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265 Cards in this Set
- Front
- Back
Where is electron transport chain on prokaryotes?
|
cell membrane
|
|
Viruses are this type of pathogen which means they have to be in a cell
|
Obligate intracellular
|
|
Fungal nucleic acid can be ____
|
haploid or diploid
|
|
Dimorphic means what?
|
yeasts or filaments
|
|
What is the most common parasitic infection?
|
toxoplasmosis
|
|
What are single celled parasites called?
|
Protozoa
|
|
What is the definition of a carrier state in normal flora?
|
Colonized by pathogen, but the interaction doesn't result in a disease state.
|
|
Are micro-organisms a source of carcinogens? Why or why not?
|
Yes, they convert chemicals of diet into active carcinogens
|
|
LD50 means...
ID50 means... |
Id=infectious dose
Ld=lethal dose |
|
Koch's postulates
1-4 |
Organism found in diseased but not in healthy
Organism isolated from disease and grown in pure culture outside Organism must be taken from culture, put into animal, and cause disease Organism must now be reisolated |
|
What does gradient to sterility mean in terms of constitutive defenses?
|
some regions of the body are heavily colonized while others are not
|
|
Give 5 examples of physical and chemical barriers to innate immunity
|
Tissue barrier
pH barrier (stomach) design of respiratory tract (muco-ciliary; epiglottis) Secretions (microbicidal) Complement system |
|
What is the chemotactic agent of the complement system?
|
C5a
|
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What is the opsonization component of the complement system?
|
C3b
|
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What is a secondary infection
|
Infection made possible by a primary infection
|
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Is prokaryotic cell geared for high or low metabolic rate?
|
High
|
|
What colors are Gram + and Gram - stains?
|
+: purple
-: red |
|
Compare membranes for gram + and - bacteria
|
Gram +: 1 membrane (inner)
Gram -: 2 membranes (inner+outer) |
|
How are pili arranged structurally (e.g. in a star shape, in a string shape)
|
helical fashion
|
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What bacteria uses type 1 pili
|
uropathogenic E. coli
|
|
Adhesive pili direct what of the invading bacteria?
|
tropism
|
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What structural feature prevents bacteria from being phagocytosed?
|
capsule
|
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What type of infections do most encapsulated bacteria cause?
|
pyogenic
|
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Which is more virulent: encapsulated pneumococci or nonencapsulated pneumococci?
|
encapsulated
|
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flagellum is a _____ helix that rotates like a ______
|
rigid; propeller
|
|
Three components of the flagellum are:
|
1)basal body
2)hook 3)filament |
|
Clockwise rotation of flagellum lead to what kind of motion?
|
random tumbling
(counter-clockwise leads to progressive movement) |
|
Process by which bacteria move toward chemoattractants?
|
chemotaxis
|
|
Where is LPS found?
|
outer leaflet of outer membrane of Gram - bacteria
|
|
LPS structural components
|
O-antigen
Core Lipid A |
|
What are the gram - strains called that do not express the O antigen?
|
rough strains
|
|
What component of LPS is responsible for host-cell toxicity and gram - sepsis?
|
lipid A
|
|
Why does lipid A cause septic shock?
|
interacts with immune cells that leads to the release of inflammatory mediators and cytokines
|
|
In terms of E. Coli, what do porins allow?
|
Ions and hydrophilic molecules to pass through water-filled channels
|
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What type of microorganism has teichoic acid
|
Gram + bacteria
|
|
How does teichoic acid cause sepsis?
|
Causes host cells to release inflammatory mediators like cytokines
|
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What are the three principal functions of the cell membrane in gram + cells?
|
Osmotic barrier
Site of selective permeability Site of cytochrome activity and proton motive force generation |
|
Where is periplasm found, what type of microorganism?
|
In gram - bacteria
|
|
What does the periplasm contain? looking for 4 things
|
proteases, de-toxifying enzymes, chaperones, and binding proteins
|
|
Where is the only place that D amino acids are found?
|
Peptidoglycan
|
|
What are the repeating units of peptidoglycan?
