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Flashcards in Antimicrobials Deck (62)

Name all the ways drugs achieve selective toxicity against bacteria

1. Disrupt DNA & Cell Division

2. Disrupt Protein Synthesis

3. Damage Bacteria's Plasma Membrane

4. Damage Bacteria's Cell Wall


5. Concentrate in Target Cells

6. Be a Pro-drug that's Activated Only in Target Cells

7. Administer Systemically Toxic Drug Only Locally


What are the ways that drugs can disrupt DNA & Cell division?

1. Interfere with topoisomerase II gyrase & topoisomerase IV supercoiling to prevent coiling of DNA: Fluoroquinolones, Nitroimidazoles.

2. Inhibit DNA-dependent RNA polymerase: Rifampin

3. Inhibit viral DNA polymerase: Acyclovir (NB anti-virus, not antibacterial)

4. Interact with DNA to cause chain breakage: Nitroimidazoles.

5. Prevent cell division by interfering with microtubule structure, thus mitosis, preventing cell growth: Griseofulvin (anti-fungal) & Benzimidazole

6. Disrupt DNA synthesis with nucleic acid analogue (base analogue): 5-Flucytosine aka Ancobon, used against yeast

Fluoroquinolones, Nitroimidazoles, Griseofulvin & 5-Flucytosine are more important.



What are ways drugs can disrupt protein synthesis?

1. Initiation of translation: Block tRNA binding to amino-acyl site on ribosome by binding to 30S subunit of ribosome - Tetracyclines.

2. Peptidyl-transferase step: Inhibit peptidyl-transferase step in protein synthesis, binding to 50S subunit of ribosome - Chloramphenicol.

3. Misreading of mRNA, leading to nonsense/truncated proteins - Aminoglycosides

4. Prevent peptide translocation on ribosome - Fusidic acid

5. Bump off peptide chain from ribosome during translocation - Macrolides

6. Prevent peptide elongation on the ribosome - Lincosamides

7. Cause distortion of amino-acyl/tRNA binding site & block production of peptide - Streptogramins


Name some antimicrobial drugs or drug groups that work by inhibiting or disrupting DNA synthesis and repair.

1. Fluoroquinolones & Nitroimidazoles - supercoiling, gyrase, transcription

2. Griseofulvin & Benzimidazole - prevent cell division by interfering with microtubule structure & mitosis

3. 5-flucytosine - analogue of DNA base Pyrimidine


Name the seven antimicrobial drug groups that work by disrupting protein synthesis. Think PROTEIN = CAT DIETS

Tired Cats Ate Fresh Meat Like Steak

1. Tetracyclines

2. Chloramphenicol

3. Aminoglycosides

4. Fusidic acid

5. Macrolides

6. Lincosamides

7. Streptogramins


Name antimicrobials that work by damaging or disrupting the synthesis of bacteria or fungi's cell membranes.

1. Polymyxins - destabilise membrane

2. Ionophores - form ion pores in membrane

3. Azoles - inhibit synthesis of ergosterol (anti-fungal)

4. Nystatin - binds to ergosterol, disrupting membrane (anti-fungal)


Which antimicrobials work by damaging the bacteria's cell wall ie., targeting peptidoglycans (remember fungi/yeast don't have cell walls). Name in chronological order of cell-wall formation.

1. Cycloserine: Inhibits initial peptidoglycan-formation step of D-ala chain

2. Bacitracin: Inhibits transport of early peptidoglycan subunits across membrane

3. Glycopeptides: Inhibit transport of later peptidoglycan chain across cell membrane

4. Beta-lactams (Penicillins & Cephalosporins) - Inhibit final step of X-linking of peptidoglycans polymer D-Ala-D-Ala  


Which antimicrobials work by concentrating in a target tissue?

Tetracyclines- concentrate strongly in bacteria vs. host cells, ie., good against intracellular pathogens. Tetracyclines disrupt protein synthesis by blocking tRNA binding to amino-acyl site on ribosome. They binds to the 30S subunit of the ribosome.


What are pro-drugs that are activated only when it's in its target cells?

