Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

353 Cards in this Set

  • Front
  • Back
what are the 2 types of control measures?
sterilization and disinfection
what is sterilizatoin?
process that eliminates through destruction or removal, ALL VIABLE microorg. including viruses
what is disinfection?
physical or chemical process used to destroy vegetative pathogens but not endospores
*reduces the infectious dose present (doesn't destroy some parts of pathogen)
what is the diff. b/n disinfectant and antiseptic?
disinfectant: used on inanimate objects (table)
antiseptic: used on animate objects
what do bacteriostatic drugs do?
prevents the growth of bacteria on tissues or on objects in the environment
what do bacteriocidal drugs do?
destroy bacteria (only a few destory endospores)
decrease infectious dose
what are the 3 factors affecting microbial control/death?
1. nature of microorg
2. # of microorg. at start
3. concentration of antimicrobial agent (dosage, half life, absorption)
in terms of the concentration of antimicrobial agent, what is impt to know?
dosage: what is a safe initial concentration to give and how often does it need to be re-administered
half life: how quickly excreted from body
absorption: is it absorbed into all tissues? if doesn't cross BBB, know the effective conc. diff in CNS and blood
what are the 6 mechanims of antibacterial action?
1. inhibition of cell wall synthesis **
2. disruption of PM
3. inhibition of protein syn
4. inhibition of nucleic acid syn
5. antimetabolites
6. target regaulatory molecules
what are 4 impt. antibacterial drugs that inhibit cell wall synthesis?
what are 4 impt. antibacterial drugs that inhibit protein synthesis?
*aimed at ribosomes b/c they are different in prok
what mode of antibacterial action is the best for highly selective toxicity?
inhibition of cell wall synthesis
what 2 impt antibacterial drugs target inhibition of sythesis of essential metabolites?
what 2 classes of antibacterial drugs target inhibition of nucleic acid replication and trancription?
what impt. antibacterial drug targets injury to plasma membrane?
polymyxin B
what are 5 methods of antibiotic resistance used by bacteria?
1. target tissue alteration (ex bacteria alter target and penicillin can no longer bind cell wall)
2. active efflux (excretion of drug)
3. inactivation or degradation of antimicrobial agent (enzymes that cleave drug)
4. decreased uptake (mutations in permeases or porins)
5. production of decoy molecules (generated to look like drug)
where are most drug resistant genes encoded?
on transposons and plasmids- things that can move around
what is selective toxicity?
ability to kill pathogen instead of or before killing the host
what is high selective toxicity?
when biochemical target is absent in host cells Ex. penicillin targets peptidoglycan that is not present in eukaryotic cells
what is broad spectrum activity?
ability to kill many different types of microbes
what is narrow spectrum activity?
drug taht kills only a few types of microbes
what is minimum inhibitory concentration (MIC)?
lowest concentration of a drug that prevents growth of a particular pathogen
what is therapeutic index (TI)?
the ratio of drugs toxic dose (toxic to host) to its minimum therapeutic dose (MIC)
*ratio b/n effective and toxic dose
is tetracyclin cidal or static? penicillin? when the 2 are combined?
tetracyclin: static
penicillin: cidal
combo: static overpowers cidal by blocking bacterial growth, now cidal can't act b/c it requires growth to work
what is this describing: the lower concentration of a drug that prevents growth of a particular pathogen?
minimum inhibitory concentration (MIC)
what is therapeutic index?
is a comparison of the amount of a therapeutic agent that causes the therapeutic effect to the amount that causes toxic effects. Quantitatively, it is the ratio given by the dose required to produce the toxic effect divided by the therapeutic dose. A commonly used measure of therapeutic index is the lethal dose of a drug for 50% of the population (LD50) divided by the minimum effective dose for 50% of the population (ED50).
*measurement for appropriate use and dosage
*see if org is resistant or sensitive to drug
what are the axis for antibiotic combination graphs?
x axis: hours
y axis: log # viable org.
describe antibiotic synergy
Antibiotic A has no effect (same as control) b/c high number organisms
Antibiotic B has some effect (static) b/c less org but some still present
then when A added to B, they act cidal and there are no more org
descibe what is happening in antibiotic antagonism.
the control and antibiotic C have same result= no effect
D decrease # org, but some still present
C+D: instead of having no effect on D, C makes D less able to work and the combo increases the amt of org
what does indifference mean in terms of antibiotic combos?
each antibiotic alone has an effect or doesn't, but when together the result isn't different
what are the 3 major classes of antibacterial inhibitors of cell wall synthesis?
1. beta-lactams
2. glycopeptides
3. bacitracin
mode of action of beta-lactams?
binds to and blocks PBP's
(inhibit cell wall syn)
mode of action of glycopeptides
bind to and block tetrapeptide linkage
(inhibit cell wall syn)
mode of action of bacitracin?
interferes w/ recycling of transport proteins
(inhibit cell wall syn and interferes w/ cytoplasmic membrane integrity)
what are the special antimicrobials taht affect acid fast cell wall sytnthesis?
isoniazid: block syn of mycolic acid
ethambutol: block syn of arabinogalactan
organism that are penicillin resistant produce what?
beta lactamase to destroy beta lactam
action of Augmentin?
combo drug that inhibits beta lactamase
augmentin is composed of beta lactam + clavulanic acid
to be effective, the cell wall inhibitors (antibac) must?
bind/associate w/ bacteria
penetrate outer memb and periplasmic space in G-
interact with PBP's
activate autolysin
*they are cidal b/c they cause lysis
how do organisms resist cell wall inhibitors?
1. production of enzymes (beta lactamases)
2. alteration of target
what are the 4 major classes of inhibitors of protein syn (antibac)?
1. aminoglycosides
2. tetracyclines
3. macrolides
4. oxazolidones
mode of action of aminoglycosides?
inhibit protein syn by interfering with binding of f-met tRNA
aminoglycosides, static or cidal?
mode of tetracyclines?
inhibit protein syn by inhibiting tRNA elongation
are tetracyclines static or cidal?
mode of action of macrolides?
inhibit protein syn by block translocation
mode of action of oxazolidones?
inhibit protein syn by inhibiting ribosomes
to be effective antibacs, the protein syn inhibitors must?
penetrate outer mem of G-
be transported
bind to ribosomal subunits and block fxn
what are the 5 major mech. of resistance used against protein syn inhibitors?
