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85 Cards in this Set
- Front
- Back
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Latent (hidden) Infection
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intermittent acute episodes of virus production b/w which there may be an absence of virus particles and very limited macromolecular synthesis, i.e. Herpes simplex
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Chronic Infection
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continued presence of virus during periods in which overt clinical disease is absent, i.e. HBV
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Transforming Infection
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cells are immortalized and properties altered (transformed) to those of cancer cells, i.e. HPV and cervical cancer
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Capsomere
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small protein subunits that combine in groups to form the capsid
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Surface eclipse
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direct fusion of capsid with host membrane
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receptor-mediated endocytosis
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uptake in clathrin coated pits --> fusion with lysosomes --> removal of capsid
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one-step growth curve
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1. latent period
2. rise 3. yield (burst size) |
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what does CPE stand for?
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cytopathic effects
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CPE of Rabies?
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negri bodies
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CPE of herpes, RSV (respiratory syncytical virus), and measles
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all create multinucleated giant cells -- syncytia formation
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hemadsorbtion
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RBCs stick to surface of infected cells that express the viral hemagglutinin
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Creutzfeldt-Jakob disease (CJD)
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human disease caused by prions
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how does Cold Eeze/Zicam work?
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they contain zinc gluconate, which antagonizes virion uncoating. it freezes the virion to the cell by blocking the pocket factor so it can't uncoat
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what is the weakness of Cold Eeze and how did Zicam overcome this?
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it can't get into the nose (where most of the viral particles are!). Zicam is a nasal spray
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how does Picovir (Pleconaril) work?
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binds to virion in canyon pocket, prevents receptor binding and proper virion uncoating. still not approved for general use
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how do 3C protease inhibitors work?
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prevent maturation of virus by halting intracellular virus protease activity
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Name 2 treatments for RSV infection
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1. Ribavirin (a guanosine analog) used in more severe cases
2. Passive immunization with anti-RSV Ig in pre-mature infants. Given in 5 monthly doses commencing in November |
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how does Amantadine and Rimantadine work?
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1. effective against Type A virus only
2. stops uncoating/penetration 3. M2 inhibitor - blocks H+ from entering the endosome which prevents the HA conformational change and uncoating |
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how do neuraminidase inhibitors work?
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1. active on both influenza type A & B
2. block neuraminidase active site, prevent sialic acid cleavage - leaves uncleaved sialic acid residues on the surface of both the host cell and viral envelopes -- HA binds uncleaved sialic acid, thus this leads to viral aggregation at the cell surface and inhibits the cell-to-cell spread of infection 3. must be applied w/in 48 hours of disease onset |
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what is Zanamivir?
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1. neuraminidase inhibitor
2. relenza 3. inhaler, use with caution with severely asthmatics |
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what is Oseltamivir?
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1. neuraminidase inhibitor
2. tamaflu 3. oral |
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TIV
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-trivalent inactivated for pts >6 mths y/o
-could be whole virus, split, or subunit |
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LAIV
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-live, attenuated for pts 2-49 y/o
-Flumist -cold-adapted, temp sensitive and no preservatives |
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Fluzone
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-TIV with 4-fold increased antigen dosage levels for pts >65 yo
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Intradermal TIV
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decreased levels of antigen and injected dose volume
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what is the other agent (besides Hib) that causes epiglottitis in adults?
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strep pneumoniae
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what is the clinical course of epiglottitis?
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-rapid and explosive
-mild to severe in 6-12 hours |
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what is the molecular makeup of the Group A Lancefield group?
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NAG + rhamnose
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where does streptolysin O hemolyze?
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-deep cuts in the BAP since it is Oxygen labile
-this is also immunogenic - ab are formed to it |
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where does streptolysin S hemolyze?
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-on the BAP - surface colonies
-not immunogenic -Serum induced |
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S. pyogenes:
reservoir? peak ages? prevalence? |
-humans only! - can have carriers
-5-15 yo -winter and early spring |
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S. pyogenes transmission
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1. respiratory droplets
2. person-to-person -- skin --does NOT survive well in environment, i.e. fomite transmission is a low probability |
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4 features of pyogenic inflammation from s. pyogenes in infants/small children
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1. subacute nasopharyngitis - serous discharge (not pus like adults)
2. tendency to extend to middle ear and mastoid 3. cervical lymphadenopathy 4. illness persists for weeks |
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6 features of pyogenic inflammation from s. pyogenes in older children/adults
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1. high fever, >101
2. cervical lymphadenopathy 3. purulent exudate 4. acute nasopharyngitis; tonsillitis (- cough) 5. intense erythema and edema - mucous membranes 6. self-limiting infection (~5 days) |
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describe the details and course of scarlet fever rash
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--it can superimpose on the strep pharyngitis (since it is d/t to the SpeA exotoxin)
It is a punctate, blanching erythematous rash. Lesions/pimples form within rash to give a "sandpaper skin" appearance. Pt will also develop pastia lines (Thomson sign), which are petechial lesions in the flexor skin folds. The rash will spread from the ears, axilla, neck and chest to the trunk and extremities |
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list 3 distinct features associated with scarlet fever
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1. desquamation - after rash has subsided the pt will notice peeling in the axilla, groin, tips of fingers and toes
2. circumoral pallor - there will be blanching around the mouth 3. strawberry tongue - yellow-white coating --> shed --> erythematous and have enlarged papillae |
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what are the 4 minor manifestations of ARF?
