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250 Cards in this Set

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What bug infects CF patients?
pseudomonas aeruginosa
Pseudomonas aeruginosa facts
Oxidase positive
Glu non-fermenter
gram negative rod

Produces blue-green pyocyanin

Resistant to wide variety of antimicrobials
What type of growth of p. aeruginosa is via single celled, motile organisms?
What causes tissue damage in p. aeruginosa infected CF patients?
Intense immune respponse that overwelms the protease inhibitors that normally protect the lung form cell damage
Name 3 multi-drug resistant, glucose nonfermenting gram negative rods in nosocomial infection?
Stenotrophomonas maltophilia
Acinetobacter sp.
Burkholderia cepacia
Name some nosoccomia multi-drug resistant gram positive cocci
Vancomycin resistant enterococci (VRE)
oxacillin resistant S. auereus (ORSA)
vancomycin resistant S. aureus (VRSA)
Wich s. aureus strain is resistant to all drugs but linezolid?
S. aureus
name a common agent of UTI in patients with indwelling catheters?
E coli
What is the most ocmmon cause of gram negative nosocomial bacteremia, due in part to its ability to infect catheters?
Bacillus antracis characteristics
Aerobic, G+, spore forming bacilli
non motile
non hemolytic (unlike other bacillus)
appears in long chains
Bacillus antracis epidemiology
Usurally related to handling spore contaiminated animal products

No evidence for human-human spread

Inhalational antrax more seen in older population
Bacillus antracis virulence factors
1) anti phagoctyttic capsule
2) "protective antigen": helps tranport toxins into mammalian cells
3) Lethal toxin
4) Edema factor
Whtat does b. antracis "protective antigen" do?
Binds to cell and is proteolytically modified to create a binding site for either lethal toxin or edema factor
What does b. antracis edema factor do?
Acts on calmodulin-dependent adenylate cyclase, stimulating the enzyme and --> edema
3 kinds of antrax disease
1) cutaneous. Most common, least mortality. Lesion forms black eschar with little purulence
What does b. antracis edema factor do?
Acts on calmodulin-dependent adenylate cyclase, stimulating the enzyme and --> edema
What does b. antracis edema factor do?
Acts on calmodulin-dependent adenylate cyclase, stimulating the enzyme and --> edema
3 kinds of antrax disease (continued...ended last one too early)
1) cutaneous
2) inhalational. Inhaled spores enter blood stream and cause septic shock and death. High bacteremia. High number of spores must be inhaled. High mortality.
3) GI. Rare. Occurs after eaing contaminated meat. High mortality.
Antrax vaccine and treatment details
Free filtrate including Ab against protective antigen. Efficacy of > 90%.

Treatment with Penicillin G, ciprofloxacin, tetracycline.
Yersinia pestis organism characteristics
Small, oval, G- pleomorphic rods

Bipolar staining

Grows on MacConkey
Y. pestis epidemiology
Worldwide distribution
Rodents are natural hoasts
Spread via fleas
Fleas may spread to humans
Respiratory drops MIGHT spread human to human
Y. pestis virulence factors
1) Fraction 1 (surface envelope protein that protects org from phagocytosis)
2) Yops: Yersinia outer membrane proteins. These are proteins involved in evading host immune response. Fraction 1 is one of 11 Yops. Yop genes are thought tobe found on plasmid pathogenicity island
3) Pla protease: plasminogen activator. A protease that degrades complement components. Important in spread via dissolving clots
4) endotoxin
Y. pestis pathogenesis
1) Bacilli injected into host by fleas
2) most ingested by PMNs and killed
3) bugs ingested by MONOCYTES will SURVIVE.
4) Fraction 1 + bugs resist lysis and are released from monocytes
5) bug dissiminates
6) causes pneumonia and DIC (disseminated intraascular coagulation)
7) the hemorrhagic changes in the skin (DIC, hypoxia, cyanosis) give name "black death)
3 forms of disease (Y. pestis)
1) bubonic. Characterized by grossly enlarged and tender nodes near site of bite. Untreated mortality is 50%.

2) septicemic: usually secondary to bubonic. Bugs grow in blood. Intermediate before pneumonic.

3) Pneumonic. No focus of lymphadenopathy. High fever and dyspnea. Most dangerous. 15% mortality in treated patients.
Y. pestis lab diagnosis
grows on most media.

Take care not to aerosolize it.
Prevention and treatment of Y. Pestis
Quarantine infected.

Control animal reservoirs.

Killed vaccine efficacy: <60%. Crude.

Antibiotics: Streptomycin/gentamicin and doxycycline given parenterally in combination. DO NOT use amp or pen.
Brucella organism characteristics
1) G-, bacillus or coccobacillus
2) aerobic, facultative intracellular parasite
3) killed at pasteurization temp.
Brucella epidemiology
1) infect dairy cattele, sheep ,goats, hogs, dogs, caribou
2) cuase infections in vets, farmers, packers
3) can be shed in cow and goat milk if unpasteurized
4) more likely to be used against animals than humans
Brucella portal of entry
1) contact with infected animal tissue and skin abrasion, oropharynx, conjuntivae
2) ingestion of contaminated & unpasteurized milk
3) possibleinfection via inhalation in attack
Clinical manifestations of brucella
1) bug is phagocytozed by not killed
2) bug localized in the RE system (reticuloendothelial (spleen, liver, bone marrow, etc)
3) can cause granulmoatous and necrotic lesions in lymph nodes, spleen, liver, marrow (like tuberculosis)
4) acute, febrile illness with chills, sweats, pain, weakness, HA
5) lymphadenopathy, hepatosplenomegaly
Lab diagnosis of brucella
1) lysis centrifugation blood cultures
2) serology: febrile agglutinins, problem with cross-reactivity
Prevention and treatment of brucella
1) vaccinnate cows with live attenuated virus
2) Therapy: oral doxycycline (severe cases: streptomycin/gentamicin IM--need drugs to penetrate WBC)
Is brucella categgory A or B agent of bioterrorism?
Possible misdiagnosis of yersinia pestis
Pain may be diagnosedas as acute appendecitis
Principle Staphylococcus species
S aureus
S. epidermidis
S. Saprophyticus
Characteristics of Staphylococcus species?
Catalase positive
Grows on mannitorl salts or blood agar
May produce hemolysis on BA
Other staphylococcus characteristics

can survive hi salt
can survive at 65 deg C
Can survive on inanimate objests
S. Aureus characteristics
Gram + cocci (like all staph)
Lives on skin, nasal pass, inanimate surfaces

