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224 Cards in this Set
- Front
- Back
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Quinolones
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ciprofloxacin and moxifloxacin
active against G- enteric bacilii, G+ cocci, and pseudamonas, anthrax, UTIs inhibits DNA gyrase bacteriocidal resistance, damage to developing bone |
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nitroimidazoles
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metronidazole
cidal vs anaerobics, protozoans has to be used anaerobically |
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Rifampin
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cidal, broad spectrum
inhibits beta subunit of RNA polymerase rapid resistance development when used alone excreted in saliva, used prophylactively |
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ethambutol
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TB drug
static |
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pyrazinamide
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TB drug
cidal requires mycobacteria amidase for activation |
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When is it correct to use more than one antibiotic?
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1. synergism
2. susceptibility pattern 3. reduces development of resistance 4. reduce dose of toxic agent 5. polymicrobial infection |
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What are the common mechanisms of resistance?
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1. antibiotic is inactivated
2. antibiotic is pumped out of cell 3. bacteria contains resistance enzyme 4. enter the cell but no drug target 5. altered membrane permeability 6. antibiotic efflux from cell 7. alteration of ribosomal targets 8. alteration of cell wall precursors 9. alteration of target enzymes 10. bypass pathways |
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Common enzymatic mechanisms of inactivation?
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1. cleave beta-lactam ring
2. acetylation, adenylation, phosphorylation 3. chloramphenicol acetyltransferase 4. erthyromycin esterase |
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enzyme inactivation
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beta-lactamase
aminoglycoside modifying enzymes chloramphenicol acetyltransferase erythromycin esterase |
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altered membrane permeability
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beta-lactams
nalidixic acid chloramphenicol amino glycosides |
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antibiotic efflux from cells
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tetracycline
fluconazole |
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alteration of ribosomes
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erythromycin (23S)
streptomycin (30S) |
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altered cell wall precursors
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vancomycin
teichoplanin |
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altered target enzymes
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methicillin (PBP)
sulfonamide (dihydropteroate synthetase) |
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bypass pathways
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trimethoprim
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Mechanisms of antifungal drug activity
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1. alter membrane permeability (bind to sterols in CM, amphotericin B [cidal], nystatin [static])
2. inhibit membrane synthesis (inhibit ergosterol synthesis [static], fluconazole, ketoconazole) 3. inhibit cell wall synthesis (inhibit glucan synthesis [cidal], caspofungin) 4. antimetabolite activity (flucytosine [either/or]) |
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Define sterilization
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killing of ALL microorganisms (bacteria, fungi, viri)
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What is the difference between antisepsis and disinfection?
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antisepsis happens to people; disinfection happens to objects
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Define sanitize
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lowering bacterial content of objects without necessarily killing all bacteria
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Phenol coefficient
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measure of killing capacity of agent, compared to phenol (min killing concentration of phenol is used as standard)
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What are the three physical agents used for santization?
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1. heat (wet or dry)
2. filtration 3. radiation |
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How is pasteurization performed and how effective is it?
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boiled 30 min at 63C reduces path level to 1-3% of baseline. kills tubercle bacillus, salmonella, streptococcus, brucella. Does not kill spores. Verified by testing for alkaline phosphatase.
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by what mechanism does UV light kill bacteria?
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1. creates thymine dimers in DNA interfering with replication (but does NOT cause lethal mutations)
2. causes intracellular peroxide formation |
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pros and cons of UV
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pro:
1. simplicity con 1. poor penetrative capacity (doesn't work through glass) 2. damage to human skin |
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gaseous sterilization
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ethylene oxide
alkylating agent toxic to humans used with high CO2 to prevent explosions |
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Describe the action of alcohol in sanitization
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denatures proteins
not reliable against all organisms isopropyl more potent than ethanol, also more expensive doesnt kill spores |
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halogens
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iodine - surgery
chlorine - food |
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cationic detergents
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active against all types of bacteria
disrupts cell membranes and lipid films most effective = quaternary ammonium salts cidal not effective against pseudamonas, yes vs TB |
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oxidizing agents
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hydrogen peroxide - vs anaerobes in mouth except those with catalase (staph)
K permanganate - urethral antiseptic |
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phenols
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denatures proteins killing wide variety of bacteria but only in high concentrations
triloscan |
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soaps
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nonantibacterial soaps - anionic, remove bacteria from skin
antibacterial - triloscan! |
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heavy metals
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ie - bind to -SH groups
silver nitrate in preventing gynococcal organisms |
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dyes
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gentian violet tx candida and tinea
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aldehydes
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formaldehyde - vaccines
glutaraldehyde - tx areas where hep virus might be present |
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preservatives
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short chain fatty and organic acids preserve food
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Salmonella and shigella are what type of pathogens? Metabolism?