|
N-acetylglucosamine (GlcNAc)
N-acetylmuramic acid (Mur-NAc) |
|
Compare how many layers of peptidoglycan a gram + microorganism has versus a gram - organism
|
Gram +: 40 layers
Gram -: 1 layer |
|
What is produced when Bordetella sloughs off peptidoglycan fragments? What is the eventual pathology?
|
tracheal cytotoxin-->whooping cough
|
|
What facilitates the cross-linking of the cell wall?
|
Transpeptidation enzymes known as penicillin binding proteins
|
|
What does penicillin do that makes it an antibiotic. What happens to the microorganism?
|
Penicillin binds transpeptidase; cell wall cross-linking stops; cell wall becomes weak; cell is lysed
|
|
What test differentiates Streptococcus and Staphylcoccus?
|
Catalase test
Strep (-) Staph (+) |
|
What differentiates S. aureus from the other staphylococcus?
|
Coagulase test
S. aureus (+) S. saprophyticus, epidermis et al. (-) |
|
What's a Lancefield antigen?
|
Classification based on C carbohydrate (antigen) on cell wall
|
|
What is Lancefield classification of Streptococcus pyogenes?
|
Group A
|
|
What causes strept throat?
|
Streptococcus pyogenes
|
|
What happens if you don't treat strept throat?
|
Leads to scarlet fever, if it produces scarlet fever toxins
|
|
What happens if you get a lot of strep infections?
|
Rheumatic fever and acute glomerulonephritis
|
|
What is rheumatic fever?
|
Inflammatory disease of heart, joints, skin, and brain
|
|
What is the B Streptococci and what does it cause?
|
streptococcus agalactiae; meningitis and bacteremia
|
|
Enterococcus [what does it cause]
|
nosocomial infections like UTI; unusually resistant to antibiotics
|
|
Corynebacterium [cause?]
|
Diptheria
|
|
Corynebacterium [produces?]
|
diptheria toxin
|
|
Diptheria toxin [symptoms/pathology]
|
sore throat, brassy cough, pseudomembrane formation
|
|
Bacillus [causes?]
|
anthrax
|
|
Anthrax toxin [patho]?
|
local necrosis, tissue damage
|
|
Listeria [who is at risk?]
|
pregnant women
|
|
Listeria [symptoms?]
|
fever, headache, vomiting, ab pain, cramps in lower back
|
|
Classification for gram - bacteria that are part of normal flora?
|
enterobacteriaceae
|
|
Who are important members of enterobacteriaceae?
[3] |
E. Coli
Shigella Salmonella |
|
Pathogenic strains of E. coli?
[5] |
Uropathogenic E. coli
Enterotoxigenic E. coli Enterpathogenic E. coli Enteroinvasive E. coli Enterohemorrhagic E. coli |
|
4 important virulence factors for enterobacteriacae
|
pili
type 3 secretion mechanism toxins LPS |
|
Pseudomanas [claim to fame?];[important to this class of people]
|
most frequent cause of nosocomial infxn in patients hospitalized for 10 days or longer
cystic fibrosis patients susceptible to its pneumonia |
|
Virulence factor of pseudomanas [3]
|
extracellular proteases
pili alginate capsule |
|
Legionella [causes; claim to fame]
|
major cause of community acquired pneumonia
|
|
What is so special about Legionella's relationship to the immune system?
|
can survive within alveolar macrophages
|
|
What is Legionella's key virulence factor?
|
type IV secretion
|
|
What does bordetella cause?
|
Whooping cough
|
|
Vibrio [causes]
|
Cholera
|
|
Important virulence factor for vibrio?
|
pili and cholera toxin
|
|
Neisseria [virulence factor (5)]
|
pili, LOS (lipooligosaccharide), outer membrane proteins, capsule, proteases
|
|
What happens if gonococci don't have pili and try to initiate urethral disease?
|
Doesn't happen
|
|
H. influenzae [pathology (2)]
|
meningitis and upper respiratory tract infections
|
|
H. influenzae [virulence factors (4)]
|
capsule
LOS pili secreted proteases |
|
Helicobacter [causes (3)]?
