• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/127

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

127 Cards in this Set

  • Front
  • Back
What is the difference between an Antibiotic, Antibacterial and Antimocrobial?
* Antibiotic is a substance produced by a micro-organism that kills or inhibits other micro-organisms

* Antibacterials are synthetic agents which have activity against bacteria

* Antimicrobials are any substance (natural or synthetic) that kills or inhibits growth of a micro-organism without damaging the host.
What are the five mechanisms of action for microbials?
1) Inhibition of protein synthesis (at bacterial ribosome)
2) Inhibition of nucleic acid synthesis (DNA or RNA)
3) Disruption of cell walls
4) Disruption of cell membranes
5) Interfere with metabolic pathways
What are the types of resistance that micro-organisms have to antimicrobials?
* Inherent
* Chromosomal mediated
* Transferable drug resistance
Give three examples of the inherent resistance of micro-organisms to antimicrobials?
1) Mycoplasma resistance to Beta Lactams via lack of cell wall
2) Anaerobic organisms (F. necrophorum) resistance to aminoglycosides
3) Aerobic organisms resistance to nitromidazole, which requite oxygen to function.
Describe how Chromosomal Resistance takes place.
A mutation in one bacteria allows it to survive and multiply when other non-resistant bacteria have been killed off with the antimicrobial.
How is transferable resistance conferred?
Plasmid replicate autonomously and contact genes which allow it to transfer from one bacteria to another. These genes may encode antimicrobial resistance for one or more drugs.
Name five mechanisms that make micro-organisms successful in resisting antimicrobials.
1) Produce enzymes which inactivate the drug
2) Alter the drugs binding site on self
3) Reduce drug uptake
4) Develop enzymes with low drug affinity
5) Increase production of competitive metabolites (ex:PABA)
Define Minimal Inhibitory Concentration (MIC).
The highest dilution at which there is no growth of microorganisms after incubation (in vivo). This is a quantification that is used in determining dosing.
Explain the difference between a Time Dependant and a Concentration Dependant antimicrobial.
Time Dependant antimicrobial require that the hosts plasma concentration of the drug remain above the MIC for a specific period of time for effictiveness, where as Concentration Dependent antimicrobials require that the peak serum concentration of the drug exceed the MIC for effectiveness.
Give three examples of Time Dependent antimicrobials.
1) Beta-lactams
2) Macrolides
3) Lincosamides

* Key that a dose is not missed as drugs have short half-lives.
Give three examples of Concentration Dependent antimicrobials.
1) Aminoglycosides
2) Fluoroquinolones
3) Metronidazole

* Infrequent, but HIGH dosing
What are the four major groupings of Beta-Lactams?
1) Penicillins
2) Cephalosporins
3) Monocatams*
4) Carbapenems*

* Not used in vet med. Saved for SERIOUS human situations.
What are the three types of Penicillins and their Method of action?
* Narrow Spectrum
* Broad Spectrum
* Antipseudomonal

Bactericidal
- Inhibits transpeptidase enzymes by irreversibly binding to the active site. Halts cell wall production.
- Disrupt cross linking of glycopeptide polymer in bacterial cell wall.

~Prevents cell wall formation
~Lyses cell wall of growing cells
What four things determine Penicillins activity against a bacteria?
1) Tranpeptidase
2) Ability to penetrate LPS cell wall (Gram -)
2) Resistance to Beta-lactamase
4) Amount of peptidoglycan in cell wall
What is Beta lactamase? Where does it come from?
An enzyme produced by certain bacteria that can cleave the betalactam ring of Betalactam antimicrobials.