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1. arthralgia
2. elevated ESR or C-reactive protein 3. fever 4. prolonged PR interval |
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what are the clinical sxs of acute poststreptococcal glomerulonephritis?
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1. periorbital edema -- fluid retention/kidney damage
2. hematuria -- dark urine + blood 3. possible hypervolemia -- secondary to fluid retention this has a good prognosis, esp in peds pop, compared to ARF |
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what are the 3 mechanisms of pathogenesis of s. pyogenes
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1. pyogenic inflammation (suppurative) -- pharyngitis
2. toxin-mediated -- scarlet fever 3. immunologic disease -- ARF and AGN |
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why would we incubate s. pyogenes in an increased CO2 environment?
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favors beta-hemolysis
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what is the DOC for s. pyogenes?
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penicillin VK for 10 days
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what other drugs are used for GAS in cases of beta-lactam hypersensitivity?
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1. 2nd or 3rd generation cephalosporins
2. macrolides 3. clindamycin if allergic to macrolides |
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most common bacterial causes of otitis externa
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1. pseudomonas aeruginosa
2. staphylococcus aureus |
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Pseudomonas aeruginosa
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gram -
bacilli motile -- single flagellum aerobic encapsulated clinical isolates possess pili (lose when grown in lab; just like how we lose the capsule of s. pneumoniae when grown in lab) pigment producer: pyocyanin (virulence factor) and pyoverdin |
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Staphylococcus aureus
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gram +
cocci (in clusters) encapsulated coagulase positive beta-hemolytic facultative halophile and mannitol fermentor -- MSA (7.5-10% salt) will turn it yellow |
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most common bacterial causes of otitis media and sinusitis
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1. streptococcus pneumoniae
2. haemophilus influenzae 3. moraxella catarrahis (in this order too) |
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Streptococcus pneumoniae
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gram +
lancet-shaped diplococci virulent strains are encapsulated alpha hemolytic bile will lyse (bile won't lyse any other alpha hemolytic strep) optochin sensitive |
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Haemophilus infuenzae
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gram -
coccobacilli non-motile contain LOS instead of LPS requires factors from RBCs for growth but don't have hemolytic properties non-typeable strains capable of losing capsule and still causing disease non-typeable strains responsible for otitis media/sinusitis. Hib (type B) is responsible for epiglottitis, meningitis and pneumonia in infants and young children |
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Moraxella catarrhalis
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gram -
diplococci oxidase positive |
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Corynebacterium diphtheriae
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gram +
pleomorphic bacilli, often club-shaped -- "chinese letters" appearance metachromatic granules -- volutin (storage of inorganic phosphate) |
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what is the pseudomembrane composed of in diphtheria?
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network of fibrin + bacteria + WBC + necrotic epithelial cells
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what are the 3 culture mediums used to grow C. diphtheriae?
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1. blood agar -- r/o hemolytic streptococcus
2. Loeffler's medium - reveals typical colony morphology 3. cysteine-tellurite agar - black colonies |
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Bordetalla pertussis
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gram -
coccobacilli grow aerobically on enriched agar |
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catarrhal stage
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-1-2 weeks
-inflammation of mucous membranes -presents like a nonspecific URT infxn with insidious onset -- looks like common cold pts are highly contagious during this period |
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paroxysmal stage
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-attacks or spasms
-paroxysmal coughing, often followed by vomiting --whooping cough -- attacks last for 1-2 minutes; up to 50x/day -- excess mucus (d/t to epithelial cells extruded) contributes to airway restriction -sxs lasts 2-4 weeks |
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convalescent stage
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-recovery
-paroxysms decrease in number and severity with gradual recovery -lasts 3-4 weeks or longer -secondary complications include pneumonia, seizures, encephalopathy and death |
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what culture medium do you grow b. pertussis?
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Bordet-Gengou or Regan-Lowe agar
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what culture medium is required for H. influenzae?
