CIC EXAM CORRECT QUESTIONS &
ANSWERS(GRADED A+)
Chain of Infection - ANSWER 1)Infectious agent= organism with ability to cause
disease; greater virulence, invasiveness, and pathogenicity => increased odds of
infection
2) Reservoir: place where microbes can persist and reproduce
3) Portal of Exit: way for microbe to leave the reservoir
4) Mode of transmission: method of microbe transfer from one place to another
5) Portal of entry: opening that allows microbe to enter host
6) Susceptible host: Lacks immunity or physical resistance to prevent invasion by
microbe
Is a circle; each link must be present in sequential order for infection to occur
Virulence - ANSWER Measure of microbe's ability to invade and create disease
Depends on ability to:
Survive in environment between hosts
Transmit between hosts (moving; adherence)
Proliferate
IgM - ANSWER Pentamer; primary response, short-lived (<6 months); best at fixing
complement
IgG - ANSWER Monomer; main blood antibody, secondary response; longer lived.
opsonization and toxin neutralization. 4 subclasses
Physical barriers - ANSWER Skin; fever; secreted antimicrobials; innate immunity
Complement system - ANSWER 11=protein cascade; classically activate by ab:ag
complexes; alternate by pathogen surfaces
Skin defects; examples and associated pathogens - ANSWER Wounds, burns, trauma,
serious derm problems, indwelling devices, injections. Skin flora- S. aureus, CNS, strep
pyo, corynebacteria, malassezia furfur
Mucous membrane barrier defects; examples and associated pathogens - ANSWER
chemo-induced mucositosis, head/neck trauma, smoking, inhalational injury,
antacids/PPIs. Resident flora- anaerobes, aerobic GNR, candida, enteroccus, bovis
Body passage obstruction; examples and associated pathogens - ANSWER Tumors,
foreign bodies, stones, cystic fibrosis. Resident flora overgrow or invade; site-specific.
,Abnormal number or function of granulocytes - ANSWER Leukemia, chemo, congenital
disorders, diabetes. If short term (< 2 wks) then aerobic GNR, Sa, CoNS. IF long term,
add fungi (candida, t. glabrata, aspergillus)
Abnormalities of cell-mediated immunity - ANSWER BMT, HIV, steroids, malnutrition,
3rd tri pregnancy. Bacteria: Intracellular pathogens (listeria, salmonella, mycobacteria,
nocardia, legionella).
Fungi: candida, Cryptococcus, coccidioides, histoplasma. Virus: Herpes group
Also toxoplasma and strongyloides.
abnormalities of humoral immunity - ANSWER BMT, HIV, some cancers, aging. Strep
pneumo, encapsulated H. flu, Neisseria meningitidis
Preventing infection for immunocompromised patients - ANSWER Take thorough
patient history. Prepare before starting with all vaccines, procedures, line placement,
screening. Support gastric acidity. Prevent exposures with awesome hygiene, approp
food and water precautions, visitor education, no flowers or plants, and possible abx
prophy (for infections that might reactivate or high-risk for pneumocystis)
Mycoplasma spp. - ANSWER No cell wall --> limited abx choices. Cause atypical
pneumonia. Usually diagnosed by serology
Chlamydiae - ANSWER obligate intracellular parasites. Elementary body=infectious,
reticulated= intracellular. DFA or ELISA for detection of antigen is most common. Can
also detect antibodies.
Rickettsiae - ANSWER obligate intracellular parasites. arthropod vectors. Rarely
culturing; detected by serology using ELISA for antibodies.
Textbook viral replication cycle - ANSWER 1. Attachment 2. penetration/entry 3.
replication 4. maturation/assembly 5. release
Sensitivity - ANSWER % of true + who test +; inherent to test
Specificity - ANSWER % of true neg who test neg; inherent to test
PPV - ANSWER Likelihood that a + test represents a true case (% T+/all+); depends on
the test and on prevalence of disease in population
NPV - ANSWER Likelihood that a negative test result is a true non-case (%TN/allN);
depends on test and population prevalence
CSF analysis- bacterial mening - ANSWER 1000-5000 WBCs, mostly PMNs. Increased
pressure. Increased protein . Decreased glucose. Bacteria seen on smears.
,CSF analysis- viral mening - ANSWER Pressure, glucose normal. Lymphocytes seen,
but few WBC in general. Protein normal-elevated. Nothing on smears.
CSF analysis- fungus mening - ANSWER Pressure variable. Glucose low, protein high.
WBCs vary, but lymphocytes predominate. India ink smear +.
CSF analysis- TB mening - ANSWER Pressure variable. Glucose low to megalow.
