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Flashcards in micro Unit 3 Deck (82):

Mantoux Skin test

subcutaneous injection to test for TB antibodies;
= Delayed-type hypersensitivity rxn (shows in 48-72 hours).
* can be "false" positive if have previous exposure
OR have received BCG vaccine.


Mycobacterium Leprae

bacilli bacteria causing leprosy;
virulence factors: similar to TB (wax D, etc.)
2 disease types:
a) Tuberculoid (delayed hypersensitivity)
b) Lepromatous (overwhelmed and shut down immune system)
* treat w/ dapsone, clofazimine, and rifampin (1 year)


tuberculoid leprosy

milder of 2 forms of leprosy, caused by mycobacterium leprae;
-- hypo/hyper-pigmented rash sites
-- loss of touch sensation.
treat w/ dapsone, clofazimine, and rifampin (1 year)


Lepromatous leprosy

more severe form of leprosy, from mycobacterium leprae;
Th1 response = overwhelmed --> immune system shuts down;
-- AFB in tissues
-- tissue damage (rash, skin and PNS nerve thickening, etc.)
-- secondary infections


mycobacterium ulcerans

acid fast rod that causes ulcers, from fresh water...
make mycolactone (a cytotoxin) --> tissue and CD4 cell apoptosis
--> non-healing lesions.
* treat w/ rifampin and streptomycin for 8 weeks


Dieterle silver stain

Used to reveal small rods that do NOT stain well by gram stain



filamentous gram neg. rod, with NO capsule;
*doesn't take gram stain well --> use Dieterle silver stain or Direct fluorescent antibody instead;
Motile w. polar flagellum, slow growing (will grow on BCYE).


BCYE (buffered charcoal yeast extract)

a type of plate often used to grow legionella,
but have to use antibiotics (vancomycin and polymycin B) to minimize growth of OTHER bacteria (ie: strep) on the plate so can see legionella growth.


Legionella transmission

the bacteria = intracellular parasite of aquatic amoebae;
--> often to humans by aerosolization of pond water
no human-human spread;
most commonly affects smokers/elderly/immune-compromised.


legionnaire's disease

more severe clinical disease/manifestation of legionella infection (in immuno-compromised);
--> pneumonia, cough and fever
treatment: quinolones, macrolides, or tetracycline (+ hospitalized)


pontiac disease

less severe clinical disease caused by legionella infection
(usually in healthy ppl, low infectious dose);
--> flu symptoms, no pneumonia
treatment: none (spontaneous resolution)


legionella pneumophila

gran negative bacteria, = facultative intracellular pathogen of naive macrophages and dendritic cells;
immunity: Th1 response (CD4 activated macrophages)
disease: intracellular invasion, endotoxin (LPS) --> inflammation;
*LPS of L.pneumophila << potent that E. Coli or neisseria*


legionella pneumophila virulence factors

1. LPS = endotoxin --> inflammation
* 50 serotypes!
2. MIP (macrophage invasion potentiator): binds to C3 (complementR) on phagocytes
*3. Dot/Icm system: embeds in membrane after MIP binds to C3R, allows coiling endocytosis and prevents fusion of vacuole with endosomes


listeria monocytogenes

non-spore forming gram + rods, motile (by actin & polar flagellum)
(similar to corneybacteria)
- Catalase +, beta-hemolytic
= facultative anaerobe
* found in soil and livestock (ie: even contaminate cantelope)


Listeria monocytogenes infection

* usually from contaminated cheese/dairy/meats (non pasteurized)
mostly in infants and elderly;
--> nausea, abdominal pain, diarrhea, fever;
also (if severe): encephalitis and meningitis, purpural rash
*vertical transmission (across placenta or in birth canal) -> ~lethal
treatment: penicillin G, ampicillin, trimethoprim/sulfamethoxazole;


