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Bacteriology > exam 2 > Flashcards

exam 2 Flashcards

1
Q

General defense of Respiratory tract (4)

A

Epithelial cells
Mechanical
Intraepthelial Lymphocytes
normal flora

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2
Q

function of normal flora in URT vs LRT

A

URT- similar function to GI tract

LRT: sterile (no normal flora), contains alveolar macrophages

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3
Q

an example of a localized, upper respiratory infection due to a contagious pathogen

A

Canine tracheobronchitis - Bordetella bronchiseptica

kennel cough

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4
Q

B bronchiseptica in cats, pigs

A

more likely to cause pneumonia in cats and other species than dogs
-significant pathogen of swine (involved in atrophic rhinitis)

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5
Q

Encounter of B. bronchiseptica

A
  • NOT normal flora, obligate pathogen
  • obligate parasite - of URT (sole reservoir of infection is other infected animals)
  • highly contagious (aerosolized, needs close contact)
  • disease enhances transmission (coughing, puppies shed for up to 3 months post infection)
  • can become carrier if not enough immunity to clear organism completely
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6
Q

exogenous

A

not from normal flora

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7
Q

endogenous

A

from normal flora

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8
Q

B. bronchiseptica (entry)

A
  1. exogenous
  2. Pili - specific adhesion to ciliated epithelium
  3. doesn’t penetrate cells (not intracellular pathogen, doesn’t invade across epithelium)
  4. primary damage from viruses (PI2,CAV 1 &2)
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9
Q

B bronchiseptica (multiplication and spread)

A
  1. usually localized to URT, no bacteremia, doesn’t extend beyond mucosal surface, multiplies on cilia and spreads
  2. rarely speads to lungs: immunosuppression with canine distemper, toy breeds, immotile cilia syndrome
  3. pneumonia is more common in cats/guinea pigs where B bronchiseptica acts as primary pathogen
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10
Q

B. bronchiseptica (mechanism of damage)

A
  1. endotoxin - minor component, may cause mild fever if absorbed through damaged mucosa
  2. exotoxin - cytotoxin (damages ciliary epithelium, accumulation of debris)
    Adenylate cyclase (increases cAMP that inhibit phagocytosis)
  3. IgA binds to pili, loss of adhesion leads to clearance
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11
Q

ciliostasis from B. bronchiseptica

A

happens within 5 minutes

impairs mucociliary elevator

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12
Q

B. bronchiseptica (diagnosis)

A
  1. based on clinical signs

2. may culture if concerned about LRT (bronchoalveolar lavage/trans-tracheal aspirate)

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13
Q

clinical signs of B bronchiseptica

A

dry hacking cough, exposure to other dogs

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14
Q

B bronchiseptica (treatment)

A
  1. antibiotics??? most are self limited, treat if there is risk of pneumonia, AB do not affect course of URT(ampicillin, tetracycline, aerosol therapy)
  2. primary treatment is supportive (warm and dry, anti-inflammatory, cough suppressants)
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15
Q

B bronchiseptica (prevention)

A
  1. improved ventilation
  2. control exposure (stress)
  3. vaccination
  4. sanitation
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16
Q

B bronchiseptica (types of vaccinations)

A
  1. systemic bacterin - while killed bacteria, elevated circulating IgG, less protective, no surface IgA, included in canine parainfluenza, canine adenovirus, distempter vacines
  2. intranasal vaccine- live avirulent, elevates local IgA titers, blocks binding of bacteria to cilia, booster required
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17
Q

how long are dogs protected after natural infection from B. bronchiseptica

A

up to 16 weeks (can become reinfected)

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18
Q

B bronchiseptica - enhances transmissibility

A

transmitted readily by aerosol in less ventilated, indoor environement.
warm, humid air enhances transmissibility

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19
Q

when should you vaccinate for B bronchiseptica

A

previoiusly exposed adult dogs can be vaccinated once 2 weeks prior to moving indoor (stress)
assume effectiveness for 4 months

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20
Q

An example of lower respiratory infection due to normal flora

A

Bovine Respiratory disease complex (shipping fever)

