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245 Cards in this Set
- Front
- Back
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T/F: most vaccines do not prevent you from getting infected, they prevent you from getting sick.
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True
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Which component of the immune response do vaccines affect?
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Vaccines try to speed up the specific immune response (vs. the already fast innate response)
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Trace the general pathway of action for effector immune cells?
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Dedritic cells present antigen to CD4(helper) T cells who either stimulate B cells to create antibody or Cytotoxic T cells (killer Ts)
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What facets of host and virus define picornavirus serotypes?
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the neutralizing antibodies of the host and the epitopes of capsid proteins on the virus
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What are the three genera of the family Picornavirus?
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Enterovirus
Rhinovirus Hepatovirus |
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What is the main route of tranmission for Picornavirus?
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fecal-Oral (Rhinovirus: fomites-hand-eye or aerosol)
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What are the common enteroviruses?
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poliovirus
coxsackievirus (A and B) echovirus enterovirus |
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What is the primary site of infection for Picornaviruses?
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Pharynx/Intestine
Rhinovirus: upper respiratory |
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Which genus of Picornavirus is the leading recognizable cause of aseptic meningitis?
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enteroviruses account for >60% of cases
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What time of year does the transmission of enteroviruses peak?
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late summer
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From where do the majority of HAV outbreaks occur?
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fecal-contaminated food (salad/oyster bars) or childcare centers
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How does the picornavirus produce more than one protein if it only has one reading frame?
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Viral proteases (2A and 3C) break the reading frame into smaller pieces for translation
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Which strand of the viral RNA is replicated?
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the (+) strand
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Viral genomic RNA functions as what upon entering the host cytoplasm?
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mRNA -> viral replicase
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T/F: Most people infected with poliovirus are aymptomatic. Thereofre the virus can circulate unnoticed for long periods of time.
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True
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Briefly trace the pathogenesis of poliovirus
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Day 0: ingest fecal material
Day 1-2: Viremia (feces excretion begins) Day 2-7: amplified replication supporting one or both pathways to the CNS\ Day 7-14: paralysis |
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What are the advantages/disadvantages of the inactivated poliovirus vaccine?
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Advantages: induces the B cell (IgG) immunity; acceptable for immunocompromised
Disadvantages: cost, poor mucosal immunity |
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What are the advantages/disadvantages of oral poliovirus vacine?
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Ad: induced mucosal (IgA) and systemic (IgG) immunity, cheap
Disad: causes VAPP |
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What is the current CDC reccomendation for polio vaccinations?
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exclusive IPV
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How do VAPP reactions occur in OPV?
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attenuate virus of the vaccine will revert to the neurovirulent forms of the virus during replication in the host
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For whom is OPV contraindicated?
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B cell compromised (e.g. Bruton's)
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A pt presents to your office with sore throat and fever. The lab reports back to you a gram +ive cocci in chains. What is the most likely cause of your pt's symptoms?
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Strep throat from S. pyogenes (Group A, beta-hemolytic)
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Which cell wall feature of S. pyogenes gives it its group specificity?
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C-carbohydrate
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What is the main reason for why a pt may have repeat infections of S. pyogenes?
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there are over 90 different serotypes specificities for the M protein (the major virulence factor) on S. pyogenes
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What are the 2 main functions of M protein?
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(1) orients LTA to be more adhesive; (2) antiphagocytic - won't let complement bind
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What are the 3 extracellular virulence products of S. pyogenes?
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(1) Steptolysin O, (2) pyrogenic exotoxins, (3) Strep spreading facotrs (e.g., streptokinase, DNAase, proteinanses)
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What is the function of Streptolysin O in S. pyogenes?
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binds to RBC membranes and inserts a pore cell to lyse the RBC (ASO antibody titer is proof of infection)
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S. pyogenes forms what type of exudate?
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Thin and watery
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T/F: treatment for strep is done to prevent the sequelae that may result from a S. pyogenes infection
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True: 99% of people would recover from a strep infection with no sequelae whether they are treated or not
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A 25-year-old woman comes to your office complaining of aching joints and fever. 4 weeks prior she recalls having a very bad sore throat that kept her from work for two days. What is the most likely diagnosis?
