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Bac T > Test 2 > Flashcards

Test 2 Flashcards

1
Q

what are the 4 main viral causes of shipping fever

A
  • IBR (infectious bovine rhinotracheitis)
  • PI3 (parainfluenza)
  • BRSV (bovine resp. syncitial virus)
  • BVDV (bovine virus diarrhea virus)
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2
Q

what damage do the following viruses cause to lead to shipping fever
• IBR (infectious bovine rhinotracheitis)
• PI3 (parainfluenza)
• BRSV (bovine resp. syncitial virus)
• BVDV (bovine virus diarrhea virus)

A

PI3 - damages ciliated epithelium, macrophages

IBR and BRSV - damage ciliated epithelium

BVDV - immunosuppressive: infects lymphocytes and
enhances growth of bacteria

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3
Q

What is the name of each of these viruses

PI3
IBR
BRSV
BVDV

A
  • IBR (infectious bovine rhinotracheitis)
  • PI3 (parainfluenza)
  • BRSV (bovine resp. syncitial virus)
  • BVDV (bovine virus diarrhea virus)
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4
Q

what are the 4 virulence vactors of M. haimolytica

A

• Fimbriae: Enhances colonization of URT
• Polysaccharide capsule: Inhibits phagocytosis and
complement mediated lysis
• Endotoxin (LPS): Induces proinflammatory cytokines,
toxic to bovine endothelial cells, etc.
• Leukotoxin (Exotoxin): cytolytic activity for leukocytes
and platelets and impairs macrophage function

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5
Q

what is the classic lesion caused by shipping fever

A

Fibrinous necrotizing bronchopneumonia and pleuropneumonia

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6
Q

what would you generally treat acute pneumonia with from shipping fever

A
  • antibiotics will reduce mortality and development of
    chronic pneumonia if treated early
  • Oxytetracycline and Sulphonamides are usually
    effective
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7
Q

what does MIMS stand for

A

Maximum Immunity, Minimum Stress

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8
Q

what are some effective antibiotics against Psittacosis

A

macrolide
quinolone
tetracycline

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9
Q

is Clamydophilia psittaci intra or extracellular

A

Gram (-) bacteria (intracellular)

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10
Q

what is the source and reservior for C. Psittaci

A

• source and reservoir are infected birds
• does not REPLICATE in the environment, but infective
forms (ELEMENTARY BODIES)

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11
Q

what cells does C. psittaci infect

A
  1. Systemic infection
    a. infects monocytes and macrophages
    key cells that allow systemic spread to target tissues
    b. also local spread in intestine, upper/lower respiratory
    tract
    main clinical signs depend on site of damage
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12
Q

similar to erilichia and rekettsia viruses C. psittaci evades the immune system by…..

A

Phagolysosomal fusion blocked

- prevents killing of bacteria

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13
Q

why must C. psittaci act as an obligate intracellular pathogen

A

Replication within the phagosome as reticulate bodies (RB)
• cannot make ATP (energy), lacks cytochromes
→ intracellular space provides protection from host
defenses, and a source of energy for replication

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14
Q

how is C. psittaci able to persist in the environment

A

Differentiate into elementary bodies (EB) and lyse cells
- Elementary bodies are the infective forms, invade new
cells
Elementary body is stable in the environment;
are “spore-like”

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15
Q

is C. psittaci a reportable Dz?

A
  • If proven, or suspected, C. psittaci infections are a reportable disease
  • signs may be very non-specific, should be considered in any bird with lethargy and nonspecific signs of illness
  • Serous ocular and nasal discharge,
  • diarrhea with excretion of green to yellow urates
  • typical differentials are other systemic bacterial and viral infections
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16
Q

how do you test for C. psittaci

A

Cloacal swab – DIRECT antigen detection

i. ELISA: detection of antigen in secretions and feces
- rapid test, commercial human kits
- lack sensitivity and specificity, especially on normal birds

ii. Culture on cell lines
- sensitive, but takes a long time
- recommended to avoid limitations of other tests

iii. Polymerase chain reaction (PCR) to detect Chlamydophila
DNA
- sensitive and fast

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17
Q

how is psttaciosis treated

A

Tetracyclines are the drugs of choice, very effective –
• Tx must be prolonged (45 days)
• Dietary calcium should be removed from food because calcium chelates tetracyclines
• Doxycycline more commonly used because it is better absorbed and more slowly eliminated.
• Treated birds should be monitored for signs of doxycycline toxicosis
• depression, decreased appetite, green yellow stained urine and altered hepatic functions).