1. Nitroimidazoles

2. Flucytosine converts to 5-fluoracil in fungal cells

3. Acyclovir is activated by viral kinases


What are some Fluoroquinolones?

Enrofloxacin (animals)

Naladixic acid (quinolone)




How do Fluoroquinolones work?

Nucleic-acid (DNA) synthesis inhibitors: Interfere with topoisomerase II gyrase & topoisomerase IV supercoiling to prevent supercoiling of DNA necessary for transcription.


Are Fluoroquinolones lipophilic? How is fluoroquinolone excreted? What are the side effects?

Highly lipophilic with ability to concentrate heavily in bacterial cells vs host cells. Despite being lipophilic, they are excreted unchanged in urine & bile. Side effects: Damage cartilage in growing animals esp puppies.


What are Fluoroquinolones used to treat?

Gram (+) cocci eg. Staphylococcus

“Difficult” Gram (-) Obligate anaerobes

Poor against infections involving Streptococci or enterococci


Name two antimicrobial drug groups that work by preventing bacteria from synthesizing folate, which they need for carbon metabolism.

1. Sulphonamides: PABA analogue / competitive inhibitor that prevents enzyme catalysis of PABA → folate

2. Trimethoprim - Prevents action of dihydrofolate reductase (DHR) to reduce FH2 to FH4 tetrahydrofolic acid for use as nuclei-acid building block.

Sulphonamide & Trimethoprim are best used together to interfere with both enzymes that catalyse usable folate.


Which antimicrobial drugs are highly hydrophilic, not metabolised by liver & thus pass unchanged in urine?

1. All the beta-lactams: Penicillin, Cephalosporin, Carbapenem.

2. Aminoglycosides (Gentamicin, Neomycin, Streptomycin, Tobramicin)

3. 5-Flucytosine


Which antimicrobial drugs are lipophilic and metabolised by liver but to varying degrees only and are thus excreted in urine &/or faeces?

1. Tetracyclines

2. Sulphonamides 

3. Potentiated sulphonamides

4. Fluoroquinolones - even though highly lipophilic


Explain the differences between beta-lactams in terms of resistance and sensitivity to beta-lactamase.

Beta-lactamase is an enzyme secreted by Staphylococci & Gram (-) bacilli such as E. coli. Some beta-lactams are sensitive to it & thus should not be used to fight Staph, while others are resistant & are effective in fighting Staph.

Beta-lactamase sensitive: Amoxycillin, Penicillin G NB NEVER give Penicillin G to guinea pig or it will die.

Beta-lactamase resistant: Cloxacillin, Cephalosporin, Amoxycillin + Clavulanic acid combo (*** Clavulanic aid INHIBITS beta-lactamase! & allows Amoxy to work)


Why would you choose Amoxycillin + Clavulanic acid to treat a kidney infection in a cat?

A kidney infection could be could be caused by Escherichia coli, a Gram (-) bacillus bacteria that can cause UTI. Beta-lactams such as penicillins & cephalosporins have wide spectrum activity to treat both Gram (+) & (-) bacteria. Also, since penicillins are very hydrophilic, they are filtered in the kidney unchanged, so they are still biologically active when they reach the urinary tract. Fluoroquinolones are also effective, with wide spectrum activity, against Gram (-) bacilli bacteria, and is filtered unchanged by the kidney even though it's lipophilic, but E. coli has shown some resistance to it with efflux pumps. 

Since E. coli secretes ß-lactamase, a ß-lactamase-resistant penicillin must be used. However, in order to avoid resistance, you could use Amoxycillin (broad spectrum), which is susceptible to ß-lactamase, along with clavulanic acid, which inhibits production of ß-lactamase but has no other antimicrobial qualities.


Why are drugs that target bacterial cells' cytoplasmic membranes have less selective toxicity than those that target the cell wall?

All bacteria have cytoplasmic membranes so it's non-selective to target them, while not all bacteria have cell walls of the same thickness (Gram-neg have thin walls, Gram-pos have thick walls).