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ARF
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Which consequence of untreated Group A, beta hemolytic strep can result from either a skin or pharyngeal infection?
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Nephritis (post-strep glomerulonephritis)
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Which consequence of prolonged strep infection (ARF or PSGN) is related to the ASO titer?
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ARF (PSGN has no link to ASO titer)
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What is the mechanism of action for PSGN?
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immune complex (Type III hypersensistivity)
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What type of hemolysis is most common in Group B strep?
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beta-hemolysis (not as strong as Group A)
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What is the prototypical species for Group B strep?
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S. agalactiae
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What is the strucutral feature of Group B strep that gives it its Lancefield type?
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The Group B polysaccharide
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Which extracellular factor is used for the indentification of GBS?
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CAMP factor
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What percentage of pregnant women are colonized with GBS in their rectum or vagina?
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20%
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Which capsular subtype of GBS is resonsible for the majority of neonatal infections?
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Type III (70% of neonatal infections)
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What unique feature do Group D enterococci share that makes them difficult to treat?
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they are resistant to penicillin
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Group D strep are a frequent cause of what type of infection?
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Urinary tract infection
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Which strep is a frequent cause of dental caries?
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S. mutans (viridian streptococci)
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50% of bacterial endocarditis are caused by which class of streptococci?
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Viridians
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What are the two main viruses responsible for gastroenteritis in humans?
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Calicivirus
Rotavirus |
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In the family of calicivirus, which genus is responsible for gastroenteritis in humans?
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Norovirus (including the Norwalk serotype)
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State the Nucleic acid, capsule symmetry and coating (naked/enveloped) of the Norovirus.
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Nucleic acid: Double stranded RNA
Capsule symmetry: icosahedral Coating: non-enveloped (naked) |
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Individuals that are homologous non-secreters of what gene are highly resistant to norovirus infection?
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FUT2 (20% of Europeans)
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Where in the host cell are rotavirus virons assembled?
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RER
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Which enzyme is required for the activation of rotavirus in a human host?
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Trypsin; in the gut, trypsin cleaves the capsid and allows for virus uncoating
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Outline the pathophys of rotavirus.
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NSP4 (non-strucutral viral protein) raises intracellular Ca levels in the host cell altering signal transduction and thus ion transport, resulting in diarrhea
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What are the two main tests used to diagnose rotavirus?
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rotavirus ELISA
PCR |
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Which experimental drug has been shown to reduce the duration of severe diarrhea from rotavirus in infants?
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nitazoxamide
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T/F: Norovirus can be grown in animals and cell culture.
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False
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Rotavirus is a member of which virus family?
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Reovirus
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Briefly outline the mechanism of congenital adrenal hyperplasia (CAH)
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inherited defect causes deficiency in any of the enzymes necessary for the synthesis of cortisol -> decreased cortisol synthesis -> lack of feedback at hypothalamus/pituitary -> increased ACTH in utero
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Which enzyme deficiency is the most common cause of CAH?
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21-OHase deficiency
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Which zones of the adrenal cortex are affected in 21-OHase deficiency and what are the clinical manifestations?
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Glomerulosa: salt-wasting (no aldo)
Fasciculata: hypoglycemia (cortisol) Overstimulation of Reticularis by ACTH causes virulization in girls |
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Which zones of the adrenal cortex are affected in 11-OHase deficiency and what are the clinical manifestations?
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Glomerulosa: accumulation of 11-deoxycorticosterone (good mineralcorticoid), salt-retaining and HTN
Fasciulata: cortisol deficiency Reticularis: overstimulation from ACTH causes virulization |
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Bacterial meningitis is caused by which three pathogens?
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Strep pneumoniae
H. influenza Nessieria meningitidis |
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What is the classification of H. influenza?
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Gram (-) coccobacillus
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What compnents of blood are required for bacterial factors of H. influenza and what are those factors?
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V Factor = NAD
X Factor = Heme |
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What is the classification of S. pneumoniae?