S. aureus is tehe primmary pathogenic staph
Associated diseases of s. aureus
1) Pyogenic. Most start as minor infections. Can lead to tissue destruction, inflammation, abcess. May become systeic (mastitis, phlebitis, meningitis, UTI, endocarditis, etc).

2) Toxinoses.
Describe S. Aureus toxin mediated diseases
1) food poisoning. Quick onset. Due to enterotoxin, so generally self limiting. Vomiting.

2) scalded skin syndrome. Seen in newborns, burn victims; skin sloughs off. Not fata. Caused by EXFOLIATIN toxin.

3) TSS. Due to entry of s. aureus via abrasions. TSST-1 responsible for syndromes of shock (pyrogenic superantigen exotoxin)
S. Aureus virulence factors
1) avodiance: capsule, Protein A (binds Fc terminus inhibiting opsonization), Coagulase/clumping factor clots plasma and prevents phagocyte access, catalase inhibits ROS

2) adhesins: matrix binding factors promote colonization and transport cross tisssues

3) Host damage: Peptidoglycan/teichoic acid activate complement and induce inflammation. Secreted factors: proteases, lipases, hemolysins (pore forming toxins), leukocidin (degranulates and kills neutrophils/macrophages). Superantigen toxins: nonspecifically activate T cells. Examples: Enterotoxins A-E (food poisoning, encoded by lysogenic phage), Exfoliatin exotoxin, TSST-1 (a pyrogenic superantigen exotoxin)

NOTE: most virulence factors are controlled by AGR (accessror gene regulator) system that reponds to density via quorum sensing.
Staph epidermidis details
1) found on skin; rarely disease assocated
2) opportunistic pathogen associated w/noscomial infections of prostheses/valves
3) produces slime layer, forms biofilms on foreign body
4) hard to treat (Ab resistant)
5) can cause endocarditis, septicemia in immunocompromised patient
6) not all strains pathoggenic
Staph saprophyticus details
causes UTI; expecially cystitis in young women
Staphylococcus treatment
1) Ab needed for all systemic infection
2) most have beta lactamase production (via transposon) and are thus penn resistant
3) methicillin may be used (semi synthetic, b-lactamase resistant penn)
4) but MRSA exists due to strains with meca gene (-->altered PBP2 that does not bind methicililn as well)
5) also some VRSA exists. Vancomycin is treatment of choice for MRSA.
Legionella pneumophila characteristics
1) Gram neg rods
2) fhard to grow in lab
3) often grow inside amoeba and ciliated protozoa
4) usual outbreak source=contaminated HOH distribution systems
What diseases does legionella pneumophila cause?
Legionaires disease (severe pneumonia)
Pontiac fever (acute onset, flulike, nonpneumonia)
Legionnaires disease details
1) no person to person transmission
2) low infection rate (higher if old, immunosuppressed, sick)
3) begins with flulike symtoms, prgresses to pneumonia symptoms
4) some have diarrhea; may need vent
5) associated wiht Pontiac fever (high exposure/infection rate; self limiting, treatment not needed)
L. pneumophila virulence
Inhaled ia contaminated aerosols
2) bug ingested by phage but survive
3) macrophage gets packed with bug and ruptures, releasing bugs to infect other cells
4) infected macrophages recruit monocytes and neutropils into lung air spaces; may develop into abscesses and cavities.
5) lung damage occurs mainly due to vigorous immune response in the lungs
Host defenses agains LEgionella
1) macrophages make TNF-alpha that inhibits intracellular bugg growth
2) once infection established, cell mediated immune response nneeded
Diagnosis and treatment of LD
Diagnosis difficult. Hard to culture bug, and no rapid tests exist

Recommended Ab: Erythromycin
Mycoplasma, generally:
Lack rigid cell wall
No cell wall peptidoglycan
Bounded by modified membrane
Few pathogenic species
Most infection mild
Clinical features of m. pneumoniae infections
1) causes walking pneumonia (primary atypical pneumonia) compared to pneumonia caused by streptococcus pneum.
2) WP is usually less abrupt onset and milder course
3) HA, fever, chest pain, scanty sputum, paatchy infiltrate, persistant cough, resolves untreated in 3-4 weeks
4) moderately contagious
Prooess of M. pneumoniae infection
1) bug attaaches to ciliated respiratory epithelial cell using specialized structure at bug tip
2) makes toxins (H2O2) that cause cilia to stop beatin in the area
3) infection limited to respiratory mucosa
Mycoplasma, M infections in general
1) no rigid cell wall, no peptidoglycan
2) most are nonpathogenic
3) a few are not, but disease is usually mild, especially in normal patient
Immune response to M. pneumoniae
1) mechanism unknown
2) Some infected people make IgM antibodies that agglutinate RBC at low temp
Treatment of mycoplasma tuberculosis
1) erythromycin treatment of choice
2) can't use Ab that are beta lactams or other cell wall inhibitors--they have no rigid cell wall or peptidoglycan!
Mycoplasmas causeing infection of GU tract (list)
1) m. hominis
2) ureaplasma urealyticum
3) mycoplasma genitalium
Info on GU infecting Mycoplasmas
(M. hominis, ureaplasma urealyticum, mycoplasma genitalium)