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21
Q

shipping fever host factors

A
  • more common in growing cattle (6 mo -2 yrs)
  • non immunized calves more susceptible (no neutralizing antibodies)
  • outbreaks after arrival in feedlot (7-10 days)
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22
Q

shipping fever Environment/management factors

A
  1. Stress ( transportation)
  2. mixing of cattle from different sources
  3. feed and water deprivation
  4. inclement weather
  5. confinement in poorly ventilated barns
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23
Q

shipping fever - Pathogen factors

A
  1. complex of viral and bacterial respiratory pathogens

2. multi-agent disease, 1+ infections, bacteria from family Pasteurellaceae

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24
Q

Shipping fever- principal viruses

A

IBR, PI3, BSRV, BVDV

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25
Q

shipping fever - principal bacteria

A

gram negative

  • Mannheimia hemolytica is principally associated
  • can be pasteuella multocida, histophilus somni
  • also Mycoplasma bovis (neither gram + or -)
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26
Q

Shipping fever - encounter

A
  1. all principal bacteria are normal flora of bovine nasopharynx (except M. bovis- pathogen)
  2. All principal bacteria are obligate parasites: only habitat is mucous membranes of URT, very short survival in enviroment
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27
Q

Shipping fever - Entry (into lung)

A
  1. endogenous infection
  2. stress alters ecology and immune competence of nasopharynx (transport, castration)
  3. inhaled into trachea/bronchioles (multiply/spread to alveoli)
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28
Q

shipping fever- Entry (how stress alters ecology)

A

a. M. haemolytica type A1 overgrows serotype A2

b. stress predisposes to viral infection - viral damage to innate respiratory defenses

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29
Q

shipping fever- frequency of Mannheimia haemolytica isolations from nasal swabs are

A

serotype 2 predominant isolate at teh farm

serotype 1 predominant at feedlot

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30
Q

shipping fever- multiplication and spread

A
  1. strictly extracellular bacteria - phagocytosis by neuts, macs, very important in control
  2. do not multiply or invade the normal trachea or lung - infection disrupts pulmonary defenses, prevents clearance of bacteria
  3. spread is aerogenous, bacteria localize preferentially in ventral portions of cranial lobes (gravity)
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31
Q

PI3

A

damages function ciliated epithelium, macrophages

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32
Q

IBR and BRSV

A

damage (loss of) ciliated epithelium

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33
Q

BVD

A

Immunosuppresive: infects lymphocytes, enhances growth of bacteria

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34
Q

shipping fever - when is it most severe?

A

within 4-7 days of viral infection

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35
Q

Shipping fever - Damage

A
  1. bacteria proliferate rapidly in the lungs
  2. Exotoxin
  3. Local release of endotoxin
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36
Q

4 virulence factors of M. haemolytica

A
  1. Fimbriae - enhances colonization of URT
  2. Plysaccharide capsule: inhibits phagocytosis and complement mediated lysis
  3. Endotoxin: induces proinflammatory cytokines, toxic to bovine nedothelial cells
  4. Leukotoxin(exotoxin) : lethal for leukocytes and platelets and impairs mac function
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37
Q

Shipping fever - exotoxin (damage)

A
  • leukotoxin or cytotoxin

- inserts pore into cell membrane, destroys cells in the area - TISSUE NECROSIS

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38
Q

Shipping fever - release of endotoxin (damage)

A
  • vasculitis, fibrin exudation and thrombi
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39
Q

shipping fever - Immune response

A
  1. Antibody to leukotoxin prevents cell damage
  2. Ab+complement kill bacteria directly (extracellular)
  3. if survive acute infection see fibroplastic healing
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40
Q

shipping fever - fibroplastic healing

A

a. pulmonary fibrosis - lost lung function

b. chronic poor weight gain = poor doers

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41
Q

shipping fever - Diagnosis

A
  1. history of stress and sudden onset of respiratory disease
  2. gross pathological findings
  3. bacteria culture for Antibiotic sensitivity (tissue blood from septic animal, trans tracheal aspirate/ bronchoalveolar lavage, cytospin)
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42
Q

shipping fever - clinical signs

A 
7-14 days after arrival in feedlot
fever
anorexia
respiratory distress
some found dead
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43
Q

shipping fever - treatment of acute pneumonia

A
  • antibiotics reduces mortality and development of chronic pneumonia if treated early
  • oxytetracycline and sulphonamides
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44
Q

shipping fever- treatment of chronic pneumonia

A

Rx of little value

has permanent lung damage

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45
Q

MIMS - shipping fever

A

maximum immunity - minimum stress

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46
Q

Shipping fever - prevention

A
  • management (vaccinate against virus(IBR, PI3, wean 2 wks before shipment, distribute stressors like branding/castration, isolate upon arival)
  • Mannheimia vaccines
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47
Q