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Gram (+) diplococcus
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Spinal tap of a pt with H. influenza will show what features?
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PMNs and bacteria
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What is the main test used to distinguish between S. pneumoniae and viridians?
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Optochin - viridians are resistant to this chemical
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What is the classification of Neisseria meningitidis?
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Gram (-) diplococcus
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What is the most critical virulence factor needed for H. influ, S. pneum, and N. mening to conduct invasive disease?
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polysaccharide capsule; if no capsule then only focal infections
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Which serotype of H. influenza most frequently causes invasive disease? Which type is most prominent?
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Type B
Type A (due to vaccine for Type B) |
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Of the 9 serotypes of N. meningitidis, which ones are responsible for the majority of dz?
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A,B, and C
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What is the significance of the N-acytl neuroamidic acid polymer in the N. meningitidis, Type B capsule?
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Our bodies also produce this molecule; cannot make vaccine since we would not want antibodies against ourselves
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Why is IgA protease a requirement for pathogens causing bacterial meningitis?
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These pathogens initiate infection in the mucosal surfaces where IgA is the only antibody in town; need to be able to break IgA down
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Why doesn't S. pneumoniae produce LPS/LOS (lipo-oligosaccharide)?
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It is an endotoxin and therefore can only be made by Gram (-) pathogens such as N. meningitidis and H. influenza
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What pathogen is the most common cause of bacterial meningitis in children and young adults?
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N. meningitidis
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What pathogen is the most common cause of bacterial meningitis in adults?
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S. pneumoniae
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What is the most common cause of otitis media in children?
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S. pneumoniae (50% of all cases)
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Between encapsulated and unencapsulated, which strains cause the highest incidence of disease? the most serious/lethal disease?
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highest incidence: unencapsulated
most severe: encapsulated |
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What is the primary site of colonization for the organisms that cause bacterial meningitis?
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upper respiratory tract
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Which class of antibiotics are used to treat H. influenza?
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3rd generation broad spectrum cephalosporins
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Which class of antibiotics are used to treat N. meningitidis?
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Third and fourth generation cephalosporins
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If a person has come in contact with another person who has bacterial meningitis, what drug is used to limit the spread (and as prophylaxis)?
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Rifampin or ciprofloxacin
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An unknown virus is placed in a tube with tissue culture medium and 5-bromo-2'-deoxyuridine (BrDU). Replication persists. What can be said about this virus from the results of this test?
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It's nucleic acid is RNA
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What is the function of 5-bromo-2-deoxyuridine (BrDU)?
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inhibits the replication of viral DNA. (BrDu, Breaks down DNA)
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An unknown virus is treated with chloroform (or ether). The virus becomes ineffective after a short period of time. What can be said about the virus from the result of this test?
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The virus contains a lipid viral envelope. (non-enveloped/naked viruses will not be affected by the solution)
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What 5 tests are available to identify the serotype of a virus?
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1. Neutralization test
2. Hemagglutination inhibition (HAI) 3. Immunoelectron microscopy 4. RIA or ELISA 5. direct immunoflourescence of infected cells from clinical specimen |
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A reference antisera is mixed with a virus and incubated. The virus was then innoculated into a new tissue and replication continued. What test is described and what can be inferred from this result?
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Neutralization test. The virus being tested is not the same as the reference virus
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A flask containing cells infected with virus X are treated with an antiserum to the virus you are looking for. RBCs are added to the culture. If hemadsorption is NOT observed, what can you conclude from the test?
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The virus in question IS your virus
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For what types of viruses is hemadsorption effective?
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ortho and paramyxoviruses
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Amantadine and rimantadine are drugs used to reduce the spread of which orthomyxovirus? What is their target?
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Influenza, Type A
The M2 protein |
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Oseltamivir and zanamivir are drugs used to reduce the spread of which orthomyxoviruses? What is their target?
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Inlfuenza, Type A and B
The neuraminidase enzyme activity |
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Treatment with appropriate antiviral drugs must be administered in what time frame to have clinical value?
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within 48 hours after onset of symptoms ("The First 48")
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Describe an ELISA. why is it used?