Produced by:
- Staphylococci (Gram +)
* Plasma mediated
- E.Coli, Klebeisella (Gram -)
* Chromosomal mediated
What are the Pharmokinetics of Penicillin? How does this effect its activity?
- Vd
- pKa
- t1/2
- Exclusion
- Excretion
- Post antibiotic effect
* Vd 0.2-0.3L/Kg - Low
* pKa 2.7 - Acid
* t1/2=0.5-1.2 hrs (Short)
* Excluded from CSF & aqueous humor
* Renal excretion (good for UTI's)
* Time Dependent - maintain [high]
What are the three types of Narrow Spectrum Penicillins?
- Penicillin G
- Penicillin V
- Cloxacillin & Nafcillin
Which Narrow Spectrum Penicillin is described by:
- Gram + only
- Acid labile (NOT orally available)
- Beta lactamase susceptible
Penicillin G
Which Narrow Spectrum Penicillin is described by:
- Gram + only
- Acid stable (Orally available)
- Beta lactamase susceptible
Penicillin V
Which Narrow Spectrum Penicillins are described by:
- Gram + only
- Acid stable (Orally available)
- Beta lactamase stable
Cloxacillin & Nafcillin
Often salts are combine with Penicillins, why?
Salt change how long the antimicrobial acts in the body.
Benzylpenicillin is most commonly used in Vet. Med.
* What type of Penicillin is it?
* Why is Procaine added to Benzylpenicillin to make Procaine benzylpenicillin?
* Penicillin G
* Procaine is added to reduce the pain of IM or SQ injections
What bacteria is Methicillin and/or Cloxacillin used to combat? Why?
Staphylococci

A Gram + bacteria that produces Beta lactamase
Name two groups w/ two examples Broad Spectrum Penicillins.
Aminopenicillins
* Ampicillin
* Amoxycillin

Antipsuedomonals
* Carbenicillin
* Ticarcillin
Which Penicillin group is described by:
- Targets Gram + & -
- Acid stable
- Beta lactamase susceptible
Broad Spectrum Aminopenicillins
* Ampicillin
* Amoxycillin

~Routinely Used
Which Penicillin group is described by:
- Targets Gram + & -
- Beta lactamase susceptible
- Effective against Pseudomonas
Broad Spectrum Antipsuedomonals
* Carbenicillin
* Ticarcillin
Why is Clavulanic Acid added to Amoxycillin?
Clavulanic Acid is a "suicide drug". It uses up the Beta latamase freeing up the Amoxycillin to attach the bacteria.
What is the function of administering Aminopenicillins in:
- Sodium Salts
- Trihydrate salts
- Depot preparations?
Sodium Salts - Highly soluble for oral and IV admin.

Trihydrate Salts - Longer acting for IV & SQ admin.

Depot prep - Long acting in oily vehicle
Name the two groups/three drugs or Antipseudomonal Penicillins. How do the two groups differ?
Dicarboxylic Acid derivative
- Ticarcillin
- Carbenicillin
*Synergistic with aminoglycodides
*Sensitive to Beta latamase from P. aueruginosa
*Sensitive to gastric acid (given parentrally)

Ureidopenicillins
- Piperacillin
*Broader spectrum that ticarcillin
Name three Beta lactamase suicide inhibitors often paired with penicillins. What is their mechanism?
1) Clavulanic Acid
2) Tazobactam
3) Sulbactam

* Irreversibly bind to Beta lactamase enzymes.
~Weak antibiotics on their own
How toxic are penicillins? What circumstances?
Very Safe
- occasional anaphylaxis/mild hypersensitivity
- Fatal clostridial colitis in guiena pigs & rabbits due to loss of normal gut flora
What is the big advantage of Cephalosporins?
Resistant to Betalactamase enzymes
What are the key differences between the 4 generations of Cephelosporins?
1st Gen
- Good Gram + and anaerobes
- Moderate Gram -
- Orally available

2nd Gen (Cefuroxime)
- Similar to 1st
- better w/ E.coli, Klebsiella, Proteus

3rd Gen (Cefovecin, Ceftiofur)
- Reduced Gram + activity
- Excellent Enterobacteriaceae
- fair Pseudomonas