Mannheimia (pasteurella) vaccines

A

bacterins moderately effective at best

-not enough cytotoxin to produce neutralizing antibody titers

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48
Q

Systemic infection (caused by obligate intracellular pathogen) where respiratory tract is primary target

A

Psittacosis (Chlamydiosis)
Chlamydophila psittaci
Gram - bacteria

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49
Q

psittacosis

A

infection in psittacine birds or humans

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50
Q

ornithosis

A

infection in non-psittacine birds

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51
Q

Psittacosis - encounter

A
  1. obligate parasite - of intestinal and respiratory tract of birds
  2. adult psittacines may be carriers
  3. aerosols of feces and respiratory secretions -> elementary bodies
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52
Q

reservoir for Psittacosis

A

infected birds

doesn’t replicate in enviro, but infective forms can persist there for months (elementary bodies)

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53
Q

Psittacosis - entry and multiplication

A
  1. systemic infection
  2. receptor mediated endo/pagocytosis into epithelial cells
  3. phagolysosomal fusion is inhibited by chlamydophila
  4. Chlamydophila replicate as reticulate bodies within the phagosome
  5. differentiate into elementary bodies and lyse cells releasing them to invade new cells
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54
Q

obligate intracellular parasites

A

must replicate within, and not be killed by, a living host cell

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55
Q

Psittacosis - systemic infection - entry and multiplication

A

infects monocytes and macrophages (allow systemic spread)
epithelial cells of GI
local spread in intestine, URT or LRT

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56
Q

elementary bodies

A

environmentally resistant infective form

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57
Q

Extracellular bacteria

A

B bronchiseptica, S. Equi, M. Haemolytica

- replicate outside of cells (blood, mucus membranes, abscess fluid, environment)

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58
Q

Facultative intracellular

A

R. Equi

replicates either outside of cell or within cell (has a choice)

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59
Q

Obligate intracellular

A

C. psittaci

replicates only in cell, never outside of cell

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60
Q

Psittacosis - Damage

A
  1. gram (-) cell wall -> endotoxin release
  2. cell lysis
  3. clinical severity related to number of infected cells
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61
Q

Psittacosis - clinical severity

A

a. age of bird (young psittacines have higher mortality in outbreak)
b. species of bird - new world more susceptible than old world
c. strain - 8 serotypes, different levels of virulence

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62
Q

Psittacosis - Immunity

A

cell mediated immunity important to kill cells with intracellular organisms
sensitized T cells secrete gamma I, FN: activate macrophages, enhances intracelllular killing
infection not eliminated but maintained at subclinical levels

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63
Q

Psittacosis - diagnosis

A

must be reported to public health if suspected

  1. Antemortem test
  2. postmortem necropsy
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64
Q

clinical signs of Psittacosis

A

non specific - bird with lethargy

  • serous ocular and nasal discharge
  • diarrhea with excretion of green to yellow urates
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65
Q

Psittacosis Antemortem tests - Cloacal swab

A

cloacal swab - direct Ag detection

i) ELISA - detection of antigen in secretions and feces, lac sensitivity and specificity
ii) culture on cell lines - sensitive, takes time, most specific
iii) PCR - sensitive and fast

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66
Q

Psittacosis antemortem tests - serology

A

serology to detect antibodies to the organism (CFT, ELISA, IFT)

i) positive titer: exposure to antigen, (prior infections, prior vaccination, current infection)
ii) Rising titer: recent infection or immunization
iii) IgM antibodies - rises early during acute exposrue, detected by elementary body agglutination test (single positive titer (>1:20) with EBA indicates current infection

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67
Q

Psittacosis Postmortem diagnosis

A

air sacculitis, hepatomegaly, splenomegaly

a. look for inclusions (intracellular bacteria) with giemsa stain
b. histio lesions with intracellular organisms
c. culture of spleen

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68
Q

Psittacosis - treatment

A

Tetracyclines - Tx must be prolonged (45 days)

acute infections- replicating organisms most susceptible = good response

carriers - metabolically quiescent organisms more resistant to antibiotics

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69
Q

Psittacosis - Prevention

A

no vaccine

  1. aviary managment - quarantine and treat new additions
  2. importation - treat in quarantine station, USDA protocols
  3. Sanitation/disinfection (quats, bleach, chlorphenols)
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70
Q

Psittacosis - public health

A 
concern is for bird owners  (70% cases from cage birds)
infection by inhalation of elementary bodies
interstitial pneumonia (common), septicemia(less common) - case fatality ate about 1%, morbidity ~90% with hospitalization
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71
Q

