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Bacteriology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Basics of Chlamydophila psittasi (Psittacosis or Ornithosis)

A
  1. obligate parasite of intestinal and respiratory tract of birds
  2. obligate intracellular
  3. gram (-)
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2
Q

Encounter, Pathogenesis, Damage of Chlamydophila psittasi (Psittacosis or Ornithosis)

A

ii. Encounter
1. asymptomatic adult bird carriers
2. doesn’t replicate in environment, but elementary bodies can persist & expose via aerosol
iii. Pathogenesis
1. local spread in intestinal and upper/lower respiratory epithelium ->
2. receptor mediated endo/phagocytosis into epithelial cells and macrophages 
->
3. phagolysosomal fusion is inhibited ->
4. differentiate into elementary bodies and lyse cells releasing elementary bodies to invade new cells
iv. Damage
1. Endotoxin release -> cell lysis -> severity dependent on age of bird, species of bird, virulence of strain

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3
Q

Immunity against, diagnosis, treatment & prevention for Chlamydophila psittasi (Psittacosis or Ornithosis)

A

v. Immunity
1. Cell mediated by T cells is most important
vi. Diagnosis
1. REPORTABLE (health concern for bird owners)
2. Cloacal swab & antigen ELISA
3. Serology of antibody
4. Necropsy
vii. Treatment
1. Tetracycline!
viii. Prevention
1. Quarantine of affected birds
2. Imported birds treated prophylactically
3. sanitation

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4
Q

3 Types of anti-microbials

A
  • synthetic anti-metabolites
  • natural products of bacteria & fungi (bacteriocins)
  • natural products of higher eukaryotes
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5
Q

Antibiotic Vs Antimicrobial

A

Antibiotics
a. substance produced by a microorganism that inhibits or kills other microorganisms, but causes little or no damage to the host

Antimicrobial
a. Any substance of natural or synthetic origin that inhibits or kills a microorganism, but causes little or no damage to the host

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6
Q

6 Questions to ask when selecting antibiotics

A

a. Is dz infectious?
b. Is dz bacteria caused?
c. Which antibiotic works for this bacteria?
d. Will the antibiotic penetrate the site of infection?
e. Is the antibiotic toxic to the patient?

f. Will antibiotic use promote development of resistance?

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7
Q

Bactericidal Vs Bacteriostatic antibiotics

A

bacteriostatic:
i. reversible inhibition of bacterial growth

bactericidal:
i. irreversible inhibition of bacterial growth (usually bacterial lysis)

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8
Q

Examples of Antibiotics that can be both static & cidal

A

a. chloramphenicol is usually bacteriostatic but is bactericidal at high doses 

b. penicillin is cidal at recommended doses, but static at low doses 


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9
Q

When are bactericidal drugs preferred

A

a. immunosuppressed or immunodeficient animals 


b. infections such as endocarditis or meningitis where reliance on an inflammatory response can be detrimental 


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10
Q

Why use multiantibiotic therapy?

A

a. Obtain synergistic effect
b. Prevent or delay emergence of persistent organisms
c. Treat polymicrobial infections
d. Treat serious infection before pathogen is identified

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11
Q

4 Potential effects of antimicrobial combinations:

A

a. indifference: combined antibiotics are no more effective than the more effective antibiotic used alone.
b. additive: combined action is equal to the sum of the actions when used alone
c. synergism: combined action is significantly greater than the sum of both effects (ideal)
d. antagonism: combination is less effective than individual

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12
Q

Why not to use cidal and static drugs together?

A

Drugs antagonize each other = less effects of both

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13
Q

Describe the difference between obligate parasite, obligate pathogen, opportunistic pathogen, extracellular pathogen, facultative intracellular pathogen and obligate intracellular pathogen.