4th Gen (Cefquinome)
- Broad Spectrum
- Not destroyed by Beta lactamase producing spp.(Klebsiella or Pseudomonas)
What are the key Pharmacokinetics of Ceftiofur?
- No milk withdrawal, as it binds to acute phase proteins and doesn't readily cross into milk
- Highly protein bound -> increased t1/2
- Rapidly metabolize to active compound
Cephalosporins
- Mechanism of Action
- Post antibiotic effect & t1/2
- Vd
- Exclusions
- Excretion
- Same as penicillins (Bactericidal)
- None - Time dependent; short t1/2, frequent dosing required
- Same as penicillins
- Prostate, CSF, aqueous humor (except later generations)
- High concentration in urine & bile
How have the Pharmacokinetics of Cephalosporins changed in subsequent generations?
- Less oral bioavailability
- Glomerular excretion and tubular secretion
- Some de-acetylated in liver -> to active metabolites (ex: Cephalothin>>ceftiofur
Name a Cephalosporin that is good for UTI's, and skin and soft tissue infections in companion animals? What generation is it?
Cefovecin - 3rd generation

* Parentral Admin. only
* Tx every 14 days (long t1/2)
* Must keep refrigerated
Name two Cephalosporins used in Food Producing species and their key difference.
Good Gram - activity

* Ceftiofur (3rd gen) - highly PPB, hepatic metabolism

* Cefquinome (4th gen)
What antimicrobials were developed to deal with Beta lactase producing Gram - organisms? What are they used for?
* Carbapenems
* Monbactams

*** Saved for human medicine ***
Name five Aminoglycosides.
1) Streptomycin
2) Dihydrostrptomycin
3) Neomycin
4) Gentamicin
5) Amikacin
What are the structural properties and associated pharmokinetics of the Aminoglycosides?
- Big Bulky Sugars
- Polar

* Poorly absorbed from GI tract (Great for treating GI infection)
* Well absorbed with IM or SQ admin.
* Small Vd
Aminoglycosides
- Mechanism of action
* Inhibits protein synthesis
- Penetrates through bacterial cell membrane (requires 02)
- Binds to a non-enzymatic site on ribosome
- Alters codon/anticodon recognition
- defective bacterial protein is produced

* Induces RNA breakdown
* Damages cell membranes
* Effects DNA metabolism
Aminoglycosides
- Post antibiotic effect
Concentration Dependent
Why are Aminoglycosides synergistic with Beta lactams?
Beta lactams interfer with cell wall synthesis allowing the Aminoglycoside easier penetration into the cell.
Why do the Aminoglycosides bind to the non-enzymatic site on the bacterial ribosome?
Increases drug movement into the cell
Why is Aminoglycoside activity decreased by pus, inflamed tissue and abscesses?
The low oxygen environment blocks the oxygen dependent active transport of the drug into the bacterial cell.

Other factors include - low pH, divalent cations & hyperosmolar conditions
What is the spectrum of Aminoglycosides antimicrobial activity?
Narrow to Moderate Spectrum
- Some Gram +
- Mycoplasma
- Some mycobacteria (not Strep)

Relative Activity
Amikacin> Toramycin> Gentamicin> Neomycin> Streptomycin
Aminoglycosides Pharmacokinetics
- t1/2
- Vd
- PPB
- Excretion
* t1/2 - short (1-3hr)
* Small (<0.35l/kg)
* Low PPB (25%)
* Renal excretion unchaged
Why is alteration of dosing for Aminoglycosides more important that Beta lactams?
Aminoglycosides are excreted via Glomular filtration only. Impaired renal function will decrease rate of excretion - dose must be adjust for toxicity.
What type of bacterial resistance currently occurs for Aminoglycosides?
* Plasmid mediate resistance - coding for enzymes that deactive Aminoglycosides and prevent ribosomal binding
* Chromosomal mutation that alters binding site (Streptomycin)
Which Aminoglycoside is relatively free of resistance issues and why?
Amikacin
- infrequent use
What are the toxicity issues associated with Aminoglycosides?
* 8th Cranial Nerve Toxicity
- Vestibular
- Cochlear
* Nephrotoxicity
* Neuromuscular blockage (non-depolarizing)
* Collapse (IV Injection)
* Hypersensitivity
How does 8th Cranial Nerve Toxicity occur in Aminoglycosides and how does it manifest itself?
* Vestibular Toxicity (Reversible)
- damage to sensory cells of the labyrinth
- Issues with balance, ataxia, incoordination, nystagmus