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enteric, gram negative rods
facultative anaerobes, glucose fermenters |
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What result would you expect from an oxidase test of shigella?
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Negative -
they lack cytochrome oxidase, which is required to turn TMPD purple |
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What are the diagnostic characteristics for salmonella?
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1. ferment glucose but not lactose
2. produce H2S --> black precipitate 3. motile (flagellated!) |
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Describe MacConkey Agar
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1. bile acid as selectieve agent
2. lactose 3. red in color below pH of 6.8 |
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What color colonies does salmonella make on MacConkey agar? E. coli?
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Salmonella - relatively white
E. coli - pinkish |
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Describe EMB agar
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1. contains lactose
2. eosin inhibits G+ 3. methylene blue as pH indicator 4. similar fxn to MacConkey |
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Sources of salmonella?
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feces, blood, urine, gallbladder
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How do you diagnose salmonella?
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1. G-
2. glucose fermenter, not lactose 3. produces H2S 3. motile 4. indole negative 5. urease negative |
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How man serotypes of salmonella are there and how are they defined?
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typhi = 1
choleraesuis = 1 enteritidis > 1500 surface antigen-antibody rxn: O (A or I; polysaccharide component of LPS) H (I or II, flagella) Vi (capsular component,salmonella typhi) |
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What are the features of a S. typhi (or paratyphi) infection?
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1. incubation 7-14 days
2. seen earlier in stool 3. episodic fever, bradycardia, rose spots, leukopenia, large liver, spleen 4. intestinal hemorrhage (late phase) 5. may hide in gallbladder |
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Route of infection of S. typhi?
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only infects humans
infects via contaminated food or water resistant to stomach acid adhesins to attach to epithelium bacterially-mediated endocytosis to apical epithelial cells |
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Define a pathogenicity island
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pathogenicity islands are acquired through horizontal gene transfer
extra genetic content, non-native sequences |
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What is encoded by SPI-1
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encodes genes for invasion and type III secretion system
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What is encoded by SPI-2
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intracellular survival genes
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Define the type III secretion system
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A specialized form of secretion wherein a protein moves across the bacterial cytoplasmic and outer membrane AND across the host cell membrane through an injection needle
Effector proteins are delivered into the host cell cytoplasm via the secretion apparatus. Effectors vary by species and strain. In Salmonella, the T3SS delivers toxins that induce membrane ruffling by stimulating actin polymerization, and endocytosis. |
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What mediates a salmonella infection?
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lipid A
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What is the course of typhoid fever?
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1. early: invasion of peyers patches, ingestion by macrophages, survival inside macrophage vacuoles, lysosome resistance
2. bacteremic phase: kill macrophage and disseminate , LPS related fever and shock 3. late GI - reinvasion of GI tract, GL bleed and diarrhea |
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How do you treat typhoid?
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fluoroquinolones or 3rd gen cephalosporin --> inside macrophages
tx chronic carriers with ampicillin or cipro rate of relapse = 10% |
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How do you prevent s. typhi infection?
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control water supplies and sewage disposal
pasteurize milk vaccines 1. oral attenuated 2. Vi capsular polysaccharide vaccine - injection |
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Source of s. choleraesuis?
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swine
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Describe the course of bacteremia related to s. choleraesuis
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6-72 hr incubation
high fever bacteremia gastroenteritis microabscesses on body tissue increased risk with sickle cell anemia and cancer |
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What is caused by s. enteritidis
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diarrheal disease confined to GI tract, rarely + blood culture
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What is the route of transmission of s. enteritidis?
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raw or undercooked eggs, but also other food products, reptiles, peanuts
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How do you treat salmonella gastroenteritis?
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fluid replacement
ampicillin sulfa drugs cepholosporin ciprpo |
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Describe shigella
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1. does NOT ferment lactose
2. nonmotile 3. yes glucose fermentation, but no gas 4. no H2S 5. contains O antigens only, no H 6. indole and urease negative 7. colorless colonies on MacConkey agar 8. 4 different species |
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What are the features of a shigella infection?
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1. children under 10 most susceptible
2. human disease, no animal reservoir 3. spread by 4 Fs (food, fingers, feces, flies) 4. LOW inoculum (100 bugs) 5. acid tolerant 6. incubation period of 1-4 days |
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How does shingella infect a person?