1) trasmitted by sex contact
2) cause urethritis in males and cervicitis/salpingitis in females
3) can be transmitted to baby in birth
4) can cause chorioamniotits (fetal membrane inflammation) and postpartum fever
5) can cause spontaneous abortion and premature delivery
Classification of Strep
1) alpha hemolytic: partial zone of hemolysis, maybe eren discoloration
2) beta hemolytic: complete hemolysis
3) gamma hemolytic: no hemolysis
Characteristic of Streptococci? Gram stain and shape
Gram positive, cocci
What kind of strep grows in pairs?
Streptococcus pneumoniiae
Diseases associated with strep pneumoniae
1) leading cause of bacterial pneumonia
2) ear infection
3) pneumococcal meningitis
4) bacteremia
Route of s. pneumoniae infection
1) spread by aerosols
2) colonizes nasopharynx
3) infection often follows lowered host defens (classic 2ry infection arfter viral URI)
4) Inhaled into lung/enters auditory tube
5)avoids phagocytosis
6) in lung, triggers response that damages lung (complement activation, fluid accumulation, etc)
7) may enter blood, cross BBB and cause meningitis
S. pneumoniae virulence factors
1) antiphagocytic capsule
2) Cell wall components like peptidoglycan and teichoic acid elicit inflammatory response, Ab recognition-->complement activation
3) PNEUMOLYSIN: cytotoxin causes RBC lysis. Also can activate complement
S. pneumoniae treatment/therapy
1) usually Penn sensitive
2) Infection-->ab protection against SAME serotype
3) VACCINE: polyvalent capsular vaccine. Adulte: protects agains 23 most common strains. Children: protects against 7 serotypes.
S. pneumoniae diagnosis
1) rusty sputum
2) G+ diplococci
3) Alpha hemolytic
4) sensitive to P disc (optochin), unlike other alpha hemolytic strp
What causes cavities?
Streptococcus mutans, a viridans streptococci
Types of viridans streptococci
S. oralis
S. sanguis
S. Gordonii
S. mitis
S. mutans
Viridans streptococci charactersitcs
1) normal inhabitants of oral cavity
2) most common cause of SUBACUTE BACTERIAL ENDOCARDITIS (affecting abnormal heart valves or prostheses)
Viridans streptococci route of infection
(s. oralis, s. sanguis, s. gordonii, s. mitis, s. mutans)

1) enter circulation thru minor trauma
2) andhere to thrombotic vegetation or valve endothelium via stick polysaccharides
3) proliferate and avoid immune response
4) promote platelt aggregation and fibrin deposition
Symptoms of viridans streptococci induced subacute bacterial endocarditis
Feve, sweats, weoight loss, fatigue rsulting from bacteremia, cytokine release, fragmentation of vegetations into circulatino
Preventative therapy for viridans streptococci
At risk patients (=heart valve lesions) should be put on prophlyaxis prior to dental procedures or invsive GI or GU tract procedures, as it may be opportunity for these bugs to get in blood stream and colonize the lesions
Beta hemolytic strep classification
Subdivided into groups A-U according to C-SUBSTANCE (cell wall carbs)
What is the sp. name for Group a strep?
Streptococcus pyogenes
What carb is on surface of group A (beta hemolytic) strep?
n-acetylglucosamine-rhamnose polymer
Illnesses associated with group A strep
(S. pyogenes)

1) no illness
2) mild illness strep)
3) skin infection (impetigo, cellulitis)
4) severe illness (necroising fasciitis, Streptococcal TSS (STSS))
5) scarlet fever, postpartum sepsis (used to be serious)
6) immune-mediated post-streptococcal diseases (rheumatic fever, acute glomerulnephritis)
Strep throat infection route
2) colonization in throat-->inflamed throat/tonsils and patches of pus. (exudative pharyngitis). Symptoms due to inflammation at site of infection. Self limiting
Streptococcal skin infections
(s. pyogenes: group A strep)

1) impetidgo: infection of epidermal layers
2) cellulitis: when infection spreads to subcutaneous tissues
3) erysipelas is infection of dermis. This may lead to more disseminated disease (5%)
Rheumatic fever: relevance to s. pyogenes
This may be a sequelae of s. pyogenes infection

1) can occur 1-4 wks after resolution of untreated strep throat
2) Autimmune reaction to epitopes shared by s. pyogenes and eart tissue. Damage llikely due to autoreactive T cell attack o fheart cells.
3) the shared epitope likely in the M protein of S. pyogenes
4) SLO (STREPTOLYSIN O), secreted by s. pyogenes, may also cause direct damage to heart via lysis
5) Fever may leed to inflammation/subsequent scarring of heart valves leading to lifelong endocarditis or heart failure risk
What does acute glomerulonephritis have to do with?
1) can follow a strep throat or strep skin infection (s. pyogenes, group a beta hemolytic)
2) kidney disfunction
3) immune cooomlexes resultin from sstrep infection deposit into kidney-->inflammation-->glomerulus damage. This only happens wiht a few GAS strains
GAS virulence factors
(s. pyogenes - beta hemolytic group A)

1) M protein: numerous types. See other card.
2) hyaluronic acid: capsule on bacteria. Also foud in joints, so it looks like host. Also antiphagocytic.
3) Adhesins (M protein, LTA, F protein)--promote adherence to mucosal cells in pharynx or keratinoctes on skin
4) C5a peptidase: degradation prevents c5a recruitmaent of Phagocytes
5) peptidoglycan induces inflammation
6) extracellular products (see other card)
GAS M protein
(Group A strep (s. pyogenes, beta hemolytic)