1. mutation of ribosomal binding site (target)**
2. enzymatic modification of antibiotic
3. decreased uptake via porines, permeases
4. active efflux
5. production of proteins which mimic bacterial elongation factors
what are the 3 major classes of inhibitors of nucleic acid synthesis?
rifampin and rifamycins
mode of action of quinolones?
act to inhibit nucleic acid syn by inhibiting gyrase in G+ and topo in G-
are quinolones static or cidal? why?
cidal b/c they accumulate ds breaks in DNA
mode of action of rafampin or rifamycins?
act to inhibit nucleic acid syn by inhibit DNA dependt RNA pol
mode of action of metronidazole?
act to inhibit nucleic acid syn by binding DNA
to be effective, nucleic acid syn inhibitors must what?
penetrate outer memb if G-
be transported
bind to nucleic acid and block fxn
what are the 2 major mech of resistance to nucleic acid syn inhibitors?
1. change DnA gyrase subunit structure/mutation to alter binding
2. affect permeases: change cell wall perm leading to decreased uptake
what are the 2 major classes of antimetabolites?
mode of action of sulfonamides?
antimetobolit that competes with PABA
mode of action of trimethoprim?
antimetabolite that inhibits dyhydrofolate reductase so can't produce tetrahydrofolate which is needed for dna, rna syn
which drug is trimethoprim used in conjxn with?
sulfamethoxazole b/c when used together it is harder for bacteria to mutate
what are the 4 major mech of resistance used against antimetabolites?
1. permeability barriers
2. alteratin in target enzyme (dihydrofolate reductase)
3. exogenous source of folic acid
4. intrinsic resistance in org which use exogenous thymidine
what are the 3 major classes of inhibitors of cytoplasmic membrane fxn?
mode of action of polymyxins?
act as inhibitor of cytoplasmic membrane fxn by inserting to increase cell permeability
mode of action of lipopeptides?
act as inhibitor of cytoplasmic membrane fxn by inserting to trigger rapid depol
mode of action of bacitracin?
act as inhibitor of cytoplasmic membrane fxn and cell wall syn
what are the 3 major mech of resistance to inhibitors of cytoplasmic membrane fxn?
1. mutation in biding site (target)
2. enzymatic modification of the antibiotic
3. decreased transport
what are the 3 major reasons as to why there are less antiviral drugs than antibacterial drugs?
1. b/c viral infxn involves human cells, selective toxicity is mandatory
2. viral illness proceeds undetected over many generations so it becomes advanced before detected
3. rapid mutation of viruses
what are the 6 targets for antiviral agents?
1. attach/penetration-fusion inhibitors
2. uncoating-neutralizing agents
3. nucleic acid syn-base analogs, inhibt NT syn, inhibit DNA pol, inhibit reverse transcriptase
4. protein syn-interferon
5. assembly-protease inhibitors
6. release-inhibit neuraminidase or hemagglutinin
what are the 3 majre mech of resistance to antiviral agents?
1. mutation of the binding site (target)
2. enzymatic modification of antibiotic
3. decreased uptake of the antibiotic
why will antimycotic agents usually have serious side effects on host?
b/c mammals and fungi are both eukaryotic and biochemical makeup and metabolism are similar
*problem is that mammalian cells do not contain the enzymes which will degrade teh cell wall of fungi
which is different about cytoplasmic membrane of funi and mammals? why is this impt?
fungi cell membrane: ergosterol
mammalian cell membrane: cholersterol
*impt b/c if drug is highly selective for ergosterol it will not harm host cells
what are the 4 major classes of antifungal drugs?
1. polyenes
2. imidazoles
3. echinocandins
4. base analogs
mode of action of polyenes?
Amphotericin B, Nystatin
insert in fungal membrane near ergosterol cusing ion leakage
mode of action of imidazoles?
ketoconazole, fluconazole
affect syn of ergosterol
mode of action of echinocandins?
inhibits syn of glucan
mode of action of base analogs?
inhibits RNA fxn and/or DNA syn
what are the 3 major mech of resistance to antimycotic agents?
1. decreased perm
2. active efflux
3. decreased production of target enzyme
which antiviral agent targets attachment/penetration by inhibiting fusion?
Enfuviritide *for HIV
which antiviral agent targets uncoating?
Amantadine, Rimantidine *for Influenza-neutralizing agents that inhibit uncoating
which antiviral agent targets nucleic acid sythesis by acting as a base analog?
which antiviral agent targets nucleic acid syn by acting as a inhibitor of nucleotide biosyn?
which antiviral agent targets nucleid acid syn by acting to inhibit viral DNA polymerase?
Acyclovir, Ganciclovir
which antiviral agent inhibits nucleic acid syn by inhibiting reverse transcriptase?
action of Nevirapine?
antiviral agent that inhibits nucleic acid syn by inhibiting reverse transcriptase
which antiviral agent inhibits protein synthesis?
interferon alpha (sets up antiviral state and can be used to treat ppl with viral infxn to limit spread)
which antiviral agent inhibits assembly by acting as a protease inhibitor?
Ritonavir-for HIV b/c HIV needs to use protease
which antiviral agent inhibits nucleic acid syn by inhibiting Neuraminidase or Hemagglutinin?