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18
Q

provide a brief overview of Clamydophila psittaci…

A
  1. Systemic infection, affects respiratory tract of parrots and humans (psittacosis) or other birds (ornithosis)
  2. Obligate intracellular parasite
  3. Receptor mediated uptake, avoids killing by preventing phagosome-lysosome fusion
  4. Replicates as reticulate bodies, released from cell as resistant, infectious elementary bodies
  5. Damages cells by endotoxin, cell lysis, and production of cytotoxins
  6. Diagnosis in live birds based on direct detection of antigen (ELISA, Culture and PCR) or serology
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19
Q

what are the most common UTI pathogens found

A

a) >75% are E. coli, Proteus, Klebsiella

b)

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20
Q

what is the source of the most UTI

A

usually normal flora of the lower UT (distal urethra)

1) usually normal flora of the lower UT (distal urethra)

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21
Q

what is the #1 defense against an UTI

A

Flushing by urine - URINE FLOW is #1 host defense!

- prevents access to and colonization of the bladder

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22
Q

what are some pathogenic causes of an UTI

A
  1. urinary stasis
  2. mechanical impediments to flow
  3. damage to epithelial surface that impedes urine flow and promotes bacterial colonization
    4 late gestation
    virulence factors that prevent bacteria from being washed away
  4. diseases that decrease urine osmolality (renal failure, cushing’s, diabetes)
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23
Q

what are some common pathogens associated with an UTI dependent on PH

A

acid - rods - E. coli
acid - cocci - Strep, Enterococcus
alkaline - rods - Proteus
alkaline - cocci - Staph

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24
Q

what is the primary source of leptospira?

A

• Carrier animals and rodents are the main source of infection for other animals
c. Infected animals shed Leptospira through urine (contaminate environment)
• Acutely infected cattle may shed up to 108 / ml
• Recovered dogs can excrete for many months

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25
Q

what is the difference between direct and indirect transmission of lepto

A 
i. Direct transmission:
• Contaminated urine
• Venereal or trans-placental
transfer
ii. Indirect transmission:
• Contaminated waters
(ponds, river, moist soil etc)
• Contaminated environment
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26
Q

how does lepto gain entry for infection

A

a. Leptospira penetrate through:
• intact mucous membranes of mouth, nose or eyes
OR
• abraded, scratched or water softened skin
b. Enter the blood vascular space (systemic circulation)
c. Multiply rapidly and spread to many tissues:
• Kidneys, liver, spleen, lungs, eyes, genital tract, CNS

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27
Q

what are the virulence factors associated with lepto

A
  • LPS: causes significant damage

* Hemolysins: lysis of cells

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28
Q

what are some common clinical findings with uremic type lepto

A

Uremic Type
• Inappetance, lethargy, vomiting, polyuria, polydipsia (excessive thirst), fever
• Oliguria, anuria and severe renal azotemia (↑N)
• UA: glucose, protein, active sediment, granular casts
– An “active” urinary sediment is a sediment that contains numerous RBCs, WBCs, RBC casts, and WBC casts.
– Indicative of glomerulonephritis, intersitial nephritis, or vasculitis.

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29
Q

What are some common clinical findings with icteric type lepto

A

Icteric types (icterohemmorhagiae, pomona, grippotyphosa)
• Focal hepatic necrosis
• Icterus (“jaundice”), mild-moderate hypoalbuminemia
• Chronic active hepatitis, fibrosis, liver failure
• Peak signs 6-8 days post-onset (lags behind renal signs)

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30
Q

how is immunity to Lepto achieved

A

Immunity to Leptospira is conferred via antibodies directed
against LPS.
• Adequate antibody response within 7 to 10 days PI

There is little cross protection between serovars, although sera from animals infected with one serovar may have some
cross reactivity against other serovars.
• Cross reactivity vs cross protection!?

IMPORTANT: seroreactivity does not equate to protection

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31
Q

what bacteriological findings are associated with lepto

A

Bacteriology (difficult and not routinely performed)
• Can be isolated from blood (first 7 to 10 days)
– Citrate anticoagulant should be avoided
• Urine (two weeks after infection)
– Urine should be alkalinized (pH 7.0) before transport
– Multiple samples may be required (intermittent shedding)
– Cultured in enrichment media (EMJH media)
• Dark field microscopy: (can be performed on urine or tissues)
– Requires >10^5 organisms/ml

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32
Q

what serological findings are associated with lepto

A

Serology
• Microscopic agglutination test (MAT)
– Most commonly used method
– Single high titer (>1:800) in unvaccinated dog is indicative of infection
– Preferred: rising antibody titer (look for four fold rise in 2 to 4 weeks interval)
– Dogs may have antibody titers against several different serovars (potential for cross-reaction)

Does not discriminate organisms at serovar level

33
Q

is there any zoonotic risk with lepto?