1) anchored at C terminus to cell surface
2) antiphagocytic: prevents opsonization--binds Factor H, triggers degradation of C3b, prevents C3b deposition on bug
3) antigentic variation in M protein: ensures that some strains won't be reconized by Ab
4) adhesin: it is involved in adhering to site of infection
GAS extracellular products
(S. pyogenes)

1) Streptococcal pyrogenic exotoxins (Spe A, B, C): causes red rash of scarlet fever. Causes STSS rash/fever/shock symtomes; involved in necrotizing fasciitis. Spe is a SUPERANTIGEN (nonspecifically stimulates T cells). Spe A and C are on lysogenic phage.
2) Streptolysin: responsible for RBC lysis. Streptolysin S not involved in virulence. Streptolysin O lyses cells including cardiac cells; may contribute to rheumatic fever
3) hydrolytic enzymes: -ases that damage tissue and cause inflammation.
Treatment/prevention of GAS
(s. pyogenes, beta hemolyic)

1) penn sensitive
2) but invasive things like necrotizing fasciitis hard to stop, since the bugs are done growing but are pumping out Spe toxins
3) vaccines in development
1) beta hemolytic
2) Latex particle agglutination assay for group A antigen)
3) A disc sensitive (baciitracin)
Group B strep example
Stretococcus agalactiae
Diseases associated with Group B Strep
1) neonatal meningitis and sepsis
2) postpartum sepsis
3) asymptomatic carrier infections
Virulence factors of Group B strep
(strep agalactiae)

1) capsule (antiphagocytic)
2) c5a peptidase (inactivates complement)
Group b strep treatment
(strep agalactiae)

1) penicillin. Can consider treating infected preg mom with pen in last trimester or during labor to prevent postpartum/neonatal disease
Gamma hemolytic strep example
Enterococcus faecalis
Descriptoin of e faecalis
1) gamma hemolytic
2) Gram pos
3) cocci
4) pairs or short chains
Route of infection of gamma hemolytic strep
(e. faecalis)

1) normal inhabitant of GI/GU tract
2) nosocomial infection can cause disease when introduced into tissue or bloodstream (often via catheters)
Diseases associated with Gamma hemolytic strep
(E. faecalis)

1) subacute bacterial endocarditis
2) urinary tract infections
3) bacteremia
Identification of Gamma hemolytic strep
(E. faecalis)

1) either non-hemolytic (but may be alpha hemolytic)
2) hardy bacteria
Treatment of gamma hemolytic strep
(e. faecalis)

1) a lot of antimicrobial resistance
2) Need antibiotic synergism--e.g., penn to weaken the cell wall and let in 2d Ab; then add aminoglycoside (streptomycin and gent)
3) note there is even some VRE (cancomycin resistant enterococci)
4) this is a SIGNIFICANT antibiotic resistant nosocomial infection
Disease path for e. faecalis
(gamma hemolytic strep)

1) lives in intestinal, GU tract
2) introduced into bloodstream
3) causes subacute endocarditis or UTI
Haemophilus influenza bug stats
1) Short gram neg rod
2) need X factor and V factor
3) Six capsular serotypes (A-F) and "non-typeable" (no capsule)
4) CAN be normal flora
What is the type b capsular carb for h. influenzae?
PRP (polyribosephosphate)
Invasive hemophilus diseases
1) meningitis (ONLY encapsulated strains)
2) epiglottitis
Infection route of h. influenza
1) colonize URT by adhering to non-ciliated epithelial cells
2) Encapsulated strains can invade sub-epithelium and enter the bloodstream
Meningitis due to h. influenza
1) bug crosses BBB
2) meninges infected
3) Cerebral edema occurs
4) CSF elevated
5) causes HA, stiff neck, vomiting, fever, altered mental state
Non typable hemophilus details
1) not likekly invasive
2) may be associated with ottitis media, bronchitis, sinusitis
3) may be hard to eradicate bc bug grows in biofilm
Meningitis due to h. influenza
1) bug crosses BBB
2) meninges infected
3) Cerebral edema occurs
4) CSF elevated
5) causes HA, stiff neck, vomiting, fever, altered mental state
Are non typeable H. influenzae strains likely to be invasive?
What diseases are non typeable H. influenzae strains associated with
Otitis media, bronchitis, sinusitis.

Can be hard to get rid of due to biofilm growth
How does kid Hib vaccine work?
PRP (b capsule carb) is conjugated to a protein antigen. This increases the immune response to PRP and increases response duration, because it can activate a T-dependent response instead of just a T-independent response. (PRP alone is NOT immunogenic, since young kids dont mount effective anti-polysaccharide responses.)
Who can get Hib conjugate vaccine? Who can't.
Kids over 2 months.

Developing country kids DON'T get is b/c the $3 is too expensive.
How much of the world population is infected with m. tuberculosis
What are Koch's postulates?
To prove that m. tuberculosis was the infected agent, he had to:

1) isolate the bacillus
2) grow it in pure culture
3) administer it to animals to reproduce the disease
What was the first tuberculosis vaccine made with?
Attenuated strain of m. bovis (the "BCG" vaccine)
Quick facts on MTB
(Mycobacterium tuberculosis)

1) Rod shaped bacillus
2) unique cell wall that can't be gram stained
3) will retain basic stain during acid wash, so can be stained via "acid fast" method
4) obligate AEROBE (makes sense!)
5) Slow growth
6) facultative intracellular pathogen (can grow in macrophage)
Types of MTB infection
1) pulmonary
2) non-pulmonary
3) disseminated
MTB infection of a healthy individual (versus HIV)
1) PRIMARY TUBERCULOSIS: iusually self limiting and undiagnosed. Infection goes to lower lung.