* Cochlear Toxicity (irreversible)
- damage to sensory cells in the cochlea
What two drugs are most commonly associated with Vestibular Toxicity?
Aminoglycosides
1) Streptomycin
2) Dihydrostreptomycin
What four drugs are most commonly associated with Cochlear Toxicity? What can potentiate this?
Aminoglycosides
1) Streptomycin
2) Neomycin
3) Kanamycin
4) Amikacin

* Loop diuretics and other diuretics (Avoiding using together)
What four drugs are most commonly associated with Nephrotoxicity?
Aminoglycosides
1) Neomycin
2) Gentamicin
3) Kanamycin
4) Amikacin
What are the clinical signs of Nephrotoxicity?
- Acute tubular necrosis
- Proteinuria
- Hyaline & granular cast in urine

***Reversible IF caught early on via blood/urine sampling***
What causes collapse during IV administration of Aminoglycosides? How can this be avoided?
Decreased heart rate
Decrease cardiac output

* Administer slowly
How does the potential for Nephrotoxicity of Aminoglycosides affect the dosing regime of the drug?
A single injectable daily does will expose the kidneys to drug once a day. Interim time allows them to "recover" before next dose.
What are three important uses for Neomycin? Why is it not given parentrally?
Mastitis - Intramammary
Skin infection - Topical
GIT infection - Orally

* Too toxic for pareteral use
What drug is typically used to treat Actinobacillosis (TB)?
Streptomycin
Name two Aminocyclitols.
Apramycin
Spectinomycin
Apramycin
- Type of drug
- Active against
- Resistance
- Common use
Aminocyclitol Aminoglycoside
* Gram - (S. Aureus), some mycoplasma
* resist R-plasma mediated degradative enzymes
*Treatment for Gram - infections in calves/piglets
Spectinomycin
- Type of drug
- Mechanism of action
- Resistance
- Common use
Aminocyclitol Aminoglycoside
* Inhibition of protein synthesis at translocation step
* Chromosomal mutation confers resistance in bacteria
* Common Use - diarrhea in piglet, mycoplasma in poultry
Sulphonomides
- Mechanism of Action
- Spectrum
- Competitive inhibition of PABA, which inhibits the folic acid cascade. (Bacteriostatic)
- Broad Spectrum
What types of microbials do Sulphonmides cover?
- Gram +
- Gram -
- Chlamydophila
- Protoza