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1. invades intestinal epithelium macrophages via T3SS plasmid
2. uptake by macrophages into phagocytic vacuoles 3. escape from vacuoles into cytoplasm 4. macrophage apoptosis 5. IL-1 and TNF --> fever and systemic infection ALSO: intestinal ulceration due to shiga toxin PMNs in stool indicative of disease bacteremia is rare |
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What is shiga toxin?
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1. produced by s. dysenteriae
2. exotoxin 3. A and B subunits 4. B binds receptor on intestinal cell 5. A interferes with 60S ribosomal RNA 6. diarrhea due to fluid malabsorption 7. ulcer due to mucosal cell apoptosis |
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What is the clinical presentation of a shigella infection?
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fever (LPS)
diarrhea abdominal cramps (shiga toxin) self-limiting organisms persist in feces up to 4 weeks |
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Dx of shigellosis
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NOT by clinical symptoms
isolation of microorganism in feces PMNs in stool |
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What would a Kligler slant-fermentation look like for shigella? E. coli?
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shigella
red at the top, yellow at the bottom -- acidic under anaerobic conditions, alkaline when aerobic E. coli acidic throughout -- no reversion cause lactose can be metabolized |
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What is the treatment for shigella infection?
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1. fluid and electrolyte replacement
2. cipro and trimethoprim 3. test for antibiotic susceptibility |
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What should you do to prevent shigella?
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improve sanitation
no effective vaccine recombinant O-antigen vaccine for shiga toxin is a promising vaccine candidate |
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Name the key features of enterohemorrhagic e. coli
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1. causes bloody diarrhea
2. extracellular, do not disseminate 3. EHEC toxin spreads via blood stream 4. causes hemolytic uremic syndrome |
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How do you catch enterohemorrhagic e coli?
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low infectious dose
food - leafy veg, cookie dough house pets can be reservoirs person to person is an important mode of transmission |
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Describe legionella
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1. G- pleomorphic rod
2. intracellular growth 3. neutritionally fastidious 4. slow growth (hard to isolate) |
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What is legionella's relationship with ameoba?
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Replicate within vacuole within ameoba in water supply
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How to do you contract legionella?
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inhale the free living and ameoba-associated legionella which then infect the lung
not transmitted person to person growth in ameoba thought to prime for infection in the lung |
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What is the clinical presentation of legionaire's disease?
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most infections are insignificant - "cold-like symptoms"
4% of the pop has legionella antibodies symptomatic: fever, chills, cough, muscle aches. headache, tiredness, loss of appetite |
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What are the cellular targets of legionella?
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infects macrophages and epithelial cells --> infection results in cell death via apoptosis (early) or necrosis (late) but always kills cells
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What is Pontiac Fever?
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milder disease associated with legionella infection
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Does legionella trigger an immune response?
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yes! very strong response. also, people with immune deficiency are more likely to be infected.
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What is the test of choice for legionella? What are the alternative tests?
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direct fluorescent antibody test to detect in the sputum
alt: antigens in urine samples antibody levels -- 6 week turn around time |
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Describe the corynebacteria shape etc.
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pleomorphic G+ rods
aerobes do not form spores rods are often club shaped - array looks vaguely like chinese characters 2 main groups: diphtheriae and other |
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Does diphtheria have an animal reservoir?
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no, humans are the only natural hosts
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What is the clinical presentation of diptheria?
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local inflammatory response in throat with fever, cough, and sore throat
a grey pseudomembrane composed of fibrin, necrotic epithiu, and white cells pseudomembrane + edema --> resp issues can also cause necrotizing skin infection |
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What type of toxin does diptheria carry?
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encoded by lysogenic bacteriophage beta --> example of lysogenic conversion
has 2 domains - binding (B and T) and toxin (A) domains blocks protein synthesis by inactivating EF2 - elongation enzyme lethal to eukaryotic cells, targets heart, kidney, nervous system |
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Can you immunize against diptheria?
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yes - antibody against toxin
formaldehyde tx of toxin makes toxoid - used to stimulate immunogenicity part of DTaP - lasts 10 years |
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How do you diagnose diptheria?
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growth on specialized media to identify *metachromatic (phosphate) granules
*stains differentially to rest of bug with the same stain definitive diagnosis is based on demonstration of toxin production also PCR test and immunoassay |
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How do you treat diptheria?