WBCs vary, mostly lymphocytes. Protein elevated. AFB stain +
Fecal leukocytes - ANSWER For determining whether diarrhea is from an invasive or
noninvasive infection. Leukocytes indicate the pathogen is breaking the mucosal barrier.
Concentration vs time dependent antibiotic dosing - ANSWER CD means you want to
spike the initial concentration really high, and if it dips below MIC before next dose it's
ok because of "post-antibiotic effect" still killing. aminoglycosides, fluoroquinolones are
[dependent].
Time dependent means you don't need a high [], just to keep the [] above the MIC for a
long time. B-lactams dosed this way.
Antifungal mechanism of action - ANSWER Echinocandins (casopfungin) work on the
cell wall synthesis process. Azoles work to prevent sterol synthesis, which affects the
cell membrane
Biofilm treatment and prevention - ANSWER Prevent adherence with antimicrobial
surfaces, exemplary sterile technique. Probiotics may help.
Once exist: physically remove/debride the biofilm, abx to prevent regrowth. Removing
devices.
Viral hemorrhagic fever pathogens and pathogenesis - ANSWER Yellow fever, dengue,
hantaviruses, Ebola, etc. 4 virus families (flavi, bunya, filo, and arena). The exact
pathogenesis varies by virus; generally target vascular endothelium. May or may not
involve immunopathology. Fever, unexplained bleeding, shock common features.
Viral hemorrhagic fever transmission - ANSWER Most have another mammal host
reservoir, and many have arthropod vectors. Spread person to person by direct contact
with infected fluids
Viral hemorrhagic fever diagnosis - ANSWER Travel history important. Antibody titers to
diagnose, need BSL-4 to isolate/culture.
Viral hemorrhagic fever infection prevention - ANSWER Isolate ASAP and use
droplet+contact+standard precautions. Increase PPE for very wet patients, lots of
coughing, or aerosol-generating procedures. Log all staff+visitor contact. Special
recommendations for lab staff. Vaccine for yellow fever exists.
Hepatitis A epidemiology - ANSWER Incidence has tanked since VACCINE introduced.
Fecal oral spread; poor hygiene and intimate contact are risk factors. Kids usually
, asymptomatic. Contagious before symptoms start. No chronic carriage. incubates15-50
days.
Hepatitis A diagnosis - ANSWER Serology. IgM antibodies within 3 wks of exposure,
present at onset of jaundice. IgG should be detectable at onset of jaundice, will remain
positive for life (indicates immunity to Hep A)
Hepatitis A infection prevention - ANSWER Vaccination. Hand hygiene. Standard
precautions fine, but if patient diapered or incontinent contact precautions
recommended. PEP in outbreak situations.
Hep B epidemiology - ANSWER Transmitted by blood, sexual contact, or perinatally.
Infectiousness increased if HBsAg, HBeAg +. Chronic carrier state much more common
with kids. Chronic infection more likely to have severe outcomes. 30-180 days
incubation
Hep B diagnosis - ANSWER Acute HBV indicated by anti-HBV core IgM
Chronic HBV involves positive serum HBsAg for 6+ months. IgG anti HBs + in both
chronic active carriers and those who have cleared the virus.
HBV DNA, HBeAg indicate lots of replication and high infectivity.
Hep B prevention - ANSWER Vaccination. BBP rules have protected HCP a lot.
Standard precautions are fine. PEP with HBIG is recommended after a needlestick.
Hep C epidemiology - ANSWER Transmitted by blood (injection) and blood products.
Inefficiently transmitted by sex. Most HCV becomes chronic. Incubates 15-160 days,
usually more like 5 wks. Often asymptomatic. Alcohol use increases likelihood of severe
outcomes
Hep C diagnosis - ANSWER EIA for anti-HCV antibodies. Acute indicated by IgM,
chronic by IgG. PCR done for HCV RNA detection, but is not specific for acute vs.
chronic. qPCR is important for treatment monitoring and genotyping.
Hep C infection prevention - ANSWER Modern blood screening practices prevent most
transfusion-associated cases. In general, avoiding exposure is the best prevention.
Standard Precautions adequate in the hospital.
Hep D epidemiology - ANSWER Parasite of HBV, dependent on HBV for transmission.
Infects ~10% of HBV cases, but more common among IVDU. Almost exclusively
transmitted by blood. Increases the chances of fulminant hepatitis. Incubation 30-180
days; usually just looks like HBV infection.