2) 10% go on to get CLINICAL/SECONDARY/REACTIVATION tuberculosis within 2+ years. HIV patients have a 10% YEARLY risk.
Course of MTB infection
1) Inhale droplet of 1-3 bacilli
2) bug ingested by macrophages in alveoli
3) If phage is activated, bugs die in the phage. If NOT, bugs multiply and explode phage
4) released bugs taken up by new phage
5) infecte phages then A) migrate thru lymph to nodes, where they disseminate; B) make IL-12 that stimulates TH1 response; C) present MTB antigens to elicit a cell mediated response
6) cell mediated response occurs 2-8 wks after infection; recruited phages form granuloma that seals off infection (but you now have Delayed-type hypersensitive response
7) latent bacilli in granulomas can reactivate with a vengence due to age, HIV, malnutrition, etc.
What is a MTB granuloma?
Central region of macrophages, extracellular bacilli, and dead phhage. Surrounded by newly recruited activated macrophages and T cells. Eventually gets a fibrin coat and is called a TUBERCLE (which can calcify).
What are the disease symptoms of classical TB?
Weight Loss
Night sweats
What are the disease symptoms of MTB due to?
(tissue destruction, fever, weight loss)

Due to host immune response to organism
How does MTB survive in the body?
It gets inside macrophage, where it inhibits PHAGOSOME-LYSOSOME fusion and acidification. So it can survive in a phagosome.
How do you diagnose MTB?
1) positive tuberculin skin test
2) sputum examination
3) antibiotic resistance testing
Describe PPD test
1) PPD = purified protein derivative (of tuberculin protein--crude extract of mycobacterial protein)
2) DTH response to tuberculin indicates cellular immunity to MTB
3) DTH response seen by redenning and thickening of skin within 2-3 days
4) note tho: MTB+ AIDS patients may not show PPD+ response
5) also MOTT can elicit cross-reactive response--and this may include people immunized with old BCG vaccine
Describe problem re. BCG and PPD
People vaccinated with BCG (an attenuated live virus vaccine made from m. bovis) have immune response that is cross reactive with the tuberculin in the PPD test. So people having had this vaccine may show positive PPD.
How do you do the sputum exam part of MTB diagnosis?
1) acid fast stain to visualize any mycobacterial species in smear
2) you can then do a culture, but it takes 3-6 weeks
3) Or do the "RAPID RADIOETRIC BALTEC METHOD" where you inculbate with labeled palmitate and measure released labeled CO2 as evidence of active MTB. Takes 1-2 weeks
Treatment of MTB
1) rif, isoniazid, ethambutol, pyrazinamide
2) multidrug regimen for 6-8 MONTHS
Cure rate for MTB therapy?
What is "DOTS"?
Directly observed therapy short course.

Administered by health department to monitor patient compliance in med regimen
How is leprosy spread?
Most likely inhalation
What is the incubation period of M. leprae
5 years before symptoms
What tissues does m. leprae affect?
Skin, appendages, peripheral nerves

Loss of sensation in affected regions can lead to inadvertent traumas, secondary infection, and disfigurement.
Two types of leprosy
Tuberculoid leprosy: Active cell mediated T cell response damage

Lebromatous leprocy: Weak cell mediated response; olarge number of bug on surface areas
Is m. leprae culturable?
M. leprae treatment
Use MDT: Multidrug therapy. Cures in 6-12 months
Is there a m. leprae vaccine?
BCG MAY protect against leprosy
General facts on MOTT
1) 1/3 to 1/2 have been infected
2) predominant in soil and water of S and MW USA
4) all are acid fast
5) infection generally will NOT produce positive tuberculin PPD skin test
General facts on MOTT
1) 1/3 to 1/2 have been infected
2) predominant in soil and water of S and MW USA
4) all are acid fast
5) infection generally will NOT produce positive tuberculin PPD skin test
Overview of Runyon Classification of MOTT strains
(based on growth rate and colony pigmentation on agar)

1) Group I photochromogens: Slow grow, yellow pigment when grown in light
2) Group II Scotochromogens: Slow grow, pigment in or out of light
3) Group III Nonchromogents: Slow grow, no pigment
4) Group IV: Rapid growers
Group I MOTT examples
(Slow grow, yellow in light)

1) M. Kansasii: TB-like pulmonary disease common in HIV patients in midwest

2) M. marinum: Causes granulomatous skin lesions/draining ulcer. Associated with trauma in contaminated water.
Group II MOTT examples
(Scotochromogens: Slow grow, pigment in light OR dark)

1) M. scrofulaceum: causes lymphadenitis
2) M. ulcerans: causes necrotizing skin ulcer (Buruli ulcer)
3) M. gordonae: nonpathogeneic, common sputum contaminant
Group III Mott examples
(nonchromogens: slow gro, no pigment at all)

1) M. avium complex (MAC): found in water, common in SW. Inhaled or ingestion, but not communicable. Causes either TB-like pulmonary disease or disseminated disease. More common among HIV or COPD individuals. Hard to treat.
Group IV MOTT examples
(rapid growers)

1) M. fortuitum, M. chelonei, M. abcessus: pathogens that cause SKIN ABSCESSES
2) Not pathogenic: m. smegmatis
What is MAC?
M. Avium complex.