* NO Activity against Mycoplasma, enterococci, & Pseudomonas
Describe the three ways in which microorganisms have become resistant to Sulphonmides.
1) Chromosomal mutation
- impair penetration
- enzyme in folic acid cascade (Dihydropteroate) becomes insensitive to drug
- increase PABA production to out compete
2) Plasmid mediated
- impaired penetration
- Dihydropteroate becomes insensitive to drug
3) R Factor resistance (similar to streptomycin)
How are Sulphonamides administered? How can you improve their effectiveness in the lower GI tract?
- They can be administered in ANY way
- Being weak acids they are easily absorbed from the upper GI tract. A bulky amino nitrogen group can be substituted on the drug, which must be hydrolysed in the lower GI before being absorbed.
Sulphonamides
- Vd
- Penetration ability
- PPB ability
* Good Vd - can reach significant level in CSF
* Penetrate milk & synovial fluid
* Low PPB
How do Sulphonomides differ from Aminoglycosides & Beta Lactams in metabolization?
Sulphonomides are metabolized to less soluble, inactive compounds via acetylation (except dogs), glucuronidation & hydroxylation in the liver. Aminoglycosides & Beta Lactams are not metabolized.
How are Sulphonomides excreted? What is the main concern surrounding excretion?
* Sulphonomides are excreted by filtration & active tubular secretion, unchanged in the urine. Gut active sulphonomides are excreted in the feces.
Sulphonomides are capable of crystallizing in urine (especially acidic urine from carnivores) when solubility is exceeded. Alkalinisation of the urine enhances elimination & decreases ppt.
How can Renal Crystalluria be reduced in patients receiving Sulphonomides?
- Use of longer acting compounds
- Use of more potent drugs
- Using combinations of Sulphonomides as they have independent solubility properties.
What types of toxicity issues are associated with Sulphonomides?
1) Diarrhoea in ruminants (decreased flora)
2) Hemorrhagic Syndrome (Vit K antagonist)
3) Reversible non-spec. polyarthritis (Dobermans)
4) Keratoconjunctivitis sicca (Small breeds susceptible; 10-15% of animals develop dry eye)
5) Fatal arrhythmias w/ alpha2 agonists (horses) AVOID
6) Shoft shelled eggs (CaCl3 interference)
7) Diuresis
What local factors can affect to efficacy of Sulphonomides?
* Pus - Free thymidine & purines produce PABA
* Local Anesthetics (procaine) are PABA esters which can compete with Sulphonomides
There are five different Sulphonomide preparations that can be created, what are they?
1) Rapid onset, short duration
2) Rapid onset, long duration
3) Ocular
4) Lower GI (require hydrolysis)
5) Upper GI
Name four Diaminopyrimidines. Which one is most significant in Veterinary Medicine?
1) Trimethoprim ***
2) Ormetoprim
3) Baquiloprom
4) Pyrimethamine
Diaminopyrimidines
- Mechanism of Action
- Spectrum
- Inhibits dihyrofolate reductase (DHFR) in the folic acid cascade. (Baterioscidal)
- Spectrum varies on drug - some are better against bacteria, others against protozoa.
Trimethoprim
- Spectrum of activity
- Administration
* Broad Spectrum Bacteriostatic (via DHFR inhibition)
* Can be given orally, except with ruminants (drug degraded by flora)
What is the Vd for Diaminopyrimidines? Do they experience ion trapping?
* Vd good - lipid soluble
* Ion trapping readily occurs in the mammary gland and prostate are they are acidic and the drug is a weak base.
Why is Baquiloprim a better Diaminopyrimidines to give ruminants than Trimethoprim?
* Baquiloprim is not degraded by rumen flora and has a longer half-life than Trimethoprim.
* Is often give as a bolus to cattle in combination with Sulfonamide.
What known toxicities are there to Diaminopyrimidines?
Uncommon, but
Erythrocyte dysfunction due to folic acid deficiency. More common in humans and treated with folic acid.
Why is it advisable to use Diaminopyrimidines with Sulphonamides?
By using a combination it is possible to use 1/8 of the usual dose of Sulphonamides, reducing toxicity risks. Drugs are synergistic and bacteriacidal and resistance is lower.
What is the newest class of antibiotics? Name two.
Fluoroquinolones
- Enrofloxacin (Baytril)
- Ciprofloxacin
Nalidix Acid is a Quinolone like Fluoroquinolone. Why is Fluoroquinolone better?
Nalidix Acid is a narrow spectrum bacterialcidal with limited distribution and serious CNS side effects.
What are the positive qualities of Fluoroquinolones?
- Broad spectrum Bactericidal
- Good oral bioavailability
- Large Vd (lipid soluble)
- No plasma mediated resistance
Are there any toxic effects to Fluoroquinolones?
Arthropathy can occur in growing animals. Modification of use can avoid side effects.
Are Fluoroquinolones an acid or base?
Can be either, depending on environment. (Amphoteric)
Each group of the molecule provides a function, what are they?
- 6 Fluoro Group
- 7 Piperazine Group
- a Alkyl or Ring Group
- 6 Fluoro Group(Broad Spectrum)
- 7 Piperazine Group(Pseudomonas)
- a Alkyl or Ring Group (improved distribution)
Fluoroquinolones
- Mechanism of Action
- Post Antibiotic Effect
* Inhibits bacterial DNA gyrase, but is less effective against the analogous mammalian Topoisomerase (enzyme that breaks DNA during negative supercoiling & transcription).