Zanamivir *specific for influienza NA by blocking active site and shaving off sialic acids
action of Enfuviritide?
antiviral target that acts as a fusion inhibitor
action of Amantadine or Rimantidine?
antiviral targets that act as neutralizing agents to inhibit uncoating
action of AZT?
antiviral target that acts as a base analog to inhibit nuclic acid syn
action of Ribavirin?
antiviral target that inhibits NT biosyn
action of Acyclovir and Ganciclovir?
antiviral targets that inhibit viral DNA pol
action of Nevirapine?
antiviral target that inhibits reverse transcriptase
action of Ritonavir?
antiviral target that is a protease inhibitor to inhibit assemble
action of Zanamivir?
inhibits Neuraminidase or Hemagglutin **specific for influenzea
what are Amphotericin B, and Nystatin?
antifungal drugs (polyenes) that insert into fungal membrane next to ergosterol causing pore formation, ion leakage
whate are Ketoconazole and Fluconazole?
antifungal drugs (Imaidazoles) that target Cyt P450 demethylase that is necessary for ergosterol syn
action of Caspofungin?
antifungal drug (Echinocandins) that inhibts syn of glucan components
action of Flucytosine?
antifungal drug (Base analog) that inhibits RNA fxn and/or DNA synthesis
what is chloroquine?
antiparasitic drug (Animoquinoline analogues) that interfere with DNA replication; hemoglobin digestion
what is Pentamidine
antiparasitic drug (Diamidine) that binds DNA and prevents synthesis
what is Metronidazole?
antiparasitic drug (Nitroimidazole) that inhibits DNA syn
wht is Pyrimethamine?
antiparasitic drug that inhibits biosynthetic pathway therefore inhibiting folic acid biosyn
what is paramomycin?
antiparasitc drug that inhibits protein syn by binding to the ribosome
what is Benzimidazole-Medendazole?
antiparasitic drug taht disrupts transport by inhibiting glucose transport and fumorate reductase, and disrupting microtubules
what is Pyrantel pamoate?
tetrahydropyrimidine antiparasitic drug taht inhibits neuromuscular action by blocking fumorate reductase (enzymes only parasites have)
tetrahydropyrimidine antiparasitic drug taht inhibits neuromuscular action by blocking fumorate reductase (enzymes only parasites have)
pyrantel pamoate
what is Piperazine?
antiparasitic drug (piperazines) that acts as a GABA antagonist and stimulates phagocytic cells
antiparasitic drug that acts as a GABA antagonist and stimulates phagocytic cells
wht is Ivermectin?
antiparasitc drug (Avermectin) that blocks nuromusclar action; GABA antagonist
waht is Praziquantel?
antiparasitic drug (pyrazinoisoquinoline) that is a calcium agonst (nueromusclar) and disrupts tegument
what are the 3 limitations to antiparasitic drugs?
1. low selective toxicity due to euk natrue of organism
2. cuticles limit effectiveness, prolong administration
3. complex life cycles with multiple developmental stages so that they may require more than one antiparasitc drug (dugs might attok 1 stage and not the other)
what are some targets for antiparasitic drugs?
folic acid biosyn (bacteria also)
DNA replication
protein syn inhibition
interference w/ neuromediators
interaction with transport
what are the 4 mech of resistance to antiparasitic drugs?
1. efflux mechanisms
2. mutations in targets
3. alternative pathways
4. life cycle alteration
what does sensitivity measure?
how often a test turns out positive when it is being used on ppl that we KNOW have the disease (TP)
what does low sensitivity result in ?
what does specificity measure?
how often a test turns out negative when it is being used on ppl that we know DO NOT have the disease (TN)
what does low specificity result in ?
false positives
what is the incubation period?
interverl b/n the time of exposure and development of symptoms of the disease
what is the prodromal period? when does it occur?
early, feeling of "not well"-malaise, anorexia, sore throat
what is the def of clinical disease?
full expression of signs and symptoms
what is the def or recovery period?
remission of signs and symptoms; may also be a stage of disability (not always fully recovered from effects, but immune system has cleared)
what is the difference b/n signs and symptoms?
signs are measurable, visible Ex: fever
symptomes are subjective, what we ask the pt, can' measure Ex: malaise
what is a syndrome?
a group of signs and symptoms associated with a disease state
what are the 7 transmission routes for disase?
person to person
vector borne
parenteral (via bite, needlestick)
Fomites (inanimate objects)
Zoonoses (contact w/ animals)
who is the primary case/index case?
the person who brings that disease into a population-infects the secondary case
in a pt. source outbreak, when do all cases occur?
w/n one incubation period
what is a point source outbreak?
all exposed at one time
cases occur suddenly after minimum incubation period
all cases occur w/n one incubation period
outbreak stops unless secondary spread occurs
*often associated with consumption of contaminated food or water
describe the curve of a point source outbreak?
fewer number of cases
steep upslope
more gradual downslope
what is an example of a propogated outbreak?
chicken pox
explain propagated oubreaks
typical of person to person oubreaks (chicken pox)
secondary cases appear one incubation pd after first peak of first wave
Taller successive waves of cases
often associated with disease transmitted via the respiratory route
how are propagated outbreaks often transmitted?
via the respiratory route
explain the curve of propogating outbreaks
large number of cases compared to point oubreak
waves of cases: successive
what is the best disease prevention strategy?
primary prevention: to prevent the occurenc of the disease
ex: vaccines
what is a secondary prevention ?
cure, block transmission, slow the progress
what is a tertiary prevention?
to limit disability and to provide rehabilitation
ex: botulism, can't cure of disbility, but limit severity w/ antitoxin
public education/infomation is what type of prevention?
primary and secondary(if outbreak then do public education)
vaccines -active immunization is waht type of prevention?
primary: prevent spread of outbreak
immune globulin (IG)-passive immuniztion is waht type of disease prevention?
prophylactic antibiotics and vector control are waht type of disease prevention?
prophylactic : 2ndary
vector control: primary
what types of disesaes are reported immediately? w/n one working day? w/n weeks?
immediately: anthrax, botulism, pertussis, polio
w/n one day: HAV, TB
w/n week: AIDS, chicken pox, mumps
what percent of deaths are due to infectious diseases?
25% but cancers, cardio and resp deaths can also be caused by infections and raise the percentage of deaths due to infectous disesase
what are the leading infectous disease killers?
acute resp infxns including pneumonia, and influenza
what are the defense mechanisms of the resp tract?
nasal cavity with mucociliary lining; inside of nose lined with hair to filter larger particles, those not filtered by hair will be collected by mucus
adenoids and tonsils in the upper resp tract
layer of mucus and ciliated cells in lower resp tract
what happens to pathogens trapped in teh lower resp tract w/n mucus?
they are drived upwards by mucociliary elevator to the back of the throat
what is the most common site for infxn and why?
respiratory tract b/c it is exposed to many potential pathogens via the smoke, soot and dust that is inhaled
how can microorg evade defenses of resp tract?
avoid being caught in mucus layers of upper tract
if it makes it to lower resp tract it must avoid phagocytosis or survive and multiply in phagocytic cell
what are the 4 mechanmisms of resp tract pathogens used to cause disease?