Listeria virulence factors

1. internalin: surface protein helps w/ invasion of host
2. PLC (phospholipase C): cytolysin
3. listeriolysin O: redox + pH-sensitive cytolysin
--> allows bacteria to escape phagosomes
(*so need CD8 response)
4. ActA and VASP: recruit + polymerize host actin, use to propel through cytoplasm and penetrate adjacent cell


immune response to listeria monocytogenes

* listeria can infect many cell types:
endothelial cells, enterocytes, hepatocytes, fibroblasts, etc.
T-cell mediated response:
Th1 -- macrophages and dendritic cells
** need CD8 to kill cells



gram neg. curved rods (s-shaped), motile w/ polar flagella;
nitrate reductase +, catalase +, oxidase +
*microaerophilic (--> low CO2 output)


Campylobacter jejuni

most prevalent Campylobacter species,
--> acute gastroenteritis + associated w/ Guillan-Barre syndrome;


minor Campylobacter species

C. rectus, C. fetus, C. coli, C. upsaliensis;
* C. fetus --> septicemia in immune-compromised (ie: newborns)
--> can cause miscarriage in pregnant women
**all campylobacter infections peak in summer **


Campylobacter virulence factors

1. acid tolerant --> low infectious dose
2. LPS (similar to gram -): molecular mimicry
(sugar = cross-reactive w/ PNS myelin --> Guillain-Barré syndrome)
3. flagella --> motility (ie: invade more cells)
4. exotoxin that destroys gut mucosa (??)


Campylobacter infection mech:

cramps, fever, bloody diarrhea (1-7 days after ingestion),
*usually self-limits after 3-5 days, can last 1-2 weeks;
usually DO have immunity after infection;
** diagnosis confirmed: stool test
treatment: macrolides and quinolones (B-lactam resistant!)


Helicobacter pylori

gram neg spiral rods, motile w/ polar flagella;
micro-aerophilic and slow growing (needs some CO2);
transmission: fecal-oral
* considered a carcinogen!!!


diseases from Helicobacter pylori infection

* the most common infection in humans (in world)
- Chronic gastritis - peptic ulcer disease
- gastric adenocarcinoma - gastric MALT lymphoma
might be treated w/ antibiotics, but usually persists life-long :(


H. pylori virulence factors

1. motility: penetrates gastric mucus
2. adhesin: attach to gastric epithelium
3. urease: increase gastric pH => chronic infection, ulcers, cancer
4. VacA: converts lyso/endo-somes into vacuoles
5. TSS4: intracellular delivery of cytotoxins (CagA, L, Y)
--> oncogenic and inflammation (IL-8)


H. pylori diagnosis and treatment

urease colorimetric (pH) test, rapid (labeled) urease breath test, immunodetection, etc.
- triple therapy (proton pump inhibitor + clarithromycin + amoxicillin OR metronidazole)
* follow up w/ urease test bc: human-human possible
--> drug resistance = concern!)


Salmonella enterica

motile gram neg. rods, part of enterobactericeae family;
- oxidase neg., bile salt tolerant, produce H2S, but NO lactose fermentation;
- facultative anaerobe;
* primary pathogen, facultative intracellular => need Th1 response


virulence factors for salmonella enterica

1. O antigen (LPS) flagella, K Ag --> capsule; variable but not VIRULENT factors)


Salmonella disease characteristics

* humans = only reservoir for S. typhi; mostly in children;
transmission: fecal-oral (human to human OR animal to human)
severe consequences:
septic shock, typhoid fever (48 hrs)


Typhoid and paratyphoid fevers

from salmonella typhi infection; * rapid invasion of epithelium
- 3 week incubation time
- gram neg shock (sepsis)
- week 1: fever, lethargy, malaise, constipation
- week 2: high fever, sepsis, biliary tract infection, tender abdomen (maybe also petechia and DIC)


treatment for typhoid/paratyphoid fever

treat w/ antibiotics, but must be wary of drug-resistance;
- ciprofloxacin, amoxicillin, cotrimoxazole
- supportive care


shigella illness

transmission: fecal-oral, direct contact, ingest contaminated food/H2O
symptoms: fever, bloody diarrhea, maybe hypotension/shock
* temporary arthritis if not self-resolving
treatment: self-limiting 2-5 days, supportive therapy (esp. hydration), and ~antibiotics