Group III Mott infection (slow grow, no pigment). CCasues TB-like disease in HIV patients or preexisting lung disease patients.
Is bordatella pertussis part of normal body flora?
How contagious is B. pertussis
Disease process of b. pertussis
(Whooping cough)

1) bug enters by inhalation
2) Attach to ciliated cells in nasopharynx
3) Secrete toxins tat paralyze cilia and cause inflammatory response
4) this causes 2 week catarrhal phase; patient highly contagious here
5) Bug proliferates and immune response increass
6) thick mucus accumulates in airway and cilia elevator impaird--this leads to characteristic paroxysms of coughing. 2 wks.
7) Convalescent stage: 4-8 weeks, things gradually get better
Morph. and stain of bordatella pertussis
Small aerobic gram neg rod
Common complications of whooping cough
(b. pertussis)


Can be life threatening in kids with cardiac or pulmo disease

Milder in adults, but they may infect susceptible/unvaccinated kid
Treatmetn of b. pertussis infection
1) Abs effective to clear bug and prevent further transmission
2) but they don't really help that patient because bacteria usually have already released the toxins responsiblef for URT damage
Where does b. pertussis growth occur
ONLY on the mucosal surface of RT. It DOES NOT invade into sub-eptihelium.
How does b. pertussis colonize?
Attaces to ciliated cells
Makes adhesins first to attach
Then makes toxins that impair netrophils and kill immune cells
Pertussis toxin details
1) most important virulence factor of b. pertussis
2) protein exotoxin
3) ADP-ribosylates host G-proteins causing inncreased cAMP in neutrophils, which inhibits their bactericidal ability
4) Also causes dramatic increase in lymphocyte number (lymphocytosis)
B. pertussis toxins other than PT
TCT kills ciliated respiratory cells
LPS endotoxin causes fever
Hemolysin kills respiratory epith cells
B. pertussis vaccines
1) Killed whole cell vaccine: good protection, but rare and serious side effects have led to decreased use

2) Acellular vaccine: made of purified bug components. Less serious side effects, but not 100% efficacy. Does at least moderate disease in kids who still get it.

NOTE: immunity wanes 5-10 years after vaccination
Which b. pertussis toxin causes most of the systmeic effects of infection?
PT: ADP-ribosylator that inhibits neutrophil function systemwide
General transimsision route of enteric pathogens
Fecal-oral. Often thru contaminated food or water; also person-person, animal-person
Non-specific host defenses to enteric pathogens
1) Gastric acidity
2) normal gut flora: colonizes mucosal surfaces leaving no room for pathogen attachment; also produce BACTERIOCINS (FA, H2S) that inhibit pathogen growth
3) gut motility
4) bile salts
Primary mechanisms of enteric pathogen cause of disease
1) enteroinvasive
2) enterotoxic (adherence and toxin production, but no invasion of host cells)
3) enteropathogenic (destrow miicrovilli, disrupt epithelial disruption, but no actual cell invasion)
Primary mechanisms of enteric pathogen cause of disease
1) enteroinvasive
2) enterotoxic (adherence and toxin production, but no invasion of host cells)
3) enteropathogenic (destrow miicrovilli, disrupt epithelial disruption, but no actual cell invasion)
List of enteroinvasive enteric pathogens
1) samonella
2) shigella
3) yersinia
4) campylobacter
5) Francisella
6) Listeria
7) enteroinvasive E. coli ("shigella like)
List of enterotoxic enteric pathogens
1) Vibrio cholerae
Enteropathogenic enteric pathogen list
2) Helicobacter pylori
What does virulence of enteroinvasive enteric pathogens depend on?
Ability to penetrate and grow in host cells (though they CAN survive outside)
Salmonella basic characteristics
Gram negative bacillus; lactose negative, facultative anaerobe
3 species of salmonella
S. typhi
S. enteritidis
S. cholerae-suis
Host range of salmonella
All can infect humans

All except typhi can infect other animals
Kinds of salmonella infection/disease
1) Typhoid fever
2) Gastroenteritis
3) septicemia
What is typhoid fever caused by?
Either s. typhi or s. paratyphi (milder)
What is the infectious dose for typhoid fever
10^5 of s. typhi
What is the reservoir for typhoid fever?
What is the disease mechanism for typhoid fever?
1) bug ingested
2) proliferates in GI tract
3) penetrates and crosses epithelium
4) taken up by macrophages, where they multiply and are taken to mesenteric lymph nodes
5) enter blood and are filtered by mononuclear phagocyte sytem (aka RES - reticuloendothelial system)
6) continued growthh in these cells
7) after 1-2 weeks incubation in phages, emerge and invade bloodstream, causing clinical illness
8) usual course untreated: 4-6 weeks
What is a problem that can be associated with Typhoid fever
Ulceration or intestinal perforation, due to good coloniztion of biliary tract that empties into the small bowel
What is the most common kind of salmonella infection?
What is the infectious dose of salmonella for gastroenteritis?
10^6 (high)
How is gastroenteritis usually started?
Ingesting contaminated food
What is disease process of gastroenteritis
Salmonella invades gut mucosa, leading to damage and fluid secretion
What are the symptoms of gastroenteritis
From mild diarhea to sudden onset of severe diarrhea with nausea, vomiting, and fever
What are the symptoms of septicemia (salmonella)
high fever, bacteremia
Who is more likely to get salmonella septicemia?
AIDS patients
Virulence factors of samonella
1) facultative intracellular pathogens: ability to livev inside macrophage is ESSENTIAL for virulence
2) Smoothe (complete) LPS also NECESSARY for virulence
3) Flagella (H antigen) synthesis also has role in intracellular survival. On/off switch regulated by DNA rearrangement. Switching off may help evade immune responses
4) May also be able to turn off other genes in coordinate fashion
S. typhi vaccine
1) oral (live attenuated)
2) injectable (killed)

Neither confers complete protection--you can still be overwhelmed by large inoculum.

