Exam one: L5-L8 Flashcards

1
Q

L5: what is the definition of epidemiology?

A

It is the study of disease and populations of factors that determine its occurrence overtime

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2
Q

L5: what is the historical origin of epidemiology?

A

John Snow identified the cause of the London epidemic because he believed that sewage and water could contaminate water. Snow removed the pump eliminated in the area 

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3
Q

L5: what are the roles and applications of epidemiology in public health?

A

It studies the etiology of disease to determine positive factors for assist, and understanding pathogenicity, it identifies describes and determines infection, patterns and disease and populations. It assists in the development of health, initiatives and prevention.

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4
Q

L5: what is an agent? What are its characteristics and what is the intervention for it?

A

An agent is a microorganism that causes disease if characteristics are variance, dose, toxicity, and living conditions, the intervention is to control/eliminate infection at its source

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5
Q

L5: what is a host? What are its characteristics and what is the intervention for it?

A

A host is the thing that gets a disease. It depends on exposure/behavior, susceptibility and response, intervention, for it is treat infection immunize, and behavior modification 

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6
Q

L5: what is an environment? What are its characteristics and what its interventions

A

An environment is backwards that affect the agent and exposure opportunities. Characteristics depend on place insects/biological factors and socioeconomic patterns, it’s interventions or sanitation water, prevention, services, and bug pillows.

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7
Q

L5: what is the reservoir?

A

Is an environment where infectious agent lives and multiplies

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8
Q

L7: What are the different B-lactams and common ending?

A

cilin, cef/ceph, penem, cefiderocol

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9
Q

L7: What are the ways that a bacteria resists B-lactams?

A

By using beta-lactamases, mutating PBPs, efflux pumps, decreasing membrane permeability

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10
Q

L7: How do we combat B-lactamases and which bacteria make B-lactamases?

A

We use combination therapy with B-lactamases, a bacteria that makes B-lactamase is enterococcus and acinetobacter

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11
Q

L7: What bacteria mutates their PBPs and how does it work?

A

MRSA mutates its PBP by acquiring mecA which encodes for PBP2a which decreases affinity for common B-lactams

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12
Q

L7: What drug resistant bacteria uses efflux pumps and decreased membrane permeability as a defense?

A

Pseudomas Aeruginosa

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13
Q

L7: What is the most common glycopeptide and what class of Ab is it?

A

Vancomycin, it is a cell-wall inhibitor

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14
Q

L7: What does vancomycin do?

A

It binds D-ala D-ala to block Tpase activity

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15
Q

L7: What does vancomycin resistance look like? And what does it?

A

VR enterococcus, it mutated D-ala into D-lac so that vancomycin does not recognize it anymore

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16
Q

L7: What are DNA targeting antibiotics called? And what do they do? What do the drugs end with?

A

Fluoroquinolones, interfere with topoisomerase t2 to cause double stranded breaks. Drugs end in floxacin

17
Q

L7: What is a common resistance mechanism against flouroquinolones?

A

Mutating topoisomerase and gyrase, efflux pumps and permeability barriers

18
Q

L7: What are the ribosomal inhibitors and where do they act?

A

A site: tetracycline and aminoglycosides
B site: oxazolidinones
C site: macrolides/lincosamides

19
Q

L7: What do nitromidazoles do and what is unique about them?

A

nitromidazole is a prodrug that when inside an anaerobic cell, makes extremely reactive nitroso intermediates that cause ds breaks in DNA

20
Q

L7: What does rifampin do and what is it good for?

A

Rifampin blocks RNA polymerase to prohibit translation, it is commonly used in combination bc resistance is easily acquired and it can penetrate osteoblasts and biofilms

21
Q

L7: What do sulfonamides do? What bacteria has intrinsic resistance?

A

Sulfonamides block the folate synthesis pathway, altering DNA synthesis. Enterococcus has intrinsic resistance because it can take up folate from the environment.

22
Q

L7: What do polymyxins do?

A

Polymyxins act in G(-) cells to disrupt the outer membrane with hydrophillic cationic ring and hydrophobic tail.

23
Q

L7: What is the good polymyxin and which is the bad one?

A

pmB is good, in Neosporin
pmA is bad, very toxic and should be used as a last resort.

24
Q

L8: When testing antibiotic susceptibility, which genes do we look for in VRE, MRSA, and TB?

A

VRE: vanA and vanB
MRSA: MecA
Mycobacterium TB: rpoB