|
chronic gastritis, duodenal ulcers, gastric ulcers
|
|
Helicobacter [virulence factors (4)]?
|
flagella
adhesins urease vacuolating cytotoxin |
|
If someone is infected with H. pylori and has microbial colonization, what is the risk?
|
gastric carcinoma
|
|
What is colonization of host tissues usually mediated by?
|
adhesins
|
|
Why inject virulence factors into the host cell anyways?
|
Helps to evade host defenses
|
|
How does "injection" of virulence factors happen, what's the mechanism?
|
type 3 secretion mechanisms
|
|
What do Enteropathogenic E. coli use during neonatal diarrhea to remain extracellular
|
type 3 secretion mechanism
|
|
where does Salmonella typhimurium inject virulence factors and why?
|
allow pathogen to invade and survive in macrophages
|
|
where are the genes that encode type 3 secretion systems?
|
pathogenecity islands
|
|
what is cystitis?
|
pain or burning upon urination
|
|
what is pyelonephritis
|
above plus fever, flank pain, nausea/vomiting
|
|
main microorganism that causes UTI?
|
uropathogenic E. coli (80%)
|
|
what is at the tip of type 1 pili expressed by UPEC?
|
FimH adhesins
|
|
what happens if UPEC type 1 adhesins don't have FimH?
|
don't adhere to bladder surface
|
|
host innate defenses to UPEC expressing type 1 pili [5]
|
urine flow
antimicrobial substances within urine and uroepithelium resident immune effector cells exfoliation neutrophils |
|
how does exfoliation happen, to prevent UPEC expressing type 1 pili
|
apoptosis-like mechanism
|
|
key bacterial products involved in H. pylori pathogenesis [5]
|
adhesins
urease flagella vacuolating cytotoxin CagA protein |
|
what does vacuolating cytotoxin do?
|
induces cell apoptosis and suppresses immune system
|
|
how does H. pylori cause neoplastic event?
|
proliferating stem cells express sialic acid containing receptor, that is recognized by H. pylori second adhesin
|
|
what mediates bacterial invasion of UPEC?
|
type 1 pili adhesin, FimH
|
|
What does E. coli invasion into bladder epithelium activate?
|
toll like receptor 4
|
|
what does activation of toll-like receptor 4 cause
|
cytokine induction
|
|
what is important movement mechanism that UPEC uses to subvert host defenses?
|
fluxing out of infected cells and invade underlying epithelium
|
|
what can UPEC do in terms of activity to subvert host defenses?
|
enter quiescent state
|
|
community acquired UTI pathogens
3 Gram + 2 Gram - |
-: Esch. Coli, Proteus mirabilis, Klebsiella
+: Staph. saprophyticus, Enterococcus |
|
Top 3 pathogens of acute otitis media?
|
Strep. pneumoniae
H. Influenzae Moraxella catarrhalis |
|
What does Dx of AOM require [2]
|
Middle ear effusion
Inflammatory changes |
|
Where does AOM caused by H. inf begin?
|
colonization of nasopharynx
|
|
What is Hap [2]?
|
H. inf adhesin secreted by autotransporter pathway; serine protease w/ autoproteolytic activity
|
|
What does Hap do?
|
augments aggregation of H. inf and causes formation of microcolony formation in presence of SLPI
|
|
What's SLPI
|
secretory leukocyte protease inhibitor
|
|
example of beta-lactamase inhibitor?
|
Augmentin
|
|
What is EPEC?
|
enterpathogenic E. coli
|
|
What is major result of EPEC infxn
|
infantile diarrhea in developing world
|
|
what happens when it interacts with epithelium
|
produces effacing and attaching lesions
|
|
what are effacing and attaching lesions?
|
pedestal like structures on the apical surface of epithelium
|
|
what's the result of effacing and attaching lesions [2]?
|
loss of microvilli from the epithelial surface and formation of actin rich pedestals beneath adherent bacteria; leads to fluid release
|
|
why does EHEC form pedestals?