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1. antigen in question is bound to the well
2. sera containing antibodies are added (incubate and wash) 3.anti-antibody is added (incubate and wash) 4. chromatogenic substrate is added and the color generate is directly proportional to the of antigen-specific anitbody present **you can also reverse the first two steps and place a differnet antigen-specific antibody on the plate, sandwhiching the antigen between pt's and lab antibodies |
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If a virus cannot be grown in culture, what tests do you still have at your disposal?
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These viruses can usually be diagnosed with RAI or ELISA
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What is the most common method for rapid viral diagnosis?
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PCR
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Describe PCR.
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1. DNA or RNA is isolated from a pt's specimen
2. Reverse transcriptase transcribes RNA to make a cDNA copy 3. Pt's viral DNA or cDNA is amplified with oligonucleotide primers specific for the suspected virus 4.Amplified DNA is id'd in agarose gels and nucleotide sequence is determined |
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Western blots are used to detect what component of a virus?
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Protein
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What test can be used to determine if a pt's illness is caused by a virulent, wild type virus or a reverted vaccine?
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PCR can look for markers of a vaccine strain, temperature sensitivity
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Corynebacteria diptheriae has what bacterial classification?
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Gram + rod, pleiomorphic (cna appear in L of V shapes)
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What is the distinctive feature of a diptheria infection that would cause you to alert the lab of a possible case?
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the distinct wet mouse smell
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Why must the labs be informed of a possible case of diptheria?
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the tests for diptheria can only be performed at a state health lab or a the CDC in Atlanta. These two locations are the only places to get antitoxin, as well
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The expression of diptheria toxin is controlled by what two factors?
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1. phage conversion (bacteriaphage carries the structural gene needed for encoding the toxin)
2. Iron levels (increased levels will shut off toxin synthesis) |
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While diptheria infection is primarily located in the _______, the toxin primarily affects the ______, ________, and ________.
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Upper respiratory tract
Heart, Peripheral nerves, Kidneys |
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What is the antitoxin for diptheria?
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Equine antitoxin
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What is the necessary timeframe for delivery of dipetheria antitoxin in order for it to be effective?
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within 4 days of dz onset, or else death rate is as high as not treating at all (do not wait for lab dx to give antitoxin!)
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What is the protective antigen for diptheria?
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The toxin itself
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Diptheria toxoid is coupled to what other toxoid in the vaccine?
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Tetanus
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What is the bacterial classification of Bordetella pertussis?
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Gram (-) coccobacillus
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When is the pertussis bacteria best captured on culture?
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in the catarrhal or early paroxysmal stages
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What is the major toxin in pertussis?
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the portion of the toxin that transfers the ADP-robose portion of NAD onto the inhibitory subunit of the adenylate cyclase complex on the host cell --> increases cAMP
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Name 3 other virulence factors of pertussis.
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1. tracheal cytotoxin - destroy UR cilia
2. adenyl cyclase toxin - prevents macrophages from coming 3. filamentous hemaglutinin - adherence problems for host cell |
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Regulatory genes for the expression of pertussis toxin are on what locus?
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The vir locus
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Name the 3 stages of Whooping Cough and describe the symptoms.
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1. Catarrhal stage - minor respiratory illness, highly communicable, dry cough
2. Paroxysmal stage - 1 to 6 weeks; intensification of symptoms, spasms, seizures, whoop (whoop can be diminished in neonates, adolescents and adults) 3. Convalescent stage - decreasing symptoms that may last for months |
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Where is the most common site for invasive infection caused by Bordetella pertussis?
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Lung
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What antitoxin therapy is used against pertussis?
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There is no current antitoxin therapy, must use antimicrobials in the early catarrhal stage
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Which antimicrobial is used in the treatment of pertussis?
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Erythromycin (penicillin cannot reach the target)
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In the lab, what makes pertussis difficult to distinguish from viral infections?
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Bacterial infections usually produce PMNs, viral produce WBC and lymphocytes.
Pertussis can attract WBCs and lymphocytes |
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What does the "a" stand for in DTaP?