1. bacterial adherence factors
2. extracellular toxins
3. intracellular growth in host tissue
4. evasion of host defense mech via capsules and M protein
upper respiratory tract infxns
common cold
otitis media
acute laryngitis
whooping cough
mumps croup
common airway infxns?
diptheria, whooping cough
laryngo-tracheo bronchitis (croup)
lower resp tract infxns?
pneumonia and brochopneumonia
pulmonary Tb
most resp tract infxns are __?
viral making them more serous than if bacterial
whch type of infxns are life threatening and are treatable with antibiotics?
bacterial infxns
common cold is mostly caused by?
actue otitis media is caused by what?
virus and bacteria (more serious)
sinusitis is mainly cuased by what?
bacteria: S penumoniae
H influenza, M. catarrhalis
pharyngitis is due 90% to?
viruses but the impt bacteria are S. pyogenes and C diptheriae
bronchitis, tracheobronchitis, bronchiolitis, croup are mostly ___
pneumonia is due to large number of ___ in adults?
bacterial infxns
which virus (4) and bacteria (3) typcially cause pharyngitis?
epstein barr virus
Strep pyogenes
C. diptheriae
Neiseeria gonorrhea (rare)
which viruses (6) and bacteria cause common cold?
coxsackie viruses
mycoplasma pneumoniae
chlamydohilia pneumoniae
which bacteria (3) cuase sinusitis?
strep. pnuemoniae
haemophilus influenzae
moraxella catarrhalis
which bacteria (3) and viruses (2) cause otitis media?
step. pneumonia
haemophilis influenza
moraxella catarrhalis
respitory syncytial virus
what is the pathogen for epiglottitis?
Haemophilus influenzae
what is the pathogen for Diptheria?
Corynebacterium diptherieae
what is teh pathogen for whooping cough?
Bordetalla pertussis
what are the 2 viral pathogens for Croup?
parainfluenza viruses
respiratory syncytial virus
what are the most numberous and obvious microbial components of the normal flora?
what are the 9 common componets of normal flora?
actinomyces (filamentous shaped bacteria)
fungi, yeasts
what do asymptomatic pts have?
they carry pathogens!
what does it mean that normal flora could potentially be pathogens?
they are opportunistic if they get to a diff site then where they are normally
40-60% of pharyngitis is caused by what?
virus: adenovirus, rhinovirus, coxsackie virus
what is the most common bacterial throat infxn and what is it casued by?
strep throat caused by Group A beta-hemolytic streptococcus (GAS or GABHS)
signs and sympotoms of pharyngtitis?
sore throat (primary symptom)
pain when swallowing
enlarged lymph nodes in your neck
runny nose and postnasal drip
in rare cases, difficulty breathing
what percent of pharyngitis is due to virus? bacteria? no pathogen isolate?
virus: 40%
bacteria: 30%
no pathogen isolated: 30%
what are the 2 complications of strep. pyogenes (GAS)?
scarlet fever
bacteremia and strep toxic shock syndrome from exotoxin
what are the sequelae of strep. pyogenes?
rheumatic fever
what is the diff b/n complications and sequelae?
complications: while the person has the disease there is serious effect
sequelae: person has recovered from infxn and weeks later have disease which is direct result of disease
characteristics of strep. pyogenes?
gram + cocci
facultative anaerobe, extracellular
normal habitat upper resp tract
what is teh route of entry for strp. pyogenes?
respiratory droplet spread-crowded conditions, daycare facilities
how is the presence of Strep. pyogenes confirmed ?
beta-hemolysis (total lysis of RBC) on agar plate that is red: when colonies are growing see clear area b/c RBC lysed
what percent of healthy children and adults assymptomatic carriers of strep. pyogenes?
what are the 5 virulence factors of strp pyogenes?
1. M protein and lipotechoic acid
2. Group A-specific carb
3. capsule-hyaluronic acid that avoids phago
4. enzyme-hyaluronidase that destoys basement meembrane
5. pyrogenic (erythrogenic) exotoxins-cause rash and fever
what are the cell suface structurs and extracellular substances of s. pyogenes?
Pyrogenic exotoxins
Peptidoglycan (cell wall)
Pili M protein type
glomerulonephritis is rare, postinfectious sequelae to what? what is glomerulonephritis?
pharyngitis or impetigo (skin infxn by strep pyogenes)
it is acute inflammation of teh renal glomeruli due to immune complex accumulation on the BM
what symptoms are associated with glomerulpnephritis?
edema, hypertension, hematuria, proteinuria
differnce of glomerulonephritis in young vs adult
young: uneventful recovery
adults: progressive, irreversible loss of renal fxn
how does post-strep glomerulonephritis affect GFR and RBF
reduces GFR and RBF
get bumpy depostiion of immune complexes
why are the presence of leukocytes in association with strep pyogenes necessary for lab diagnosis?
b/c strep pyogenes is a part of normal flora
how is strp. pyogenes antigen detected? high or low specificity? sensitivity?
2 ways: enzyme immunoassay or latex aggultination both rapid strep tests
high specificity, low sensitivity (more FN)
after rapid strep test, how is confirmation made?
by culture, beta hemolysis, catalase negative, bacitracin specific, PYR test positive
what is the PYR test? how does strep. pyogenes repsond to it?
a filter paper contains PYR. if the bacteria has the enzyme pyrrolidonyl peptidase it will hydrolize the PYR yeilding the yellow color
what are the characteristics of presumptive identification of strep Group A?
beta hemolysis
bacitracin sensitivity
hydrolysis of PYR
how do you extract pathogen for rapid strep? how do you identify? accuracy of rapid strep?
extract: by using enzyme (more sensitive) or with acid (faster)
identify: enzyme immunoassay (more common) or latex agglutination
accuracy: sensitiviy 90% specificity 98%
why is the throat culture for strp pyogens not recommended as primary test?
b/c takes 24hr minimum for growth
used for confirmatory testing when negative strep rapid to make sure really negative
*throat cultures are NOT recomended for the routine primary eval of adults with pharyngitis
who do you test with a rapid strep test?
test if 2 or more signs and symptoms of GABHS are present but treat only if positive
when is it acceptable to treat presumed GABHS?
when 3 or 4 signs and symptoms are present WITHOUT testing
what do want to administer to Tx GABHS?
limit antibiotic treatment to only those with GABHS
Tx penicillin G, Erthromycin or oral Cephalosporin
*immediate treament shown to prevent rheumatic fever but not progression to acute glomerulonephritis
what are some S&S of sinusitis?
thick colored post nasal drainage or nasal discharge
congested nasal passages (stuffy nose)
facial pain, tenderness, swelling
loss of sense of tast and smell
Halitosis (bad breath
ear stuffiness, clogging
most sinusitis occur as a result of what?
common cold of viral origin
usually follows URT viral infxn
50% of acute OM and sinusitis are caused by what?
strep. pneumoniae
what is happening in otitis media?
