Bacteriology Treatment Flashcards

1
Q

CHAIN OF INFECTION

infectious agents
reservoirs
portals of exit
modes of transmission
portals of entry
susceptible host

infectious agents (microbes capable of causing diseases or illness)
- bacteria, ?, parasites, ?

reservoirs (place in which infectious agents grow, live and reproduce)
- ?, ?, ?

portals of exit (ways in which infectious agent leaves the reservoir)
- blood, secretions, ?, skin

modes of transmission (ways in which the infectious agent is spread from the reservoir to the susceptible host)
- ?, contact, ?, airborne

portals of entry (ways in which the infectious agent enters the susceptible host)
- ? membranes, ? system, digestive system, ? skin

susceptible host (individuals have traits that affect their susceptibility and severity of diseases)
- ? deficiency, ?, burns, surgery, age

! this chain could stop at any stage !

A

CHAIN OF INFECTION

infectious agents
reservoirs
portals of exit
modes of transmission
portals of entry
susceptible host

infectious agents (microbes capable of causing diseases or illness)
- bacteria, fungi, parasites, prion

reservoirs (place in which infectious agents grow, live and reproduce)
- people, water, food

portals of exit (ways in which infectious agent leaves the reservoir)
- blood, secretions, excretions, skin

modes of transmission (ways in which the infectious agent is spread from the reservoir to the susceptible host)
- physical contact, droplets, airborne

portals of entry (ways in which the infectious agent enters the susceptible host)
- mucous membranes, respiratory system, digestive system, broken skin

susceptible host (individuals have traits that affect their susceptibility and severity of diseases)
- immune deficiency, diabetes, burns, surgery, age

! this chain could stop at any stage !

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2
Q

Different uses of antimicrobials

THERAPEUTIC (relating to healing of disease) USE:

Treatment
Control Metaphylaxis
Prevention/Prophylaxis

metaphylaxis: a large number of animals w or w/o disease so protecting rest that aren’t sick and in close contact to the sick and treat those that are sick.- TO ALL OF THEM
- (metaphylactic treatment aka antimicrobial control of disease: the treatment of group of animals after the diagnosis of disease has been made in part of the group.)

(thus, prophylaxis/prevention and metaphylaxis involve administering antimicrobials to healthy individuals to PREVENT infections but for prophylaxis/prevention, there is a perceived risk whereas metaphylaxis could be a DEFINABLE hazard.

Prophylaxis/PREVENTION: preventing before the disease comes

NON-THERAPEUTIC USE
- growth promotion

(production uses include “feed efficiency” and “growth promotion” uses, which are unrelated to disease management. These uses typically involve the administration of subtherapeutic antimicrobial agents in the feed or water of an entire herd or flock to promote faster growth with less feed.)

farm animal will feed with antibiotic to grow faster and stronger as u control .. Prophylaxis and we CONTROL MICROBIOTA of animal and less opportunistic subclinical disease will raise and affect those animals and then will better use their.. thats y called growth promoters

A

: )

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3
Q

“BAN on antibiotics as growth promoters in animal feed enters into effect; antibiotic use plummets on US farms after ban on using drugs to make livestock grow faster”

y? promotes antibiotic resistance (selecting all the time the most .. organisms so resistant ones, we are only bullet we have to treat pathogen ..for sum else so wasting bullet .. in developing nations still using .. so this can travel to other developed nations and so we need to span these to all countries

A
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4
Q

Antimicrobial agent = any substance of ?, ? or ? origin that kills microbes (bacteria, fungi, virus) or prevents their ?/?, reducing their pathogenic effect

ANTIMICROBIALS
- antibiotics/antibacterials: against bacteria e.g. drugs for bacteria pneumonia
- antivirals: against viruses eg. drugs for herpes and HIV
- antiparasitic agents: against parasites e.g. drugs for malaria
- antifungals: against fungi e.g. drugs for yeast infections

  • Natural: produced by ? or ? (e.g., streptomycin, penicillin, tetracycline)
  • Semi-synthetic: ?-altered natural compound (e.g., ampicillin, amikacin) (e.g. from bacteria and then in lab)
  • Synthetic: chemically designed in the ? (e.g., sulfonamide, enrofloxacin, marbofloxacin). Based on pre-existing molecules. (this is from scratch)
A

