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Medical Micro > new facts for jan > Flashcards

new facts for jan Flashcards

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USMLE® Step 1 flashcards
1
Q

environmental reservoir of infection

A

the habitat in which the agent normally lives, grows, and multiplies

could be the source from which the agent is transferred to the host

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2
Q

chemoprophylaxis

A

the use of drugs to control disease

antibiotics

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3
Q

vector control

A

controlling the animal that transmits the disease

eg. mosquito for malaria

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4
Q

define biofilm

A

matrix-associated microbial populations adherent to each other and/or to surfaces or interfaces

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5
Q

chracteristics of primary fungal pathogens

A 
route of infection = inhalation 
localised pneumonia
healthy host
asymptomatic
progress to pulmonary dissemination
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6
Q

histoplasma

blastomyces dermatidis

A

primary fungal pathogen
thermally dimorphic
geographically limited - endemic regions - travellers can get after they come back

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7
Q

candida

A

most common fungal etiological agent in immunocompromised
4th most causative agent of nosocomial infections (Gordon Brown 2012)
azole resistance

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8
Q

apergillus mortality rate

A

60-90%

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9
Q

emergence of HIV

A

increasing the immunocompromised population

now 33 million people living with AIDS

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10
Q

ageing population

A

increases the immunocompromised therefore more people susceptible to opportunistic pathogens

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11
Q

bacterial adaptation to cold requires

A

structural flexiibilty

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12
Q

bacterial adaptations for survival

A

mutations
acquired resistance
passed down generations
selection pressures

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13
Q

gene expression changes bacterial

A

surface chemistry

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14
Q

gram -ve biofilm

A

vibrio haemolyticus

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15
Q

gram -ves are often naturally resistance to

A

penicillin

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16
Q

lipopolysaccharides can be more or less

A

water resistant

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17
Q

incidence of a disease depends on…

A

the pathogen

individual susceptibility

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18
Q

how does Histoplasma capsulatum cause host damage

A

spores inhaled from faeces in soil
form budding yeast cells in the lungs
causes coughing symptoms
can disseminate

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19
Q

effect of fever

A

heat inactivates many viruses

secretion of interferons

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20
Q

Neisseria meningitidis adherence factors

A

Adhesin complex protein (ACP)

FBP

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21
Q

cytotoxin example

A

tetanus

causes skeletal muscle spasms e.g. lockjaw

22
Q

how do infections spread after establishment

A

through bloodstream and lymphatics

23
Q

Rabies virus

A

produces P protein
JAK/STAT blocker
blocks phosphorylation of IRF3

rabies competes with host RNA
impairs neural function

body produces NO - acts as a toxin against body and attacks nervous tissue
(2004 Tara K Harper)

24
Q

educational control strategies

A

campaigns e.g. catch it, bin it, kill it
influenza
2013

25
Q

vector control

A

malaria

dengue

26
Q

surveillance of emerging infections

A

vital for early identification of public health threats

27
Q

new technology allows rapid molecular identifaction

A

important for emerging infections

e.g. pandemic H1N1 influenza

28
Q

guidlines for sterilisation and disinfection of invasive devices used in surgery have been developed (P.Patterson 2009)

A

e.g. catheter associated UTI guidlines - 2009

29
Q

commensal gut microbiota

A

promote mucosal barrier and enhance innate immune resposne

30
Q

biofilms can cause infections in blood and tissues

A 
bacteremia
UTI
pneumonia
bacterial vaginosis
endocartidis

65% infections biofilm related

act as reservoirs of contamination/infection

31
Q

biofilm resistance

A

require higher dose of antibiotics

cells are hidden from antibody or complement factor recognition due to exopolysaccharide matrix

higher persister population

e..g pseudomonas aeruginosa

32
Q

pseudomonas aeruginosa

A

biofilm bacteria

MIC and MBC hard to reach as much up to 1000x higher than planktonic counterparts
therefore much more difficult to eradicate