[4] |
promote attachment
facilitate delivery of toxin produce diarrhea kidney toxicity |
|
What do Tir and Esps do with EHEC
|
activate host signals to produce actin polymerization
|
|
What does EHEC lead to, what other syndrome?
|
Hemolytic Uremic Syndrome
|
|
Where is typhoid fever acquired from?
|
human source (feces, urine)
|
|
How does typhoid fever happen?
|
Salmonella typhi and are ingested, go to intestinal lymphatics, phagocytosed by macrophages. Travel around with macrophages. Once macrophages destroyed salmonella comes out and causes septicemia.
|
|
What type of secretion mechanism does Salmonella typhi use and why?
|
Type 3, allows survival in vacuolar compartment in macrophages
|
|
What causes hemolytic uremic syndrome?
|
Shiga toxin producing EHEC
|
|
What % of EHEC infxn result in HUS?
|
2-7%
chronic renal failure develops in 4-10% of children w/ HUS |
|
What are bacterial byproducts of metabolism [3]
|
H2S
Acetic acid Reactive oxygen species |
|
what type of bacteria produce exotoxins?
|
gram + and gram -
|
|
what is the most potent exotoxin?
|
tetanus
1 mg can kill 10,000 people |
|
Where do these toxins originate from?
|
encoded on plasmids or on phages
|
|
what regulates expression of diptheria toxin?
|
iron levels
high iron=low expression low iron=high expression |
|
most toxins have what kind of structure
|
A-B
A: action, enzymatic activity B: binding activity (specificity) |
|
_Scarlet fever_
Organism: Toxin: Mechanism: Pathophysiology: Treatment: |
Organism: Strept. pyogenes
Toxin: pyrogenic exotoxins Mechanism: superantigen Pathophysiology: lymphocyte activation, perivascular inflammation Treatment: penicillin |
|
_Scalded skin syndrome/bullous impetigo_
Organism: Toxin: Mechanism: Pathophysiology: Treatment: |
Organism:Staph. aureus
Toxin:Epideromolytic toxin A or B Mechanism: Serine protease-cleave desmoglein in CT Pathophysiology:Separation of granulosa layer of skin Treatment:anti-satphylococcal |
|
_Diptheria_
Organism: Toxin: Mechanism: Pathophysiology: Treatment: |
Organism:Corynebacterium diptheria
Toxin:diptheria Mechanism:inhibits protein synthesis Pathophysiology:cell necrosis, heart and neurons esp. susceptible Treatment: |
|
_Pertussis_
Organism: Toxin: Mechanism: Pathophysiology: Treatment: |
Organism:Bordetella pertussis
Toxin:pertussis toxin Mechanism:inactivation of G proteins Pathophysiology:unsure Treatment:macrolides (erythromyocin) |
|
_Infantile botulism_
Organism: Toxin: Mechanism: Pathophysiology: Treatment: |
Organism:Clostridium botulinum
Toxin:botulinum toxin Mechanism:Zn2+ protease, cleave synaptobrevin Pathophysiology:prevents ACh secretion at neuromuscular junction; flaccid paralysis Treatment:suppportive, antitoxin |
|
_Tetanus_
Organism: Toxin: Mechanism: Pathophysiology: Treatment: |
Organism:Clostridium tetani
Toxin:tetanus toxin Mechanism:Zn2+ protease, cleaves synaptobrevin Pathophysiology:prevents release of neurotransmitters at inhibitory neurons; tonic muscle contraction Treatment:vaccine, supportive, metronidazole or penicillin, antitoxin |
|
_Cholera_
Organism: Toxin: Mechanism: Pathophysiology: Treatment: |
Organism:Vibrio cholerae
Toxin:cholera toxin Mechanism:activates adenylcyclase Pathophysiology:Na+ and water secretion, dehydration Treatment:hydration, electrolytes, glucose, antibiotics (for diarrhea) |
|
_Toxic shock syndrome_
Organism: Toxin: Mechanism: Pathophysiology: Treatment: |
Organism:Strep. pyrogenes, Staph aureus
Toxin:TSST-1 Mechanism:superantigen Pathophysiology:Non-spec activation of T-lymphocytes, massive cytokine and NO production Treatment:supportive, anti-staph antibiotics |
|
_Necrotizing pneumonia/lung abscess_
Organism: Toxin: Mechanism: Pathophysiology: Treatment: |
Organism:Staph aureus
Toxin:Panton-Valentine leukocidin (PVL) Mechanism:pore formation Pathophysiology:tissue necrosis; inhibits phagocytosis Treatment:anti-staphylococcal (MRSA) antibiotics |
|
CDC Category A Biological Diseases List [6]
|
Smallpox
Tularemia Bubonic plague Anthrax Botulism Viral hemorrhagic fevers |
|
Is person to person spread of anthrax likely?