Hep D diagnosis - ANSWER MUST test + for HBsAg. Acute: HDV PCR, IgM. Chronic:
IgG, although short-lived and not helpful
ANSWERS(GRADED A+)
Chain of Infection - ANSWER 1)Infectious agent= organism with ability to cause
disease; greater virulence, invasiveness, and pathogenicity => increased odds of
infection
2) Reservoir: place where microbes can persist and reproduce
3) Portal of Exit: way for microbe to leave the reservoir
4) Mode of transmission: method of microbe transfer from one place to another
5) Portal of entry: opening that allows microbe to enter host
6) Susceptible host: Lacks immunity or physical resistance to prevent invasion by
microbe
Is a circle; each link must be present in sequential order for infection to occur
Virulence - ANSWER Measure of microbe's ability to invade and create disease
Depends on ability to:
Survive in environment between hosts
Transmit between hosts (moving; adherence)
Proliferate
IgM - ANSWER Pentamer; primary response, short-lived (<6 months); best at fixing
complement
IgG - ANSWER Monomer; main blood antibody, secondary response; longer lived.
opsonization and toxin neutralization. 4 subclasses
Physical barriers - ANSWER Skin; fever; secreted antimicrobials; innate immunity
Complement system - ANSWER 11=protein cascade; classically activate by ab:ag
complexes; alternate by pathogen surfaces
Skin defects; examples and associated pathogens - ANSWER Wounds, burns, trauma,
serious derm problems, indwelling devices, injections. Skin flora- S. aureus, CNS, strep
pyo, corynebacteria, malassezia furfur
Mucous membrane barrier defects; examples and associated pathogens - ANSWER
chemo-induced mucositosis, head/neck trauma, smoking, inhalational injury,
antacids/PPIs. Resident flora- anaerobes, aerobic GNR, candida, enteroccus, bovis
Body passage obstruction; examples and associated pathogens - ANSWER Tumors,
foreign bodies, stones, cystic fibrosis. Resident flora overgrow or invade; site-specific.
,Abnormal number or function of granulocytes - ANSWER Leukemia, chemo, congenital
disorders, diabetes. If short term (< 2 wks) then aerobic GNR, Sa, CoNS. IF long term,
add fungi (candida, t. glabrata, aspergillus)
Abnormalities of cell-mediated immunity - ANSWER BMT, HIV, steroids, malnutrition,
3rd tri pregnancy. Bacteria: Intracellular pathogens (listeria, salmonella, mycobacteria,
nocardia, legionella).
Fungi: candida, Cryptococcus, coccidioides, histoplasma. Virus: Herpes group
Also toxoplasma and strongyloides.
abnormalities of humoral immunity - ANSWER BMT, HIV, some cancers, aging. Strep
pneumo, encapsulated H. flu, Neisseria meningitidis
Preventing infection for immunocompromised patients - ANSWER Take thorough
patient history. Prepare before starting with all vaccines, procedures, line placement,
screening. Support gastric acidity. Prevent exposures with awesome hygiene, approp
food and water precautions, visitor education, no flowers or plants, and possible abx
prophy (for infections that might reactivate or high-risk for pneumocystis)
Mycoplasma spp. - ANSWER No cell wall --> limited abx choices. Cause atypical
pneumonia. Usually diagnosed by serology
Chlamydiae - ANSWER obligate intracellular parasites. Elementary body=infectious,
reticulated= intracellular. DFA or ELISA for detection of antigen is most common. Can
also detect antibodies.
Rickettsiae - ANSWER obligate intracellular parasites. arthropod vectors. Rarely
culturing; detected by serology using ELISA for antibodies.
Textbook viral replication cycle - ANSWER 1. Attachment 2. penetration/entry 3.
replication 4. maturation/assembly 5. release
Sensitivity - ANSWER % of true + who test +; inherent to test
Specificity - ANSWER % of true neg who test neg; inherent to test
PPV - ANSWER Likelihood that a + test represents a true case (% T+/all+); depends on
the test and on prevalence of disease in population
NPV - ANSWER Likelihood that a negative test result is a true non-case (%TN/allN);
depends on test and population prevalence
CSF analysis- bacterial mening - ANSWER 1000-5000 WBCs, mostly PMNs. Increased
pressure. Increased protein . Decreased glucose. Bacteria seen on smears.
,CSF analysis- viral mening - ANSWER Pressure, glucose normal. Lymphocytes seen,
but few WBC in general. Protein normal-elevated. Nothing on smears.
CSF analysis- fungus mening - ANSWER Pressure variable. Glucose low, protein high.
WBCs vary, but lymphocytes predominate. India ink smear +.
CSF analysis- TB mening - ANSWER Pressure variable. Glucose low to megalow.