Antimicrobial agent = any substance of natural, semisynthetic or synthetic origin that kills microbes (bacteria, fungi, virus) or prevents their multiplication/growth, reducing their pathogenic effect

  • Natural: produced by bacteria or fungi (e.g., streptomycin, penicillin, tetracycline)
  • Semi-synthetic: chemically-altered natural compound (e.g., ampicillin, amikacin) (e.g. from bacteria and then in lab)
  • Synthetic: chemically designed in the lab (e.g., sulfonamide, enrofloxacin, marbofloxacin). Based on pre-existing molecules. (this is from scratch)
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5
Q

Key definitions

SPECTRUM OF ACTIVITY

■ ** IMP Broad-spectrum antibiotics = active against both ? microorganisms
■ ** IMP Narrow-spectrum antibiotics = limited activity and primarily only useful against ? species of
microorganisms e.g. preventing ?

A

SPECTRUM OF ACTIVITY

■ ** IMP Broad-spectrum antibiotics = active against both gram + and - microorganisms
■ ** IMP Narrow-spectrum antibiotics = limited activity and primarily only useful against particular species of microbes
microorganisms e.g. preventing antimicrobial resistance (as only targeting the pathogen willing to kill and rest of the microbiota will not be under pressure to be resistant)

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6
Q

Key definitions
TYPE OF ANTIMICROBIALACTIVITY

■ ** IMP BacteriCIDAL agents = kill bacteria and reduce the total number of ? organisms
■ ** IMP BacterioSTATIC agents = inhibit ? and ? of bacteria, thus allowing the host immune system to complete pathogen ?

■ If a type of therapeutic agent is not maintained at ? concentrations in the tissues, dissociation of the drug/cell structure complex can occur, permitting bacterial survival

A

viable = capable of working succesfully

Key definitions
TYPE OF ANTIMICROBIALACTIVITY

■ ** IMP BacteriCIDAL agents = kill bacteria and reduce the total number of viable organisms
■ ** IMP BacterioSTATIC agents = inhibit growth and replication of bacteria, thus allowing the host immune system to complete pathogen elimination
■ If a type of therapeutic agent is not maintained at effective concentrations in the tissues, dissociation of the drug/cell structure complex can occur, permitting bacterial survival

w/ bacterioSTATIC drug bacteria can re-emerge

■ If a type of therapeutic agent is not maintained at effective concentrations in the tissues, dissociation of the drug/cell structure complex can occur, permitting bacterial survival

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7
Q

History line of antibiotics

Alexander Flemming
- Discovery of the ?!

hole of inhibition around fungi: what happened in the hole of inhibition?(pic)

antibiotic introduction even since 1935

Mode of action
To interfere with bacterial cell growth, antibacterial agents (antibiotics) ** must ? ** with a * ? * structure or block a metabolic pathway and preferably exhibit * ? * (i.e., without direct toxicity for hosts receiving treatment)

cell wall is a good target for interfering with bacterial cell growth (Beta-lactams e.g. penicillin; Glycopeptides: e.g. vancomycin; Bacitracin)

metabolic pathways: target it, then can’t produce essential components and then die.

Plasma membrane

ribosomes

DNA synthesis and RNA synthesis

A

History line of antibiotics

Alexander Flemming
- Discovery of the Penicillin!

hole of inhibition around fungi: bacteria were killed there in that inhibition space. (pic)

antibiotic introduction even since 1935

Mode of action
To interfere with bacterial cell growth, antibacterial agents (antibiotics) ** must interact ** with a * vital * structure or block a metabolic pathway and preferably exhibit * selective toxicity * (i.e., without direct toxicity for hosts receiving treatment)

cell wall is a good target for interfering with bacterial cell growth (Beta-lactams e.g. penicillin; Glycopeptides: e.g. vancomycin; Bacitracin)

metabolic pathways: target it, then can’t produce essential components and then die.

