Bacteria Corynebacterium Clostridium Tetani Clostridium Botulinum Vibrio Cholerae

Diphtheriae
Disease Diphtheria Tetanus Botulism Cholera
Cell Rod Rod Very long rod Rod
Structure
Differentia Gram + Gram + Gram + Gram -
l Staining
Oxygen Aerobic Strict Anaerobe Strict anaerobe Facultative Anaerobe
Requireme Catalase Positive (very sensitive to O2) (extremely sensitive to O2)
nts
Endospore No Yes Yes
Formation
Motility No Yes Yes (highly)
Misc. Tellurite agar O-Ag: O1/O139 cause chol
Reservoir Human carriers on skin or Water, normal human flora Prefer slightly alkaline Contaminated water
nasopharynx (GI), spores in soil conditions
Virulence -tox phage; regulated by Tetanospasmin Botox Flagella, mucinase, Zot (get b
Factor/Tox DtxR AB subunit exotoxin AB subunit exotoxin cells)
in FeDtxR bd to tox gene B: bd gangliosides on CNS n.n. B: protective against acid Adhesins
FeRNAP bd to tox gene A: Zn-dependent A: Zn-protease Cholera toxin/AB subunit
AB subunit exotoxin metalloprotease Potent neurotoxin exotoxin
B: bd glycoptn R, heparin- Toxinendocytosisactivation (similar to tetanus toxin) B: bind GM1 ganglioside
bding EGF, on ep surface by acidification of endosome Blocks rel of Ach at A: ADP-ribosylatesinactivat
(NAD+EF2ADP-ribosyl-EF2) cleaves synaptobrevins (ess NMJinhibits muscle G-ptnACcAMP
A: ADP-ribosylase for nt rel)block rel of contraction hypersecretion of H2O/Cl-,
(irreversibly block ptn syn) inhibitory nt Flaccid paralysis blocked absorption of Na+
Spastic paralysis explosive hypermotility, copio
watery diarrhea
Transmissi Aerosol route, sometimes Injection of spores into Food Must survive acidic pH of
on fomites deep traumatic wound, low Not person-to-person stomach, ID50~109 ; oral-fec
ID50 route
Pathogene Infl Reponseinflux of PMN, Toxin spreads thru nerve fibers Flaccid Paralysis No inflammation
sis killed by toxinneucrosis or blood to CNS Foodbourne Botulism: Rica water stools of Cholera
*anorexia, lethargy, Spastic Paralysis: locked double/blurred vision, mucus flecked, watery, no blo
 enlarged cervical lymph
nodes
Pseudomembrane in
throat (dead ep cells, bld,
leukocytes, fribin) block
respiration
Systemic Toxemia
myocarditis
Diagnosis Throat culture, difficult
Treatment Antitoxin, antibiotics,
vaccine
jaw (masseter), back and drooping eyelids, slurred or fecal leukocytes
neck, abdominal, extremity speech, difficulty swallowing,
m.m. dry mouth, m. weakness,
paraylysis, no fever
Also wound and inhalation
botulism possible
Clinical presentation Cant culture Symptoms, selective mediu
Antitoxin (human tetanus Antitoxin, most recover Replacement of
immune globulin), after supportive care fluids/electrolytes
sometimes antibiotics *improved sanitation
 Bacteria Staphylococcus Aureus Streptococcus Pyogenes
Disease Invasive: abscesses, wound infections, Direct Invasion Toxin mediated Delayed
pneumonia immunologic
Toxigenic: scalded skin syndrome, toxic reaction
shock syndrome, food poisoning Pharyngitis Toxic-Shock like Rheumatic
(Strep throat) Syndrome, Fever,
Skin & Wound Scarlet fever, Glomerulonephri
Infections Necrotizing tis
fasciitis
Cell Cocci in clusters Cocci in chains
Structure
Differential Gram + Gram +
Staining
Oxygen Facultative anaerobes Strictly fermenatative (no respiration)
Requiremen Catalase positive Catalase negative
