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Pathophysiology > Antibiotic Resistent Organisms > Flashcards

Antibiotic Resistent Organisms Flashcards

1
Q

What 4 factors contribute to the development of antibiotic resistance?

A
  1. Misuse and overuse of antibx
  2. Hospital environment
  3. Food
  4. No new antibx on the horison
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2
Q

Explain why misuse and overuse of antibx causes AROs?

A
  • Incorrect prescribing (UTI)
  • Too low of a dose
  • Treatment too short
  • Patient error (non-adherence/sharing)
  • Agricultural use in livestock
  • Over-availablility
  • Manufacturing plants leaching
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3
Q

Explain why the hospital environemnt can cause AROs?

A
  • Large amount of immunicompromised people
  • Close pt proximinity
  • Invasive procedures
  • Teaching hospitals have the sickes and highest acuity patients
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4
Q

Explain how food causes AROs?

A
  • More meals are consumed outside the home (easier spread)
  • Contamination of food source with pathogens (ie: melons and recall)
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5
Q

Explain how lack of new antibx contributes to AROs?

A
  • No new pathways to tackling bacteria as there is no particular financial gain
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6
Q

What is drug resistence?

A

An adaptive response in which microorganisms beging to toelrate an amount of antibx that would normally inhibit or kill it

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7
Q

What is the ability to resist antibx due to?

A

Genetic versatility and adaptablity of the microbial population

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8
Q

What are the two types of ARO resistence?

A
  1. Inherent (natural) resistnace
  2. Aquired resistence
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9
Q

Explain inherent resistance

A

Bacteria may be naturally resistant due to structural advantage
Can also be called “insensitivity” since it occurs in organisms that have never before been suspectible to that dtug

Ex: Gram - bacteria are immune to vano
Ex: Microplasm have no cell wall so no antbiotic that targets cell wall will work

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10
Q

Knowledge of the intrinsic resistance of a pathogen is of great importance to clinicians?

A

Avoid prescribing inappropaite or ineffective therapies

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11
Q

What is aquired resistence?

A

When bacteria become resistent to antibx due to vertical gene transfer or horizontal gene transfer

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12
Q

Describe vertical gene transfer

A
  • Spontanous mutation happens that results in resistence
  • Resistence advantage is then tranferred directly to its offspring
  • Bacteria have fast growth rate so this change gets passed on quick
    ** Is an example of natural selection*
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13
Q

Define horizontal gene transfer?

A

DNA is transfered between indivddual bacteria of the same species (staph aureus to staph aureus) or even different species (enterococcus facieals to staph aureus)

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14
Q

What 3 methods can horizontal gene transfer occur?

A
  1. Conjugation
  2. Transformation
  3. Transduction
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15
Q

Explain conjugation in horizontal gene transfer

A

This process is mediated by a plasmid, a part of DNA that replicates independently

It occurs when there is a direct contact between 2 bacterias and facilitated by a hollow bridge called sex pillus that forms to allow plasmids to transfer between bacterias

Genes for ARO or virulence (toxicity, enzymes, adhesion molecules) can be transferred

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16
Q

Describe conjugation in gram negative bacteria

A

Gram negative bacteria have a specialized plasmid called a fertility factor or F factor, once cell, the donor bacterium (F+), gives up DNA; and another bacterium, the recipient cell (F-), receives the DNA.

17
Q

What is a resistance factor? (R factor)

A

A plasmid containing multiple genes for drug resistance

18
Q

Explain the process of transformation in horizontal gene transfer

A

When a bacteria is lysed and breaks apart, DNA gets released into the surrounding environemnt. Other bacteria can scavenge this free floating DNA and incorporate it in. This can have advantageous genes.

Genes transfered from one bacteria to another are called naked DNA

Cells capable of accepting new DNA are called competent, once the donated DNA is inserted into the reciepient (competent) cell it is now transformed

19
Q

Explain the process of transduction in horizontal gene transfer

A

Bacterial DNA is transfered from one bacteria to another INSIDE a virus that infects bacteria (bacteriophage).

Phage enters bacteria and produces more pahge, during this process bacterial DNA can be plugged into the phage.

Phage then goes and invades another bacteria

Phage goes and invades another bacteria and now the NEW bacteria gets genes from the first bacteria

20
Q

What are the three specific methods of antibiotic resistence?