To which antimicrobial group do the following antibiotics belong? Gentamicin Streptomycin Neomycin Tobramicin

Aminoglycosides. These disrupt protein synthesis (the hint is in "amino") by causing a mis-reading of the mRNA, leading to a nonsense code and/or truncated protein in translation. Aminoglycosides are cidal & filtered in kidney, excreted in urine. Effective against Gram (-) bacilli such as Pseudomonas aeruginosa, which is resistant to many other types of antibiotics.


Which antimicrobials undergo enterohepatic recirculation, and why is this important in their use?

Macrolides & Lincosamides undergo enterohepatic recirculation aka enterohepatic recycling: Recirculation of drugs from the liver to the bile, followed by entry into the small intestine, absorption by the enterocyte and transport back to the liver. This causes an increased drug effect, like another dose. Macrolides & Lincosamides are lipophilic, so they are metabolised by the liver & excreted in faeces. Macrolides & Lincosamides interfere with protein synthesis: Macrolides are big and bump off peptides from ribosomes during translocation while Lincosamides prevent elongation of the peptide chain.


What are the names of some Macrolides?

Erythromycin Tylosin (pigs, dogs) Tulathromycin Azithromycin (human)


What are some names of Lincosamides?

Clindamycin Lincomycin


Why are Macrolides effective against Gram (+) bacteria but not Gram (-)?

Macrolides are really big so they can't make it through the outer cell membrane. An exception is Azythromycin, used in human Gram (-) bacilli bacteria infections, which can enter the outer membrane. Macrolides are used more against Gram (+) cocci like Streptococci uberis, which causes mastitis, if beta-lactams don't work.


What antimicrobial drugs can be used to treat ringworm (Microsporum canis, a dermatophyte)?

1. Griseofulvin - Interferes with microtubule structure, thus mitosis, preventing fungal-cell growth. However, it is teratogenic. 2. Azole (eg. Ketoconaozole) - Inhibits synthesis of ergosterol & thus fungal-cell membrane. Also teratogenic.


Name 10 families of antimicrobial drugs.

1. Penicillins 2. Cephalosporins 3. Aminoglycosides 4. Macrolides & Lincosamides 5. Glycopeptides 6. Fluoroquinolones 7. Tetracyclines 8. Nitroimidazoles 9. Chlorampenicols 10. Sulphonamides & Potentiated Sulphonamides


Of the 10 families of antimicrobial drugs, which are cidal (kill bacteria)?

Five families are bacteriocidal: The beta-lactams are cidal: - Penicillin - Cephalosporins - Fluoroquinolones - Nitroimidazole - Aminoglycosides


Of the 10 families of antimicrobials drugs, which are static (inhibit growth)?

Five families are bacteriostatic: Most of those that inhibit protein synthesis are static except for Aminoglycosides: - Tetracyclines - Chloramphenicol - Macrolides & Lincosamides - Glycopeptides - Sulphonamides & Potentiated Sulphonamides


Which families of antimicrobial drugs ONLY have narrow-spectrum of activity?

Most drugs that inhibit protein synthesis have narrow spectrum except Tetracyclines & Chloramphenicol: - Aminoglycosides - Macrolides & Lincosamides and - Nitroimidazoles


Which families of antimicrobial drugs ONLY have broad spectrum activity?

- Tetracycline - Chloramphenicol - Cephalosporins - Sulphonamides & Potentiated Sulphonamides


Which families of antimicrobial drugs have BOTH broad & narrow spectrum of activity?

- Penicillins - Quinolones (narrow) & Fluoroquinolones (broad)


Penicillins are really the only main antimicrobial family that have both narrow and broad spectrum activity. Give examples in each spectrum.

Narrow: Penicillin G, Cloxacillin Broad: Amoxycillin


Cephalosporins are cidal beta-lactams that interfere with formation of the peptidoglycan polypeptide chain. Give an example of a cephalosporin, whether it's broad or narrow spectrum and what it can be used to treat.

Cephalexin is a broad-spectrum beta-lactam that can be used against Gram (+) & Gram (-) bacteria. It's also resistant to beta-lactamase, so can be used against Staphylococcus pathogens.


What do Fluoroquinolones & Nitroimidazoles have in common?