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1. antitoxin-produced in horses
2. antibiotic tx (penicillin) 3. reimmunization |
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Characterize mycoplasma
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1. smallest known organism able to grow and reproduce autonomously
2. stains poorly, cannot be identified by gram stain (no cell wall, pleiomorphic shape, no peptidoglycan in these organisms) 3. only bacterial membrane to contain cholesterol (from the host, resp. for osmotic rigidity) 4. fried egg colonies |
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What is a variable lipoprotein?
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anchored to the cell membrane
helps stabilize bacterial structure provides immune diversity |
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What is the clinical presentation of mycoplasma infection?
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1. usually mild respiratory infection rather than pneumonia
2. slow onset, nonproductive cough, low amounts of sputum 3. can progress to primary atypical pneumonia, pts do not respond to penicillin or sulfonamide - diffuse changes on xray 4. rarely fatal |
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Can mycoplasma disseminate?
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yes! they can get into the CNS. can also cause arthritis and there is autoimmune potential.
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How common are mycoplasma outbreaks?
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5-20% of pneumonia cases
50% of summer pneumonia outbreaks in places where people live in close contact most common in people aged 4-20 |
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How is it transmitted?
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transmission by respiratory droplets
P1 complex attaches to host epithelial cells (cell glycoproteins) |
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What is the mechanism of mycoplasma cell damage?
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1. produces hydrogen peroxide and superoxide --> damages host cell membranes, disrupts nucleic acids and metabolism, leads to ciliostasis
2. inflammation and prior immunity worsen symptoms |
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How do you diagnose mycoplasma infection?
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sputum stain - no prominent bacteria, yes monocytes and PMNs
PCR cold agglutination test - autoagglutination of RBCs at a low temp but not 37 present in serum of about half of infected patients |
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Does mycoplasma have a cell wall?
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NO
you can't use antibiotics that target the cell wall |
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How do you treat mycoplasma infections?
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1. erythromycin
2. tetracycline |
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What is caused by mycoplasma hominis?
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associated with inflammatory situations in the genital tract
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Can you use erythromycin to tx m. hominis?
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nope - you have to use tetracycline
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what is caused by m. arthritidis?
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causes rheumatoid arthritis
produces a super antigen |
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What is caused by ureaplasma urealyticum?
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common inhabitant of the genital tract - causes nongonococcal urethritis
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Describe the general characteristics of haemophilus influenzae
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small
nonmotile G- pleiomorphic |
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What are the 2 main strains of H. influenzae?
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encapsulated (typeable) - cause bacterial meningitis in children under 4
there is a vaccine has a large antiphagocytic polysaccharide capsule responsible for virulence AND for vaccine B, C, D, E, F strains unencapsulated (non-typeable) - causes earaches and respiratory disease |
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What is the Quellung Reaction? Would unencapsulated bacteria be positive?
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antibody-based visualization of the capsule
nope, they would not |
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How is encapsulated H. influenzae transmitted?
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reservoir is the nasopharynx of humans
harbored in healthy children and adults transmitted as an aerosol |
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Does exotoxin play a significant role in H. influenzae pathogenesis
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no exotoxin!
endotoxin is covered by capsule and is less significant part of initial disease. does contribute to systemic infection and meningitis. |
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What is the clinical presentation of an encapsulated H. influenzae infection?
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initial:
nasopharyngitis otitis media sinusitis late: bacteremia to meninges epiglotitis or obstructive laryngitis cellulitis polyarthritis |
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Describe vibrio cholerae
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G- enteropathogen
250 serogroups (O1, O139) O1 has 2 biotypes: classical and El Tor currently in its 7th pandemic |
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How is cholera transmitted?
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Water born disease caused by vibrio cholerae
ingestion of contaminated water or food colonizes upper small intestine - secretes an enterotoxin |
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What is the clinical presentation of cholera?
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painless, copious diarrhea
hypovolemic shock and death if not treated |
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Describe the course of cholera infection
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1. oral ingestion - passage through the gastic acid parrier into the small intestine, expression of colonization factors
2. multiplication: expression of colonization factors and secretion of cholera toxin 3.diarrhea facilitates return to aquatic environment |
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What determines cholerae virulence?
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1. toxin co-regulated pilus
2. cholera toxin 3. critical colonization factor 4. type 4 pilus 5. composed of polymerized pilin (TcpA) subunits 6. AB5 type toxin 7. assembled in the periplasm and secreted by a type II secretion system |
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What is the mechanism of action of the cholera toxin?
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mediated by g-protein receptors upregulating chloride export through the CFTR
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Is there a vaccine for cholera?