Shigella virulence factors

1. LPS (endotoxin)
2. Shiga toxin --> hemolytic uremic syndrome (inactivates protein synthesis by depurinating A residue on 28S ribosomal RNA)
-- bacteriophage carries shiga toxin genes
3. large plasmid (type III secretion system) --> internalize
4. hemolysin
5. F-actin tail --> motility


Escherichia coli

gram neg., part of enterobacteriaceae family;
Oxidase neg., facultative anaerobe;
* a normal gut commensal BUT can be extracellular pathogen;


E. coli virulence factors

(depend on the strain, typing is difficult)
1. invasiveness
2. Exotoxin (many, affect disease state caused)
3. LPS (endotoxin)
4. Pili


Disease caused by Enterotoxigenic E. coli

--> traveler's diarrhea: watery diarrhea, like cholera;
* usually self-limiting -> treat w/ fluids or peptobismol
=only sm. intestine (NO fever/inflammation/cramping/blood/leuks)
1. need pili (CFA) for attachment (encoded by plasmid)
2. Heat-Labile (LT) and Heat Stable (ST) enterotoxins cause diarrhea


Enteropathogenic E. coli (EPEC)

2nd cause of traveler's diarrhea, via H2O/beef/chicken;
* type IV ("bundle-forming") pili + other adhesin. No CFA, LT/ST
- limited cell invasion, self-limiting,
- usually only very young children


Enteroinvasive E. coli (EIEC)

causes mild dysentery, humans = natural reservoir;
attach to epithelium of large intestine via adhesins and invasins;
* NO exotoxin, but replication in epithelial cells --> tissue damage
** low infectious dose!, self-limiting (no antibiotic treatment)


Enterohemorrhagic E. coli (EHEC)

* major food-borne outbreak (like salmonella)
--> bloody diarrhea + low fever
1. adhere to large intestine
2. make Shiga-like toxins (target blood vessels of GI, kidneys, lungs, etc) *encoded by bacteriophage
treatment: NO antibiotics (can cause hemolytic uremic syndrome)


E. coli and UTIs

E. coli = most common cause of urinary tract infection,
* specific virulence factors: pili for attachment, cytolysin (RTX)
- cystitis (bladder infection 2nd to UTI -- poly/dysuria, no pain)
- pylonephritis (kidney infection -- + fever, chills)


"rice water stool"

white-ish color w/ no normal stool material or blood,
indicative of vibrio cholera infection
* contains HIGH titre of viable bacteria!


Rapid cholera test

similar to rapid strep test, dip into stool sample...
- tests for presence of Cholera antigen
* use only in early stages of infection, when bacterial replication is highly active in the body
(can give false positive)


Vibrio Cholera virulence factors

- cholera toxin (encoded by phage), = A:B5
--> similar to E. coli LT
- pili: co-regulated w/ toxin
--> helps bacteria remain in lumen of small intestine
(all have common H antigen, and varied O antigens -- used to classify subspecies)


Mechanism of cholera toxin

Spontaneous toxoid production...
1. toxoid binds to GM1 ganglioside in small intestine lumen,
2. activates adenylate cyclase
3. increase cAMP levels
--> massive loss of fluid (diarrhea) => hypovolemic shock


bacteria that can cause UTIs (urinary tract infections)

#1. E. coli
- enterobacter aerogenes
- pseudomonas aeruginosa
- proteus vulgaris (*can cause kidney stones)
- klebsiella pneumoniae
- staph. aureus
- enterococcus faecalis


signs of dehydration + severity

- skin doesn't flatten when pinched
- sunken eyes
- "thready" (fast and weak) pulse
* irritable/restless --> lethargic/coma
* Eagerly drink --> unwilling to drink (need IV)


Vibrio cholerae

gram neg. curved rod w/ 1 polar flagellum,
facultative aerobe;
transmission: fecal-oral (human:human, also assoc. w/ algal blooms + shellfish)
--> causes cholera


Cholera (disease)

acute severe diarrhea caused by vibrio cholerae bacteria;
can be fatal --> hypovolemic shock (MASSIVE loss of fluids),
- short incubation period, EASY fecal:oral transmission
- "disease of poverty," equally affects children and adults
--> 75% asymptomatic but can still transmit via fecal matter
treatment: fluids and electrolytes, NO antibiotics