They both disrupt DNA transcription by interrupting topoisomerases responsible for unwinding and supercoiling of the DNA strands. They are both cidal; they work effectively against obligate anaerobes such as Clostridium & Actinomyces; Differences: Fluoroquinolones are broad spectrum. Nitroimidazoles are narrow spectrum and can only work against obligate anaerobes & nothing else. They are both highly lipophilic but Fluoroquinolones are excreted unchanged in urine.


Give an example of a pro-drug in the Fluoroquinolone family of antimicrobials.

Enrofloxaxin is metabolised in liver to Ciprofloxaxin


Which antimicrobial family is made up of amphoteric molecules? Ie., moderately hydrophilic and strongly lipophilic (water soluble & lipid soluble)



What does is the Minimum Inhibitory Concentration mean in terms of antimicrobial resistance?


MIC describes the sensitivity of a particular microorganism or group of organisms (eg., bacteria, yeast, fungi) to a drug. It is the minimum about of drug required to cause COMPLETE cessation of growth. It applies only to a given strain under standarised conditions.


What is Minimum Bacterial Concentration?

It is lowest concentration of antibiotic required to reduce the viability of bacteria by at least three logs, so that less than 0.1% of the viability remians.

It refers to the amount of drug that can reduce the viability of bacteria by at least three logs. Disinfectants use MBC to claim they kill 99.9% of household germs (bacteriacidal).

It's used less than MIC (Minimum Inhibitory Concentration).


Antimicrobial drug A has a very high MIC50 and high MIC90 against Bacteria X.

Antimicrobial B has a low MIC50 and a very low MIC90 against Bacteria X

Which antimicrobial drug is more effective against Bacteria X? 

Drug B. 

MIC50 & MIC90 are the minimum concentrations of drugs expected to inhibit 50% & 90% of bacterial isolates, respectively. Ie., lower concentrations of Antimicrobial B would inhibit the growth of  50% & 90% of the whole range of strains of Bacteria X.

From perspective of bacteria, MIC50 & MIC90 indicate relative sensitivity of a particular species for a given antimicrobial drug.


What are the two main types of antimicrobial resistance? 

Innate & Acquired



What is innate resistance & give examples.

A bacteria's innate resistance to an antibiotic drug is a result of its natural insensitivity, due to its structure. Primarily, innately resistant bacteria are protected by having NO cell wall or by having outer membranes. 

Remember that Gram (+) bacteria have thick cell walls & are thus targeted by drugs that block formation of the peptidoglycan cell wall, as Cycloserine, Bacitracin, Glycopeptides & the ß-lactams, Penicillins & Cephalophorins. The most widely used with wide spectrum are the hydrophilic ß-lactams.

Gram (-) bacteria have outer membranes & only thin cell walls.

1. Mycoplasma - has no cell wall/peptidoglycan target, thus naturally insensitive to ß-lactams

2. Escherichia coli - Gram (-) with outer membrane that keeps out big molecules, thus insensitive to Macrolides

3. Enterobacteria, such as Salmonella & E. coli, are Gram (-) bacilli, with outer membranes that are resistant/insensitive to Penicillin G, which is non-polar & hydrophobic, thus repelled by the membrane, unable to penetrate porins. Other penicillins such as Ampicillin are more hydrophilic, polar, thus able to penetrate porins. 




How do bacteria develop acquired resistance (three ways)?

It's resistance that develops from mutation - simple genetic changes in DNA that occur spontaneously, & NOT in response to the drug. Selection occurs in response to the drug, but that's not the same as mutation, which occurs first & independently of the drug.

Three types of mutation that cause resistance:

1. Altered ribosome structure

2. Decreased permeability

3. Alteration of target enzyme


Give examples of the three ways in which bacteria MUTATE to develop acquired resistance to antibiotics.

1. Altering ribosome structure: Streptomycin resistance

Mutation causes ribosome to RE-DISTORT mis-reading of mRNA, caused by Streptomycin, indirectly back to normal, so protein synthesis proceeds normally. Streptomycin is an Aminoglycoside. This mutation is pretty rare.

2. Decreased permeability: Tetracycline resistance

Mutation causes bacteria to prevent Tetracycline from getting in, reducing the concentration (Tetracycline works by concentrating in target cells/tissue). MIC increases, need to increase dose, causing resistance. 