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acellular - the only form of pertussis vaccine now used.
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Which DTaP vaccine is approved as a booster for 11-18 year olds? 19-64 year olds?
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11-18:boostrix
19-64:adacel |
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What are the defining characteristics of Staphylococcus?
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Gram + cocci that grow in clusters, catalase +
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What enzyme does s. aureus have that distinguishes it?
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coagulase
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Name the cell wall elements of s. aureus that are also virulence factors.
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Protein A, aggressin, capsule, clumping factor, techoic acids
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How does protein A in s. aureus act as a virulence factor?
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binds Fc portion of Ab and prevents opsonization
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How does clumping factor in s. aureus act as a virulence factor?
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cleaves fibrinogen and protects bacteria from phagocytosis
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What part of s. aureus cell wall binds to epithelial cells?
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Techoic acids
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What enzymatic virulence factors does s. aureus have?
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catalase, coagulase, hemolysins
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Which strains of s. aureus are generally positive for Panton-valentine leucocidin?
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MRSA - PVL makes strain more invasive, severe
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What is the preferential colonization site for s. aureus? What about coagulase neg staphs?
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anterior nares; skin
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Erythromycin resistance in staph can induce resistance to which other antibiotic?
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Clindamycin - ERM gene
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What is the most common cause of osteomyelitis in children?
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staph infection (localized infection -> bacteremia -> osteomyelitis)
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What skin infections are associated with staph?
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furunculosis, abcesses
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How does staph usually colonize the blood in disseminated staph septicemia?
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endocarditis or septic thrombophlebitis -> particles of infection break off and circulate
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What is a positive Nikolsky's sign, seen in staph scalded skin syndrome?
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skin sloughs off when toched (at granular layer, whereas drug induced syndrome sloughs at basal layer)
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How can you distinguish staph from strep scarlet fever?
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No strawberry tongue in staph dz
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What are the clinical findings in a patient with Toxic shock syndrome?
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fever, shock, erythroderma, mutliorgan involvement, strawberry tongue
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Why does the TSS toxin grow well in the vagina?
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high pH, high protein with menses, high pO2 and pCO2
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What does coagulase do?
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Clots the plasma -> walls off the abcess
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What preformed toxin leads to the clinical symptoms (nausea, vomiting, diarrhea) in food poisoning?
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Enterotoxin
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What does the exfoliatin toxin do?
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Separates the skin at the granular cell layer -> desquamation
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What accounts for the varying degree of methicillin resistance seen in s. aureus?
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combinations of alleles of the FEM (factors essential for Methicilin resistance) genes
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What clinical course is seen in patients with Chronic Granulomatous Disease who acquire s. aureus?
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unchecked skin infection because no neutrophils present to clear bacteria
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Why do patients with Job's defect get cold abcesses with s. aureus infection?
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because they switxh to IgE Ab too soon, no IgM or IgG to opsonize bacteria
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What is Ritter's disease?
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Systemic staph infection in newborns
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When do coagulase negative staph become dangerous pathogens?
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When associated with an inserted foreign body
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What do h. influenzae, N. meningiditis, and s. pneumoniae have in common?
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polysaccharide capsule that is a virulence factor, age-related causes of meningitis, contain IgA protease
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Describe h. influenzae.
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gram neg coccobacillus
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Describe s. pneumoniae.
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gram pos diplococcus, lancet shaped, alpha-hemolytic, optochin sensitive
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Describe n. meningiditis.
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gram neg diplococcus, coffee-bean shape
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How can you detect the polysaccharide capsule shed by encapsulated pathogens?
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latex agglutination or concurrent immunoelectrophoresis
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Where does a culture have to be from to be diagnostic in growing encapsulated pathogens?
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A normally sterile site
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What is Lipo-oligosaccharide?
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virulence factor in gram neg encapsulated pathogens - ass'd with meningitis, bacteremia, DIC, sepsis
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Why is there no vaccine availabe for N. meningiditis serotype B?
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serotype factor = N-acetyl neuraminic acid, which is present in humans and therefore non-immunogenic
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Why do vaccines have to induce IgG/IgM antibody to protect from encapsulated pathogens?