Chlamydophila pneumoniae

A

human pneumonia

koala and equine biovars ( pneumonia)

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72
Q

Chlamydophila abortus

A

enzootic abortion in sheep, cattle, goats and other mammals

most common in the USA

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73
Q

Chlamydophila felis

A

conjunctivitis, rhinitis, pneumonia in cats
endemic among house cats worldwide
30% cats with conjunctivitis were reported to have Chlamydia infection

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74
Q

Antimicrobial therapy

A

selective chemotherapy (targeting microorganisms specifically) without damaging host cells and tissues

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75
Q

synthetic antimetabolites

A

-synthetic dyes that bind bacteria (arsphenamine against syphilis)
discovered by Paul Ehrlich in 1906
-sulfonamide

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76
Q

Natural products (bacteriocins) of bacteria and fungi

A
  • Penicillium produced in 1940 - B-lactam antibiotics with both natural and semi-synthetic members
  • cephalosporins: a second family of naturally occurring B lactam antibiotics
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77
Q

Natural products of higher eukaryotes (sources of anitimicrobials)

A

-potential sources for new antimicrobials

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78
Q

Antibiotic

A

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

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79
Q

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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80
Q

principles for antibacterial selection

A
  • potential interactions between the antimicrobial, microorganisms and host
  • static/cidal? spectrum? toxicity? in vivo effectiveness? Gram +/-
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81
Q

bacteriostatic

A

reversible inhibition of bacterial growth

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82
Q

bactericidal

A

irreversible inhibition of bacterial growth- meaning bacteria are killed

-preferred for immunosuppressed or immunodeficient animals

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83
Q

bacteriostatic and bactericidal

A

distinction is not absolute - depends on species and dose (penicillin is cidal at recommended doses, but static at low doses)

both classes rely on competent host immune system

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84
Q

indifference: antimicrobial combination

A

combined are more effective than the more effective antibiotic used alone

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85
Q

additive: antimicrobial combination

A

combined action is equal to the SUM of either used alone

- two antibiotics with the same mech of action

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86
Q

Synergism: antimicrobial combination

A

combined action is greater than the sum of both effects

  • number of different mechanisms
  • example: Clavamox: a penicillin adn a monobactam
    1. block sequential steps
    2. one prevents inactivation of 2
    3. one promotes uptake of 2
    4. penicillin damages the cell wall and enhances uptake of aminoglycoside antibiotics
    5. one antibiotic reduces resistance to 2nd
87
Q

Antagonism

A

combination is less effective than the most effective individual antibiotic
-common with bactericidal and bacteriostatic together
(tetracycline blocks protein synthesis, penicillin cannot incorporate and block cell wall synthesis)

88
Q

Absorption - pharmacokinetics

A

new B lactams, aminoglycosides are not absorved from the GI tract
ex- penicillinG is acid susceptible so can’t be used orally

89
Q

Tissue distribution - pharmacokinetics

A

depends on antibiotic properties - passive diffusion, polarity
- BBB - modified by inflammation

90
Q

Function in tissue conditions - pharmacokinetics

A

aminoglycosides DO NOT function at low ph (

91
Q

Excretion

A

many antibiotics require normal renal and hepatic function

  • ex. aminoglycosides are renally excreted
  • can use mode of excretion to help treat some infections (high concentrations of ampicillin in urine due to renal excretion)
92
Q

Antibiotic toxicity - damage to eukaryotic cells

A

damage is dose -dependent

93
Q

elimination of normal flora -antimicrobials

A
  • esp a problem with intestinal flora (penicillin induced fatal diarrhea in guinea pigs)
  • allows overgrowth of resistant bacteria
  • allows fungal proliferation (candida)
94
Q

Allergy - antimicrobials

A
  • major problms with penicillins and sulfas
  • penicillins bind plasma proteins, act as carries, produces IgE antibody in susceptible individuals, upon re-exposure to penicillin, mast cell degranulation is triggered
95
Q

site of actionof antibacterical drugs

A
  1. inhibitors of cell wall synthesis
  2. inhibitors of protein synthesis
  3. inhibitors of nucleic acid synthesis
  4. cell membrane function - (increase permeability)
96
Q

Beta-lactam antibiotics families

A

3 families:

  • Penicillins
  • Cephalosporins
  • Carbapenems, monobactams, B-lactamase inhibitors
97
Q