A

Obligate parasite:
- can only persist & replicate on mucus membranes

Obligate pathogen:
- exogenous pathogen

Opportunistic pathogen:
- endogenous flora that causes disease when there is opportunity

Extracellular pathogen:
- replicates and survives outside of host cell

Facultative intracellular
- can replicate inside or outside of host cell

Obligate intracellular
- replicates and survives inside of host cell

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14
Q

Bordatella bronchseptica (kennel cough) Basics, entry, spread, damage, diagnosis, treatment, prevention

A
  • Exogenous obligate pathogen
  • extracellular
  • gram (-)
  • highly contagious (inapparent carriers)

Entry

  • coughing & sneezing
  • Pili attach to but don’t penetrate ciliated tracheal epithelial cells 


Spread

  • Localized to mucosal surface
  • Cause pneumonia in cats & others but not dogs (unless underlying issue

Damage

  • Endotoxin: fever
  • cytotoxin (exotoxin): damages ciliary epithelium = ciliostasis = inflammation = coughing
  • Adenylate cyclase (exotoxin): inhibits phagocytes = facilitates multiplication & spread

Diagnosis
Dry hacking cough

Treatment

  • Usually self-limiting (IgA)
  • does not require antibiotics unless pneumonia
  • Supportive care

Prevention
- Improved ventilation, reduce exposure, Vx, sanitation

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15
Q

Vaccines available for Bordatella bronchseptica (kennel cough)

A

systemic bacterin:

  • IgG to B. bronchiseptica

  • Less protective
  • included w/ vx for parainfluenza virus, adenovirus-2, & distemper

intranasal vaccine (live avirulent strain)

  • elevates local IgA
  • Blocks binding of bacteria to cilia 

  • available for cats
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16
Q

Basics of Bovine Shipping Fever & associated bacteria

A
  • Growing, non-immunized calves after arrival @ feedlot
  • Due to stress, mixing of cattle, poor nutrition, poor ventilation
  • Many viruses + Mannheimia involved
  • Mannheimia: Normal flora, extracellular, gram (-), obligate parasite (must live on mucus membrane, short survival in environment),
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17
Q

Entry & Spread of Bovine Shipping Fever (Mannheimia)

A

Entry
- Decreased immune competency due to stress (normally phagocytized)
Inhaled into trachea & bronchioles

Spread

  • Gain entry to lung due to viral infection/damage
  • Inhabit ventral portions of cranial lung lobes
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18
Q

Mannheimia Virulence 4 Factors

A

Fimbriae:
- enhances colonization

Polysaccharide capsule:
- Inhibits phagocytosis

Endotoxin:

  • alters bovine leukocyte function

  • can cause vasculitis and associated thrombosis

Leukotoxin (exotoxin):

  • cell lysis of leukocytes and platelets
  • destroys immune cells,-> tissue necrosis
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19
Q

Diagnosis of Shipping Fever

A
  • History of exposure to stress factors and sudden onset of respiratory disease (clinical signs w/in 7-14 days after arrival in feedlot)
  • Lung tissue or blood from septicemic animals
  • collect Trans-tracheal wash & culture
  • cytology: degenerate neutrophils w/ gram (-) rods
  • bacterial culture for antibiotic sensitivity 

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20
Q

Treatment & Prevention of Shipping Fever

A

Treatment

  • acute pneumonia - antibiotics will reduce incidence of mortality and development of chronic pneumonia if treated early 
(Oxytetracycline)
  • chronic pneumonia – Treatment is of little value 
due to permanent lung damage

Prevention

  • Maximum immunity & minimum stress
  • minimize multiple sources of cattle 

  • vaccinate 3 weeks prior to transport
  • minimize transport stress 

  • segregate upon arrival and feed highly palatable feed 

  • Mannheimia (Pasteurella) bacterins are not very effective
  • New bacterin/toxoid Vx effective against leukotoxin
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21
Q

Similar Conditions to Shipping Fever in other Species

A
  • Canine infectious respiratory Disease Complex (CIRDC)

- Feline Lower Respiratory Tract Infection

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22
Q

Compare Penecillins Group 1, 3, 4, 5: Do they work on gram (-) or gram (+)? Are they resistant to β-lactamase?