* Concentration dependent (Once daily dosing)
What activity of Quinolones have bacteria become resistant to?
Fluoroquinolones enter bacterial cells via porins. Bacteria have been seen to reduce porin permeability as a form of resistance. Additionally, they can change the DNA gyrase structure.
** Plasmid mediated resistance is no believed to occur.
Fluoroquinolones are known as Broad Spectrum. What do they cover?
- Gram negative aerobes
- Gram positive aerobes
- Intracellular bacteria (due to lipid soluble nature)
- Mycoplasma
* Ciprofloxacin is good against mycobacteria
Fluoroquinolones are known to concentrate in specific tissues/areas. Which ones?
1) Lung & Bronchosecretions
2) Urine
3) Prostate
4) Bone
5) CSF
Name two antimicrobial groups that are good for treatment of prostate infections.
- Diaminopyrimadines
- Fluoroquinolones
What is meant by saying that a drug concentrates in a tissue?
The tissue can achieve higher concentrations than plasma.
Fluoroquinolones
- Bioavailability
- PPB
- Excretion
- High oral bioavailability (except in rumenant, perentral admin.)
- Low PPB
- Liver metabolism to active/inactive metabolite & kidney
***Enterohepatic Recycling may occur**
Why should Fluoroquinolones be avoided in young animals?
Erosion of weight bearing cartilage has been known to occur in dogs & cats. Dog are more susceptible, esp. Giant Breeds.
What toxicity concerns surround Fluoroquinolones?
* Decrease dosing in animals with renal impairment
* Erosion of weight bearing cartilage
* Avoid with other drugs requiring liver clearance (methylxanthines)
* Neurotoxicity - blindness in cat from Enrofloxacin

****Stick to recommended dose ranges*****
Name five Macrolides licensed for use in veterinary medicine.
1) Tylosin
2) Tilmicosin
3) Tiamulin
4) Spiramycin
5) Tulathromycin
Macrolide
- Mechanism of Action
Inhibits protein synthesis via binding to 50S subunit and inhibiting translocation..
What is the spectrum of activity for Macrolides?
Moderate
- Gram +
- Some Gram -
- Anaerobes
- Mycoplasma
- Some Chlamydophila
- Non-tubercular mycobacterial orgs.
How are Macrolides similar to narrow spectrum Penicillins?
Both can cover:
- Gram +
- Some Gram -
- Anaerobes
What types of resistance have come up against Macrolides?
* Chromosomal - but bacteria can revert back to sensitive if drug is removed.

* Plasmid mediated
- Change in drug binding site
- Decreased permeability
- Esterases which hydrolyse drug
Macrolides
- Solubility -> Metabolism
- Acid or Base -> Vd
* Which drugs have best Vd.
- Highly lipid Soluble
-> Hepatic Metabolism (to mostly inactive metab.)
- Basic
-> Large Vd
* Spiramycin & Tilmicosin
Marcrolides have a high Vd, how does this aid in their antimicrobial activity?
They are able to achieve high concentrations inside of Macrophages, which aid in the killing of an organism after phagocytosis.
What is the parent drug in the Macrolides and what are the potential routes of administration?