ts
Motility No
Misc. -hemolytic, high salt media, form golden Bacitricin-sensitive, -hemolytic (complete lysis of RBC),
colonies Lancefield groupings (cell wall carbohydrate Ag: not
capsule)
Reservoir Human anterior nasopharynx, skin, normal Human nasopharynx, (normal flora)
microbiota, thrive in high salt environment
Virulence Surface Ags: capsule (prevent phago/chemotaxis by Surface Ags: hyaluronic acid capsule (mucoid-antiphag),
Factor Toxin PMN), slime layer (bioflims), ptn A (prevent lipoteichoic acid (bd fibronectin, attachment to pharayngeal
opsonization), peptidoglycan (act. alt C), Teichoic acid cells), M ptn (adh, anti-phag, degrade C C3b, bd IgM), M-like ptns
(bd fibronectin, act. C), MSCRAMM (bd IgM, IgG, 2-microglobulin), Ptn F, G (bd fibronectin)
Toxins: Toxins:
-hemolysin: pore-forming Streptolysin O- O2 labile: pore-forming , lyse WBC, RBC,
-toxin: sphinogomyelinase C, hydrolyze mem P.lipids immunogenic
-toxin: dermonecrotic toxin, acts as surfactant Streptolysin S-serum soluble: O2 stable, non-immunogenic
P-V leukocidin & -toxin: pore-forming, damage Pyogenic exotoxins, SPE: superAg
PMN/m Extracellular enzymes: streptokinase A & B (lyse blood clots),
Super Ag Toxins: Toxic shock syndrome toxin (TSST-1, hyaluronidase (degrades capsule), C5a peptidase (degrade C),
 system toxicity), Enterotoxins: heat-resist, resist gastric DNAses (degrade free DNA, viscosity in pus)
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
Transmissio Direct contact or aerosol Direct contact or aerosol
n
Pathogenes Attachment: FNBP, CBP, EBP; Toxins: tissue damage; Avoid phag/opsonizationmultiplication/invasion into
is spread: further damage tissuesspread
Pyogenic Diseases (Pus forming disease): locally Localized epithelial After spread 1-3 weeks after
destructive boils, carbuncles, folliculitis, impetigo damage before erythrogenic scarlet fever
*Toxic Shock Syndrome: no bacteremia; toxin spread toxin lead to Rheumatic Fever:
released fever, rash, hypotension, desquamation, *impetigo scarlet fever (1-2 infl of heart, joints,
diarrhea, vonmiting, sore throat, m. pain, purura (pyoderma), days after bld vessels, chronic
fulminans puerperal childbed pharyngitis) progressive damage
*Scalded Skin Syndrome: large blisters, fluid-filled, fever, erysipelas, Toxic shock-like Glomerulonephriti
complete desquamation of epithelium, no scarring cellulitis, necrotizing syndrome: s
Food poisoning: no ingestion of organisms necessary; fasciitis pyogenic exotoxin, Accumulation of
rapid onset of vomiting, diarrhea, nausea SpeA (bacteria are immune complexes
Others: osteomyelitis, septic arthritis, endocarditis, systemic) in kidneys, acute
pneumonia, empyema (pneumonia complication) infl, blood, ptn in
urine, edema,
hypertension
Diagnosis Easily cultured, yellow on MSA, no lasting immunity Easily cultured
Treatment Penicillin resistant, Vancomycin (only useful one) Penicillin is drug of choice! Add aminoglycoside if serious,
vancomycin if penicillin allergy (no affect on
glomerulonephritis)
 Bacteria Streptococcus Pneumoniae Legionella Pneumophila Mycobacterium Tuberculosis
Disease Pneumonia Legionnaires Disease Tuberculosis
(also Sinusitis, Otitis Media, Pontiac Fever (also Leprosy, M. avium
Meningitis, Bacteremia) complex)
Cell Cocci Rod Rod