Plasma membrane

ribosomes

DNA synthesis and RNA synthesis

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8
Q

Cell wall synthesis inhibitors

β-lactam antibiotics (e.g. penicillin, ampicillin, cephalosporin, carbapenem, monobactam)

Mode of action:
■ ** !! IMP Inhibit the ? ** by binding to
? that are involved in this process
■ Promote ? activity causing cell lysis

Glycopeptides (e.g., vancomycin, teicoplanin)

■ Mode of action:
■ ** !! IMP inhibit the ? ** by binding to amino acids (d-alanyl-d-alanine; resemble the structure of d-ala..) in the cell wall, preventing the addition of new units
■ Differences in the cell wall [Gr(+) vs Gr(-)] determine ? to these antibiotics. Some agents cannot penetrate ? of Gr(-) bacteria, their antimicrobial spectrum is confined to Gr(+)

A

Cell wall synthesis inhibitors

β-lactam antibiotics (e.g. penicillin, ampicillin, cephalosporin, carbapenem, monobactam)

Mode of action:
■ ** !! IMP Inhibit the peptidoglycan synthesis ** by binding to
penicillin-binding proteins (PBP) that are involved in this process
■ Promote autolysin activity causing cell lysis

Glycopeptides (e.g., vancomycin, teicoplanin) - resemble structure of amino acids (d-alanyl d alanine)

■ Mode of action:
■ ** !! IMP inhibits the peptidoglycan synthesis ** by binding to amino acids (d-alanyl-d-alanine; resemble the structure of d-ala..) in the cell wall, preventing the addition of new units

■ Differences in the cell wall [Gr(+) vs Gr(-)] determine susceptibility to these antibiotics. Some agents cannot penetrate outer membrane of Gr(-) bacteria, their antimicrobial spectrum is confined to Gr(+)

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9
Q

Protein synthesis inhibitors

? (e.g. gentamicin, amikacin) -> Inhibit 30Ssubunit of bacterial ribosome

? (e.g. oxytetracycline, chlortetracycline) -> Inhibit 30Ssubunit of bacterial ribosome

? (e.g. erythromycin, azithromycin) -> Inhibit 50S subunit of bacterial ribosome

? -> Inhibit 50Ssubunit of bacterial ribosome

? (e.g. clindamycin) -> Inhibit 50Ssubunit of bacterial ribosome

A

AT 30s

MCL 50s

(50s 30s -> 70s bacterial ribosome
60s 40s -> 80s eukaryotic ribosome)

Protein synthesis inhibitors

Aminoglycosides (e.g. gentamicin, amikacin) -> Inhibit 30Ssubunit of bacterial ribosome

Tetracyclines (e.g. oxytetracycline, chlortetracycline) -> Inhibit 30Ssubunit of bacterial ribosome

Macrolides (e.g. erythromycin, azithromycin) -> Inhibit 50S subunit of bacterial ribosome

Chloramphenicol -> Inhibit 50Ssubunit of bacterial ribosome

Lincosamides (e.g. clindamycin) -> Inhibit 50Ssubunit of bacterial ribosome

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10
Q

DNA synthesis inhibitors

?: Nalidixic acid, enrofloxacina
■ Inhibit enzymes which separate DNA strands (e.g. DNA ?)

Metronidazole
■ Causes breaks in DNA strands and is particularly effective against ** IMP ? ** (e.g. Clostridium)

?
■ Inhibit RNA polymerase during transcription
■ Active against “ ** IMP ? “ tuberculosis

?
■ Inhibit tRNA synthetase during translation

A

Quinolone”s”: Nalidixic acid, enrofloxacina
■ Inhibit enzymes which separate DNA strands (e.g. DNA gyrase)

Metr”o”nidazole
■ Causes breaks in DNA strands and is particularly effective against ** IMP obligate anaerobic bacteria ** (e.g. Clostridium)

“R”ifa”m”pin
■ Inhibit RNA polymerase during transcription
■ Active against “** IMP Mycobacterium tuberculosis “

Mupirocin
■ Inhibit tRNA synthetase during translation

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11
Q

Folic acid synthesis inhibitors

?
■ Interfere with formation of folic acid, essential precursor for ? synthesis. Inhibitors of ? (PABA) in the folic acid metabolism cycle.

?
■ Interfere with formation of folic acid, essential precursor for nucleic acid synthesis. Blocks the reduction of ? to tetrahydrofolate, the ? form of folic acid

A

Folic acid synthesis inhibitors

Sulphonamides
■ Interfere with formation of folic acid, essential precursor for nucleic acid synthesis. Inhibitors of p-aminobenzoic acid (PABA) in the folic acid metabolism cycle.