Yersinia pestis

non-motile gram neg. coccobacilli that causes bubonic plague;
(= in enterobacteriaceae family)
- facultative anaerobe, oxidase negative;
- facultative intracellular pathogen (Th1 response)
Transmission: 1. rodent flea bites (bubonic), then person-person aerosol (pneumonic)


Extended mechanism of Yersinia pestis infection

1. flea colonized --> biofilm over gut --> voracious flea
2. flea runs out of rodent host, so bites human
3. bubonic: Ag into bloodstream, localizes to lymph nodes (swell)
--> buboes and gram neg. shock (4-5 days)
*4. infection can move to lungs --> pneumonic:
-multiply in lungs
- cause gram neg. shock (2-3 days) **high fatality!


treatments for yersinia pestis infection

antibiotics: aminoglycosides, doxycycline or floroquinolones;
also: supportive care.


Francisella tularensis

gram neg. rod, grows best on cysteine-glucose blood agar plate;
= facultative intracellular pathogen of macrophages
--> Th1 immune response
transmission: by wild rabbits, rats, etc.
* causes tularemia (complex symptoms, ie: high fevers, granulomas, etc.)


enterobacteriaceae family

gram negative rods, grow on MacConkey plates;
a) lac neg (tan):
- primary = Salmonella, shigella, yersinia
- opportunist = Pseudomonas, proteus
b) lac positive (pink):
opportunists = E. Coli, Enterobacter, klebsiella


Causes of meningitis (by age)

newborns: E. coli and grp B strep
3 mo - 7 yo: Haemophilus influenzae
All ages: Strep. pneumoniae, Neisseria meningitidis


Most common causes of Pneumonia

1. Strep. pneumoniae
2. klebsiella pneumoniae
3. mycoplasma pneumoniae
4. Staph. aureus
5. Chlamydia tracomatis/chamydophila pneumoniae
*6. legionella pneumophila (rare)


Top 5 causes of gram neg. shock

1. E. coli
2. Klebsiella
3. Enterobacter
4. proteus
5. pseudomonas aeruginosa


basic pathway of gram neg. shock

1. LPS binds to LPS binding protein
2. transfer LPS to TLR4 ==> signal cascade --> up-regulate NFkB
3a. increase IL-1B transcription --> fever
3b. synthesize and release TNF-a --> hypotension


Pseudomonas aeruginosa

motile gram neg rod, obligate aerobe, from soil and water;
-- oxidase +, grows white on MAC plate;
= opportunisitic pathogen for ppl w/ no f(x)ing PMNs.
--> septicemia, pneumonia (esp in CF pts), arthritis, abcesses, etc.
* high antibiotic resistance


virulence factors for pseudomonas aeruginosa

Colonization (3): fimbrae/pili, proteases, exopolysaccharide
Invasion (3): Alginate (biofilm against lympho/phagocytes),
pore-forming cytotoxin, hemolysins
Dissemination (3): LPS, Exoenzyme S, Exotoxin A


Exoenzyme S

impairs phagocyte function


Exotoxin A

Inhibits protein synthesis (like diptheria toxin)
* necrotizing


Burkholderia cepacia

nosocomial gram neg. rod, similar to pseudomonas;
often a co-infection with pseudomonas aeruginosa
--> high mortality in CF patients
* high antibiotic resistance
treatment: trimethoprim and sulfamethoxazole



hospital-acquired pathogen


Bacteroides fragilis

most common ANaerobe, gram neg. rod;
==> forms abcess(es) in peritoneal space;
* Capsular polysaccharide (CPC) --> attaches to peritoneal wall
treatment: cephalosporins/carbepenems (if clindamycin resistant)


clinical signs of treponema pallidum infection

==> syphillis.
** lesions on skin of palms and soles of feet,
also fever, swollen lymph nodes, and lesions on tongue and lips
--> gram stain: ambiguous results
---> darkfield wet mount: motile, elongated corkscrew-like cells