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yes!
killed whole cell + CT-B - 50% efficacy, widely used live, attenuated microorganisms with the toxin gene deleted |
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What is the story with camplyobactor jejuni?
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begins as rod, 48 hours later becomes coccoid
zoonosis (cattle, swine, goat, dogs, cats, rodents, all fowl) cannot withstand freezing or drying but survives 4 degrees well 1:1000 guillain-barre |
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What are the diagnositic criteria for c. jejuni?
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Campylobacter jejuni is a species of curved, rod-shaped, non-spore forming, Gram-negative microaerophilic, bacteria commonly found in animal feces.
can pass through small filters, plate on chocolate agar w/o abx 10^6-10^9/gram stool in infected individuals |
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What are the stages of c. jejuni infection?
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1. adherence
2. invasion 3. vacuole passage 4. exocytosis 5. CDT-induced cell death and IL8 release 6. lymphocyte enlistment from lamina propria 7. basolateral reinvasion |
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What are ways to prevent c. jejuni spread?
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avoid raw chicken and unpasturized milk
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How do you treat c. jejuni?
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usually self-limiting
oral rehydration occasionally antibiotics |
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Are there any vaccines for c. jejuni?
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None
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What are the stages of an h. pylori infection?
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1. invasion
2. neutralization of acid via urease action 3. colonization 4. mucosal damage by bacterial mucinase, inflammation, mucosal cell death by cytokines and ammonia |
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What are the virulence factors associated with h. pylori?
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1. flagella
2. cag pathogenicity island 3. adherence 4. LPS 5. nitrogen metabolism enzymes: urease and arginase 6. secreted proteins: VacA and paralogs |
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By what mechanisms does h. pylori lead to cancer?
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intestinal metaplasia --> dysplasia --> gastric adenocarcinoma
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How do you diagnose h. pylori infection?
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1. stool culture
2. seroconversion 3. PCR 4. endoscopy 5. carbon urea breath test |
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How do you treat h. pylori?
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antibiotics: amoxicillin, clarithromycin, tetracycline, metronidazole
plus pepto bismol |
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What makes vitamin K?
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E. coli
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What is caused by enterohemorrhagic E. coli?
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1. causes bloody diarrhea
2. remains largely extracellular 3. EHEC toxin can spread via the blood stream |
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What causes hemolytic uremic syndrome acute renal failure?
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EHEC
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How do you catch EHEC?
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low infectious dose
illness associated with eating undercooked meat veggies house pets as reservoirs person to person contact is important |
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What determines the virulence of EHEC?
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common pilus
T3SS and LEE pathogenicity island (locus of enterocyte effacement) |
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What is the role of type III secretions?
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allows the bacteria to deliver proteins to the host. induced by host cell contact.
EspA forms type III pili EspB/D pass through pili and form pore Tir (cell side) and Intimin (e.coli side) in LEE locus mediate bacterial adhesion to cell |
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Is there a vaccine for H. influenzae
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Hib vaccine
in use for >20 years very successful capsule linked to proteins is key for long-term immunity as of 04 - conjugate vaccine with synthetic carb moiety |
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Sites of typeable H. influenzae infection?
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meningitis
epiglottitis bacteremia |
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By what mechanisms does unencapsulated H. influenzae infect?
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three routes of invasion:
1. macropinocytes 2. paracytosis (btwn tight jxns) 3. LPS-platelet activating factor |
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What are the adhesins that promote H. influenzae infections?
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Hap - both
HMW1/2 - nontypeable Hia - nontypeable Hsf LPS |
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Course of H. influenzae infection?
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restricted to respiratory tract and ear
colonization starts in nasopharynx can cause resp disease in pts with existing issues otitis media in children |
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Is there a vaccine for untypeable H. influenzae?
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no
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What is unique about H. influenzae's metabolism?
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facultative anaerobe
no diangostic fermentation patterns very fragile very fastidious only grows on chocolate agar (X and V factors) |
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What are the diagnostic criteria for H. influenzae type b?
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1. culture blood and CSF
2. hx and age of pt 3. Type B capsular Ag+ -immunoscreening, PCR, latex agglutination |
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How do you treat H. influenzae meningitis?
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Apicillin with chloramphenicol
3rd generation cephalosporins rifampin prophylaxis |
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How do you treat H. influenzae otitis media and sinusitis?
|
amoxicillin
resistant strains tx w/ amoxicillin w/ b-lactamase inhibitor |
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Can H. influenzae form a biofilm?
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yes!
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What kind of bacteria is Bordatella pertussis?