3. Altering target enzyme: Sulphonamide resistance 

Mutation of dihydropteroic acid synthetase, so active sites binds PABA more effectively than Sulphonamide, which then can't go on to prevent catalysis of PABA to folate. The altered enzyme competitively inhibits Sulphonamide. 


Give three ways in which bacteria that INHERIT NEW GENES develop antimicrobial resistance?

1. Inactivating enzymes: New genes produce "inactivating enzymes" that don't catalyze the drug to work

ß-lactamases - "the bottom falls out of the garage" when new genes turn penicillin into peniciolloic acid

Chloramphenicol acetyl transferase & Aminoglycoside O-phosphotransferase

2. Efflux mechanism: Active transport (pump) of drug out of bacterial cell

Tetracycline pumped out of bacterial cell - concentration too low inside so A-site on ribosome is free to bind to amino-acyl-tRNA

3. Bypass mechanism - Plasmid encodes new target enzyme that can't easily be inhibited by the drug.

Sulphonamide resistance: Plasmid-encoded dihydrofolate reductase (DHFR) enzyme encoded has lower affinity for sulphonamide, so inhibition of NATURAL DHFR is bypassed & FH4 is synthesized.


What is MRSA? 

Why is it important?

Methicillin-Resistant Staphylococcus Aureus

Normally S. Aureus, a Gram (+) cocci, is naturally resistant to penicillin & ampicillin, which are sensitive to ß-lactamase. However it is also NORMALLY SENSITIVE to cloxacillin, flucloxacillin & methicillin, which are NOT SUSCEPTIBLE to ß-lactamase. Normally, these bind to transpeptidase enzyme on D-Ala-D-Ala polypeptide & together block formation of peptidoglycan cell wall.

But MRSA produces MecA transpeptidase, which has a higher affinity to the polypeptide than regular transpeptidase for the drug, so it doesn't bind to the drug. Ie., the drug doesn't work. 


What is Fluoroquinolone resistance?

Fluoroquinolones work by disrupting DNA transcription (gyrase & supercoiling disruption) & therefore synthesis & repair. It is a wide-spectrum, fluorinated form of the quinolone, Nalidixic acid. Generally they have low toxicity and very low MIC, ie, very effective. Examples are Enrofloxaxin, which is metabolised to Ciprofloxacin. 

Basically, since it was so successful, it was overused in the 1990s instead of being held back for difficult infections. 

MUTATION alters the target enzymes, DNA gyrase & topoisomerase enzymes in the bacteria, so they become less inhibited by Fluoroquinolones. Some of this resistance is transferable on plasmids.

Some bacteria develop, through genetic modification, efflux pumps that expel drug out of bacterial cell: Staphylococcus (eg. S. intermedius), Pseudomonas & E. Coli



What is an effective drug combination for overcoming antimicrobial resistance in Gram (-) bacilli bacteria or Gram (+) cocci bacteria to Cloxacillin, Methicillin & other drugs that are usually insensitive to ß-lactamase?

Amoxicilllin + Clavulanic Acid.


Amoxillin (eg., Synulox) is susceptible to ß-lactamase but has wide-spectrum activity against Gram (+) & Gram (-) bacteria. 

Clavulanic acid inhibits production of ß-lactamase, which is secreted by Gram (-) bacteria such as E. Coli, allowing Amoxicillin to work.  


What is VRE in terms of antimicrobial resistance & why is it important?

Vancomycin-Resistant Enterococci. 

These refer specifically to Gram (+) Streptococci that cause enteric disease, ie., S. faecium & Enterococcus faecalis.  

DO NOT confuse with Enterobacteria, which refer to Gram-negative bacilli such as Salmonella & E. coli.

Normally, Gram (+) cocci are susceptible to Vancomycin, the main drug in the Glycopeptide family (disrupts peptidoglycan cell-wall synthesis). However, some enterococci have become resistant, and can't be treated by anything.


An English Bulldog dog enters your clinic pyoderma in its skin folds, showing red pustules on the skin. You swab some of the pus and pustules & grow it on culture, finding the colonies are Gram (+) cocci. 