A

Group 1 Gram (+) Not resistant
Group 3 Gram (+) resistant
Group 4 Gram (+) & Gram (-) not resistant
Group 5 Gram (-) resistant

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23
Q

Penicillins (Group 1): Basics

A

a. Bactericidal
iii. Narrow window against gram (+) anaerobes
vi. Killed by beta-lactamases & acid hydrolysis
viii. not taken up by cells
viii. New generations less susceptible to acid hydrolysis

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24
Q

Sites of action of antibacterial drugs

A

a. Inhibitors of cell wall synthesis
b. Inhibitors of protein synthesis
c. Inhibitors of nucleic acid synthesis

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25
Q

ß-lactam antibiotics: site of action, example drugs, bactericidal or static, structure, action

A

inhibitors of cell wall synthesis

a. penicillin, cephalosporins, carbapenems, monobactams 

b. bactericidal
c. high therapeutic index

Structure

i. ring structure
ii. enzymes that catalyze hydrolysis of beta-lactam bond

Action
e. inhibit final cross-linking of peptidoglycan in cell wall formation

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26
Q

Beta-lactams (beta-lactamase inhibitors): drug examples, cidal or static, work against gram (+) or (-)

A

a. Cephalosporins and Cephamycins
b. Bactericidal
c. greater resistance to ß-lactamases
d. improved penetration of membranes 

e. work against gram (+) and Gram (-)
f. can be used in penicillin-allergic individuals

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27
Q

Differences between generations of beta-lactams

A

1st Gen (Pen G) - gram (+)
2nd Gen - gram (-) or (+)
3rd Gen- gram (-) more than (+)
4th Gen (Beta-lactmase inhibitors) - gram (-) or (+)

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28
Q

Glycopeptides; drug, cidal or static, mechanism of action, gram (+) or (-)

A

a. Vancomycin
b. Bactericidal
c. blocks cell wall synthesis 

d. effective against Gram positive bacteria 
(especially cocci)
g. is not taken up by cells
h. should be reserverd for serious resistant infections in humans!!

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29
Q

Antibiotics that block protein synthesis

A
  • Tetracyclines
  • macrolides
  • chloramphenicol
  • aminoglycosides
30
Q

Tetracyclines; cidal or static, mechanism, work against

A

i. Bacteriostatic
ii. inhibit protein synthesis
iii. broad-spectrum
iv. negative effect on normal flora
b. Can enter cells

v. resistance is widespread among bacteria due to plasmid encoded membrane pump

31
Q

Aminoglycosides; cidal or static, mechanism, work against

A

i. Bactericidal
ii. inhibits protein synthesis
iii. aerobes
Iiii. Do not penetrate cells
iv. resistance in older aminoglycosides is widespread

32
Q

Macrolides / Lincosamides; static or cidal, mechanism, drugs, active against, special treatment considerations

A

i. Bacteriostatic
ii. inhibit protein synthesis
iii. Erythromycin (macrolide)
iv. Clindamycin (lincosamide)
v. Gram (+), mycoplasmas, anaerobes
ix. Resistance is common 

x. do not use in horses or rabbits!
xi. use for wounds, abscess, periodontal Dz

33
Q

Chloramphenicols

A

i. Bacteriostatic
ii. inhibit protein synthesis
iii. can’t use in food animals (florfenicol can)
iv penetrates cells
iiv. broad spectrum

34
Q

Antibiotics that inhibit nucleic acid synthesis

A
  • quinolones/fluroquinolones
  • sulfonamides
  • trimethroprim / ormetoprim
  • rifampicin
35
Q

Quinolones / Fluroquinolones

A

i. Bactericidal
ii. inhibit nucleic acid synthesis
iii. aerobes, facultative anaerobes, rickettsia, mycoplasmas
vi. Penetrate mammalian cell

36
Q

Sulfonamides

A

i. Bacteriostatic
iii. Inhibit nucleic acid synthesis
iv. broad spectrum 

v. ineffective in the presence of pus or necrotic tissue
vi. Resistance widespread, but overcome by combining sulfonamides with trimethoprim 


37
Q

Trimethoprim / Ormetoprim

A

i. Bacteriostatic

ii. Bactericidal when combined w/ sulfonamides

38
Q

Rifampicin

A

i. Bactericidal
ii. Inhibits nucleic acid synthesis
iii. Gram (+) bactereia 

iv. Used in combo w/ others to avoid resistance

39
Q

Constituative Vs Acquired Resistance

A

constitutive resistance:
• bacteria resistant to antibiotics because they normally lack the uptake systems or targets of the antibiotics
• not related to prior exposure to antibiotics
• ex: Penicillin G cannot enter members of the family Enterobacteriaceae

acquired resistance:
• bacteria become resistant to antibiotics by mutation resulting in alteration of uptake systems or targets of the antibiotics
• dependent on prior exposure to antibiotics 