A
  1. Destruction or inactivation of an enzyme
  2. Expulsion of the antimicrobial agent from the cell using efflux pumps
  3. Alteration of drug binding sites
21
Q

Explain destruction or inactivation of enzymes

A
  • Bacteria possess genes that can make enzymes to deactivate the antibiotic
  • When the beta-lactam ring of is destroyed by the enzyme beta lactamase the antibx no longer works

Pencilinases destroy the beta-lactum ring in pennicilin
Cephalosporinases destroy the beta-lactam ring in cephalosporin

22
Q

Explain efflux pumps in AROs

A
  • Both gram - and + can become resistent to antibx through efflux
  • Efflux pump is a cahnnel that activesly transfport substances out of the cell (gram - transport toxins out)
  • Antimicrobial enters the bacteria through a porin channel and then gets pumped out by the efflux pump preventing the accumulation inside the cell
  • Some pumps can only pump out one type of antibx while others can be Multi Drug Resistant Pumps (MDRP)
23
Q

Explain alteration of drug binding sites in AROs

A

Drugs bind mostly on a specific target such as a portien, RNA, DNA or membrane structure. By changing the nature of these targets, you can prevent the drugs from binding and having an effect

24
Q

Explain aminoglycosides

A

Aminoglycosides work by binding to 30s ribosomes so if the ribosome binding
site is changed this antimicrobial can’t bind thus has no effect

25
Q

What is an alteration on 50S ribosomal binding site assocaitated with?

A

Erythromycin and clindamycin resistance

26
Q

What makes MRSA pencilliin resistent?

A

MecA gets changed that alters the PBP to become PBP2a and prevents penicillins from binding to it

27
Q

Explain ciproflaxin and mexifiosin resistence

A

cipro and mexi bind to the DNA gyrase enzyme to prevent the bacteria from replicating

Bacteria changes the DNA gyrase enzyme so cipro and mexi can’t bind

28
Q

How does sulfonamide resistance develop?

A

when microbes deviate from the usual pattern of folic acid synthesis

29
Q

What is virulence

A

is a measure or degree of pathogenicity (ability to cause disease)

30
Q

What 4 mechanisms do microbes vary in thier ability to cause disease?

A
  1. Ability to infect the host
  2. Ability to protect itself from the host defenses
  3. Ability to invade and multiply in tissues
  4. Ability to cause damage or destruction
31
Q

Define and list virulence factors

A

The properties or characteristics that contribute to virulence of a pathogen are called virulence factors

  • Adhesion factors
  • Evasive and invasion mechanism
  • Toxins
32
Q

Explain adhesion factors in virulence

A

Pathogens have surface molecules called adhesins or ligans that bind on surface receptors on certain host tissues.

Some organisms have pilli that help to attach to host tissue, some have microtubules like c-diff

Microbes HAVE to attach to cell to colonize host

33
Q

Explain evasive factors in virulence

A

Evasive factors refer to the methods bacteria apply to evade the host’s immune system

Flagella: motile can move away from the defence mechanism (play tag)
Capsule: form anti-phagocytic function

34
Q

Explain c-diff’s evasive factor

A

C-diff has a polysaccharide coat that makes it hard to phagocytose

35
Q

Explain S.aureus’ evasive factors

A

Strains of S. aureus produce a surface protein (protein A) that immobilizes
IgG and IgM, holding the antigen-binding region harmlessly away
from the organism

S. aureus – secretes a unique enzyme called coagulase – coagulase converts
soluble human coagulation factors into a solid clot which envelops and protects
the organism from phagocytic host cells and antibodies

36
Q

Explain invasive factors in virulence

A

The infectious agents produces substances that facilitate penetration of anatomic barriers and host tissues such as enzymes that destroy cellular membranes or connective tissue

Ex: necrotizing facisitis

37
Q

Explain toxins as a virulence factor

A

The ability of pathogens to damage host tissues and cause disease can be dependent on poisonious substances known as toxins

38
Q

List and describe the 2 types of toxins

A
  1. Exotoxins: proteins released from baterial cell wall during growth that inactivate cellular fucntions in the host, genens for this are carried in the plasmid. Eg: botulism/tetnus
  2. Endotoxins: these are weak toxins in gram neg bacteria but can be fatal in large quanities. They produce the same signs andsymptoms because they all activate the inflamatory process (chills, fever etc), also activate the blood clotting mecahnisms and can result in septic SHOCK

Pathophysiology (9 decks)

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