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-chocolate agar enriched with X (hemin) and V (NAD) factors
-incubated at 37C in CO2 incubator |
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Klebsiella pneumoniae
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gram -
bacillus non-motile can cause both CAP and NP, but mostly in alcoholics and DM -- often seen in homeless coated by a thick, mucoid (slimy) capsule |
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distinct features of K. pneumoniae pneumonia
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-aggressive necrotizing CAP with predilection for the upper lobes
-often fatal, even with antimicrobial tx -productive cough with a thick, blood tinged sputum -- currant jelly sputum --leads to abscess formation and cavitation |
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Mycobacterium tuberculosis
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acid-fast
bacilli non-motile obligate aerobe intracellular pathogen heat sensitive -- killed by pasteurization |
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what is a mycoside?
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a mycolic acid + a CHO = glycolipid
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what is a cord factor?
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-a disaccharide sandwiched b/w 2 mycolic acids
-produces parallel growth of bacteria -inhibits neutrophil migration -damages host cell mito -induces release of TNF -- promotes phagocytosis by macrophages |
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what is a sulfatide?
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-same as cord factor with a sulfate attached to the trehalose
-inhibits fusion of the phagosome with lysosome |
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what is wax D?
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-complex mycoside
-acts as an adjuvant -may activate CMI and DTH |
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what does lipoarabinomannan (LAM) do?
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-may suppress macrophage presentation of MHC II
-may suppress T-cell proliferation -provides resistance to ROI -may interfere with macrophage activation via IFN-gamma |
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what are the 3 potential outcomes of MTB infection?
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1. the immune system may be able to entirely destroy the microbes -- no active case of TB -- 90% of individuals colonized
2. Granulomas form and control the pathogen -- infection: Primary Infection - granulomas form and MTB eliminated or Latent TB Infection (LTBI) - MTB becomes persistent and secondary or reactivation can occur with immunosuppression 3. Immune system unable to form granulomas -- macrophages quickly disseminate MTB hematogenously leading to miliary TB. seen in active HIV or medical immunosuppresion |
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positive PPD if >5mm?
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1. HIV positive
2. Pt on immunosuppressives 3. Recent contact with TB pt 4. Pt with abnormal fibrotic CXR |
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positive PPD if >10mm?
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1. Recent immigrants from countries with high-prevalence
2. IV drug users 3. Residents and employees of high-risk setting 4. Persons with conditions of high risk 5. Children <4 yo |
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positive PPD if >15mm?
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persons at low risk for TB
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what culture medium is used for M. tuberculosis?
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-lowenstein-jensen and middlebrook -- took 1-7 weeks
-now use BACTEC -- takes 6-10 days |
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Aerobic Actinomycetales
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gram +
aerobes bacilli catalase + colonizes humans & animals |
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what is the most common cause of infection by NTM?
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1. MAC --Mycobacterium avium complex: m. avium & m. intracellulare
2. Mycobacterium kansasii |
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MAC
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gram +
aerobic bacilli acid-fast ubiquitous slow growing -- 10-12 hrs doubling time colonization does not equal disease grow optimally at 41C not killed by drinking water chlorination |
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what culture medium is used for norcardia?
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this is a slow grower (~1 wk) obscured by fast growers. this is prevented by using:
-BCYE agar (for Legionella) -- buffered charcoal-yeast extract -modified Thayer-Martin medium (Neisseria gonorrhoeae) |
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Norcardia
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gram +
weakly acid-fast branche hyphae in tissues and culture strict aerobic bacilli catalase + gelatin liquefaction growth on nonselective media |
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Legionella pneumophila
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gram -
pleomorphic bacillus fimbriae single, polar flagellum catalase & oxidase + beta-lactamase producer aerobic |
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what culture medium does L. pneumophila need?
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buffered charcoal yeast extract (BCYE)
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what two diseases are caused by legionella pneumophila?
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1. pontiac fever -- self-limited illness; sxs last 2-5 days and resolve spontaneously w/o tx
2. legionnaires' disease -- a severe, acute atypical pneumonia with a high mortality rate (up to 75% w/o tx) -- GI and neurologic sxs common -- death d/t shock or respiratory failure |
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Mycoplasma pneumoniae
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-smallest of free-living bacteria
-don't have cell walls; PM contains sterols -stain poorly and are pleiomorphic in shape -have a fried egg appearance |
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what culture medium is used for m. pneumoniae?
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Eaton's agar - contains serum, abx, and sterols
cultures grow slowly (2-6 wks) and are often insensitive |
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Chlamydia
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gram - but have no peptidoglycan in their cell walls
very tiny non-motile cocci-shaped obligate intracellular parasites found within intracytoplasmic inclusions |
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Francisella tularensis
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gram -
aerobic coccobacilli small thin, lipid capsule fastidious has LPS, but weak activity no flagella, no pili beta-lactamase producer facultative intracellular pathogen -- inhibits phagolysosome formation (survives and replicates w/in endosome) |
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what culture medium is used for F. tularensis?
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Thayer-Martin agar -- chocolate agar supplemented with abx
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Coxiella burnetti
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small
aerobic gram - pleomorphic bacilli non-motile no exotoxins weak endotoxin activity |