• ex: Staphylococcus aureus resistance to penicillin G (due to bacterial production of enzymes that inactivate penicillin)

40
Q

3 Mechanisms of acquired resistance

A

Alter the target for the drug

Alter uptake of drug

Inactivate drug

41
Q

Multi-antibiotic resistance Vs cross-resistance

A

multi-antibiotic resistance
• presence of different mechanisms of resistance 

• antibiotics must be in different classes (aminoglycosides Vs penicillin)

cross-resistance
• resistance to one antibiotic implies resistance to others due to common mechanisms 

• antibiotics in same class

42
Q

Acquired Resistance via DNA Mutation

A
  • Usually lethal
  • When not lethal result in:
  • Disadvantageous = loss of mutant from pop
  • No advantage = mutant in pop in low levels
  • Selective advantage = resistant to host defense & antibiotics = growth until dominant in pop
43
Q

Acquired Resistance via Genetic Transfer

A
  • Done by transduction or conjugation
  • Transfer of DNA (resistance genes) between bacteria
  • Responsible for multi-antibiotic resistance

Transduction
• transfer of DNA following infection with a bacteriophage
• bacteriophage inserts its genetic material into bacterial chromosome

Conjugation
• direct interbacterial transfer of DNA (plasmid) thru sex pilus
• plasmids (extrachromosomal DNA): encode mechanism of antibiotic resistance
• plasmids transferred horizontally
• plasmid transfer uncommon in gram (+)
• transfer of chromosomal genes when plasmids obtain chromosomal genes using transposons 


44
Q

Selecting antibiotics effective against bacteria

A
  • Gram related spectra 

  • History of sensitivity


in vitro sensitivity
• shows which antibiotics not to use
• obligate anaerobes, obligate intracellular, & slow growing bacteria not suitable for routine testing

in vitro susceptibility testing
• MIC: min conc. of antibiotic that completely inhibits bacterial growth
• disk diffusion (Kirby-Bauer) test provides an estimate of MIC: the diameter of the zone of inhibition is inversely proportional to the MIC 


3 categories of results for MIC
o susceptible
o moderately susceptible
o resistant

45
Q

UTIs in Dogs

A

o Lower UTI (cystitis) most common

Most frequent pathogens
•	Most common (75%)
•	E. coli
•	Proteus
•	Klebsiella
  • Less common
  • Staphylococcus psuedintermedius/aureus
  • Streptococcus
  • Pseudomonas
  • Any bacteria
  • Fungus
  • May see candida w/ long-term antibiotic use
46
Q

UTIs in Cats (common pathogens)

A

o Less common than dogs

Most common pathogens
•	E. coli
•	Proteus
•	Staphylococcus aureus
•	Pasturella multocida
47
Q

UTIs in Horses

A

o Uncommon

Most common pathogens
• E. coli
• Staphylococcus aureus
• Streptococcus

48
Q

UTIs in cattle, cheep, pig

A

o Uncommon
o E. coli most common

periparturient cows:
o Corynebacterium pilosum & C. cystitidis

49
Q

Encounter, Spread, & Immunity for UTIs

A

Encounter
o Normal flora of lower urinary tract (opportunistic)

Spread beyond lower urinary tract (Pyelonephritis)
• Ascend ureters & colonize renal pelvis
• = pyelonephritis (very serious condition)
• can result in renal damage & loss of function

Immunity
• Limited Ab & cell mechanisms
• No immunity following UTI

50
Q

Bacterial entry & reasons for entry in UTI

A

o Ascending from exterior
o Colonization of urinary tract
o Usually limited to urethra & caudal bladder (uncomplicated cystitis)

Due to breakdown of urinary defenses
•	Urinary stasis
•	Mechanical block of flow
•	Damage to epithelial surface
•	Late gestation
•	Bacterial factors
•	Diseases that cause decreased osmolarity
51
Q

Diagnosis of Lower UTI: tests & rule-out differentials

A
  • Abdominal pain or painful urination
  • Small firm bladder

Dysuria (frequency (pollakiuria), blood, etc)
• Blood at beginning = urethra
• Blood at end = bladder