Oral vaccine should not be given to pregnant or immunocompromized people
Basic stats on shiella
Gram neg
Lac negative

Causes bacillary dysentary
most virulent strain of shigella
s. dysenteriae
Characteristics of bacillary dysentery

1) from mild diarrhea to dysentery; painful bloody mucosal diarrhea of relatively small volume, fever
Transmission of shigella

Fecal oral. Can be transmitted via roaches and flies due to low infective dose
What is infective dose of shigella?
ONLY 10-100: LOW!! this means roaches and flies that have been contaminated can spread it
Where is shigella dysentary most common?
Institutionallized populations and kids 1-5
What is the shigella reservoir?
What is the shigella disease process?
1) attach to and invade epithelium of intestines
2) multiply within epithelium
3) spread cell to cell
4) cause necrosis
5) this leads to acute inflammation and ulcceration
6) invasion confined to lining of colon and ileocecal valve
Is gastric acidity an important resistance factor for salmonella? shigella?
Salmonella: yes
Shigella: no
Shigella virulence factor
1) #1 factor is ability to invade host cells and survive. Noninvasive=aviruent
2) invasive ability requires large virulence PLASMID
3) Shiga toxin: enteroxic, cytotoxic to several cell lines, lethal in some animals
Whoops: what else does shiga toxin do?
1) enterotoxic
2) cytotoxic to some cells
3) also inhibits PROTEIN SYNTHESIS in eukaryotic cells by CLEAVIN the 28S rRNA in the ribosomes. No evidence for an ADP-ribosylating activity of the toxin)
Shigella vaccine
Attenuated vaccines have been developed, but it has been hard to isolate safe/non-reverting shigella strains
Campylobacter jejuni quick facts
Gram negative
curved rod
enteroinvasive enteric pathogen
What does campylobacter cause?
Major cause of human gastreoenteritis
What is the source of campylobacter sp.
Birds, dogs, farm animals, chickens especially, also UNPASTEURIZED MILK
What is the infectious dose of campylobacter?
500 organisms
What are campylobacter reservoirs?
animals, livestock, cats, dogs, rodents
What are the characteristics of campyloacter gastroenteritis?
From watery diarrhea to shigella-like dysentery.

Usually self limiting, lasts several days.
What is the disease process of campylobacter?
Invade epithelial cells. Produce cytotoxin wiht unknown disease role.

NOTE: there is a correlation between Campylobacter infection and later development of Guillain-Barre syndrome. Therefore, known infections are treated with antibiotics in an attempt to shorten duration of contact.
What are 2 yersinia sp. enteroinvasive enteric pathogens?
Y. enterocolitica
Y. pseudotuberculosis
Quick facts on enteroinvasive Yersinia
Gram negative bacilli
Characteristics of enteroinvasive yersinia infection
1) distinctive acute watery diarrhea
2) mesenteric lymphadenitis (mimics APPENDICITIS)
What is the infectious does of enteroinvasive yersinia?
10^6 organisms
What is the reservoir of enteroinvasive yersinia??
mainly domestic animals and pigs
Quick facts on Listeria monocytogenes
1) eneteroinvasive enteric pathogen
2) gram positive coccobacilli (often confused on slide with Group B strep)
3) grows at cold temperature
4) host range: humans mammals, birds, fish, crustaceans
Characteristics of Listeria infection
1) associated with contaminated foods (dairy, processed meats)
2) I guess it causes dysentery
Listeria vaccine
Who is at most risk of Listeria infection?
Pregnant women, neonates, fetuses
Virulence factors of Listeria:
1) must be able to survive in macrophage
2) Must make LYSTERIOLYSIN O, which disrupts phage vacuole membrane but leaves PM intact.
Francisella tularensis quick facts
1) gram negative
2) aerobic
3) nonmotile coccobacillus
4) need cysteine to grow
5) enteroinvasice enteric pathogen
Tularemia characteristics
(Francisella tulearensis)

1) more commmon in Russia, N europe
2) can occur via skin contact, inhalation, or ingestion
3) Most VIRULENT bug known. 5 bugs enough to cause disease via skin or inhalation (10^6 for ingestion)
Transmission of tularemia
(francisella tularensis)

Transmitted by inoculation of skin, conjunctiva, or mucus membrane with blood or tissue from infeted animal. Also via mosquito, fly bite, tick bite, inhaling dust, eating/drinking contaminated stuff
Symptoms of tularemia
(Francisella tularensis)

1) initiated by contact with skin
2) begins with an ulcer at inoculation site
3) regional lymph nodes swell
4) septicemia ensues
5) sudden onset of fever
What disease process leads to highest tularemia fatality rate?
Inhalation -->tularemic pneumonia
What is systemic tularemia similar to?
Typhoid fever
Where does freancisella best survive and infect?
survives in macrophages and infects the RES?
Quick stats on Vibria cholerae
Gram negative
comma shaped rod
History of cholera infections
7 pandemics