|
No
|
|
Three kinds of botulism
|
Foodborne, Infant, Wound
|
|
Organism of plague
|
Yersinia pestis
|
|
Types of plague [3]
|
Septicemic (complication or primary), pneumatic (air), bubonic (skin)
|
|
Two clinical forms of smallpox [2]
|
Variola major (severe)
Variola minor (less severe) |
|
Types of variola major [4]
|
ordinary (most frequent)
modified (mild and occurs in vaccinated) flat (rare and severe) hemorrhagic (rare and severe) |
|
Tularemia [caused by]?
|
Francisella tularemia
|
|
Symptoms of tularemia
|
sudden fever, chills, headaches, muscle aches, joint pain, dry cough, progressive weakness, and pneumonia
|
|
Where do Viral hemorrhagic fevers normally reside?
|
arthropod vector
|
|
bacteriostatic requires what to kill bacteria?
|
host's defenses
|
|
what are beta lactam antibiotics considered to be structural analogs of?
|
D-Ala-D-Ala of the peptidoglycan unit
|
|
Why do drug companies bring a lot of beta lactam drugs to market [3]
|
differences in target bacteria
differential inhibition of PBP differential sensitivity to beta-lactamases |
|
why is the mycobacteria cell wall different?
|
it is Gram + but has much less peptidoglycan; contains carbohydrate polymers and a waxy mycolic acid coat
|
|
what do most eukaryotes carry?
|
a symbiotic prokaryote
|
|
what is most common protein synthesis inhibitor; why are they special?
|
aminoglycosides; bacteriocidal
|
|
side effects of aminoglycosides [4]
|
hypersensitivity rxn
ototoxicity nephrotoxicity neuromuscular blockade |
|
target of quinolones?
|
DNA topoisomerases
|
|
what do toposiomerases do?
|
essential enzymes for the packaging and segregation of DNA strands
|
|
what is Ciprofloxacin?
|
inhibitor of topoisomerase 2
|
|
What do antimetabolites do?
|
inhibit metabolic pathway
|
|
Most prominent antimetabolites [2]
|
sulfonamides
antifolates |
|
key function of antifolates?
|
inhibits Dihydrofolate Reductase which is required for tetrahydrofolate synthesis
|
|
what's key feature of sulfonamides and antifolates?
|
synergy as well as additivity
|
|
why is it difficult to develop antibiotics that target viruses?
|
viruses use cellular machinery/enzymes to function
|
|
Since viruses need special DNA and RNA polymerases, what is an attractive strategy?
|
nucleoside analogs
|
|
what is selectivity of nucleoside analog determined by?
|
how efficient viral enzymes activate the drug
degree of potency to inhibit viral polyermase |
|
what is the critical step in viral maturation and so what is the target?
|
cleavage of precursor proteins; protease inhibitors
|
|
what is the major membrane difference between fungi and other organisms?
|
sterol component: ergosterole instead of cholesterol
|
|
How can microbe become resistant to drugs [2]?
|
change the drug target
change how drug is handled |
|
How to change drug targets [4]
|
mutation
over-production sequester target borrow a resistant target |
|
how to change transport of drug in viruses [5]
|
increased efflux
decreased uptake decreased activation increased detoxification sequestration of drug |
|
major role of chloroquine
|
parasites ability to detoxify heme
|
|
what are transposons?
|
mobile gene elements
|
|
how to prevent spread and emergence of drug resistance
|
understand mechanisms of resistance
use drug combos use drugs properly keep microbial populations low reduce transmission |
|
how do pathogenic organisms differ from non-pathogenic organisms?
