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162 Cards in this Set

  • Front
  • Back
E coli as an opportunistic pathogen
-95% of all UTI (cystitis-lower, pyelonephritis-upper), meningitis, GI

-VF: capsular antigen (neonatal meningitis), pili (UTI, GI), exotoxin (GI)

-binds mannosides on epithelial cells

-can replicate inside epithelial cells and cause persistant infections due to pods
E coli adhesis
P pili- pyelonephritis, cystitis
Prs pili- cystitis
Type 1 pili- cystitis
S pili- cystitis

F adhesin- pyelonephritis
Dr adhesin- cystitis
P pili
Ecoli pili that cause pyelonepthritis by attaching to Gal-gal of glycolipids on uroepithelial cells and RBC. Encoded on the chromosome
K1 capsule
A polysialic acid capsule (similar to Neisseria's) for E coli that can lead to bacteremia (when urinary flow is obstructed), neonatal meningitis (by crossing BBB and surviving in CSF). Host has sialic acid, so don't get immune rxn.
Klebsiella pneumoniae
G- opportunistic infection that causes respiratory problems. Has a capsule that reduces phagocytosis and complement rxn.

Id on a mucoid colony
Enterobacter cloacae
G- Similar to Kleb but is motile with less capsule.

Common socomial infection after antibiotic therapy.

Burn, wound, resp, UTI infections.
Proteus (vulgaris, mirabilis)
Causes UTI.

Pathogenicity due to flagella and urease synthesis (causes stone formation leading to infection)

Serratia marcesens
G- opportunistic pathogen that causes UTI and resp moreso than GI.

Get pneumonia after contaminated respirator. Can lead to spetic arthritis.

See in heroin addicts.

VF: Has Ig protease.
Pseudomonas aeruginosa
G- opportunistic pathogen that can cause bacteremia, eye and burn infections.

Aerobic or can use N as an e- acceptor.

Occurs in association with resp disease, esp. CF. Causes biofilms in the lung. In CF, P aeru makes alginate capsule that results in mucoid strains.

VF: few nutritional req, endotoxin, plasmid resistance, exotoxin A, S, T, U; elastase & phospholipase, alginate capsule (mucoid)
P. aeruginosa exotoxins
ExoA: ADP-ribosylates elongation factor 2 which stops phagocytosis and causes apoptosis of infected cells.

ExoS/T: ADP-ribosylating enxymes that targets host regulatory proteins

ExoU: cytotoxin with phospholipase activity that causes cell membrane breakdown and death.
Legionella pneumophila
G- opportunistic pathogen that causes pneumonia.

Lives inside amoebas in water of cooling towers (seen in summer with A/C use). Slow growing with alot nutritional req.

Induces apoptosis in macrophages and alveolal epithelial cells, then forms pores in phagocytes.

Diagnose with direct florescent Ab of sputum, antigen in urine.

facultative anaerobe Lac-
Lac + G- opportunistic pathogens
E coli
Klebsiella pneumonia
Enterobacter cloacae
Lac - G- opportunistic pathogens
Serratia marcescens
Proteus mirabilis
Legionella pneumphila
pseudomonas aeurginosa
E coli virulence factors
1. adhesins
2. Shiga-like toxin (encoded on lysogenic phage)- inhibits protein syn
3. LT toxin (heat labile)- identical to cholera toxin
4. ST toxin (heat stable)- acts on guanylate cylase and causes diarrhea
5. endotoxin LPS
6. siperophobe (nutrient uptake systems)
7. hemolysins, cytotoxins
8. K1 capsule- serum resistance that leads to neonatal meningitis.
E coli sources
contaminate farm products, undercooked meat, leafy vegetables

unpasteurized milk/juice

contaminated wading pools

petting zoos
E coli symptoms
Asymptomatic carrier

Diarrhea, sometimes bloody

Sever, cramping ab pain

vomiting- 50%

HUS (hemolytic uremic syndrome)
0157: H7
Strain of E coli that causes bad disease.