WBCs vary, mostly lymphocytes. Protein elevated. AFB stain +
Fecal leukocytes - ANSWER For determining whether diarrhea is from an invasive or
noninvasive infection. Leukocytes indicate the pathogen is breaking the mucosal barrier.
Concentration vs time dependent antibiotic dosing - ANSWER CD means you want to
spike the initial concentration really high, and if it dips below MIC before next dose it's
ok because of "post-antibiotic effect" still killing. aminoglycosides, fluoroquinolones are
[dependent].
Time dependent means you don't need a high [], just to keep the [] above the MIC for a
long time. B-lactams dosed this way.
Antifungal mechanism of action - ANSWER Echinocandins (casopfungin) work on the
cell wall synthesis process. Azoles work to prevent sterol synthesis, which affects the
cell membrane
Biofilm treatment and prevention - ANSWER Prevent adherence with antimicrobial
surfaces, exemplary sterile technique. Probiotics may help.
Once exist: physically remove/debride the biofilm, abx to prevent regrowth. Removing
devices.
Viral hemorrhagic fever pathogens and pathogenesis - ANSWER Yellow fever, dengue,
hantaviruses, Ebola, etc. 4 virus families (flavi, bunya, filo, and arena). The exact
pathogenesis varies by virus; generally target vascular endothelium. May or may not
involve immunopathology. Fever, unexplained bleeding, shock common features.
Viral hemorrhagic fever transmission - ANSWER Most have another mammal host
reservoir, and many have arthropod vectors. Spread person to person by direct contact
with infected fluids
Viral hemorrhagic fever diagnosis - ANSWER Travel history important. Antibody titers to
diagnose, need BSL-4 to isolate/culture.
Viral hemorrhagic fever infection prevention - ANSWER Isolate ASAP and use
droplet+contact+standard precautions. Increase PPE for very wet patients, lots of
coughing, or aerosol-generating procedures. Log all staff+visitor contact. Special
recommendations for lab staff. Vaccine for yellow fever exists.
Hepatitis A epidemiology - ANSWER Incidence has tanked since VACCINE introduced.
Fecal oral spread; poor hygiene and intimate contact are risk factors. Kids usually
, asymptomatic. Contagious before symptoms start. No chronic carriage. incubates15-50
days.
Hepatitis A diagnosis - ANSWER Serology. IgM antibodies within 3 wks of exposure,
present at onset of jaundice. IgG should be detectable at onset of jaundice, will remain
positive for life (indicates immunity to Hep A)
Hepatitis A infection prevention - ANSWER Vaccination. Hand hygiene. Standard
precautions fine, but if patient diapered or incontinent contact precautions
recommended. PEP in outbreak situations.
Hep B epidemiology - ANSWER Transmitted by blood, sexual contact, or perinatally.
Infectiousness increased if HBsAg, HBeAg +. Chronic carrier state much more common
with kids. Chronic infection more likely to have severe outcomes. 30-180 days
incubation
Hep B diagnosis - ANSWER Acute HBV indicated by anti-HBV core IgM
Chronic HBV involves positive serum HBsAg for 6+ months. IgG anti HBs + in both
chronic active carriers and those who have cleared the virus.
HBV DNA, HBeAg indicate lots of replication and high infectivity.
Hep B prevention - ANSWER Vaccination. BBP rules have protected HCP a lot.
Standard precautions are fine. PEP with HBIG is recommended after a needlestick.
Hep C epidemiology - ANSWER Transmitted by blood (injection) and blood products.
Inefficiently transmitted by sex. Most HCV becomes chronic. Incubates 15-160 days,
usually more like 5 wks. Often asymptomatic. Alcohol use increases likelihood of severe
outcomes
Hep C diagnosis - ANSWER EIA for anti-HCV antibodies. Acute indicated by IgM,
chronic by IgG. PCR done for HCV RNA detection, but is not specific for acute vs.
chronic. qPCR is important for treatment monitoring and genotyping.
Hep C infection prevention - ANSWER Modern blood screening practices prevent most
transfusion-associated cases. In general, avoiding exposure is the best prevention.
Standard Precautions adequate in the hospital.
Hep D epidemiology - ANSWER Parasite of HBV, dependent on HBV for transmission.
Infects ~10% of HBV cases, but more common among IVDU. Almost exclusively
transmitted by blood. Increases the chances of fulminant hepatitis. Incubation 30-180
days; usually just looks like HBV infection.
Hep D diagnosis - ANSWER MUST test + for HBsAg. Acute: HDV PCR, IgM. Chronic:
IgG, although short-lived and not helpful