PMNs infiltrate and obstruct sinuses and ear canal
S&S of otitis media?
otalgia (middle earache)
bulging tympanic membrane (if bacterial)
middle ear effusion (fluid build up)
if bulging tympanic membrane, can almost always assume what?
due to bacteria
waht is the most common bacterial infxn in childen and the most commonly diagnosed?
otitis media
50% have episode by age 1
80% have episode by age 3
*the most freq reason for prescribing antibiotics
what is the first complaint with otitis media?
persistant severe earache
hearing loss may occur
HIGH fever up to 40.5C (105)
what is stasis? where is that seen?
stasis: normal flow of mucus from eustachian tubes is blocked
see in otitis media
what 2 syndromes have the same 3 bacterial causes? what are they?
sinusitis and otitis media
Strep. pneumoniae
Haemophilus influenzae
Moraxella catarrhalis
Sinusitis, Otitis Media, Epiglottis, Bronchitis and Pneumonia are associated with what bacteria?
Haemophilus influenzae
Haemophilus influenze: G+ or -? oxygen requirements?
facultative anerobe
what type of agar does Haemphilus influenzae grow in?
Chocolate agar bc it is fastidius (doesnt grow in normal nutrient agar) requires supplmentation of growth medium with hematin (X factor) and NAD (V factor) for growth
why called chocolate agar?
b/c RBC are heat inactivated releasing nutrients into media thefore dark brown
(can also be obtained by streaking plate with beta hemolytic bacteria that lysis RBC then streak with Hemophilus and it will grow)
Haemophilus is normally found where?
normal flora in human respiratory tract
30-50% children
75% adults
3% asymptomatic with pathogens
which of the Hemophilus influenzae infxns aren't typable?
otitis media
nontypable means no capsule
what does it mean if a strain is typable?
Ab can be made against capsular polysachharide Ag a, b, c, d, e
why type of H. influenzae is most virulent?
Hib (type B)-cause of meningitis that now has a vaccine
nontyable H. influenzae strains colonize where?
in nasopharyxn of normal ppl (ie, normal flora)
What are the virulence factors of Hib?
polyribosyl ribitol phosphate (PRP) capsule making it resistant to phago by PMNs
IgA protease
LRT infxns of H influenze are seen in what population?
cystic fibrosis pts and others with chronic pulmonary disease (bronchitis as well as pneumonia) in elderly
why is epiglottitis a medical emergency?
associated with H influenzae
begins as inflammation and swelling b/n tongue and epiglottis casing throat to push epiglottis backward which can block airway
children (peak 2-4 yrs)
adults (peak 20-40yrs)
what is the most common cuase of epiglottitis?
S&S of epiglottitis?
sore throat
dysphagia (difficulty swallowing)
muffled voice
stridor (resp distress)
most common misdiagnosis of epiglotitis?
strep throat
dianosis and tx of epiglottitis?
lateral xray of neck
cricothyrotomy for airway obstruction
IV antibiotics, blood culture
structure of H. influenze?
baccilli (rod) or coccobacilli
diagnosis of epiglottis?
rapid PRP caspular antigen for H. influenze type b only
Antibiotic treatment of epiglotitis?
amoxicillin/clavulanic acid (Augmentin) or Trimethoprin-Sulphamethoxazole (TMP/SMX) affective against beta-lactamase producting strains
prevention and control of epiglottis?
Hib vaccine (capsular polysachharide that is conjugated to be able to be given to infants
what are the 4 GABHS Pharyngitis S & S?
Tonsillar exudate: 50%
NO cough
tender anterior cervical lymphadenopathy
what causes the Scarlet Fever that is a complication of strep. Pyogenes?
S. Pyogenes produces a pyogenic exotoxin (erythrogenic) that is lysogneized
how does Scarlet Fever present?
diffuse erythematous rash on upper chest that spreads to extremities;blanches with pressure; in skin folds (Pastia's lines) and "sandpaper" feel
white and red "Strawberry tongue"
HIGH fever, nauseu and vomiting
what delayed antibody mediated disease is associated with strep. Pyogenes?
Rheumatic Fever: sequelae to untreated and/or asymptomatic pharyngitis
occurs 2-3 weeks after pharyngitis
what are the 6 major manifestations of Rheumatic Fever?
Myocarditis, Pericarditis, Endocarditis
Chorea (uncontrolled dance like movements)
what do you use to diagnose Rheumatic Fever?
Jones Criteria
is Rheumatic Fever preventable/
if treated w/n 10 days of start of pharyngitis
why is the heart susceptible to Myocarditis in Rheumatic fever?
b/c Rheumatic fever is antibody mediated. there are antigens in heart that are similar to the Ag of the Beta hemolytic group A streptococci. therefore, the Ab that form to eradicate this particular strep also cross react with Ag in the heart attackign the heart tissue
what is St. Vitus' dance?
syndenham's chorea: involuntarty dance like movements associated with Rheumatic Fever
Erythema marginatum and subcutatneous nodules are associated with what disease?