Structure
Differential Gram + Gram - Acid fast
Staining (Gram + like)
Oxygen Facultative anaerobe Obligate Aerobe Strict Aerobe
Requiremen Catalase negative Catalase positive
ts
Endospore Facultative intracellular parasite No
Formation Facultative intracellular pathogen
Motility Motile (flagella)
Misc. No Lancefield Ag, optochin Metabolize amino acids for energy, Cell Wall: Very high lipid, mycolic
sensitive heat-resistant, Cl- resistant acids, arabinogalactan,
-hemolytic lipoarabinomannan (LAM)
Reservoir Upper respiratory tract (normal flora) Fresh water streams & lakes Humans
Virulence Pneumolysin: not secreted, shed by Pili (type IV class, adh to m), outer Cord factor: trehalose dimycolate (toxic,
Factor Toxin autolysis, pore-forming, slow ciliary membrane ptn (MOMP, bd C3b), m inh PMN migration), Wax D:
beating, act. C, inh resp burst. Polysac invasion protentiator (MIP), LPS, DOT immunostimulatory Lipoarabinomannan:
capsule: anti-phag, immunogenic, (defect organelle trafficking ptnsinh (T cell prolif, prevent m act),
required for virulence maturation of phagosome/m), Icm Tuberculin: delayed hypersensitivity
Neuramindase, sIgA protease, H2O2, (intracellular multiplication ptn, Type IV -produce NO extotoxins/endotoxins
surface ptns (MSCRAMM), peptidoglycan, sec Dot), Degradative enzymes: Ability to survive in m: bd C3b on
teichoic acid, phosphorylcholine phospholipase, extracel protease, Type muptakeinh ox
II burstsulfatidesinh phag-lysosome
*can survive in m fusionfuse w/other vesicles
Transmissio Aerosol Aerosols, no person-to-person, Aerosol
n no asymptomatic carriage ID very low (< CFU)
Pathogenesi Productive cough w/ bloody sputum, Coiling phagocytosisuptake into Hypersensitivitytissue destruction
s chest pain mmultiplylyse/spread to and necrosis (heightened immune
others response: cell mediated

Diagnosis Gram stain of sputum, quelling test
Treatment Resistance against penicillin
Erythromycin, vancomycin, vaccine
Legionnaires Disease: severe,
progressive, toxic pneumonia:
necrotizing, myalgia, headache,
fever, dry coughshock,
respiratory failure
Pontiac Fever: non-progressive,
self-limiting, fever, chills, headache,
myalgia
1 Macrolides, fluroquinolones
2 doxycylcine
Penicillin resistant
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)
PPD skin text: measure DTH
reaction to Tuberculin
Culture sputum, acid-fast rods
1st line: isoniazids, ethambutol,
rifampin
2nd line: ethionamid, streptomycin,
etc
 Bacteria Treponema Pallidum Borrelia Burgdorferi
Disease Syphilis Lyme Disease
Cell Helical/Spirochetes Helical/Spirochetes
Structure
Differentia Gram - Gram -
l Staining
Oxygen
Requirem
ents
Endospore
Formation
Motility Corkscrew motility Corkscrew motility
Periplasmic flagella Periplasmic flagella
Reservoir Human mucosal surfaces, strict pathogen Deer, ticks, and rodents
Misc. Cant be cultured No person-to-person, linear genome, Fe abstinence,
no LPS, TCAC, ETC
Virulence No known toxins (some hly-like genes), adhesins, None listed
Factor hyaluronidase (anti-phag)
Toxin
Transmissi Sexually Ticks
on
Pathogene Primary Secondary Tertiary Initial (Skin) Second Chronic Phase
sis Syphilitic chancre Metastatic Bacteria hard to Phase (Systemic) Phase Immunopathologic
10-90 days after stage find, not Erythema migrans Bacteria systemic, reactions,