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IgA Ab cannot opsonize because pathogens have IgA protease
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Prevnar vaccine to s. pneumoniae has been shown to reduce what childhood illness by 10%
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otitis media
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What distinguishes a bacterial meningitis from viral?
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more severe, brain damage/learning disability sequelae, hearing loss
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What will be the result of a spinal tap in a patient with h. influenzae meningitis?
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PMNs and bacteria (PMNs usually seen in viral meningitis?)
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What cytopathic effect do cells exhibit with alpha-herpes infection?
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cells become multinucleated giant syncitial cells with intranuclear inclusions
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What is the number one viral cause of encephalitis?
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HSV1
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What does TORCHES stand for?
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Toxoplamosis, Rubella, CMV, Herpes, HIV and Syphillis all cause neonatal infection
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Why does chickenpox present with lesions at different stages at one time?
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VZV viremia leads to lesions that arise in "crops", but not all at once
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Where do chickenpox blisters generally arise first?
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on the face and trunk
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What is the number one viral cause of mental retardation in children?
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CMV
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What percent of CMV infections are asymptomatic?
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eighty
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What are the different patters of CMV-related illness in AIDS v. marrow transplant patients?
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Both get: viremia and colitis, AIDS pts get retinitis, transplant pts get pneumonitis
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What virus usually causes mononucleosis?
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EBV
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What herpes viruses are associated with malignancy?
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EBV - Burkitt's; HHV8 - Kaposi's sarcoma
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What are the three sequential stages of viral replication in herpes infection?
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Immediate early -> early -> late
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What type of proteins are encoded by the IE genes in herpes infection?
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immune evasion protiens
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What type of proteins are encoded by the E genes in herpes infection?
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proteins required for viral replication (virus circulization)
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What type of proteins are encoded by the L genes in herpes infection?
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structural proteins: capsid, shell, tegument
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Where does the herpes viral capsid assemble in the infected cell?
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in the nucleus
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WTF happens to a herpes viral capsid after it assembles in the nucleus?
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buds thru nuclear membrane, then thru Golgi where it acquires glycoproteins
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What is the primary site of infection and site of latency in the alpha herpes viruses?
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mucosal epithelium -> down axon to neuronal cell
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The beta herpes viruses (CMV, HHV6, HHV7) extablish latency in what type of cell?
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myeloid lineage, endothelial cells
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Where does EBV establish latency?
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B cells, can subsequently transform cells
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What are the shared properties of the herpes family viruses?
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spherical enveloped virions, linear dsDNA, icosahedral capsids, replicate and encapsulate in nucleus, lytic -> latent phase, don't survive well outside human body
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How does the herpes viral capsid enter the cell?
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glycoproteins tether virion to cell, also allow cell-to-cell spread
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What immune responses lead to the papule and then vesicle seen in HSV1 and 2 infection?
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papule is due to inflammation and veicle is due to cytokine induced fluid accumulation
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What is the classic description of a chickenpox lesion?
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dew on a rose petal
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What are some of the proteins seen in latent EBV infection?
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EBNA1: tethers DNA, EBNA2: Transcription factor, LMP1: mimics T-cell receptor. LMP2A: mimics B-cell receptor
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What polymerase is used in lytic infection with beta and gamma herpes? Latency?
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lytic - viral polymerase, latent -host polymerase
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What makes an obligate aerobe obligate?
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it lacks some of the genes necessary for metabolic growth and rely on a host cell to supply those proteins. CANNOT GROW IN PLATES WITHOUT CELLS
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What are the two mechanisms by which obligate bacteria enter a host cell?
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1. zipper
2. trigger |
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Describe the zipper mechanism for host cell entry. Name three examples a bacteria that use this entry.
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tight interaction between bacterial cell ligands and host cell recptors allowing closure of the host cell surface around the bacterium.
Listeria monocytogenes Mycobacterium tuberculosis Legionella pneumophila |
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Describe the trigger mechanism for host cell entry. Name two examples of bacteria that use this entry.