Additional genetic factors:
-Imtimin/Tir: part of a pathogenicity island with Tir delivered to the epithelial cell and intimin on the surface of e coli which binds to Tir
-Type III secretion system: A sort of injection needle apparatus that allows e coli to deliver proteins into the host cell.

-Shiga-like toxin (verotoxin): has 2 subunits, has RNA cleavage activity that interfered with host protein synthesis

-hemolysin: forms pores in cells for nutrient aquisisition.
Enterohemorrhagic Ecoli- a food borne pathogen that affects the large intestine. moderately invasive, produces Shiga toxin. problems with hemolytic uremia
Enterophathogenic E coli. Cause of infantile diarrhea via infection of small intestine. Forms A/E lesions, no specific toxins ided
Enteroaggregative ecoli. Causes persistant diarrhea in children via infection of small intestine. No lesions, non0invastine, produces ST toxin, hemolysin.
Important cause of diarrhea via infection large intestine with non0fimbrial adhesins. Replicates withing enterocytes leading to lysis
Enterotoxigenic ecoli that causes diarrhea worldwide via infection in small intesntion. Fimbrial adhesins
Ecoli- Lac status
Lac + (Salmonella and Shigella are Lac-)
Salmonella Lac status
Lac - (Ecoli is lac +, shigella is also lac -)
Shigella Lac status
Lac - (like salmonella but Ecoli is Lac +)
Diagnostic tool 0157:H7
Sorbital agar (this strain is negative-colorless while other ecoli is positive)

aggluntination test for 0157 antigen

biochemical test

H7 serology and toxin analysis

serotyping with pulsed field gel electrophoresis

PCR analysis of virulence factors
Salmonella Gram?
Enterobacter characs
facultative anaerobes
glucose fermenters
oxidase negative
nitrate reduces
Salmonella fermentation
Glu+ Lac-
H2S producer
Salmonella motility
Salmonella general prop
G- rods
non-spore forming
facultative anaerobes
Glu+ in anaerobic conditions
H2S producer
motility due to prescence of flagella
Salmonella species
Over 1500 serotypes, the following are importatn:
Salmonella typhi-one serotype
Salmonella chloeraesuis- one serotype
Salmonella enteritidis (many serotypes)
Lab id of Salmonella
-look at blood, feces, urine
-Differential agar: EMB, MacConkey
-biochem and serological tests to id O, H, Vi antigens
Enteric fever symptoms
Called by Salmonella typhi

-contaminated food or water
7-14 day incubation period
malaise, anorexia, headache, fever to 104
no diarrhea but have abdominal tenderness
Rose spots on trunk
leukopenia (WBC)
intestinal hemorrhages
osteomyelitis (in patients with sickle cell anemia)
Salmonella typi infectious process
Survive gastric acid, reach small intestine, multiply in MO in Peyer's pathches, travel in blood to spleen, bone marrow and gall bladder.
Cultures for Salmonella typhi
blood: positive in 1st-2nd week of disease

stool: positive from 3rd week on
Salmonella typhi diagnosis
-from blood, stool, or urie
-test for febrile agglutinins (O-sugar part LPS, H agglutinins-part of flagella)
-test for Ab to Vi antigen
Antigen found only in salmonella typhi
Vi capsular antigen
Salmonella typhi treatment
1. flouroqhinolones (cipro) or 3rd generation cephalosporins (ceftriaxone)
2. Chloramphenicol, ampicillin, tremothprin plus sulfa

chronic: ampicillin or cipro, cholecystectomy
Typhoid vaccines
For Salmonella typhi:
oral live attenuated (4 doses)
Vi capsular polysaccharadie vaccine via injection
Salmonella choleraesuis
-causes septicemia without GI infection
-occurs in patients with sickle cell anemia, cancer, or kids
-supparative lesions anywhere in body
Cultures for salmonella cholerasesuis
blood: pos during high fever
stool: rarely
Salmonella typhimurium symptoms
-causes enterocolitis in GI
-sudden onset with headache, chills, stomach pain, nausea, vomiting, diarrhea, fever
-due to endotoxin
-1 to 4 days long
Cultures for Salmonella typhimurium
blood: rarely
stool: positive soon after onset
Motility of Shigella?
non-motile no flagella