Currently rare in developed world

Epidemic in SA in 1991 caused 4K deaths
Infectious dose of cholera
Epidemiology of cholera
1) water borne
2) humans are sole host
3) not easily spread person to person
4) gastric acidity is an important defense
Clinical characteristics of cholera infection
1) painless, watery diatrrhea
2) rarely vomiting
3) may lose 10-15 L fluid per day
4) May lead to extreme dehydration, metabolic acidosis, hypokalemia
5) 60% untreated mortality; 1% with rehydration therapy
6) is NOT invasive; NEVER causes systemic disease
V. cholerae virulence factors
1) ability to specificaly adhere to host mucosa
2) cholera toxin: enterotoxin (causes net fluid secretion)
CT molecule details
1) multemeric protein; A and B polypeptides
2) A peptide processed to A1 and A2; A1 is the catalytic moiety responsible for activating target adenylate cyclase
3) B polypeptide represents binding moiety--binds to surfase ganglioside; also helps get A1 into target cytosol.
Mode of action of CT
1) A1 subunit targets adenylate cyclase
2) it ADP-ribosylates the Gs subunit of the G protein, stabilizing it in active ATP-bound form. So it constantly is associated with adenlyate cyclase, makign it always "on"
3) intracellular cAMP rises; cells secrete water and electrolyte
4) the stimulation is IRREVERSIBLE
Cholera treatmetn
1) replace lost fluid and electrolytes
2) Ab may be helpful, but do not dimnish symptoms due to existing toxin
3) current vaccines are expensive and not very effective. Current effort to engineer a knockout nonvirulent bug to make vaccine from.
Helicobacter pylori quick facts
1) gram neg
2) spiral shaped rod
3) associated with peptic ulcer disease
4) enteropathogenic
Helicobacter disease

1) Colonizes gastric mucosa
2) may lead to chronic astritis, ulceration, atrophic gastritis, gastic cancer risk
3) raises gastric pH from 1-2 to 7.6
E. coli variants:
1) enteroinvasive
2) enterotoxigenic
3) enteropathogenic
4) enterohemorrhagic
E . coli quick facts
Gram negative bacillus
Lac positive
Common features to all diarrheagenic e. coli
1) critical virulence factors on plasmids, lysogenic phage, or pathogenicity islands
2) characteristic association with intestinal mucosa
3) enterotoxins or cytotoxins often made
ETEC details
Enterotoxigenic E. Coli

1) infection similar to cholera
2) symptoms: cholera like/severe infantile diarrhea to more mild "travellers diarrhea"
3) non bloody, without pus
4) large infectious dose
Enteroinvasive E. coli
1) infection simiolar to shigellosis
2) less common than enterotoxigenic
3) Can penetrate intestinal epithelium like Shigella
4) severe ab cramps and pus/blood in stool
Enteroinvasive E. coli
1) infection simiolar to shigellosis
2) less common than enterotoxigenic
3) Can penetrate intestinal epithelium like Shigella
4) severe ab cramps and pus/blood in stool
Enteropathogenic E. Coli

1) associated with infant diarrhea
2) adhere tightly to epithelial cells
3) destroy brush border microvilli but no overt invasion like with Shigella
Enterohemorrhagic E. Coli

1) causes hemorrhagic colitis
2) bloody diarrhea and cramping
3) may cause HUS: hemolytic uremic syndrome (clots in kidneys lead to RBC destruction and kidney failure)
4) HUS might be made more likely with Ab treatment
5) Generally only O157:H7 strain
6) Only 0157:H7 can NOT ferment sorbitol
7) produces shiga like toxin that damages epithelium and mesenteric blood vessels
What is presumptive evidence of EHEC infection?
Bloody stool and isolation of sorbitol negative E. Coli
Diseases E. coli can cause OTHER than gastroenteritis
1) bacteremia
2) UTI
3) meningitis
ETEC enterotoxins
1) ST: heat stable toxin. carried on transposon. Like cholera toxin.

2) LT: heat labile toxin. Carried on plasmid. Similar to cholera toxin
EIEC enterotoxins
NOT LT or ST (like ETEC): but they do make a Shiga-like toxin
E. coli virulence factors
1) enterotoxin production
2) adherence: must be able to attach to intestinal epithelium to escape intestinal motility. Strains have specific adhesion pili designated CFA (colony factor antigens) that recognize host cell receptors
What are CFAs
Colonization Factor Antigens: E. coli

1) adhesion pili that recognize host cell receptors
2) genes for CFAs are located on a plasmid.
Prevention of enteric pathogen infection
proper food handling
control of carriers
good public health
Treating salmonella sp
1) Ab not indicated in mild gastroenteritis since disease is brief and limited to GI.
2) for Typhoid fever, Ab are used
Shigella treatment
1) Ab reserved for severe cases
Campylobacter treatment
1) has unusual antibiotic sensitivity for enterig Gram neg pathogen
2) usually use Erythromycin
E. coli treatment
Ab use is controversial: it may decrease length of illness, but it might also exacerbate hemolytic uremic disease (HUS)
Helicobacter treatment
Treat ulcer disease with Ab plus Pepto; works symptomaticallly and cures underlying infection
Koch's postulates
(to show that a given pathogen causes a given disease)

1) pathogen found in all diseased an not in healthies
2) pathoen isolated from diseased subjects and grown in pure form
3) pure culture recreates disease when innoculated into new subject
4) pathogen can be reisolated from experimentally infected subjects
Prime example of infectious origin of a chronic disease
Helicobacter pylori causing gastritis, gastric ulcer, gastric cancer risk
What kind of evidence suggests involvement of an infectious agent in a chronic disease?
1) epidemiology (prevalence change not explained by genes or lifestyle)

2) presence of pathogen in individuals with condition, and not in those without

3) continued prevalence of the condition over multiple generation (even though natural selection should be selecting it out)
What are the mechanisms potentially involved when a bacterial pathogen is associated with a chronic disease? Example?
1) persistant inflamation leading to tissue/organ damage. (periodontal disease)

2) production of autoantibodies attacking self tissues due to molecular mimicry/cross reactivity (GAS and rheumatic fever)

3) Bacteria make product that has a direct efect on host's cellular activities (H. pylori and gastric cancer)
Difficulties in determining if a particular bacterium is respponsible for a chronic disease
1) chickeen and egg: is bug causing the problem, or is it an opportunistic bystander?

2) Many suggested pathogens are ubiquitous, so people without disease may show infection evidence as well