infection, painless 6 weeks after infectious, (bulls eye), local between Autoimmunity, inh
ulceration, 1 granulomatous infl, fatigue, chills, endothelial cells, in C, neurological
elevated, Bacteria lesions fever, headache, joints, manifestations,
neucrotic systemic (skin,bones,join m./joint ache, disseminated rash difficult to cure
lymphadenopathy Diffuse skin ts) swollen lymph *skin, nervous
eruptions, Irreversible nodes system, heart,
widespread joints
rash; CMI
Asymptomatic
for
 yearslatency
Diagnosis Difficult, not culturable, darkfield microscopy Can be cultured
Treatment Penicillin, tetracycline, erythromycin, Antibiotic prophylaxis, doxycycline, amoxicillin,
cerfuroxime
 Bacteria Chlamydia Trachomatis Neisseria Gonorrhoeae Neisseria Meningitis
Disease Chlamydia Gonorrhea (localized infection) Meningitis

Cell Cocci Cocci

Structure
Differential Gram type Gram - Gram -
Staining No peptidylglycan
Oxygen Can respire, has ETC Oxidase positive Oxidase positive
Requireme Catalase positive Catalase positive
nts
Endospore Obligate Intracellular pathogen Facultative intracellular pathogen Facultative intracellular pathogen
Formation
Motility Require CO2 for growth
Reservoir Strictly human Strictly human mucosal ep Human upper respiratory tract
surfaces
Misc. Do not synthesize amino acids, do syn
ATP
Virulence Two Cell Types: Pili (type IV class, adhesin, twitch Fe-bding ptns, LOS: may be sialylated,
Factor Elementary body (EB): hardy, EC form, motility, Ag variation), Outer IgA1 protease: cleave IgA and
Toxin non-replicative, infectious form, stores ATP membrane ptns: P I (Porin, adh, lysosomal ptns in cells
Reticulate body (RB): fragile, invasion, resist C, inh phag- Type IV Pili: adh, phase/Ag variation
metabolically active, replicative, dont lysosomal fusion), P II (Opa, phase/Ag Outer membrane ptns: porins
survive EC, line up around periphery of variation, adh, invasion), P III (Rmp, (adh/invasion), PII: adherence,
inclusion, take nutrients from host block Ab), Fe-bding ptns, LOS: phase/Ag variation, LOS: 1 toxin,
1. Dormant phase endotoxin, IgA1 proteases: cleave damage ep/endo cells, infl response
2. Entry: Adherance: heparin sulfate, IgA/lysosomal ptns, Peptidoglycan: Not in GC: Capsule: polysac, -phag
estrogen rec, Invasion: actin cytotoxic
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)
Transmissi Sex Direct contact of mucosal surfaces Respiratory aerosols
on
Pathogene Men: epididymitis, prostatitis Men: epididymitis, prostatitis Meningitis: cross BBB, replicate
sis Women: vaginitis/cervicitis Women: vaginitis/cervicitis in the meningesmassive infl resp
Lymphogranuloma venereum Disseminated Gonococcal in SAS
(LGV): chronic disease caused by L1, Infection: Meningococcal septicemia:
L2, L2a, L3 Tbp: acquire Fe in blood, LOS (can Nasopharynxsubmucosabloodst
*Infl of draining lymph nodes, painful survive in PMNs), OMPs, ream meningococcemia
buboes piliGonococcal arthritis frequently fatal bacteremia
Trachoma: can lead to blindness Waterhouse-Friderichsen
syndrome:
Diagnosis Obtain infected ep cells, grow in cell, Gram stain purulent of exudates,
ELISA, PCR antibiogram
Treatment No vaccine, antibiotics: tetracycline, No vaccine, antibiotic resistance Vaccine-capsular polysaccharide