A 
Occupational
• Farming
• Abattoir workers
• Sewage workers
• Veterinary students have been infected during their clinical years of training:
– in the areas of food inspection, farm work, and contact with pet carnivores and animal traders
Exposure to animals
• Cattle, rats, dogs
Recreational water/swimming
34
Q

what is the advantage of mycobacteria’s wall structure.

A

All Mycobacteria are “Acid-Fast bacilli (AFB)”
- Differences in cell wall structure (mycolic acids and lipids in cell wall)
– Protect against phagocytosis, extreme pH and environmental stresses
- CAN NOT be stained with Gram staining method
– Zheil-Neelsen (ZN) staining: special staining technique used for identification of Mycobacteria
– Common method used for preliminary diagnosis

35
Q

all mycobacterium are Facultative _________ pathogens, and infect _____________

A

Facultative intracellular pathogens of macrophages
- Inhibit fusion of phagosome and lysosome (mycolic acids and lipids)
- Cause granulomatous infections
– e.g., M. bovis infection in cattle
- Mechanism of “granuloma” formation

36
Q

what are NTM’s (non-tuberculous mycobacterium) generally susceptable to?

A

~90 % are susceptible to Amikacin and Cefoxitin

37
Q

T or F

Culture and antibioic sensitivity is very important for accurate diagnoss and treatment of Mycobacterial infections

A

TRUE

38
Q

what are the 4 major pathogenic mycobacteria, and what Dz to they cause

A
  1. M. bovis: Wide host range
    – Primarily infects cattle (Bovine tuberculosis)
    – Humans, cervids, primates, swine, dogs, horses, sheep, goats, cats, rodents, rabbits, badgers
    – Chickens are resistant
  2. M. tuberculosis
    – Primarily human, but dogs, rodents, swine can get infected
  3. M. avium subspecies avium
    – Primarily poultry, can infect pigs, horses and wild birds
  4. M. avium subspecies paratuberculosis (Johne’s disease)
    – Cattle, sheep, goats and deer
39
Q

what is the main source of bovine tuberculous

A

other infected animals

Bacteria are in respiratory droplets, sputum, milk, feces, urine, vaginal discharge.
– 10 bacteria are sufficient to cause infection via AEROSOL route
– Need >107 bacteria to cause ORAL infection

40
Q

what is an easy test to run for the diagnosis of bovine tuberculosis

A

Caudal fold (base of tail) test: Intradermal Skin test
- Measuring delayed type hypersensitivity to intradermally injected tuberculin (PPD- purified protein derivative) of M. bovis.
- Look for swelling at 48-72 hours.
- Cows become test positive 3 to 6 weeks post infection
– False negatives: too early/too late, recently calved, old age, progressive
disease, within 1 to 8 weeks of first test.

Must be confirmed by comparative cervical test (skin test comparing reaction to PPD of M. avium and M. bovis).
– Reaction to M. bovis not M. avium is considered positive
– Often used in conjunction with interferon gamma assay

41
Q

what is the primary site of infection in Bovine paratuberculosis (johne’s disease)

A

Organisms ingested by macrophages in Peyers Patches
(lymphoid tissue of intestine) of ileum
– Primary site of infection is ileum (ileal lymph nodes).

42
Q

what is the dianostic test for Johne’s Dz

A

Direct microscopy (look for acid fast bacilli in rectal pinch smear or scraping)
• DNA based PCR test is sensitive (USDA approved).
• Serological tests (ELISA, INFγ, AGID) are of low sensitivity
• Culture of organisms from manure or ileal node definitive, but takes a long time (3 to 4 months)
IMPORTANT: organisms are intermittently shed in feces, so fecal culture may be negative despite active infection
• 10 to 15 gram fecal samples taken at 6 month intervals

43
Q

what class of antimicrobial is penicillin

A

ß-Lactam

44
Q

define antibiotic

A

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

45
Q

define antimicrobial

A

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

46
Q

what are the three ?’s you should ask before initiating any antibiotic therapy

A
  1. Is this an infectious process?
  2. If yes, what are the likely pathogens?
  3. Is antibiotic therapy indicated?
47
Q

rickettsia is uniformly susceptible to…

A

tetracyclines

48
Q

Streptococcus is uniformly susceptible to…

A

penicillin

49
Q

what antibiotic should you never use on abscesses/pus lesions, and why

A

sulfonamides

they are not able reach the desired area

50
Q

what class of ABx are known to cause iatrogenic nephrotoxicity

A

aminoglycosides

51
Q

what is the advantage of using a narrow spectrum ABx vs a broad spectrum

A

What are the effects on microbial flora? Will its use promote development of resistance?
• BROAD SPECTRUM ANTIBIOTIC will have both effects
• Can minimize these possibilities with NARROW SPECTRUM antibiotics.