Then you do a catalase test, which comes out positive, so it's Staphylococci. 

To determine its virulence, you subject it to a coagulase test, which also comes back positive. What is it likely to be?

A virulent (coagulase-positive) Staphyococci that infects dogs would be S. intermedius (the human version is S. aureus). It causes canine pyoderma.


Having determined a dog with pyoderma has Staphylococcus intermedius, how would you treat it?

1. Determine the sensitivity of the S. intermedius to antimicrobials in culture. 

2. Determine how deep the pyoderma is using histological and clinical exam; deeper infections might need higher dosages & longer treatments.

3. First-time bacterial pyoderma can be treated with empiril antibiotic therapy with Lincomycin or Clindamycin (both Lincosamides), or Erythromycin (a Macrolide). Empiric means an initial therapy before firm diagnosis is made of disease. DO NOT use Fluoroquinolones, such as Enrofloxacin or Ciprofloxacin, for empiric therapy. 

4. Surface pyoderma may be treated with topical therapy:

- 2% mupricin (protein-synthesis inhibitor) ointment, but note this is not effective against Gram (-) bacteria

- Neomycin (Aminoglycoside) is more likely to cause a contact allergy, so don't use it; Bacitracin (cell-wall-synthesis inhibitor) & Polymyxin B (cell-membrane disrupter) are inactivated in purulent exudates & more effective against Gram (-) 

5. Deep pyoderma requires systemic antibiotics for 21-30 days

- Erythromycin (Macrolide), ß-lactamase-resistant penicillins (Cloxacillin) & cephalsporins (Cephalexin) can be used; they are bacteriacidal and time-dependent, as long as MIC is maintained.

- Azythromycin (Macrolide) is cheap & has more efficacy against Gram (-) than other Macrolides but can cause V&D

- Tylosin (Macrolide) has 90.5% efficacy in dogs with S. intermedius pyoderma, esp. deep pyoderma



What are three signs of Bovine Mastitis?

1. Drop in milk yield

2. Increase in somatic cell count 

3. Inflammation of udder/teats


If you suspect a cow has bovine mastitis, you culture the milk sample & learn she is infected with Streptococcus uberis. How would you treat the disease? Locally or systemically?

1. Intramammary administration (local) of antimicrobial is the most common treatment method. It has the advantages of high concentration in target site & low systemic consumption. Disadvantage is uneven disribution about the udder. Typically intramammary preparations combine 2 or 3 antibiotics to achieve synergistic action.

2. Systemic, or parenteral treatment should be distributed better throughout the udder. Disadvantages are 1) the pharmacokinetics of the drugs after systemic admin are reduced as ruminants eliminate them very quickly & the drugs' half-lives are very short; 2) difficult to achieve & maintain therapeutic concentrations; 3) S. uberis is best killed off by long-term treatment via intramammary (local) infusion

3. ß-lactams such as Penicillins & Cephalosporins are drugs of choice, followed by Macrolides (Erythromycin, Azythromycin) & Lincosamides (Clindamycin, Lincomycin), which are intracellularly active

4. Don't use Penicillin G as it penetrates weakly into mammary gland (it's a weak acid) 

5. Other broad-spectrum antibiotics such as Tetracyclines & Fluoroquinolones have disappointing results


A group of calves show signs of pneumonia. What are the four main pathogens causing BRDC (Bovine Respiratory Disease Complex)?

1. Mannheimia haemolytica - Gram (-) bacillus, oppotunistic, secretes leukotoxin & causes fibrin buildup, influx of inflammatory cells, haemorrhage in host tissues

2. Pasteurella multocida - Gram (-) bacillus, causes atrophic rhinitis in pigs via osteolytic toxin, hyaluronic capsule, found in mouth of many animals, pathogenic & opportunistic

3. Histophilus somni (not studied by us)

4. Mycoplasma bovis (mild) - Gram (-) with no cell wall, very tiny bacterium


With bovine bronchopneumonia & BRDC (bovine respiratory disease complex), remember to treat early, treat long enough, & use the right antibiotics. With a clear diagnosis from culture that Mannheimia haemolytica &/or Pasteurella multocida are responsible, how would you treat a group of sick calves?