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small
G- coccobacillus obligate aerobe |
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How long is the incubation period for pertussis?
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7 to 10 days
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How is B. pertussis transmitted?
|
aerosol droplets
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Is there a vaccine?
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yes, very effective
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What are the steps in the infectious process of B. pertussis?
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1. inhalation via water droplets
2. interactions with ciliated epithelial cells in the trachea nasopharynx 3. adherence 4. multiplication and toxin production 5. evasion of host defenses 6. dissemination |
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What mediates attachment in B. pertussis?
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Pili
filamentous hemagglutinin (binds to galactose moieties on host cell) pertactin (surface molecule, anchored in OM) tracheal colonization factor (surface molecule, anchored in OM) |
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Name the B. pertussis toxins.
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exo:
1. pertussis toxin 2. adenylate cyclase toxin 3. dermonecrotic toxin trachael cytotoxin endotoxin (LPS) |
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By what mechanism does pertussis toxin increase infection?
|
ADP-ribosylating toxin targets a g-protein that inhibits adenylate cyclase leading to increased levels of cAMP -->
lymphocytosis increased insulin production sensitization to histamine (capillary permeability, hypotension, shock) |
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By what mechanism does adenylate cyclase toxin function?
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can be secreted or cell-associated
directly catalyzes production of cAMP from ATP in host cytoplasm toxin can lead to cell lysis impares macrophage function |
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What is the effect of dermonecrotic toxin?
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local necrosis and inflammation
acts on GTPase Pho protein via deamination of gln63 |
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Tracheal cytotoxin?
|
peptidoglycan fragment
ciliostasis stops cilia from beating kills tracheal epithelial cells proinflammatory |
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What is the DTaP vaccine?
|
component vaccine:
pertussis toxoid Fha pertactin two types of fimbrae |
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How do you diagnose pertussis?
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classic cough
isolation of organism problematic lymphocytosis pt hx |
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How do you treat pertussis?
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tx for hypoxia
erythromycin resistant to ampicillin and penicillin |
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Best way to identify bortedella pertussis in the lab?
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PCR
you need a special plate to culture it |
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What is an opportunistic pathogen?
|
pathogens capable of causing disease only in immunocompromised people
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What are the potential clinical diseases caused by E. coli infections?
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UTI
bacteremia meningitis |
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What pili are associated with E. coli cystitis? Pyelonephritis?
|
Cystitis:
type 1 Prs S Dr Pyelonephritis F adhesin Both P pili |
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To what does P pili bind?
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Glycoproteins of the human P blood group
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What is a mannose-sensitive adhesin?
|
Many E. coli UTI bacteria are capable of binding mannosides (mannans and mannoproteins) that are common constituents of uroepithelial cells and urinary tract mucus
This attachment is blocked by mannose, thus these adhesins are referred to as “mannose-sensitive” adhesins |
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What bacteria causes a positive mannose-sensitive hemagglutination test?
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type 1 e. coli pili - cystitis
P pili are negative |
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What is responsible for serum resistance in E. coli infections? What is the consequence of serum resistance?
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Correlated with the production of polysialic acid K1 capsule --> antiphagocytic (blocks complement binding)
is involved in the development of bacteremia |
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What disease is caused by Klebsiella pneumoniae
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primary pneumonia when underlying medical problems are present
(alcoholism, diabetes, lung disease) red current jelly sputum also: UTIs, wound infections, bacteriemia, meningitis, diarrhea |
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What is the main virulence factor of Klebsiella pneumoniae?
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Capsule is the main virulence factor -->
reduced phagocytosis reduced complement susceptibility helps with identification |
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What is the disease caused by Enterobacter cloacae?
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associated with burns, wounds, resp and urinary infections and catheter associated infections
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What is the major characteristic of Serratia marcesens?
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1. Orange color caused by prodigiosins
2. MS fimbrae, proteases, siderophores, swarming motility infections are secondary to antibiotic tx or implants |
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What disease do proteus infections cause?
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UTIs
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What characteristics are contribute to pathogeniciy in proteus infections?
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flagella
urease production |
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What is the clinical presentation of Pseudomonas aeruginosa?
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infects burns, eye wounds, catheters, implants
can cause (ventilator-associated) pneumonia and chronic lung infections blue green!!! |
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Can P. aeruginosa ferment sugars? What is the diagnostic significance?
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No - obligate aerobe
you have to incubate in aerobic conditions |
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What are the factors that contribute to pathogenicity in Pseudomonas infections?