Rule-outs
• Urethrocystitis
• Pyelonephritis
• prostatitis

Tests
• Urinalysis
• Microscopic exam

Bacteriologic culture of urine from cysto
• If UTI, will see WBCs

52
Q

Most likely bacteria if acidic or alkaline urine w/ rods, cocci, or coccobacili

A
  • Acid w/ rods = most likely E. coli
  • Acidic w/ cocci = most likely strep (chains) or emterococcus
  • Alkaline w/ coccobacilli = most likely proteus
  • Alkaline w/ cocci = most likely staph
53
Q

Diagnosis of Pyelonephritis & Prostatitis

A

Pyelonephritis
• systemic signs + cystitis
• may have abnormal renal function 

• casts 


• diagnostic methods:
o visualize kidneys 

o pyelocentesis 


Prostatitis
• systemic signs + cystitis
• prostate enlarged and/or asymmetrical shape 


• diagnostic methods:
o prostatic aspiration w/ culture
o biopsy 


54
Q

How to select antibiotics for UTI & know if they are affective

A

Antibiotic Selection
• urinary tract is a CONDITIONALLY SUSCEPTIBLE site
• many labs test urinary isolates at levels of antibiotics expected in the urine, not blood
• bacteria resistant in blood may be susceptible in urine because antibiotic is concentrated in urine
• effective treatment may require 10-14 days (think of toxicity)

Are they effective?
• re-culture at 48 hours:
• growth = change antibiotic

• no growth = continue another 7-10 days

55
Q

Recurrent cystitis & Chronic bacterial cystitis

A

recurrent cystitis
• sources of infection:
• relapse = infection with the same organism
• re-infection = infection with a new organism
• either case may have underlying causes

chronic bacterial cystitis
• culture at 48 hours, if no significant growth, continue antibiotics for 4- 6 weeks .

56
Q

Antibiotics used for UTI & which bacteria they work for

A

o Ampicillin
o Chloramphenicol
o Oxytetracycline
o Trimeth sulfa (long-term use = keratoconjuctavitis)
o All work on E. coli, Klebsiella, Proteus, Staph
o Most work on Pseudomonas accept oxytetracycline

57
Q

Corynebacterium renale Infection of Ruminants; basics, bacteria involved, virulence factors, spread

A

o Contagious cystitis and pyelonephritis in cattle and sheep
o No underlying problem needed to cause disease


Bacteria: 
•	all normal flora
•	C. renale, 
•	C. cystitidis
•	C. pilosum

Virulence factors:
• pili – adherence
• urease - increase pH & facilitate adherence

Spread
• Subclinically infected
• direct contact with urine or splashing of urine
• can be endemic & difficult to eradicate

58
Q

Basics of Leptospira

A

o Order: Spirocheaetales

Families
• Leptospiraceae: Leptospira,

• Spirochetaceae: Brachyspira, Borrellia, Treponema

o	Spiral shaped
o	Gram (-)
o	obligate pathogen
o	no replication but persists in environment
o	likes wet environments
59
Q

Leptospira Encounter: direct v indirect encounter, maintenance v accidental hosts

A
  • Persists in renal tubules & genital tract of carrier animals
  • Infected animals shed in urine & contaminate environment

Direct:
• From infected animal to healthy via urine

Indirect:
• from contaminated env -> healthy animal

Maintenance host
• Rodents w/ icterohaemorrhagiae 

• Cattle w/ hardjo
• Dogs w/ canicola

Accidental host
• Dogs, cattle, humans w/ icterohaemorrhagiae 

• Humans w/ canicola

60
Q

Leptospira Pathogenesis & virulence factors

A
  • penetrate thru intact mucous membranes or abraded or water softened skin ->
  • enter systemic circulation ->
  • multiply rapidly & spread to many tissues
  • renal colonization in most infected animals

Virulence Factors
• LPS: incites significant damage
• hemolysins: lysis of cells
• flagellum: for movement thru body

61
Q

Leptospira clinical findings in dogs, cattle, horses

A

Dogs

Uremic type
o Inappetance, lethargy, vomiting, PU/PD, fever 

o Oliguria, anuria and severe renal azotemia 

o UA: gluc, prot, active sediment, granular casts 


Icteric Type
o Focal hepatic necrosis 

o Icterus, mild-moderate hypoalbuminemia 

o Chronic active hepatitis, fibrosis, failure 

o Peak signs 6-8 days post-onset (lags behind renal signs) 


Cattle
• Abortion 4mo – term
• Dam: Icterus, Hemoglobinuria, fever, Mastitis
• Calf: IMHA, anemia, acute renal failure

Horses
• Recurrent uveitis
• Acute renal failure in foals

62
Q

Immunity to Leptospira & what does immunity in cattle, pigs, dogs, horses, & sheep look like?