B-lactam function

A
  • inhibit final cross-linking of peptidoglycan in cell wall formation
    - inhibit enzymes
    - inactivate an inhibitor - activates cell wall breakdown
    - requries a growing cell (BACTERICIDAL)
    - high therapeutic index
98
Q

B-lactam variation in acivity

A
  • amount of peptidoglycan in cell wall
  • unaltered penicillin-binding proteins (PBP) in bacteria
  • permeability of bacterial outer cell membrane
  • production of B-lactamases by bacteria
99
Q

Penicillin

A
  • BACTERIOCIDAL

- categorized into different groups based on activity against bacteria

100
Q

Benzyl Penicillin: group 1

A

original penicillins- (penicillin G)

  • narrow spectrum of activity (against gram +, anaerobes, cannot penetrate gram - outer membrane)
  • susceptible to B-lactamases (resistance in s. aureus is common)
  • many susceptible to acid hydrolysis (can’t give orally)
101
Q

clavulanic acid

A

group 4 penicillin extended spectrum (can penetrate gram -)
-product of Steptomyces clavuligenes, weakly anti-bacterial by itself, irreversible inhibitor of B-lactamases (except Pseudomonas aeruginosa)

102
Q

Cephalosporins

A

-B lactams
BACTERICIDAL
-greater resistance to B-lactamases than penicillin
-broad spectrum activity (gram +/-)
-less antigenic (can be used in penicillin allergic individuals)

103
Q

Glycopeptides

A

ex. Vancomycin
-block cell wall synthesis
BACTERICIDAL
- gram + spectrum (esp. gram + cocci (staph areus, enterococcus spp))
gram - are resistant
expensive (requires IV)
reserve for serious resistant infections

104
Q

Antibiotics that block Protein synthesis

A
  • anti-ribosomal - block prokaryotic ribosomal activity in some way
  • includes: tetracyclines, macrolides. chloramphenicol, aminoglycosides
105
Q

Tetracyclines

A
  • anti-ribosomal antibiotic
  • bacteriostatic
  • binds 30s ribosome
  • broad spectrum (affect normal flora)
  • resistance is widespread (not reported in rickettsia)
106
Q

Aminoglycosides

A

anti-ribosomal antibiotic
- Bactericidal
- binds 30s and 50s ribosomes (initiation of translation)
- primarily Gram - spectrum
- resistance to older generation of aminoglycosides is widespread (anaerobes), cross resistance is common
-newer aminoglycosides - efficacy vs Pseydmonas aeruginosa
(not lipid soluble, NOT effective against intracellular pathogens)

107
Q

Macrolides/Lincosamides

A
  • usually bacteriostatic
  • 50s ribosomes
  • good against gram +, mycoplasma and many anaerobes
  • highly lipid-soluble
  • well distributed in body
  • penetrate mammalian cells
  • erythromycin (macrolide)
  • clindamycin (lincosamide)
  • resistance develops readily
108
Q

Clindamycin

A

common lincosamide
-good against anaerobes
- can significantly disrupt normal GI flora, resulitng in serious diarrhea/colitis
DO NOT USE IN HORSES

109
Q

Chloramphenicols

A
  • usually bacteriostatic, broad spectrum
  • ribosome
  • can cause aplastic anemia in people
  • can’t use in food animals
  • well distributed in body
  • penetrates host cells
  • florfenicol has similar activity but lacks side effect
110
Q

inhibitors of nucleic acid

A
  1. Quinilones/Fluoroquinilones
  2. Sulfonamides
  3. Trimethoprim/ormetoprim
  4. Rifampicin
111
Q

Quinilones/Fluroquinolones

A

bactericidal
inhibit bacterial gyrase
highest activity against gram - aerobes/ facultative anaerobes
-inactive against obligate anaerobes
- penetrate mammalian cells - against rickettsia and mycoplasmas
some antimycobacterial

112
Q

Sulfonamides

A
  • inhibit nucleic acid synthesis
  • Bacteriostatic
  • interfere with synthesis of folic acid
  • broad spectrum
  • ineffective in presence of pus or necrotic tissue
  • widespread resistance
113
Q

Trimethoprim/Ormetroprim

A
  • inhibitor of nucleic acid
  • bacteriostatic on their own
  • act synergistically with sulfas -> combo is BACTERICIDAL
114
Q

Rifampicin

A
  • Bactericidal
  • inhibits RNA polymerase
  • highly lipid soluble: penetrates cells, including cells surrounding caseous lesions (can reach abscessed tissues)
  • useful for treating Rhodococcus equi; mycobacterial infections
    -not used alone - rapid development of resistance
    (used with erythromycin)
115
Q