Are there any concerns surrounding Administration?
Erythromycin
- Oral or parentral
- Highly irritant with any type of administration.
What toxicity or side effects occur with Erythromycin?
- Parasympathomemetic effects, which induces vomiting in dogs.
- GIT disturbances in herbivores
What common diseases are treated with Erythromycin?
- Staph. aureus infections with Penicillin resistance
- R. equi pneumonia in foals (combine with rifampicin)
- C. jejni enteritis
Tylosin
- Type of drug
- Primary use
- Concerns
- Macrolide
- Used in food production species (leptospirosis, rickettsia, Mastitis, Bovine pneumonia)
- Similar toxicity to Erythromycin, irritant to tissues, DO NOT use in horses
Spriamycin
- Type of drug
- Positive qualities
Macrolide
- Concentration and Long persistence in tissues
Name a Macrolide that is commonly used in the Pig Industry. How is it administered?
Tiamulin
- Orally in feed
Tiamulin
- Activity
- Contraindications
- Resistance
- Mycoplasma & Anaerobes
- DO NOT feed with ionophores in pigs & poultry as may interfere with liver metabolism of ionophores, increasing their concentration and toxicity. DO NOT use in herbivores
- One way cross resistance with Tylosin (Resistance in Tiamulin=Resistance in Tylosin)
What can be used to treat Respiratory diseases like Mycoplasma, Pasteurella, Mannheimia, & Haemophilis in pigs & poulty?
Tulathromycin (Macrolide)
Name two Lincosamide drugs and their Mechanism of Action.
- Lincomycin (antibiotic)
- Clindamycin (Synthetic)

Inhibit bacterial protein synthesis via 50S subunit binding.
Lincosamide
- Spectrum of Activity
- Gram +
- Anaerobes (Clindamycin is best)
- Mycoplasma
How do bacteria confer resistance to Lincosamides? What other antimicrobial group does resistance effect?
* Chromosomal Mutation during treatment (not common)
* Plasmid Mediated (Common)
- Methylate ribosomal drug binding site.
* Macrolides
Why are Lincosamides in effective against Gram - bacteria?
- Impervious to drug entering
- Methylated ribosomal drug binding site.
What are the Pharmokinetics of Lincosamides?
- Acid/Base
- Adminstration
- PPB
- Vd
- Basic->ion trapping
- Oral & parentral admin.
- Highly PPB (as opposed to macrolides)
- Lipid Soluble->High Vd
Where are Licosamides likely to trap in the body?
- Udder
- Prostate
- Lung
- CSF (but not as high)
What areas are Licosamides able to penetrate in the body?
- CSF
- Bone
- Eye
- Synovial Fluid
Lincosamides
- Toxicity concerns for spp. and administration
- Highly toxic to herbivores.
- Can cause Colitis X in horses
- Cat/Dog relatively non-toxic
* Give slowly IV to reduce incidence of myocardial depression.
* Oral stricture from irritation via PO
Why are Lincosamides given with food or a warm water bolus to follow?
Oral stricture can occur from tracheal irritation due to contact with the drug.
What are three main interactions (positive and negative) with Lincosamides?
* Lincosamide/Spectinomycin - cattle respiratory disease
* Clindamycin synergistic with metronidazole against anaerobes
* AVOID use with macrolides or chloramphenicols as they are antagonistic (compete for binding site)
What antimicrobial can be used like Penicillin in patients who are hypersenstive to Penicillin?
Macrolides
Name two Tetracycline most commonly used in Veterinary medicine?
- Doxycycline
- Tetracycline
Tetracycline
- Mechanism of Action
- Unique characteristic
Inhibit bacterial protein synthesis by binding to 30S ribosomal subunit.

* Enters the bacterial cell two ways:
- Passive diffusion
- Active carrier-mediated transport
Tetracycline
- Spectrum
- Element that improves drugs performance
Broad Spectrum
- Gram +
- Gram -
- Mycoplasma*
- Chlamydia*
- Rickettsia*
- Protozoa*
- Spirochaetes*
*Primary Use

- Acidic pH improves activity
Minocycline has a greater activity that other Tetracyclines, what accounts for this?
- Higher Lipid solubility which leads to greater Vd.