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bacterial products cause the host cell surface to ruffle causing membrane projections to surround the bacteria and pull it in.
Salmonella and Shigella (Gram -ive rods) |
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What are three advantages to living in a host cell (obligate bacteria)?
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1. nutritional advantages (no competition with other bacteria)
2. protection from the immune system 3. protected dissemination around the body |
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Name the three antimicrobial defenses that professional phagocytes have against obligate bacteria?
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1. NADPH oxidase (makes O2 radicals
2. NO synthases to make NO 3. O2 independent effector molecules (decreased Fe and pH) |
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Which bacteria is able to escape phagocytic vacuoles and get to the cytosol? What host defense mechanisms await them there?
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Listeria (makes actin propelling it into the cytosol); NO synthase and cytotoxic T cells
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What is a common sequela of non-fusogenic organisms?
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Granulomas (infectious agents, host cells and activated T cells)causing long-term infections balancing organism growth and host defenses
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What is the only intracellular pathogen to reside within the phagolysosome?
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Coxiella burnetti
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Obligate intracellular bacteria are most susceptible two which two classes of antimicrobials?
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Tetracyclines
Rifampicin |
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How many tests must be done within a 2-4 hour period for a diagnosis of infective endocarditis?
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3
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What is the microbiologic factor in Strep viridans leading to the development of infective endocarditis?
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extracellular polysaccharide dextran allows it to adhere to the damaged valve with fibrin
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What pertinient PE finding alerts you to a diagnosis of necrotising fasciitis (say, over cellulitis) and what are the two types of necrotizing fasciitis?
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Most common PE finding is that the pain is disproportionate to the size of the infection.
Type I: polymicrobial (anaerobes, aerobes, enterics, G-negs) Type II: Group A, beta hemolytic strep (pyogenes) |
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What are the 4 main non-invasive enterics?
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1. Vibrio cholerae
2. ETEC 3. EPEC 4. EHEC |
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All enterics are of which bacterial classification?
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Gram (-)bacilli (rods)
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Which antigenic structure is common to all enterics?
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"O" antigens, associated with the LPS of the outer membrane of the bacteria
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What is the mode of transmission of enterics?
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fecal-oral
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What is the role of the TCP (toxin co-regulated pilus)?
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serves as a receptor for the bacteriaphage to facilitate conversion to toxin inside the cell
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What is the function of AB toxin in Vibrio cholera?
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B-binding-binds to surface receptors of enterocytes
A-active-activates adenylate cyclase -> increased cAMP -> increased Cl- secretion -> decreased Na = net secretion of fluid into the gut |
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What are the symptoms and treatment of Vibrio cholera infection?
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large volume, water diarrhea "rice water"--hypovolemic shock if severe; tx = ORT
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What bug is the major cause of Traveler's diarrhea?
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ETEC
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Compare the AB toxins of Vibrio cholera and ETEC
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Vibrio and ETEC B toxins are similar
A toxin of ETEC activates guanylate cyclase -> cGMP -> increased fluid excretion A toxin of Vibrio activates adenylate cyclase |
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What are the virulence factors associated with EPEC?
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AE - attaching and effacing;
Tye III secretion systems |
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What is the name of the receptor on EPEC allowing it to form a close association between host and organism and inject effectors into the host cell?
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translocating-intimin receptor
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What is the major serotype of EHEC?
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O157:H7 (does not necessarily correlate to virulence)
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What media is used to culture EHEC?
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MacConkey w/ sorbitol (non-fermenting in sorbitol)
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What virulence factors are in EHEC?
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AE lesions
Shiga-like toxins AB toxins to inhibit protein synthesis |
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EHEC can lead to the development of what other disease in the young and elderly?
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HUS - hemolytic uremic syndrome
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Where is the site of colonization for EHEC?
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Large intestine
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What are the 4 major invasive enteric pathogens?
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Shigella
Salmonella H. pylori Campylobacter |
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What is a common diagnostic feature of all invasive enterics?
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presence fecal leukocytes
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Which Shigella bacteria is most common in the US?
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S. sonnei
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What is the site of invasion for Shigella?