Rheumatic Fever
Moraxella catarrhalis: G+or -? shape? associated with what infxns? O2 reqts?
sinusitis and otitis media
obligate parasite of the mucus membranes of humans
where is Moraxella catarhallis found?
normal pharyngeal flora in children and adults
*obligate parastie in mucus membranes of humans
diagnosis of Moraxells catarhallis? Tx?
gram stain and culture
Tx: 95% are beta lactamases and pencillin resistant thefore give them Augmentin, cephalosporins, TMP/SMX (antimetabolites)
what is the resistance mech that M. catarrhalis pathogens use agasint otitis media? H. influenza? S. pneumonia?
beta lactamase: catarrhalis
influenze: beta lactamase and altered PBPs
S pnuemonia: altered PBPs: lowest resistance as of now
if pt presents with otitis media and bulging tympanic membrane, how will you treat?
immediated Tx with high dose amoxicillin for 7 days
If pt. presents with otitis media without bulging tympanic membrane, how will you treat?
delayed antibiotic prescribing treament b/c probably not due to bacteria
wait 48-72 hrs and give acetaminophen for pain
Corynebacterium diptheria has what characteristic microscopic appearance?
chinese character grouping
why is pts. urine cloudy in strep pyogenes?
b/c of glomerulonephritis: deposition of complexes in glomerular BM where they activate complement leading to glomerular destruction thus see blood in urine
is Corynebacteria diptheriae G+or-? shape? O2 requts? where found?
corneyform (irregular or club-shaped)
normal habitat is nasopharynx, URT, GI, skin
*normally harmless to humans except when C. diptheria whch is deleterious
what enzymes does Moraxella cattarhalis produce?
oxidase pos (G-)
Virulence factors of Corynebacterium diptheria?
diptheria toxin (DT) A-B exotoxin that inhibits protein synthesis by acting as ADP ribsoylation/inactivation of EF-2 (TF)
diptheria toxin is encoded on what? how is it regulated?
bacteriophage that is lysogenized
regulated via DTxR (iron dependent repressor protein) on the chromosome responds to tissue iron levels
How are the toxins of strep. pyogenes and C. diptheriae similar
they both must first be lysogenized by a temperate bacteriophage to produce the erythogenic toxin that casues scarlet fever (pyogenes) and the one that codes for diptheria exotoxin (diptheriae)
explain the workings of the diptheria exotoxin.
it is a AB exotoxin. the B binds to target cells and allows the A subunit to enter the cell. Once inside the cell(endocytosed and acidified), the A subunit is translocated to the cytoplasm and blocks protein syn by inactivating elongation factor EF2 which is involved in tranlsation of eukaryotic mRNA into proteins
explain the response of chromosomeal Diptheria Toxin Repressor (DTxR) protein
low levels of iron, repressor inactive, toxin made
high levels of iron, repressor active, represses toxin
*want low levels of iron
how is corynebacterium diptheria spread?
respirtory or person to person spread
explain how diptheria presents clinically
2-6 day intubation
colonize the epithelial cells of pharynx
***initial damage due to exotoxin activity no to invasion of tissue
**it colonizes the pharynx, forming a grayish pseudomembrane composed of fibrin, leukocytes, necrotic epithelial cells and C. diptheria bacteria cells in a fibrin mesh
*covers tonsils, uvula and palate
what is pathognomic of C. diptheria?
pseudomembrane on pharynx
in all cases of diptheria what does the bacteria do systemiclly?
the bacteria relase the powerful exotoxin into the bloodstream, which specifically damages heart and neural cells by interfering with protein synthesis
"Bull neck", severe edema, is a sign of infxn by what bacteria?
Corynebacterium diptheria
why is microscopy of diptheria unreliable?
b/c there are a lot of normal flora that look like it
microscopy is unreliable and produces FN and FP
In microscopy of Diptheria what will you see?
chinese character grouping
**no spores
what type of culture plate do you use of diagnosis of C. Diptheria?
Potassium Telluride Medium that inhibits the growth of most NORMAL flora therefore it is a selective medium for diptheria
the Potassium Tellurite agar plate will show what if C. Diptheria is present? What type of confirmatory test do you want to do now?
gray-black colonies in 24-48hrs
now test for toxin to rule out other corynebacterium
what is the 3 step method of Tx of C. Diptheria?
1. Diphteria Antitoxin: only inactivates circulating toxin; passive immunity
2. Penicillin or erythromycin: kill bacteria preventing further exotoxin release
3. DPT vaccine: doesn't always result in immunity to future infxn by this org; requires boosters b/c its a toxoid
Elek test is what?
test for toxin production such as in C. Diptheria
form of immunodiffusion assay: Outerlony, preciptan test
Bordetella pertussis causes ___
whooping cough
characteristics of Bordetella pertussis
coccobacillus (short rod)
humans only reservoir
sensitive to drying
aerosol transmissin/direct contact
Even though there is a DPT vaccine, why is pertussis still endemic?
b/c immunity not lifelong and lack of vaccination in children
what are the virulence factors of Bordetella pertussis?
filamentous hemagglutinin (FHA)
Pertussis Toxin
filamentous hemagglutinin and Pertactin (virulence factors of pertussis) have what in common?
RGD motifs that promote binding to integrins on ciliated epithelial cells of the bronchi

the pertussis toxin binds to glycolipds
what type of toxin is pertuss toxin?
AB exotoxin that interferes with protein syn, kills resp ciliated cells, increases IL-1 and stimulates fever
structure of pertussis toxin?
AB type toxin (1 enzymatic, 5 nonidentical binding subunits)
Subunit 2 attaches to a host R: lactosylceramide
S1: enzymatic that causes ADP ribosylation of host cell protein abolishing the regulation of cellular cAMP (increass amt)
action of pertuss toxin?
A subunit transfers ADP to regulatory Gi that normally hydrolyzes GTP on Galpha. The ADP ribosylated Gi protein is inactivated and can't fxn to inhibit adenylate cyclase so cAMP levels rise
Paroxysmal cough is pathogenetic of what ?
whooping cough of Bordetella pertussis
incubation period for whooping cough? followed by how many stages of the disease?
1 week incubation
stage 1: Catarrhal(1-2wks)
2. Paroxysmal (2-4wks)
3. Convalescent
what stage of whooping cough is most contagious? desribe this stage.
Catarrhal stage (1-2wks)
similar to URT common cold: rhinorrhea, sneezing, low grade fever
Describe the Paroxysmal stage of whooping cough
Paroxysmal= (sudden, violent)
(2-4wks) develop characteristic whooping cough following serous bouts of coughing, destruction of ciliated epithelium; impairment of mucus clearing; vomiting, leukocytosis*
convalescent stage of whooping cough?
final stage: attacks of coughing become less freq and no longer contagoius
may have secondary complications: pneumonia, seizures, encephalopathy
What type of culture will you use to diagnosis whooping cough?
charcoal-cephalexin blood agar (charcoal + antibiotic therefore selective ) called Bordet-Gengou, Regan-Lowe Medium
what are the two serological tests used for whooping cough?