caused by treponema pallidum (corkscrew shaped, motile cells),
transmission: STI, congenital infection *highly infectious
testing: rapid test (Ab:Ag) being developed
treatment: 1 intramuscular penicillin G injection
(or tetracycline if penicillin allergy)
-- can be primary or secondary infection


primary syphilis infection

1 or few non-painful lesions (at site of infection, but may be anywhere on body, ie: hand, tongue...), NOT systemic
* easily transmitted
-- after 3-4 weeks of infection
* may resolve with therapy


secondary syphillis

= systemic infection by treponema pallidum 2-10 weeks after primary infection,
--> fever, rash, sore throat, headache, rash (esp. on palms and soles of feet)
secondary lesions "teeming" with spirochetes
* may develop glomerulonephritis (immune complex disease)
*** may resolve w/o treatment but likely cause chronic infection


tertiary syphilis

rare stage of treponema pallidum infection w/ delayed-type hypersensitivity reaction, causes:
- gummas (painless granulomatous lesions, no deterioration)
- neurosyphilis (paralytic dementia, blindness, ~ALS)
- aneurysms


congenital syphilis

can cause natural abortion or fatality in newborns,
if survive: mental retardation, chalky/soft teeth, thin bones


Jarisch-Herxheimer reaction

mild exotoxin shock-like reaction 2-10 hours after penicillin injection for primary or secondary syphilis,
--> bc of release of toxic dead/dying spirochetes
(headache, fever, malaise, hypotension)


Borrelia spp.

microaerophilic spirochete, causes Lyme disease.
transmission: insect vector (ticks)


Lyme disease

infection caused by borrelia (transmitted by ticks),
--> migrating erythematous rash (starts at site of bite) and arthritis
("erythematum chronicum migrans" = bullseye rash)
treatment: doxycycline
**post-treatment Lyme Disease Syndrome = long-lasting joint pain


relapsing fever

alternating symptomatic and asymptomatic periods due to Ag variation over course of replication;
caused by Borrelia recurrentis or hermsii (spirochetes):
- recurrentis: transmitted by lice, epidemic infection
- hermsii: transmitted by soft ticks (high rate), endemic infection


Neisseria gonorrheae (gonorrhea disease)

Sexually transmitted, often also w/ Chlamydia trachomatis;
--> purulent discharge, Pelvic inflammatory disease, epidydimitis, and opthalmia neonatorum (vagina --> newborn eyes)
* rapid test available (test for Ag in secretions)
Treatment: ceftriaxone and azithromycin


neisseria meningitidis

gram negative diplococci,
transmission: by aerosols or share saliva
*obligate human pathogen w/ some asymptomatic E in population
--> meningitis or meningococcemia
treatment: cephalosporin (little resistance)


clinical diagnosis of meningitis

= infection w/ neisseria meningitidis,
--> violent headache, stiff neck, irritability, fever and nausea, hemorrhagic/purpuric rash [& may have low glucose]
* cloudy/turbid CSF = diagnostic


treatment for meningitis

IMMediate treatment,
IV fluids, ceftriaxone, hydrocortisone (anti-inflammatory),
** if DIC (disseminated intravacular coagulation):
--> purpuric rash and gangrene --> treatment: ciprofloxacin


Leptospira interogans

aerobic extracellular spirochete, causes leptospirosis;
--> biphasic illness w/ jaundice, nephritis, fever, GI trouble
transmission: from urine of animals (can survive in standing water)
virulence factors: persistence in host + hemolysins (some)



infection by leptospira interogans;
--> biphasic illness w/ jaundice, nephritis, fever, GI trouble
transmission: from urine of animals
treatment: penicillin, doxycycline, or cefoxatime


potential causes of jaundice

1. Hep A, B, C, or E
2. Leptospira interogans infection
3. yellow fever virus


Disseminated Intravascular Coagulation (DIC)

from systemic immune response, *ie: from Neisseria meningitidis*
--> mis-shapen RBCs in blood,
- reduced platelets
- increased coagulation
==> causes peripheral purpuric rash and gangrene