+ Trimethoprim
■ Interfere with formation of folic acid, essential precursor for nucleic acid synthesis. Blocks the reduction of dihydrofolate to tetrahydrofolate, the active form of folic acid

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12
Q

Antimicrobial susceptibility testing AST

  • An in vitro test (performed ? an animal) of the * ? * to one or more ?
  • Three main methods (widely used):
    1. ? diffusion test,
    2. ? diffusion test
    3. ? dilution test
  1. Disk diffusion test (“Kirby Bauer”) test

■ Based on the diffusion of an antibiotic on solid cultures
■ Must use a bacterial isolate in ** IMP ? **

■ Standardized bacterial inoculum ➔ spread on agar plate (solid culture)

■ Standardized antibiotic disks ➔ amount of antibiotic in the disk and size

■ Single-concentration antimicrobial disks are placed on the plate and incubated. The antibiotic diffuses in the agar and the concentration declines as it distances from the disk.

15% even tho halo (so they compare clinical data with a particular amount of drug and see if the drug level is enough to inhibit bacteria)

A

Antimicrobial susceptibility testing AST

  • An in vitro test (performed outside an animal) of the * sensitivity of bacteria * to one or more antibiotics
  • Three main methods (widely used):
    1. disk diffusion test,
    2. concentration gradient diffusion test
    3. broth dilution test
  1. Disk diffusion test (“Kirby Bauer”) test

■ Based on the diffusion of an antibiotic on solid cultures
■ Must use a bacterial isolate in ** IMP pure culture**

If an antibiotic stops the bacteria from growing or kills the bacteria, there will be an area around the disk where the bacteria have not grown enough to be visible. This is called a zone of inhibition. The susceptibility of the bacterial isolate to each antibiotic can then be semi-quantified by comparing the size of these zones of inhibition to databases of information on known antibiotic-susceptible, moderately susceptible and resistant bacteria. In this way, it is possible to identify the most appropriate antibiotic for treating a patient’s infection.[1][2] Although the disk diffusion test cannot be used to differentiate bacteriostatic and bactericidal activity, it is less cumbersome than other susceptibility test methods such as broth dilution.

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13
Q
  1. Broth dilution test

■ A method for measuring ? concentration of ?

■ Minimum inhibitory concentration = MIC -> Highest dilution of an antibacterial agent that ? growth of an isolate in the broth (naked eye)

■ Minimal bactericidal concentration = MBC -> ✓ Highest dilution of a drug that can ? a particular bacterium (demonstrated by subcultures)

  1. Broth dilution test
A
  1. Broth dilution test
    ■ A method for measuring minimum inhibitory concentration of antibiotics

The broth dilution test is one of the earliest susceptibility tests and involves setting up twofold dilutions of antibiotics in medium with bacteria to determine the lowest concentration in which the bacteria will still grow.

■ Minimum inhibitory concentration = MIC
✓Highest dilution of an antibacterial agent that inhibits the growth of an isolate in the broth (only through naked eye but in reality, there might be some of them still there)

■ Minimal bactericidal concentration = MBC
✓ Highest dilution of a drug that can kill a particular bacterium (demonstrated by subcultures)

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14
Q
  1. Concentration gradient diffusion test

■ Method that uses both principles from diffusion and dilution

■ MIC values are obtained at the point of intersection between the strip and the ellipse of the zone of ?

(conc. will declin a/c to inoculation of that antibiotic -> gives inhibtion zone (spherical kinda)

(no growth in yellow part and growth in darker part: shown in pic in middle)

A
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15
Q

From AST to therapy success/failure

not the same as treat as skin infection, kidney and systemic infecetion as all these have to be pout there to see which drug best to use

(if black how much systemic

not the same as intravenous.. a lot

all parameters will change a/cly

lipophillic more in tissues and fatty lipids.. will penetrate easier if hydrophillic will not)

A
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16
Q

Antimicrobial resistance generation

  1. Lots of germs. A few are drug-resistant
  2. antibiotics kill bacteria causing the illness, as well as good bacteria protecting the body from infection
  3. the drug-resistant bacteria are now allowed to grow and take over
  4. some bacteria give their drug resistance to other bacteria causing more problems.
A

Become a responsible vet!

DO NOTS:

■ Providers
* Overprescription for mild and non-bacterial infections
* Over-selection of broad spectrum, costly, or last resort drugs

■ Patients/clients
* Non-compliance, self-medication

■ Industry
* Misleading promotion, competition