|
possession of virulence factors
|
|
_staphylococcus aureus_
Gram: Structure: Virulence: Epidemiology: Diseases: Lab Dx: Treatment, Control, Prevention: Virulence factors and effects: |
Gram: +
Structure:cocci in clusters Virulence: meth resist Epidemiology: normal flora, trauma, foreign body, poor hygiene Diseases:cutaneous, bacteremia Lab Dx:rapid growth on blood agar, clusters, catalase and coagulase + Treatment, Control, Prevention: penicillins Virulence factors and effects: Cytotoxins. Panton-Valentine leukocidin-->toxic for many cells, including PMN; Toxic Shock Syndrome Toxin-1-->superantigen, systemic activation of inflammatory response |
|
_Streptococcus pyogenes_
Gram: Structure: Virulence: Epidemiology: Diseases: Lab Dx: Treatment, Control, Prevention: Virulence factors and effects: |
Gram: +
Structure: cocci in chains; M-protein Virulence:/ Epidemiology:asymptomatic carry in nasopharynx Diseases:pyogenic and nonpyogenic Lab Dx: blood agar, beta-hemo Treatment, Control, Prevention: penicillin, macrolides Virulence factors and effects: capsule-->resist phagocytosis; M-protein-->adhesin, anti-phag, degrade C3b; F protein-->adhesin; pyrogenic exotoxins-->fever, mitogenic for T cells, enhance DTH, cytotoxic, scarlitiniform rash; Streptolysin S-->lysis many cell types; Streptolysin O-->lyses many cell types |
|
_Neisseria meningitidis_
Gram: Structure: Virulence: Epidemiology: Diseases: Lab Dx: Treatment, Control, Prevention: Virulence factors and effects: |
Gram: -
Structure: coccibacillus Virulence: capsule Epidemiology: humans Diseases: meningitis Lab Dx:typical morphology Treatment, Control, Prevention: penicillin Virulence factors and effects: |
|
_Salmonella enteriditis_
Gram: Structure: Virulence: Epidemiology: Diseases: Lab Dx: Treatment, Control, Prevention: Virulence factors and effects: |
Gram: -
Structure: bacilli Virulence: capsule, type 3 sec system, resistance to serum killing, survive within macrophages Epidemiology:contamination Diseases:bacterima, enteritis Lab Dx:isolation from stool or blood Treatment, Control, Prevention: no antibiotics; 3rd gen cephalosporins Virulence factors and effects: |
|
_Clostridium botulinum_
Gram: Structure: Virulence: Epidemiology: Diseases: Lab Dx: Treatment, Control, Prevention: Virulence factors and effects: |
Gram: -
Structure: spore-forming bacillus; strict anaerobe Virulence: botulinum toxin; spore formation Epidemiology: honey, soil Diseases: flaccid paralysis from botulinum toxin Lab Dx: isolation from blood or stool Treatment, Control, Prevention: supportive, antitoxin Virulence factors and effects: |
|
_Pseudomonas aeruginosa_
Gram: Structure: Virulence: Epidemiology: Diseases: Lab Dx: Treatment, Control, Prevention: Virulence factors and effects: |
Gram: -
Structure: bacillus; oxidase positive; mucoid exopolysaccharide capsule Virulence: anti-microbial resistance Epidemiology: ubiquitous Diseases: pulm infxn, burn infxn, urinary cath infxn, ear infxn, eye infxn Lab Dx: grows on agar; oxidase + Treatment, Control, Prevention: 3rd gen ceph sporins Virulence factors and effects: capsule-->resist phagocytosis; biofilm-->anti-phagocytic |
|
what does M protein in strep pyogenes do?
|
inhibits opsonization by alternative complement system
|
|
what's a virion?
|
package with virus material destined for infxn of host cell
|
|
what is a capsid and what is it made by?
|
protein shell of some viruses, made by capsomers
|
|
what is nucleocapsid?
|
genome complexed with one or more capsid proteins, wrapped up in membrane envelope
|
|
what is eclipse phase of virus infxn?