(while Salmonella is motile)
Motility of Salmonella?
motile with flagella

(while Shigella is non-motile)
H2S Shigella?
non-producer (salmonella is a producer)
Shigella LPS antigen
O antigen only (no H antigen-flagella)
Shigella spread
No animal reservoir- spread by 4 Fs:
Most common shigella in the US
Shigella sonnei
Bacteremia in shigella?
Shigella doesn't cause bacteremia because it doesn't penetrate the submucosa (unlike salmonella)
Shigella innoculum
100- low because shigella can resist killing by stomach acid
Shigella diarhea
Blood diarrhea caused by invading cells in ileum and colon causing mucosal ulcerations. Adsorptive epithelial cells are killed.
Shiga toxin
exotoxin for shigella with two subunits:
A-inactivates 60s of host, protein synthesis is stopped and cell dies
Shigella diagnosis
-id organism in feces: G- rod, Glu +, Lac -, no H2S
Shigella therapy
Gluid and electrolyte replacement

Cipro, trimethoprim-sulfa
Stages in chlymadia development cycle
1. elementary bodies: small, non-multiplying with rigid wall- transmits the infection

2. Initial bodies (reticulate bodies)- larger, they multiply, no rigid walls, noninfectious. after multiplying turn back into elementary bodies
Chylmadia psittaci
Parasite of birds trasmitted to humans in feces, resulting in interstitial pneumonia
Chylamydia pneumoniae
-causes a distinct lobar pneumonia spread by resp. aerosols
chylamydia trachomatis serotypes D-K
1. nongonoccal urethritis (venereal disease). can be asymptomatic

2. inclusion conjunctivitis & infant pneumonia transmitted at birth from infected moms
Chlymidia trachomatis STD treatment
chylamydia trachomatis serotypes A, B, C
Trachoma in Africa and Asia transmitted from finger to eye (or by flies) causes infolding eyelashes, scarring, and blindness.

These serotypes are more invasive.
chylamydia trachomatis serotypes L1, L2, L#
Lymphogranuloma Venereum (LGV): STD with an invasive serotype.

Causes painless papule turning into ulcerating vesicle leading to painful disease of regional lymph nodes.

Use FREI test to diagnose
FREI test
Test (delayed hypersensitivity) used to diagnose LGV caused by Chlymadia trachomatis. Inject intradermally to indicate prior or current disease.
Chlymadia treatment
All treated with tetracycline
Rickettsia prowazekii
Causes primary epidemic typhus: abrupt fever and headache leading to rash on body (but not on soles) transmitted by body louse. Treat with tetracycline
Transmission Rickettsia prowazekii
body louse
flying squirrel
Treatment Rickettsia prowazekii
Weil-Felix Reaction
agglutination test for Rickettsia prowazekii that isn't used anymore
Brill-Zinsser Disease
A recrudescent disease of Rickettsia prowazekii when immunity is compromised.
Rickettsia typhi
Causes endemic murine typhus which resemples epidemic typhus, but less severe. Seen in SW US with ground squirrel as host
Rickettsia typhi animal host
ground squirrels
Rickettsia rickettsii
-Causes Rocky Mountain Spotted fever: fever, headache, atrhritic pains, abdominal pains with nausa and vominiting and rash on soles.

Transmitted via ticks
Rickettsia rickettsii animal hosts
Rickettsia akari
-Causes rickettsial pox: primary skin lesion at bite that resembles chicken pox leading to systemic disease (fever, chills, headache, rash). Non-lethal.

