CIC 2024 STUDY GUIDE COMPREHENSIVE
QUESTIONS AND CORRECT ANSWERS GET ALL
RIGHT [EXAM PREPARATION] GRADE A+
The importance of collaboration between IP&C and lab in preventing HAIs
Microbiology should promptly notify IP&C of any organism's unusual resistance pattern
-CDC recommends that all healthcare organizations establish systems to ensure that
clinical microbiology labs promptly notify infection control staff or a designee when a
novel resistance pattern is detected
Immunoglobulin M
-the primary immune response after exposure to a communicable disease pathogen or
vaccine
-Sign of active infection
-IgG antibodies develop a few weeks later - these are a good indication of the
convalescence period and establishes long-term immunity to the pathogen
When are IgM antibodies to Hepatitis A (HAV) detectable in the blood?
-Within 3 weeks of exposure, at the onset of jaundice
-Clinical features of acute hepatitis are not specific to HAV infection, so serological
testing is necessary
-Titer declines over 4-6 weeks and antibodies are usually not detectable after 6-12
months
-IgG also detectable at onset of jaundice, remains positive lifelong
Chain of Infection
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
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
Pentamer; primary response, short-lived (<6 months); best at fixing complement
IgG
,Monomer; main blood antibody, secondary response; longer lived. opsonization and
toxin neutralization. 4 subclasses
Physical barriers
Skin; fever; secreted antimicrobials; innate immunity
Complement system
11=protein cascade; classically activate by ab:ag complexes; alternate by pathogen
surfaces
Skin defects; examples and associated pathogens
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
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
Tumors, foreign bodies, stones, cystic fibrosis. Resident flora overgrow or invade; site-
specific.
Abnormal number or function of granulocytes
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
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
BMT, HIV, some cancers, aging. Strep pneumo, encapsulated H. flu, Neisseria
meningitidis
Preventing infection for immunocompromised patients
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.
No cell wall --> limited abx choices. Cause atypical pneumonia. Usually diagnosed by
serology
Chlamydiae
obligate intracellular parasites. Elementary body=infectious, reticulated= intracellular.
DFA or ELISA for detection of antigen is most common. Can also detect antibodies.
Rickettsiae
obligate intracellular parasites. arthropod vectors. Rarely culturing; detected by serology
using ELISA for antibodies.
Textbook viral replication cycle
1. Attachment 2. penetration/entry 3. replication 4. maturation/assembly 5. release
Sensitivity
% of true + who test +; inherent to test
Specificity
,% of true neg who test neg; inherent to test
PPV
Likelihood that a + test represents a true case (% T+/all+); depends on the test and on
prevalence of disease in population
NPV
Likelihood that a negative test result is a true non-case (%TN/allN); depends on test and
population prevalence
CSF analysis- bacterial mening
1000-5000 WBCs, mostly PMNs. Increased pressure. Increased protein . Decreased
glucose. Bacteria seen on smears.
CSF analysis- viral mening
Pressure, glucose normal. Lymphocytes seen, but few WBC in general. Protein normal-
elevated. Nothing on smears.
CSF analysis- fungus mening
Pressure variable. Glucose low, protein high. WBCs vary, but lymphocytes
predominate. India ink smear +.
CSF analysis- TB mening
Pressure variable. Glucose low to megalow. WBCs vary, mostly lymphocytes. Protein
elevated. AFB stain +
Cold Agglutinins test
Used to detect antibodies for Mycoplasma pneumoniae or mononucleosis. Positive test
is high titer, with resp Sx indicates M. pneumo infection, viral pneumo, or primary
atypical pneumo
CRP test
Serum sample looking for the CR protein; normal value is none or low CRP. Indicates
current acute inflammation
Liver Function Tests
chemistry assays on blood; looking for various things including enzymes, bilirubin,
ammonia, and albumin. Generally higher is worse. Helps detect liver problems,
differentiate among liver problems, measure liver damage, and follow response to Tx.
Arterial Blood Gas (ABG)
blood from artery, measures oxygen and CO2 tension, pH. Assesses gas exchange,
which is helpful in recognizing pneumonia
Sedimentation rate
Measures rate of RBCs sinking; faster indicates acute infection/inflammation (among
other things, is not very specific)
Toxin production tests
Many ways of doing, including EIA and HPLC. limulus amebocyte lysate tests for
endotoxin.
Weil-Felix agglutination
Serum, test for rickettsial antibodies. High titer or 4x rise in titer indicates rickettsial
infection.
Urinalysis
Multiple tests. Normal has various chemistry values and should have no or few cells.
High WBCs, leukocyte esterase, and nitrite indicate infection.
Complete blood count: WBC count
, 4000-10000 is normal. High indicates infection/inflammation. Low indicates AIDS or
some other infections
CBC:WBC differential
Gives percents of cell types. Should be:
PMN>lymphocytes>monocytes>eosinophils>basophils. If inc PMNs and "left shift",
acute bacterial infection. If inc lymphocytes and reactive lymphs, some viral infections.
Monocytes increase with EBV, TB, endocarditis, and rickesttsia. Eosinophils increase
with allergies, parasites, and mycobacteria. Basophils shouldn't be high but it happens
with allergies, variola, and varicella.
CBC: absolute neutrophil count
Normal is >2x109/L; less indicates neutropenia. <.5x109/L is severe neutropenia
Lymphocyte subset
Additional test beyond CBC to differentiate T and B cells, and the types of T cells.
Important in monitoring HIV patients, also info about response type.
Fecal leukocytes
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
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
Echinocandins (casopfungin) work on the cell wall synthesis process. Azoles work to
prevent sterol synthesis, which affects the cell membrane
Biofilm treatment and prevention
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
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
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
Travel history important. Antibody titers to diagnose, need BSL-4 to isolate/culture.
Viral hemorrhagic fever infection prevention
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