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colonic M cells (via Type III)
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What is the function of IL-1 and IL-8 in the pathophys of Shigella?
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attraction of PMNs
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What is the treatment for Shigella?
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Antibiotics
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Serotypes of Salmonella are defined based on what marker?
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O antigen side chains
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List the three virulence factors of salmonella and the mechanism for each.
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attachment - fimbriae
invasion - pathogenicity island 1 survival in macrophages - pathogenicity island 2 |
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What are the three main sx of a Salmonella infection?
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Gastroenteritis
Septicemia Typhoid fever |
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What bug is the #1 cause of gastroenteritis in the US?
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Campylobacter jejuni
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What is the most common bacterial pathogen?
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H. pylori
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What is the main result of an H. pylori infection?
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duodenal and gastric ulcers
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What constitutes the triple therapy required for an H. pylori infection?
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PPI + bismuth + tetracycline
14 days. |
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Describe the MOA of the following antimicrobial drug: sulfamethoxazole
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inhibits DNA synthesis, folic acid analog
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Describe the MOA of the following antimicrobial drug: quinolones
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inhibits DNA gyrase
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Describe the MOA of the following antimicrobial drug: penicillins, cephalosporins, carbamapens
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inhibits cell wall synthesis
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Describe the MOA of the following antimicrobial drug: aminoglycosides and tetracyclines
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inhibits protein synthesis at 30S subunit
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Describe the MOA of the following antimicrobial drug: macrolides, chloramphenicol, lincosamides
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inhibits protein synthesis at 50S subunit
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Describe the MOA of the following antimicrobial drug: trimethoprim
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inhibits dihydrofolate reductase (step in DNA synthesis downstream from sulfonamide MOA
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Why are SMX and TMP used together?
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synergistic effect makes combination more effective than each alone - they block different steps in same reaction
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What four drugs are involved in the first-line treatment of TB?
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Rifampin, Isoniazid, Pyrazinamide, Ethambutol (RIPE)
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Why is the onset of sulfamethoxazole slow?
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DNA synthesis continues until excess substrate is used (stores of metabolites downstream from the targeted reaction)
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What antimicrobial drug predisposes to crystalluria? Why?
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sulfonamides; drug metabolite is LESS soluble than drug (inverse of usual); deposits in renal cells
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What TB drugs have gout as a potential side effect?
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Pyrazinamide, Ethambutol
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What antimicrobial drug predisposes to kernicterus in infants? Why?
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sulfonamides; drug binds albumin, displaces bilirubin into bloodstream
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In TB treatment, what does DOT stand for?
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directly observed therapy
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Describe the spectrum for drugs in the quinolone class, including trend with newer generations.
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all are good with gram neg. broader spectrum in later generations
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Why are so many drugs administered at once in TB?
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There are so many organisms (10^9) that tx with 1 drug could allow for resistance to develop due to random mutation
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What is the MOA of the following drug? Isoniazid
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blocks synthesis of myconic acids (outer layer of mycobacterium)
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What is the MOA of the following drug? Rifampin
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Inhibits RNA synthesis by binding the polymerase
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What two firstline TB drugs are KNOWN to enter the human cell?
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Isoniazid and Rifampin
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What is the MOA of the following drug? Ethambutol
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binds and inhibits the EZ responsible for arabino-galactam layer of mycobacterial cell wall
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What genetically influenced differences exist in the metabolism of Isoniazid?
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N-Acetylation
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What side effects of Isoniazid are related to genetic differences in the drugs metabolism?
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Slow acetylators - optic and peripheral neuritis, Fast - hepatic damage (pts on the drug should avoid EtOH)
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What TB drug can also be used in severe gram+ or - cocci and Legionella?
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Rifampin
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Which TB drugs are specifically effective inside lesions?
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Pyrazinamide (more active at low pH); Ethambutol (esp. lung lesions)
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What combination of drugs is used in leprosy?
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dapsone, rifampin, clofazimine
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What combination of drugs is used in mycobacterium avium?
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Amikacin, Clofazimine, Fluoroquinolones, macrolides
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