1. specific antiserum agglutination
2. titers against pertussis toxin and hemagglutinin
*both using acute and convelescent serum
describe the titer serological test for Whooping cough
take serum sample at time you first examine pt= acute serum then take convalescent serum sample 2 wks later. If see 2-4 x incresae in convalescent serum titer than org. is present (if remained the same in convalescnet titer as acute titer means not due to org)
Prevention and control of Whooping cough?
DPT vaccine: 85% effective as whole cell inactivated
DaPT vaccine: multivalent acellular(variety of virulence factors such as FHA, pertactin) to decrease the adverse affects in infants
what is the most common viral cause of pharyngitis?
Adenovirus causes what infxns (3)?
Common cold
Acute Respiratory Distress
characterstics of Adenovirus: shape? genome?
ds DNA virus
non-eneveloped (lytic, more resistant in environment), icosahedral
classified into 6 subgenera: A to F
why does the immune system produce Ab against the fiber that the capsid contains of adenovirus? what is the significance of it?
the fiber of the capsid helps the virus attach to host cells. We produce Ab that neutralize it. It has Hemagglutinating activity and attaches to the receptor
what is the R that the capsid fiber of Adenovirus attaches to?
Coxsackievirus B and Adenovirus R (CAR) which is a member of the Ig superfamily exprssed at tight jxns of polarized epithelial cells
Reservoir for Adenovirus? Transmission?
reservoir: man
transmission: aerosol, close contact, fecal-oral, direct or indirect to mucosa, fomites, poorly chlorinated pools **NOT just resp. droplets
clinical disease of Adenovirus?
URI's in children *more problematic
ARD (acute resp distress) and pneumonia (Types 4, 7, 21) *in military recruits
what are the particular sites of entry for adenovirus?
eye and upper respiratory tract but can become systemic**
While there are Subgenus A-F for Adenocvirus, what is the most oncogenic?
A and then decrease in oncogenicity to F
what serotypes make up the vaccine for adenovirus that is given to military recruits?
4, 7, 21
Diagnosis of Adenovirus can be confirmed how?
by cytoplasmic effect (CPE) in cell culture: Hematoxylin stained infected cells become rounded and the cell sheet disentigrates. Dark basophilic inclusions w/n the nuclei**
see clear area indicating lysis
Tx/Prevention of Adenovirus?
no specific antiviral therapy
there is a vaccine for ARD syndrome: life adenovirus 4, 7, 21 in enterically coated capsules (to survive in GI tract and set up mucosal immunity in both GI and URT)

** given to new military recruits b/c outbreaks occur in cramped areas(would not use on any other population b/c vaccine wasnt tested on anyone else)
Characteristics of Coxsackie Viruses? shape? genome?
Picornaviridae family, enterovirus (along with polio and Hep A)
ss + sense RNA
nonenveloped, icosahedral
2 main groups: A & B
which viruses are the 2nd most common viral infectous agents in human (after rhinovirus)?
enteroviruses (polio, Hep A, coxsackievirus)
where is Coxsackie A found? B? How transmitted?
A: oropharynx, associated with vesicular lesions
B: associated w/ pneumonia, bronchitis, UR "flu-like" illnesses
*transmitted fecal-oral and airborne
Group A Coxsackie viruses cause what?
Herpangina: sore throat with fever and vesicles in mouth
*white papules with red base on posterior of palate ***but NO exudate!
characteristics of Epstein-barr Virus. Shape? genome?
Herpesviridae family: Human Herpes Virus 4: HHV-4
Enveloped, icosahedral
ds DNA
*only affects certein epithelial cells (oro and naso-pharynx) and B lymphocyts by attaching to CD21 or CR2 Receptor
tramission and attack of Epstein Barr Virus?
transmitted by saliva, enters oropharnyx and then spreads via the blood. It then effects B cells by attaching to CD21 R
(Permissive and lytic in epithelial cells. Episomal in B cells)
Disease causd by Epstein Barr Virus?
Infectious mononucleosis. Usually asymptomatic in young ppl, but when symptoms are present see fever, sore throat (tonsillar exudates), fatigue, lymphadenopathy, accompanied by lymphocytosis (bc B cells infected)
Epstein Barr Virus is associated with what familar disease?
Burkitts Lymphoma
nasopharyngeal carcinoma
Transfomation of B cells
What is the Epstein Barr virus sign?
EBV mononucleosis sign: red throat and whitish tonisllar exudate
another name of common cold?
Acute Coryza
which viruses cause Acute Coryza?
picornaviruses (rhinovirus)
resp syncytial viruses
characteristics of common cold?
afebrile (no fever: seperates it from influenza)
viral infxn of RT w/ inflammation in any or all airways

*NO vaccines
what is the seasonality for viruses that cause common cold?
Rhinovirus: summer-fall
Coronavirus: winter-spring
Reservoir for common cold? spread by?
upper airway of young children
spread by direct contact, airborne droplets
prevention: handwashing
what % of common cold caused by rhinovirus? coronavirus?
rhino: 30-50%
corona: 10-30%
Microbiology of Rhinovirus?
non-enveloped icosahedral
ss + sense RNA
replication in cytoplasm using RNA dependent RNA pol
acid labile, resistant to drying
prefers cooler temps (URT)
what is the R on host cell that Rhinovirus binds?
trasmission of rhinovirus?
major cause of common cold
transmitted by resp droplets, hand contact and fomites
complications of Rhinovirus infxn?
symptoms of common cold ususally resolve in 1 week
*does cause viral sinusitis and otitis media
Diagnosis of Rhinovirus?
may be isolated from nasal secretions and use serology to confirm but since there are over 100 serotypes, immunity is limited
Microbiology of Coronavirus?
ss + sense RNA
2 serogroups
*2nd most common cause of common cold
*the cause of SARS
when do you treat a pt you suspect to have Acute Rhinosinusitis?
with symptoms lasting longer than 7 days b/c difficult to differentiate b/n bacterial or viral cuase
*if have unilateral facial pain, strong predictor of bacterial etiology
Measles and Mumps viruses fall under what family?