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Type III secreted effectors:
ExoA - inhibits protein synthesis ExoS and T - exoenzymes that modify regulatory proteins ExoU - phospholipase activity Extracellular elastases, phospholipases, redox-active pyoverdine - involved in iron acquisition |
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What is a major clinical issue with pseudomonas?
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Lung infections with CF patients
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What disease is caused by Acinetobacter baumanii?
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similar to pseudomonas
infection associated with medical devices, wounds, lung infections |
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What are the factors associated with virulence in Acinetobacter baumanii?
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capuslar polysaccharides, ahdesins, proteolytic and lipolytic enzymes and LPS
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Name the "other" G- opportunists and their common sites of infection
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Morganella - disease similar to proteus
Providencia - UTI, blood, resp, wound Citrobacter - neonatal meningitis, brain absesses, enterotoxigenic Edwardseilla - gastroenteritis |
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Name the "other" G- opportunists and their common sites of infection
|
Morganella - disease similar to proteus
Providencia - UTI, blood, resp, wound Citrobacter - neonatal meningitis, brain absesses, enterotoxigenic Edwardseilla - gastroenteritis |
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True or False - Chlamydia and Rickettsia are grow within cells?
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True! They are obligate intracellular organisms as opposed to facultative intracellular bacteria like Salmonella, Shigella, and legionella
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Does chlamydia have an arthropod host? Rickettsia?
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Chlamydia - no
Rickettsia - yes |
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What are the stags in the chlamydia life cycle?
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2 -
elementary bodies - 1. small and non-replicating 2. rigid cell wall 3. transmissible initial or reticular bodies - 1. larger, actively multiplying 2. lack rigid wall 3. noninfectious |
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What is the gram stain and shape of neisseria?
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G-
diplococci kidney bean shape only gram negative coccus |
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What are the histological diagnostic characteristics of neisseria?
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fastidious in its growth requirements - blood agar, 5-10% CO2 (for membrane growth)
thayer-martin is the selective medium for it 1. chocolate agar 2. vancomycin to inhibit G+ 3. colistin to stop other G- 4. nystatin - antifungal |
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How do you distinguish between hemophalous and neisseria?
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oxidase test
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What does neisseria gonorrhoea ferment? Neisseria meningitidis?
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Gonorrhoae - glucose
Meningitidis - glucose, maltose |
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What is the course of meningitidis infection?
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1. initial colonization of nasopharynx
2. carrier state - lasts a few days 3. risk increased on close exposure 4. in some no disease, in others severe CNS disease, septicemia endotoxin, multiply outside of cells but seen in phagocytes |
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What causes the seasonal variations in meningitis cases in the the meningitis belt of Africa?
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Weather patterns
Lung irritation |
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How is Neisseria transmitted?
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person to person
aerosol droplets crowded conditions |
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Does Neisseria meningitis have a capsule?
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YES
vital to infection, antiphagocytic action |
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What are the diagnostic criteria for Neisseria menigintis?
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pt hx
1. URI followed by signs of meningitis 2. petechiae 3. culture and agglutination test |
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How to you tx Neisseria meningitis?
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third generation cephalosporins
IV penicillin rifampin and cipro are used for prophylaxis |
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Is there a vaccine for Neisseria meningitis?
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Quadrivalent vaccine against A, C, Y, W135
You can't immunize against B - composed of sialic acid which is all over the human body |
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What are the three causes of bacterial meningitis?
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1. Group B strep, E. coli K1 < 2yoa
2. Haemophilus influenzae type B <5yoa 3. neisseria meningitidis - variable |
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What is the course of gonorrhea infection?
|
STD
direct genital contact rectal and pharyngeal mucosa conjuctiva in newborns rapid establishment of infection involves pili that promote attachment and inhibit phagocytosis reach subepithelial cells followed by inflammation and purulent discharge you can also become asymptomatic OR can also cause disseminated disease arthritis-dermatitis syndrome PID |
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What would you see on a gram stain of a urethral smear of someone with gonorrhea?
|
leukocytes with intracellular G- diplococci
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With what type of infection is expulsion of ciliated cells associated?
|
gonorrhea
|
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What type of pili do gonococci use to adhere?
|
type 4 --> many antigentic varieties
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What is the lifecycle of chlamydia?
|
1. Elementary bodies enter by inducing hot cells to phagocytose them
2. EBs lose their cell wall, double in diameter, and synthesize RNA to yield reticulate bodies 3. the initial bodies divide by binary fission and some of the progeny are converted back to the smaller, more infectious EBs 4. release by exocytosis and cell lysis |
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Why is chlamydia an obligate intracellular pathogen?