|
time after infxn but before progeny virions can be found
|
|
what does hemagluttinin on the influenza A virus bind to?
|
sailic acid residues of glycoproteins and glycolipids on host cell surface
|
|
Papilloma virus [type DNA/RNA and methods]
|
DNA; DNA-->DNA-->DNA
|
|
Hep B virus [type DNA/RNA and methods]
|
Retrovirus; DNA-->RNA-->DNA
|
|
HIV virus [type DNA/RNA and methods]
|
Retrovirus; RNA-->DNA-->RNA
|
|
West Nile virus [type DNA/RNA and methods]
|
RNA; RNA-->RNA-->RNA
|
|
Why is the fidelity of reverse transcriptase and RNA polymerase important?
|
implications for viral adaptation and drug resistance
|
|
what is the de facto way of identifying viruses?
|
PCR and up and coming microarrays
|
|
How to make viral diagnosis? [6]
|
Viral Culture
Detection of viral antigens Detection of nucleic acid Direct visualization Observation of effect in tissue Detection of immunological response. |
|
How does ELISA work? and what does it stand for?
|
enzyme-linked immunosorbent assay [ELISA];
detects antigen using capture antibody and enzyme labeled detector antibody |
|
What's the difference between acute and chronic infection?
|
acute infxn progress rapidly, have short incubation time, usually resolved quickly
chronic infxn much slower |
|
_Human influenza_
characteristics: |
segmented, single strand, negative sense RNA genome
|
|
why do some viruses have good vaccine but others don't?
|
the good vaccines targeted essential parts of the virus
|
|
what type of influenza virus are antivirals good for?
|
influenzavirus A
|
|
are hep B and hep C cytolytic or non-cytolytic?
|
non-cytolytic
|
|
is HIV cytolytic or non-cytolytic?
|
cytolytic
|
|
strategies to evade host defenses [7]
|
immune privileged sites
restricted gene expression inhibit innate immune response antigenic variation inhibit cytokine function interfere with antigen processing infect immune cells |
|
what kind of genome is HSV?
|
large (152kb), enveloped linear dsDNA
|
|
what is target of HSV?
|
epithelial cells; later invades the central nervous system and establishes latency in neurons
|
|
why does HCV have high rate of chronic infection?
|
HCV outpaces the immune response, maximal titers before immune system can respond
|
|
what kind of genome is HCV
|
enveloped positive sense RNA virus
|
|
what type of bacteria does MacConkey agar plate grow?
|
gram negative
|
|
cryptosporidium parvum [claim to fame]
|
severe and life-threatening diarrhea in AIDS patients; apicomplexin
|
|
Leishmania [claim to fame]
|
live inside phagolysosome of macrophages
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RBC targets:
Plasmodium falciprum Plasmodium vivax Plasmodium malariae |
falciparum: all ages RBC
vivax: reticulocytes malariae: old |
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Fungal superficial infxn [organisms]
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piedras, tinea versicolor
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Fungal cutaneous [organisms]
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tineas
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Fungal subcutaneous [organisms]
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Sporothrix schenkii
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What is candidiasis?
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opportunistic infxn, part of normal flora
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What is aspergillosis?
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opportunistic infxn, bronchopulmonary disease, lung aspergillomas?
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what are aspergillomas/
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opportunistic infxn, fungus ball, clumb of fungus which exists in a body cavity
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What is cryptococcosis?
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opportunistic infxn, encapsulated, yest form only, neurotropic
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What is Mucormycosis?
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opportunistic infxn, spores germinate and hyphae invade blood vessels of sinuses, brain, very aggressive
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What is pneumocystis carinii?
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opportunistic infxn, eukaryotic, closest to fungi
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As far as global mortality, what is the top 5?
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Infectious disease
Cancer Heart Diseases Cerebrovascular diseases Chronic lung disease |
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Top 3 infectious disease killers?
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TB, HIV, Malaria
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What are the pyogenic cocci?
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Streptococci, Staphylococci, Neisseria
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What are some characteristics of Streptococcal disease [7]?