1. Use only one antimicrobial at a time when treating cattle.

2. Ensure proper shelter & nutrition, & supportive therapy such as oral fluids.

3. When choosing method of admin, note that the drugs need to get past bronchial secretions & penetrate the stratefied columnar epithelium layer of the bronchi

3. Macrolides (Erythromycin, Azythromycin) are good because they accumulate in high concentrations many tissues such as epithelial lining fluid & easily enter the host 

4. Penicillins & Oxytetracyclines are used at higher dose to prevent resistance


A seven-year-old female Golden Retriever comes into clinic with fever & incontinence. You suspect UTI & take a urine sample via cystocentesis. Why do you use cystocentesis?


Cystocentesis is a veterinary procedure where a needle is placed into the urinary bladder through the abdomen of an animal and a sample of urine is removed. Diagnostic cystocentesis is used to prevent sample taken for urinalysis from being contaminated with bacteria, cells and debris from the lower urogenital tract. 


After using cystocentesis to take a urine sample from a dog that is incontinent, how do you culture it to determine it has UTI?

Canine UTI is commonly caused by E. coli (Gram-negative bacillus) in the urinary tract. E. Coli, as an enterobacteria, ferments glucose & can grow on MacConkey agar as it can withstand bile salts found in the gastrointestinal tract. You would conduct a bacterial count after incubating the culture on both blood agar and MacConkey for 18 hours at 37C, in an aerobic environment (E. coli is facultatively anaerobic). 

If there are more than 100,000 CFUs (colony-forming units) per mL of one single type, then you can confirm a Urinary Tract Infection.


Which antimicrobials would you use to treat UTI in a female dog?

1. Penicillins such as Amoxicillin & Ampicillin (broad-spectrum) work well as they are bacteriacidal & relatively non-toxic.

2. Amoxicillin has high bioavailability in dogs and cats & better absorbed by GIT than Amipicillin

3. Amoxycilllin + Clavulanic acid even better for UTI caused by E. coli, Klebsiella & Staphylococci that secrete ß-lactamase

4. Fluoroquinolones are the only antimicrobials that work against Pseudomonas aeruginosa-caused UTI


List therapeutic failures in treatment of canine UTI that result in relapses or re-infection.

RELAPSES - infection by same species of bacteria shortly after discontinuing therapy

1. Inappropriate choice of antibiotic.

2. Development of bacterial resistance.

3. Mixed causes of UTI in which all organisms were not eliminated due to inadequate dosage concentration to reach possible sequestered infection (in prostate or nephrons, eg) or poor client compliance.

REINFECTION - recurrent infections caused by different species

1. Impaired bacteriostatic nature of urine (glucosuria)

2. Disruption of uroepithelial layer

3. Reduced immunocompetence

4. Altered urethral function (structure) & urinary retention

5. Chronic antimicrobial therapy required to prevent further episodes


What is an MSA plate and what is it used for during microbial culture?

Mannitol Salt Agar

It contains 6% NaCl. 

Only Staphylococcus will grow on MSA plate.

If yellow colonies appear, that means the mannitol sugar is fermented, a positive identification for Staphylococcus Aureus.


What is an Isosensitest?

It's a sensitivity test to identify which antimicrobial drugs a microorganism is sensitive to. 


You've identified through culture (yellow colonies on Mannitose Salt Agar plate), catalase test (positive) and coagulase test using dog plasma (positive for coagulation) that you have a sample of Staphylococcus Aureus. 

Why would you then submit it to an Isosensitest with Oxacillin? 

To test for MRSA (methicillin-resistant S. aureus).

Oxacillin is a ß-lactamase-insensitive penicillin, like methicillin, that should be effective against S. aureus. If it's resistant to Oxacillin, then it will be resistant to methicillin & will thus be MRSA.


How do you "fix" fresh bacteria to view under a microscope (not Gram-staining)?

1. Place a drop of saline on slide

2. Mix sample from loop or toothpick into saline, spread thinly over slide.

3. Heat over bunsen burner.

4. Add Methylene Blue stain for 15 seconds & rinse off.

5. Observe by oil immersion (x100)

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