Transmitted from mouse mites
Rickettsia akari animal house
mouse mite
Coxiella burnetii
-Causes Q fever (interstitial pneumonia, fever, headache, elevated LFT, rash).

Stable to drying- humans get by inhaling it when working with animals
Coxiella burnetii transmission
Humans get by inhaling dried particle working with animals: sheep, goat, cow, cat.

high infectious dose in placental tissue
Tick-borne disease caused by obligate intracellular bacteria:
-monocytic infects monocytes
-granulocytic infects granulocytes

Results in fever, lymphocytopenia (cause that is where replication is taking place)
Happens in ehrlichiosis because bacteria invades monocytes and granuloctes, resulting in reduced WBC.
Cornebacteria diphtheria
Pleomorphic G+ rods that cause diptheria (throat infection with fever, cough, sore throuat leading to pseudomembrane).

Systemic infection not due to bacteria but to exotoxin.

Can also cause necrotizing skin infection in tropics
Formed in diptheria, made up of fibrin, necrotic epithelium and white cells. can block respiration in young.
Cornebacteria diphtheria exotoxin
Spreads from bacteria in throat in damage heart, kidney, CNS

Two subunits:
B-binds to host cell surface receptor
A- toxin domain that enters cytoplasm and inactivated protein synthesis by inactivating elongation factor two (EF2)

This is the same as Psedomonas aeruginosa
produced by G+ or G- bacteria
coded by a phage or plasmid
Denatured by boiling
from G- outer membrane
Coded by central DNA as part of membrane
Stable to boiling
Cornebacterium diptherae diagnosis
1. Growth on tellurite and Leoffler media

2. Toxin production (cross a line of bacterial growth with antitoxin and look for precipitate)
Diptheria treatment
Begin treatment immediatly, treat with antitoxin and penicillin
Schick test
Toxin and toxoid test used to determine immunity. If both rxn are -, the patient has Ab to the toxin and is immune.

If the patient has a + toxin and toxoid test, but the lesion fades, the rxn is due to hypersensitivity and the patient is immune.

Hypersensitivity is max at 1.5 days, toxin rxn stays around for 5 days.
Haemophilus influenzae
-Used to be most common cause of children bacterial memingitis.

-Small G-, non-motile, non-spore-formin bacillus with alot nutritional req.
Haemophilus influenzae virulence
no exotoxin, endotoxin not that imp

IgA protease
most common cause of bacterial meningitis until recently
H influenzae
transmission of Haemophilus influenzae
respiratory aerosols
Disease course of Haemophilus influenzae
-Starts as nasopharyngitis with otitis media, then bacteremia of meninges

-epiglottitis and obstructive laryngitis may follow
Haemophilus influenzae pathogen type
Type b is most important pathogen. It has a ribose instead of a hexose in its capsular structure.
Growth factors of Haemophilus influenzae
-facultative anaerobe

-Needs: factor X (heat-stable) and factor V (heat-labile)
Factor X
Hemin Growth factor of Haemophilus influenzae.
Factor V
NAD growth factor of Haemophilus influenzae.

Staph produces alot of V factor leading to growth of Haemophilus influenzae colonies around it on blood agar
Agar required for Haemophilus influenzae
chocolate agar- heated blood agar releases Factor X (hemin) and factor V (NAD) from RBC that are required for Haemophilus influenzae growth
Haemophilus influenzae capsulation?
encapsulated strains are virulent and grow as smooth colonies. they give rise to unencapsulated strains which are not virulent
Immunity aquisition of Haemophilus influenzae
passive immunity aquired from mother which falls off

by age 3, most children have aquired immunity from asymptomatic infections
Haemophilus influenzae vaccine?
yes- conjugate capsular vaccine linked to diptheria toxoid to increase memory
Diagnosis of Haemophilus influenzae
1. Quelling test (swelling of capsule to detect antigen type)

