disease

Staphylococcus Aureus Invasive: abscesses, wound infections, pneumonia Toxigenic: scalded skin syndrome, toxic shock syndrome, food poisoning

Direct Invasion Pharyngitis (Strep throat) Skin & Wound Infections

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

Direct contact or aerosol

Attachment: FNBP, CBP, EBP; Toxins: tissue damage; spread: further damage Pyogenic Diseases (Pus forming disease): locally destructive boils, carbuncles, folliculitis, impetigo

Direct contact or aerosol

Avoid phag/opsonizationmultiplication/invasion into tissuesspread Localized epithelial After spread 1-3 weeks after scarlet damage before spread erythrogenic toxin fever

*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)

*impetigo (pyoderma), puerperal childbed fever, erysipelas, cellulitis, necrotizing fasciitis

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

Aerosol Productive cough w/ bloody sputum, chest pain

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)


Gram stain of sputum, quelling test


Resistance against penicillin Erythromycin, vancomycin, vaccine

1 Macrolides, fluroquinolones 2 doxycylcine Penicillin resistant

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

Treponema Pallidum Syphilis Helical/Spirochetes Gram -

Borrelia Burgdorferi Lyme Disease Helical/Spirochetes Gram -

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

Difficult, not culturable, darkfield microscopy Penicillin, tetracycline, erythromycin,

Can be cultured Antibiotic prophylaxis, doxycycline, amoxicillin, cerfuroxime

Bacteria Disease Cell Structure Differential Staining Oxygen Requirements Endospore Formation Motility Reservoir Misc. Virulence Factor Toxin

Chlamydia Trachomatis Chlamydia

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

Strictly human Do not synthesize amino acids, do syn ATP

Two Cell Types: Elementary body (EB): hardy, EC form, nonreplicative, infectious form, stores ATP Reticulate body (RB): fragile, metabolically active, replicative, dont survive EC, line up around periphery of inclusion, take nutrients from host 1. Dormant phase 2. Entry: Adherance: heparin sulfate, estrogen rec, Invasion: actin arrangements, pedestal formation w/o use of trigger or zipper mech 3. EBRB: (endocyticexocytic) 4. RB multiplication 5. RBEB (Type III) IncA (necessary for inclusions): phos by host cellvacuole fusionexit (destroy vacuole or fuse with cell membrane)

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)


Oral-fecal (food handlers) ID50 very low, highly infectious

Evade Host Immune Response: 1. trigger uptake to non-prof APC 2. escape phagosome 3. spread to other epithelial cells via actin tails LPSsevere inflammatory response *Fever, abdominal pain, diarrhea (w/bright red blood and pus)

Oral-fecal ID50 very low (S. enteritidis: ID50)

Infect M cells in mucosa of lg intestine 1. trigger endocytosis in M cells 2. membrane ruffling (via inv & T3SS) 3. pass thru M cellsubmucosa 4. ingested by m (T3SS) 5. multiply in spleen/liver 6. LPS in blood streaminfl response (high fever, flushing, anorexia) Samonellosis (Gastroenteritis); S. enteritidis: nausea, vomiting, diarrhea, muscle ache and cramping, bacteremia Typhoid Fever: enter GI, travel via mfever, headache, fatigue, myalgia Enterotoxigenic E. coli (ETEC) Relatively high ID50 Watery, cholera-like diarrhea Enteroinvasive E. coli (EIEC) Require higher ID Water, sometimes bloody diarrhea Enteropathogenic E. coli (EPEC) Fever, Nausea, Vomiting, Diarrhea (mainly infant diarrhea) Enterohemorrhagic E. coli (EHEC) Low ID50 Hemorrhagic colitis: watery diarrheabloody diarrheahemolytic uremic syndrome (HUS) Uropathogenic E. coli Urinary Tract Infectionspyelonephritis SEC Sepsis Meningitis


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

Facultative anaerobe Facultative anaerobe Facultative anaerobe