33
Q

treatment of biofilm infection if no foreign body present

A

long term treatment - high doses

combination of different antibiotics with different killing mechanisms

34
Q

treatment of biofilm infection with foreign body present

A

removal of material necessary

35
Q

quorum sensing in biofilms

A

used by bacteria to coordinate gene expression according to their density
used as a target

36
Q

current research into biofilms

A

strategies to increase the efficacy of antimicrobials

use of bacteriophages

37
Q

examples of biofilm forming bacteria

A

gram +ve = listeria monocytogenes

gram -ve = vibrio haemolyticus

38
Q

listeria monocytogenes

A

gram +ve
rod-shaped
causes listeriosis
attaches to food-contact surfaces - problems in food industry
makes biofilms
disperses cells in final stage as a source of contamination

39
Q

staphylococcus aureus

A 
gram +ve
dangerous virulence
can cause pneumonia and meningitis
by 1960, 80% of antibiotics were resistant 
induces keratinocyte autophage
40
Q

mrsa

A

methicillin-resistant-staphylococcus

41
Q

methicillin resistance mechanism

A

methicillin is a beta-lactam antibiotic - broken down by beta-lactamases

staphylococcus contains cassette chromosomes - mecA - mobile genetic elements
altered penicillin binding protein (PBP’) has lower binding affinity so methicillin doesnt bind to the PBP therefore the transpep

42
Q

adaptations to ocean conditions

A

small genomes but rich in AT to reduce N-demand
microbial seas have low nutrient concentration
adapt to be oligotrophs

e. g. pelagibacter ubique
- SAR11 gene converts global primary production back to CO2

43
Q

how does salmonella enterica evade immune resposne

A

uses O2 free radicals for respiration
recognised by TLRs and hijacks them to enter protective niche - Salmonella Containing Vacuole (modified phagosome)
T3SS 1 and 2 secrete effector proteins
pH of vacuole lowered prevents fusion with lyososme

44
Q

how does listeria monocytogenes evade immune system

A

secrete listeriolysin extracellularly
lower pH causes more listeriolysin production
phagosome ruptures
bacteria now intracellular and can spread
recruits actin tails for movement

45
Q

outline recognition of bacterial pathogens by professional phagoctyes

A

PRRs e.g. NLR/TLR recognise pathogen by their PAMPS
PAMPs can lead to NF-kappaB activation (required for phagocytosis of Staph. aureus)

opsonins e.g. antibodies act as attachment sites and mediate recognition as they coat the particles
- often clathrin independent

cytokines are produced in response to recognition e.g. chemokines and interleukins which recruit more phagocytes and can stimulates inflammation

46
Q

methods used by professional phagocytes to tackle intracellular bacterial pathogens

A

phagocytosis - recognition, engulfment, degradation

secretion of ROS/NOS - degrade extracellular matrix and lipid mediators of inflammation

47
Q

what mediates bacterial engulfment by phagocytes

A

actin-myosin contractile system

48
Q

what happens once bacteria has been engulfed by phagocyte

A

pH of phagosome drops - more acidic and more hostile for bacteria
phagosome matures and binds with lysosome
rich in hydrolytic enzymes eg. lysozyme - antimicrobial
lysozyme hydrolyses links in peptidoglycan which is in gram+Ve cell walls
causes cell lysis
damage signal recruits more immune cells

49
Q

granulocytes

A

a white blood cell with secretory granules in its cytoplasm, e.g. an eosinophil or a basophil

50
Q

intrinsic resistance

A

when resistance genes are naturally encoded and expressed by all (or almost all) strains of that particular bacterial species.
e.g. gram -ve bacteria against vancomycin

51
Q

how do drug efflux pumps drive the acquisition of additional resistance mechanisms

A

they lower the intracellular antibiotic concentration

they promote mutation accumulation within the cell

Medical Micro (10 decks)

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