2. blood and spinal fluid cultures on chocolate agar

3. immonoflorescene to detect type b Ag in spinal fluid
Haemophilus influenzae treatment
ampicillin, 3rd generation cephalosporin, Augmenten if ampicillin resistant
Non-typeable Haemophilus influenzae
-No capsule: uses adhesins and LPS for colonization in nasopharynx

-infections restricted to respiratory and ear (otitis media)
Non-typeable Haemophilus influenzae colonization factors
1. peritrichous pili

2. cell-surface adhesins: Hap, Hia, HMW1/2, P2 and P5 porins, OapA OM proteins, LPS
Invasion routes of Haemophilus influenzae
1. macropinocytosis (bacteria makes host surround itself with host membrane, bacteria is internalized)

2. Paracytosis- bacteria passes between cells

3. LPS binding to PAF
mechanism of Haemophilus influenzae to get host to surround bacteria with host membrane and internalize bacteria
Treatment Non-typeable Haemophilus influenzae
amoxicillin for otitis media and sinusitis
Immunity Non-typeable Haemophilus influenzae?
If any, strain specific- no long term
Haemophilis ducreyi
emerging STD

-cause of chancroid (ragged ulcer on genitalia)
Haemophilis aegypticus
conjunctivitis in hot climates
Haemophilis parainfluenzae
cause of pharyngitis and bacterial endocarditis
cause of whooping cough
Bordetella pertussis
Bordetella pertussis
causes whopping cough
Bordetella pertussis G? aerobe?
small G- cocco-bacillus

strict aerobe that requires fresh media for growth
Bordetella pertussis virulence factors
1. pertussis toxin: inhibits adenylate cyclase leading to increased cAMP

2. adylate cyclase toxin: catalyzes production of cAMP (synergistic with pertussis toxin)

3. dermonecrotic toxin: mouse-letal or heat-labile toxin, causes SM contraction resulting in ischemic necrosis of lung tissue

4. Tracheal cytotoxin: causes ciliostasis, DNA inhibition resulting in tracheal epithelial cell death
Bordetella pertussis colonization
1. Pili allows attachment to ciliated epithelial cells of upper resp

2. FHA (pilus-like filamentous hemagglutinin) binds bacteria to host cell

3. pertactin, a surface molecule

These result in local inflam, increase mucuous, ulceration of resp epi, diminished O2 supply, pneumonia
clinical progression of Bordetella pertussis
two stages:

1. catarrhal stage (runny nose, sneezing, fever, mild cough)

2. paroxysmal stage: coughing to dislodge muscous, whoops, vomiting. coughing more frequent at night
immunization Bordetella pertussis
1. DTP vaccine, but not life long immunity

2. new acellular vaccine with PT, FHA, pertactin, pili
diagnosis Bordetella pertussis
rapid direct fluorescein-labeled Ab test
treatment Bordetella pertussis
erythromycin, tetracycline, chloramphenicol

not sensitive to penicillin or ampicillin
Bordetella parapertussis
sporatic whooping cough
Bordetella bronchispetica
resp illness in animals
Haemophilis exotoxins
Neisseria meningitidis causes...
meningocaucal meningitis
Neisseria gonorrhoeae causes...
Neisseria G? Glu? Mal? Lac? Suc? oxidase?
G- diplococci

N. gon: Glu+
N. men: Glu+ Mal+
non-path: Glu+ Mal+ Lac+

all Suc-
Neisseria virulence
1. IgA protease
2. Pili
3. LOS (like LPS but no O side chains)
4. endotoxin
5. N. men: sialic acid capsule (non antigenic)
Neisseria encapsulation
N. men: encapsulated
N. gon: unencapsulated
Neisseria menigococcus characs
-multiplies outside cells, then phag
-lives in nasopharynx
-virulent strains are encapsulated, they give rise to non-virulent unencapsulated strains