A
  • Immunity to Lepto is conferred via Ab directed against LPS.
  • Adequate Ab response within 7-10 days PI 

  • little cross protection across serovars but may have some

IMPORTANT:
• Cattle: subclinical w/ or w/o lepto in urine
• Pigs: infected w/ Pomona = subclinical w/ lepto in urine
• Dogs: infected w/ canicola = subclinical w/ lepto in urine
• Horses: recurrent uveitis & maybe blindness
• Sheep: infected w/ hardjo = subclinical w/ lepto in urine

63
Q

Diagnosis of Leptospira

A
  • U/A for Hematuria, pyuria, proteinuria, glucosuria
  • Increased BUN and creatinine, thrombocytopenia Increased serum bilirubin, ALP (icteric form)
  • Can be isolated from blood or urine
  • Dark field microscopy on urine
  • Microscopic agglutination test to look for Ab
  • NO culture
64
Q

Treatment & Prevention of Leptospira

A

Treatment
• Eliminate active infection and carrier state w/ antimicrobials
o Dogs – ampicillin / doxycycline
o Horses- PenG / Oxytetracycline
o Cattle – Oxytetracycline/ Dihydrostreptomycin 

• Treat systemic complications 


Prevention
• Bacterins
• Vaccinate in endemic areas: 2 to 3 injections, 2 or 3 weeks apart (boost every 6 to 8 months) 

• Vx effective ONLY if targeting the serovars currently in the environment

65
Q

Nosocomial V Iatrogenic Infections

A

nosocomial infection
o new infection acquired during hospitalization 


iatrogenic infection
o acquired by direct action of a veterinarian (or technician)

66
Q

Sources of Nosocomial Infections

A

o Invasive Devices
o Patient Flora
o Medical personnel
o Hospital environment

67
Q

Flora Carried by Certain Species that can cause nosocomial infection

A
  • Salmonella - horses 

  • Bordetella bronchiseptica - dogs 

  • Chlamydophila psittaci - birds 

  • Feline Viral Rhinotracheitis - cats 

  • Normal flora that gains access to a normally sterile site (E. coli pneumonia or UTI, Staph intermedius bacteremia)
68
Q

Control of Nosocomial Infections; define: sterilization, disinfection, antisepsis, germicide, sanitation, decontamination, & cleaning

A

Sterilization
• destruction of all living organisms, including spores 

• autoclave @ 121C for 15 mins; monitor w/ Bowie Dick tape test
• ethylene oxide used for heat intolerant materials

disinfection
• elimination of all vegetative organisms, but not spores from an inanimate object 


antisepsis
• treatment of living tissue in an attempt to destroy all vegetative organisms

germicide
• agent that destroys vegetative organisms on either tissue or an inanimate object 


sanitation
• removal of organism numbers to an acceptable level for public health standards 


decontamination
• removal of pathogens to allow safe handling of material 


cleaning
• removal of organic material 


69
Q

Basics of Postoperative Infections

A

o Staph aureus can invariably be isolated from operative area
o surgical procedures limit risk of surgical wound infection
o source of contamination = patient’s skin
o Surgical prepping reduces bacterial numbers on skin. 

o Minimal time in surgery minimizes tissue desiccation.
o Good technique minimizes tissue damage. 

o Can prescribe pre-operative or perioperative antibiotics
o Rate of infection doubles every hour patient is under

70
Q

1st line V 2nd line antibiotic therapy for perioperative use

A 
First Line
•	Routinely used in hospitals
•	Work 75-85% of the time
•	Older generation & low cost
•	Ie. Penicillin, trimethoprim/sulfa, gentamicin
Second Line
•	Restricted use
•	Work 85-95% of time
•	Newer more expensive drugs
•	Ie. amikacin, ticarcillin, imipenem, vancomycin

Bacteriology (2 decks)

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