|
cannot make ATP (depends on host)
induces ATP synthesis observed in infected cells |
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What are the three main species of chlamydia and what diseases to they cause?
|
psittaci - psittacosis (zoonosis from birds; blood in sputum, fever, headache, severe interstital pnemonia, no lobar pnemonia)
pneumoniae - pneumonia in adults (children don't get sick, do seroconvert) trachomatis - different serotypes cause trachoma, lymphogranuloma venereum, and a complex array of different clinical presentations including inclusion conjunctivitis, newborn infant pneumonia, and urethritis |
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How do you treat STI chlamydia trachomatis?
|
single dose of azithromycin
|
|
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What causes inclusion conjunctivitis?
|
Chlamydia trachomatis serotypes D-K
also causes infant pneumonia and chlamydia |
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What is the clinical presentation of Chlamydia trachomatis serotyples A, B, C?
|
tachoma (eye infection)
chronic reinfection of conjunctiva causes corneal scarring and blindness serotypes are particularly infectious hand to eye, eye to eye transmission prevalent in africa and asia tx with azithromycin q1year x 2 |
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What is lymphogranuloma venereum? How do you test for it?
|
veneral papule ---> ulcerating vesicle that can progress to suppurating disease of lymph nodes
FREI TEST |
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How do you treat chlamydia
|
tetracyclines
alt: single high dose azithromycin can help ensure compliance |
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|
What are the diagnostic criteria for chlamydia?
|
1. all chlamydia share group antigen
2. antigen can differentiate between c. trachomatis serotypes 3. acute vs. convalescent Ab titre 4. staining for inclusion bodies 5. flurescent Ab examination 6. PCR |
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|
What is the main vector for Rickettsia infections?
|
arthropods!
|
|
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Why is Rickettsia an obligate intracellular parasite?
|
adapted to take up ATP, NAD, and other phosphorylate metabolites
they CAN make their own ATP |
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|
What clinical disease does Rickettsia prowazekii?
|
typhus!
incubation of ~10 days abrupt onset of fever and severe intractable headache rash follows 4-7 days later untreated disease is fatal (except in children) toxin involvement |
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|
What transmits typhus?
|
lice
louse feeds and defecates at the same time - scratching drives the fecal material and rickettsia into the bite wound |
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How do you treat typhus?
|
tetracycline
|
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How do you prevent typhus?
|
DDT, louse control
|
|
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How do you diagnose typhus?
|
PCR
serological tests for R. prowazekii-specific antigens liver fxn tests antibody titers |
|
|
What is Brill-Zinsser Disease?
|
Caused by reactivation of latent R. prowazekii infection
tx - tetracycline |
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|
What animal is the reservoir for rickettsia?
|
flying squirrels
|
|
|
What disease is caused by Rickettsia typhi?
|
murine typhus - can also be transmitted to humans
|
|
|
What causes rocky mountain spotted fever?
|
Rickettsia rickettsii from dog and rocky mountain wood ticks
fever, headache, arthritic pain, abdominal pain, nausea, vomiting rash on hands and feet spreading to trunk w/out tx 20% fatality |
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|
How do you diagnose RMSF?
|
pt hx
clinical signs fluorescent Ab test |
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|
How do you treat RMSF?
|
tetracycline
|
|
|
How do you prevent RMSF?
|
clothing, removing ticks
|
|
|
What is caused by Rickettsia akari?
|
Rickettsial pox - benign chicken pox like rash
|
|
|
what is Q fever and what causes it?
|
interstitial pneumonia, fever, headache, elevated liver fxn tests, rash --> can progress to chronic state that affects other organs
caused by inhalation of Coxiella burnetii from infected sheep |
|
|
What are the diagnostic criteria for Q fever?
|
serologic testing for coxiella bunetii antigen or immunofluorescence assay/staining
|
|
|
How do you treat Q fever
|
doxycycline
quinolone chronic Q fever encocarditis requires aggressive long term therapy and perhaps surgery |
|
|
What are the mechanisms to reduce Q fever spread
|
appropriate disposal of birth products of sheep and goats
isolate infected animals vaccinate individuals who work with the virus counsel people at highest risk for developing chronic Q fever, especially persons with pre-existing cardiac disease |
|
|
What is the clinical presentation and route of infection for ehrlichioses?
|
fever, lymphocytopenia, elevated liver function tests due to liver damage
tick bites |