52
Q

what are 4 reasons you might use multiantibiotic therapy

A
  1. to obtain a synergistic effect
  2. to prevent or delay emergence of persistent organisms
  3. to treat polymicrobial infections
  4. to treat serious infections in the stage before the infectious agent is identified
53
Q

what are the different effects that multiantibiotic therapy can have

A
  1. indifference
  2. additive
  3. synergism
  4. Antagonism
54
Q

what is ment by the indifference effect?

A

combined are no more effective than the

more effective antibiotic used alone

55
Q

what is meant by the additive effect, and what might be the advantage

A

combined action is equal to the SUM of either used alone
• a. Two antibiotics with the same mechanism of action
– i. Similar to increased dosage
– ii. May reduce toxicity as compared to a higher dosage of single antibiotic

56
Q

what is meant by the synergism effect

A

combined action is greater than the

sum of both effects

57
Q

how does trimethoprim-sulfamethoxazole which are both bacteriostatic work together

A

They act synergisticly to become bactericidal

– Sulfa competitively inhibits PABA incorporation into folic acid synthesis
– Trimethoprim noncompetitively inhibits enzyme (dihydrofolate reductase) - acts at a later step

58
Q

how do ß-lactam antibiotics work, and what is an example of one

A

penicillin

• β-lactam ring mimics the substrate of the transpeptidase inhibiting formation of peptidoglycan in the cell wall.

59
Q

what is meant by the antagonism effect

A

combination is less effective than the most effective individual antibiotic

60
Q

what are the 4 primary things to keep in mind when perscribing an Abx

A
  1. Absorption
  2. Tissue distribution
  3. Function in tissue conditions
  4. Excretion
61
Q

what are the 3 families of ß-lactams

A
  1. penicillins
  2. cephalosporins
  3. carbapenemes, monobactams, and ß-lactamase inhibitors
62
Q

what is one draw back of ß-lactam Abx

A

they require cell growth, so if you use in conjunction with an Abx that slows growth it will now work well

63
Q

what is the difference between Constitutive and Acquired resistance

A

Constitutive: membrane permeability, charge of cell surface, presence of efflux pumps, enzymatic transformation of biocides
Acquired: mutation

64
Q

why is the penetration of amino glycosides into hose cells and tissues poor

A

it is not lipid soluble

65
Q

Penicillin G is active against???

A

Gram Positive 4+
Gram (-) 1+
Anaerobic 4+
Clostridium 4+

66
Q

Dicloxacilin

A

Gram Positive 4+

67
Q

Amoxicillin

A

Gram Positive 4+
Gram (-) 2+
Anaerobic 3+
Clostridium 3+

68
Q

Amox/Clav acid

A

Gram Positive 4+
Gram (-) 2+
Anaerobic 4+
Clostridium 3+

69
Q

Ticarcillin

A 
Gram Positive  4+
Gram (-) 4+
Pseudomonas 4+
Anaerobic 4+
Clostridium 4+
70
Q

Imipenem

A 
Gram Positive  4+
Gram (-) 4+
Pseudomonas 4+
Anaerobic 4+
Clostridium 4+
71
Q

cefazolin and cephalothin are 1st gen…. and are effective…

A

Gram Positive 3-4+
Gram (-) 2-3+
Clostridium 1-2+

72
Q

cefoxitin and cefadroxil are 2nd gen….. and are effective….

A

Gram Positive 2-3+
Gram (-) 2-3+
Anaerobic 3-4+
Clostridium 0-3+

73
Q

cefotaxime and ceftiofur are 3rd gen… and are effective….

A

Gram Positive 1-3+
Gram (-) 2-4+
Anaerobic 1-3+
Clostridium 0-3+

74
Q

clindamycin

A

Gram Positive 4+
Anaerobic 4+
Clostridium 2-3+

75
Q

lincomycin

A

Gram Positive 2-3+
Anaerobic 1+
Clostridium 1+

76
Q

erythromycin

A

Gram Positive 2-3+
Anaerobic 1+
Clostridium 1+

77
Q

rifampin

A

Gram Positive
Gram (-)
Anaerobic 4+
Clostridium 4+

78
Q

what are the 3 basic mechanisms for acquired resistance, and how are they generally done

A
  1. alter the target for the drug
  2. alter the uptake of the drug
  3. inactivate the drug

Changes in DNA via mutation, or acquisition of DNA through
- genetic transfer via transduction or conjugation

79
Q

define the 3 categories of results with MIC testing

A

• i. Susceptible (S)
– Bacteria are inhibited at concentrations that can be achieved in tissues using normal dosage
• ii. Moderately susceptible or Intermediate (MS, I)
– Bacteria are inhibited at concentrations achieved in tissues ONLY at a maximal dosage and/or increased frequency of administration
• iii. Resistant (R)
– Bacteria are not inhibited at concentrations achievable or tolerated in the animal

Bac T (5 decks)

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