Paramyxoviridae family
measles also called Rubeola (not Rubella)
Influenza A, B, C viruses fall in what myxovirus family?
Parainfluenza virus causes what 3 infxns?
common cold
croup (laryngitis) *problematic syndrome
S & S of laryngitis?
weak voice
tickling sensation
dry throat
dry cough
Risk factors for children less than 4 with laryngitis may have croup
what is croup?
Croup (sometimes referred to as croup syndrome or laryngotracheobronchitis) is a respiratory disease which afflicts infants and young children, typically aged between 3 months and 3 years. The respiratory symptoms are caused by inflammation of the larynx and upper airway, with resultant narrowing of the airway.
S&S of croup, viral croup, laryngotracheobronchitis?
breathing difficulty
**barking cough
seen in young children: 3 months to 5 yrs of age
Differential for Croup?
diptheriae, epiglottitis (other obstructions of airway)
80% of croup is caused by?
parainfluenza virus
What 4 viruses fall under the Paramyxoviridae family?
Respirovirus: human parainfluenza virus 1-4 (cause croup)
Morbillovirus: Measles
Rubulavirus: Mumps
Pneumovirus:Respiratory Syncitial Virus
what is the shape, genome of Paramyxoviridae family?
ss - sense RNA
cytoplamic replication
enveloped therefore buds
has fusion proteins responsible for fusing at PM (PH independent)
HN: hemagluttinin,neuraminidase
how is parainfluenza transmitted?
inhalation of large droplet, aerosols, person-person, inactivated by dryness (because enveloped therefoer can get it from fomites)
characteristics of parainfluenza infxn?
seal's bark cough
inspiratory stridor*
risk group: children 6mos-12yrs
on a radiograph, what is the classic sign of croup?
steeple sign due to obstruction to airflow that causes fatigue and requires pt on ventilation
the inflammation associated with parainfluenza in croup casues what?
inflammation of subglottic area: steeple sign obstrucing airflow, increasing fatique
inflammation of airways and lung parenchyma leading to hypoxia
80% of croup cases are cuased by?
parainfluenza virus
Because rapid diagnosis methods are poor sensitivity for parainfluenza infxns,what methods work best?
Virus Isolation:Heamabsorption
Serology: HAI, CFT, ELISA
What happens in the HAI serological test?
take pts serum and add add it to virus . if HAI is positive, RBC wont be able to bind virus and virus will be bound by Ab that are present in pts serum. this will appear as a discrete round "button"
If the HAI is negative: pts serum does not have Ab to virus (meaning they are not infected with parainfluenza) and RBC will bind virus. this will appear like a sheet of red
what does a serological test mean?
virus is the reagent
add pts serum (unknown)
If parainfluenza virus is present in pts. serum, will the HAI be negative or positive?
positive b/c it means Ab are present and RBC can't agglutinate the virus so they sit on bottom in "button" formation
if we see hemolysis in a CFT what does that mean? no hemolysis?
in CFT we mix pts serum + C' +Ag with a mixture of sheep RBC. If the pt's serum DOES NOT have Ab to the Ag, C' can't fix b'c no ICs so it lysises RBC.
If the pts serum has Ab to that Ag the C' will be fixed and no hemolysis will occur: + test
Mumps is a part of what family of viruses? what are the characteristics of this family?
paramyxoviridae family
ss- sense
enveloped, buds via PM
cell-cell fusion: multinucleated cells
***one antigenic type
how many antigenic types of mumps are there? what does mumps induce?
only 1 therefore if you are immunized (MMR) you are protected
mumps induces cell-cell fusion (multinucleated cells) bc it buds from PM (pH independent)
are Mumps localized only in epithelial cells of nasopharynx?
no!! it replicates there and regional lymph nodes (spreads systemically)****
what is the most common sign of Mumps?
Parotitis (30-40%): swelling of parotid glands, fever, self limiting
(also see Orchitis: swelling of testes)
how do you differentiate b/n Mumps and RSV (resp syncitial virus)?
they both have multinucleated cells, but when add RBC to RSV they won't stick bc it doesn't have hemaglutinating activity
Serological tests for mumps?
EIA, CFT, ****HAI (distinguishes it from RSV)
what type of vaccine is MMR?
live attenuated to stimulate cell-mediated immunity and is needed to prevent cell-to-cell spread
why don't you need a live attenuated vaccine for polio and influenza?
bc neutralizing Ab prevents flu from spreading cell to cell (normally live attuated vaccin is needed to prevent cell cell spread)
what type of population is prone to URT infxns due to fungi?
immunosuppressed (compard to a normal,healthy individual)
Both Rhizopus and Mucor are responsible for what infxns?
allergic rhinitis
Rhinocerebral mucormycosis
Zygomycosis is due to what?
Rhizopus and Mucor
The life threatening form of zygomycosis (mucormycosis) is known as _____ syndrome? What is it associated with?
Rhinocerebral syndrome which occurs with diabetic ketoacidosis (Rhizopus principal cuase)
The principal fungal cause of Rhinocerebral syndrome is what?
why is Rhinocerebral mucormycosis fatal? what is this condition? How is it transmitted?
the fatal form of Zygomycosis that begins in nasal mucosa or sinuses and progresses to the orbits, palate and the brain
Transmitted by inhalation of sporangiospores (spores in a sac) from rotting fruit, old bread, air water, soil
How do you diagnosis Mucor or Rhizopus?
Microscopically ID: NONseptate, ribbon like hyphae which branch at RIGHT angles **, sporangium
what are sporangiospores? what org are they found in?
found in Mucor and Rhizopus
spores in a sac that are what is inhalaed to cause allergic rhinitis and possibly rhinocerebral mucormycosis
What are the 4 distinguishing characteristics of Zygomycosis?
1. sporangium
2. sporangiospores
3. coencytic hyphae/aseptate
4. rhizoids
what culture do you use to determine if zygomycosis? what will it look like if +?
Sabouraud's Dextrose Agar (SDA) which will look like cotton candy
what is the antifungal therapy that needs to be given for Zyogmycosis?
Amphotericin B

*treat as lethal disease