azithromycin, trichaisis (surgery) (esp to subunit vaccine, multivalent ptn
penicillin/tetracycline/cipro, tx conjugate vaccine
with ceftriaxone, doxycycline, Antibiotics-penicillin,
azithromycin chloramphenicol
 Enterobacteriaceae
Bacteria Shigella Dysenteriae Salmonella Typhi Escherichia coli
Disease Dysentery (Bloody Diarrhea) Typhoid Fever Watery, Cholera-like diarrhea
Cell Rod Rod Rod
Structure
Differential Gram - Gram - Gram -
Staining
Oxygen Facultative anaerobe Facultative anaerobe Facultative anaerobe
Requireme Oxidase negative Oxidase negative Oxidase negative
nts
Endospore No No No
Formation Resistant to bile salts Resistant to bile salts Resistant to bile salts
Motility No, no flagella Yes
Reservoir Human intestinal tract, Human carriers, not part of the EHEC: large intestine
contaminated water/food, strict normal flora
pathogen
Misc. Glucose fermenter, not lactose Glucose fermenter, Non-lactose Glucose AND Lactose fermenter
fermenter, does not produce H2S, fermenter, produces H2S, Ag based
Ag based on O-Ag on O-Ag & H-Ag
Virulence Ipa ptns: invasion plasmid organisms LPS Enterotoxigenic E. coli (ETEC)
Factor (A-D, adh, invasion, escape endocytic Invasins Inv-H: Type III sec, PAI I/SPI-1 Heat-labile toxin (LT): LT-I, AB-subunit like
Toxin vesicle, Type III sec), IcsA, IcsB: Ability to survive in m: Type III sec, Cholera toxin, LT-II (animal disease); Heat-stable
intracellular spread on polymerized PAI II/SPI-2 toxin (ST): STa (bd GCcGMPhyper-secretion
actin tails Vi Ag: polysac capsule surrounds O Ag of H2O), STb (animal dis, HCO3-, Colonizing
Shigatoxin: AB subunitdegrade Complex regulatory cascade factors (CF)
23S RNAblock ptn synthesisNa Enteroinvasive E. coli (EIEC)
abs, excess fluid, cell death, necrosis Like Shigella but no shiga toxin, Ipas (invasion
of colonic ep, hemorrhagic colitis, ptns)
neurocytotoxin 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

Transmissi Oral-fecal (food handlers)
on ID50 very low, highly infectious
Pathogene Evade Host Immune Response:
sis 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
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)
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
 mfever, headache, fatigue, myalgia Urinary Tract Infectionspyelonephritis
SEC
Sepsis
Meningitis
Diagnosis
Treatment Samenellosis (Gastroenteritis):
spontaneously resolves in a couple of
days
Typhoid Fever: antibiotics, vaccine
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Bacteria Staining Sha O2 Requirements Toxin Disease

(only 6 G+ pe
and 1 acid
fast, the
rest are
G-)
1. Corynebacterium G+ Rod Aerobe
Diphtheriae
2. Clostridium Tetani G+ Rod Anaerobe
3. Clostridium G+ Rod Anaerobe
botulinum
4. Vibrio Cholera G- Rod Facultative
anaerobe
5. Staphylococcus G+ Cocc Facultative
aureus i anaerobe
6. Streptococcus G+ Cocc Anaerobe
pyogenes i
7. Streptococcus G+ Cocc Facultative
pnemoniae i anaerobe
8. Legionella G- Rod Aerobe
pnemoniae
9. Mycobacterium AF Rod Aerobe
Tuberculosis
10. Treponema G- Heli
pallidum cal
11. Borrelia G- Heli
burgdorferi cal
12. Chlamydia G-
trachomatis
13. Neisseria G- Cocc
gonorrhoeae i
14. Neisseria G- Cocc
meningitis i
15. Shigella G- Rod Facultative
dysenteriae anaerobe
16. Salmonella G- Rod Facultative
typhi anaerobe
17. Escherichia G- Rod Facultative
coli anaerobe