-transmitted respitarpy droplets
Neisseria menigococcus organotropism
localize preferentially in meninges, but also in skin, ees, lungs
Waterhouse-Friderichsen syndrome
uncommon occurence of meningococcus causing hemorrhage into adrenal glands leading to shock and death
Neisseria menigococcus symptoms
upper resp infection, high fever, patechiae then ecchymosis (caused by leakage of blood from small vessels)
Neisseria menigococcus diagnosis
blood, spinal fluid, nasopharyngeal cultures

sugar fermentation test

latex agglutination test
Neisseria menigococcus treatment
penicillin or 3rd gen cepahlosporin (ceftriaxone)

rifampicin for household contacts
causes of meningitis
Neisseria meningococcus
Haemophilus influenzae
Streptococcus pneumoniae (most common cause of men now)
Neisseria menigococcus vaccine?
yes- quadrivalent vaccine
Ophthalmia neonatorium
transmission of Neisseria gonorrhoeae to conjunctiva of newborns

prevented now cause all newborns treated at birth with tetracycilne or erythromycin
Neisseria gonorrhoeae infection
bacteria penetrate cells to sub-epithelial CT, inflam and yellow urethral discharge

higher rate of asymptomatic infection in females
Neisseria gonorrhoeae complications
arthritis-dermatitis: joint and skin lesions

chronic pelvic inflammatory disease in females
Neisseria gonorrhoeae diagnosis
G- stain within PMNs (intracellular)
Neisseria gonorrhoeae treatment
Problem with resistance: use cetriaxone and long term tetracycline or doxycycline (for chylamidia)
Neisseria gonorrhoeae drug resistnace
due to:

1. plasmid penicillanase
2. plasmid tetracyclina resistance
3. chromoson broad band resistance (pen, tetr, cephalopsorin)
Neisseria gonorrhoeae immunity?
low immune response due to lots antigenic variation of surface components

no vaccine
Clostridia G? aerobe? spores? cat? oxidase?
G+ rode
obligate anaerobe
catalase negative
oxidase negative
Disease mechanism of Clostridia
1. toxin-mediated disease (no organism required)

2. invasion leads to over-reactive immune response
Clostridium botulinum diseases
noninvasive, causes botulism:
1. food botulism
2. wound botulism (requires spore germination in wound)
3. Infant botulism (from honey- ingestion of spore)
botulism toxin
causes flaccid paralysis by blocking Ach release (but no sensory deficit)

also: dysphagia, diplopia, dry throat, dilated pupils

7 types


not destroyed by stomach acid

causes foot botulism in canned vegetables
Clostridium botulinum diagnosis
-detect toxin in serum, vomit, feces
-EMG (to see muscle weakness- suggestive, not diagnostic)
Clostridium botulinum treatment
Clostridium tetani disease
causes tetanus: spastic paralysis with arched back and activated flexor muscles

resp muscles can be affected leading to problems
tetanus toxin
-one serotype

-cause spastic paralysis by inhibiting release of glycine and GABA

-two subunits: B binds, A inhibits
Clostridium tetani treatment
Tetanus Ab
penicillin plus wound debridement
Clostridium tetani vaccine?
yes- part of DPT, booster every 10 years
Clostridium difficile disease
antibiotic associated diarrhea (nosomical)

pseudomembranous colitis
Clostridium difficile exotoxin
two subunits: A- binds to gut receptor
B- damages colonic mucosa (bloody diarrhea) leading to pseudomembrane formation
Clostridium difficile diagnosis
history of antibiotic use
exotoxin B detection in stool
ELISA to detect toxins
sigmoidoscopy to see plaques
Clostridium difficile treatment
Stop antibiotics
metronisazole, vancomycin
Clostridium perfringens disease
gas gangrene- a surgical disease
tissue necrosis: cellulitis, necrotizing cellulitis, necrotixing fasciitis, myositis or myonecrosis)
Clostridium difficile toxins
1. lecithinase (alpha toxin)- damages host membranes

2. collagenase

3. hyaluronidase
Alpha toxin
Clostridium difficile toxin lecithinase that damages host cell membrane
gas gangrene treatment
wound debridement, penicillin, hyperbaric oxygen