Gram: Type of infxn: Acute/Chronic: Extracellular/Intracellular: Weak/Strong Inflammatory response: Fever/No fever: |
What are some characteristics of Streptococcal disease [7]?
Gram:+ Type of infxn:pyogenic Acute/Chronic:acute Extracellular/Intracellular:extracellular Weak/Strong Inflammatory response: strong Fever/No fever: fever |
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What is normal harmless colonization rate of Streptococcus?
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30-70%
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Where does streptococci have to enter into and spread in order to be virulent in pneumonia?
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aveolar spaces
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What is the most important virulence factor of streptococcus?
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capsule
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What is the agent that the immune system reacts against with streptococcus?
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capsule polysaccharide
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Where do legionella live?
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macrophages
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What is legionella practically indistinguishable from?
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Pneumococcal pneumonia
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What are symptoms of pontiac fever?
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flu-like; no pneumonia, recover w/o Tx within 1 week
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_Legionella_
Gram: Aerobic/anaerobic: Structure: How pathogenic: |
Gram:-
Aerobic/anaerobic: aerobic Structure: coccobacilli How pathogenic: macrophages, inhibition of acidification of phagosome |
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What is the main type of antibiotic that can penetrate into white blood cells?
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erythromycin
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Where is Avian influenza endemic?
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waterfowl populations
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Where does Avian influenza normally reside inside waterfowl?
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digestive tract, via fecal-oral
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What type of Hemagluttinin are waterfowl versus human?
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H1,H2,H3: human
H5,H7,H9:domestic poultry |
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What was infection/mortality profile of 1918 flu?
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W shaped, old, young, and middle aged most affected
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What type of virus is SARS?
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Coronavirus
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Where do we think SARS came from?
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bats
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What type of organism is multi- or unicellular with membrane bound organelles?
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eukaryote
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What is a unicellular organism with no membrane-bound organelles?
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prokaryote
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what type of pathogen is a virus?
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obligate intracellular
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Why are mycobacteria called gram +?
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They have one membrane
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What color are acid-fast staining organisms?
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red
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What are the three main types of cellular morphology and what is their definition?
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coccus: spherical
bacillus: rod spirochete: spiral |
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Where are type 1 pili normally found and what do they usually have attached?
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enteric bacteria; FimH adhesin
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What is the general name of a protein that binds to a sugar residue?
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lectin (ex. FimH)
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What are type 4 pili and where are they usually found?
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found in gram - bacteria, not implicated in conjugation; Enterpathogenic E. Coli, Vibrio cholerae, Enterotoxigenic E. Coli
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What is the difference between peritrichous and monotrichous?
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peritrichous: more than one flagellum per cell
monotrichous: one polar flagellum per cell |
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What does the Quellung rxn do?
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binds antibodies to capsule of Strep. pneumoniae and allows it to be visualized under microscope
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what does the normal vaginal flora contain?
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lactobacillus
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What does passive immunization mean?
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transfer of antibodies from a donor to a host (ex. maternal antibodies to baby)
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what does cholera toxin do?
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increase cyclic AMP levels
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what is the organism that is Lancefield group A versus lancefield group B
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A: streptococcus pyogenes
B: streptococcus agalactiae |
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is streptococcus + or - catalase
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-
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hemolytic: strep pyo?
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beta
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hemolytic: strep agal?
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beta
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hemolytic: strep pneumo
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alpha
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what is the only staph that is coagulase positive?
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Staph aureus
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Does staph have a capsule?
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no
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What does bacillus cereus cause?
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food poisoning
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What is clostridium and bacillus known for?
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endospores
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is UPEC extracellular or intracellular?
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intracellular
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is EHEC extracellular or intracellular?
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extracellular
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How does your diff Dx change if something will not grow on blood agar but will grow on chocolate agar?
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Haemophilus will not grow on blood agar.
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What are three types of hemolysis?
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Acts on RBC's
alpha-halo, moderate lysis beta-full lysis gamma-no lysis |
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What's the C. dificil elevator speech?
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pseudromembranous colitis
Gram + spore former (b/c all clostridiums are spore formers) |