Antibiotic resistance

A

you do not induce antibiotic resistant bacteria, you selectively encourage their growth and survival by killing the susceptible bacteria
-exception: membrane pumps (tetracycline resistance)

116
Q

Constitutive resistance

A

bacterial resistant to antibiotic because they lack the uptake system or target of the antibiotic

  • Pennicillin G cannot enter membranes of family Enterobacteriaceae,
  • not related to previous antibiotic exposure
117
Q

Acquired resistance

A
  • bacteria become resistance to antibiotics by mutation resulting in alteration of uptake systems or targets of the antibiotics
  • ex. staphylococcus aureus resistance to Penicillin G (due to bacterial production of enzymes that inactivate penicillin)
  • depended on prior exposur
118
Q

mechanisms of acquired resistance (not how bacteria acquires resistance)

A
  1. Alter the target for the drug
    a. modify target site
    b. reduce significance of target site (develop alt. metabolic pathway)
  2. Alter the uptake of the drug
    a. inhibiting uptake (decrease pore size)
    b. increase excretion (tetracycline resistance)
  3. Inactivate the drug
    a. synthesizing an enzyme
    • b-lactamases for penicillins and cephalosporins
119
Q

multi-antibiotic resistance

A

implies multiple different resistance mechanisms = different classes
-ex. resistance to aminoglycosides (altered ribosomal protein) AND penicillin (B-lactamase production)

120
Q

Cross-resistance

A

resistance due to a common mechanism- so that resistance to one antibiotic implies resistance to others = same class

  • resistance to newer class implies resistance to older generation
  • is unidirectional, resistance to older class doesn’t imply resistance to newer class
121
Q

Acquired resistance: 2 mechs bacteria acquire resistance genes

A
  1. changes in DNA via Mutation

2. acquisition of DNA

122
Q

acquired resistance: mutations

A

changes in genotype - most frequently arise as errors during replication

  • most mutations are lethal
  • only important if they give selective advantage: increase in pop until become dominant type
  • antibiotic resistance only confers selective advantage IF antibiotics are present
123
Q

Genetic transfer : acquired resistance

A

-acquisition of dna
-transfer of dna between strains of a given species, different species, different genera
- critical in adaption of bacteria to different environmental conditions
is responsible for multi-antibiotic resistance
- transduction and conjugation

124
Q

transduction : acquired resistance

A
  • transfer of dna following bacteriophage infection
  • bacteriophage carries its own genetic material and is transferred by integration into the bacterial chromosome
  • ex. transfer of B-lactamase from resistance to susceptible S. aureus
125
Q

Conjugation: acquired resistance

A

interbacterial DNA transfer through sex pilus

  • plamids can encode multiple antibiotic resitance genes (R. plasmids)
  • transferred vertically during bacterial division and horizontally during conjugation
  • rare in gram +
  • common in gram - organisms, esp enterobacteriaceae (salmonella)
  • conjugation can also tranfer chromosomal genes via transposons
126
Q

antibiotic sensitivity can be determined by

A
  1. gram related spectra
  2. historical
  3. in vitro sensitivity
    • some not suitable for testing (obligate anaerobes, intracellular bacteria, slow growing bacteria)
127
Q

in vitro susceptibility testing

A

a. MIC
b. measured by incubating dilutions of antibiotic with standard number of bacteria
c. 3 categories of results (Susceptible, moderately susceptible, resistant)

128
Q

MIC

A

minimum inhibitory concentration

minimum concentration of antibiotic that completely inhibits bacterial growth

129
Q

susceptible MIC

A

bacteria is inhibited at antibiotic concentrations that can be achieved in tissues using normal dosage

130
Q

moderate MIC

A

bacteria is inhibited at antibiotic concentrations achieved in tissues only at maximal dosage and/or increased frequency of administration

131
Q

Resistant MIC

A

bacteria is not inhibited at anitibiotic concentrations achievable or tolerable in animal

132
Q

antibiotic selection criteria

A

a. non-resistant antibiotic with narrowest spectrum (minimize effect on normal flora, decreased risk of promoting bacterial resistance)
b. absorption (GI vs paraenteral)
c. Tissue distribution (can it get to site)
d. excretion/inactivation (Sulfa-TIMp cannot work well in purulent materials)
e. cost
f. convenience (will owners comply)

133
Q

Leptospirosis

A

single high titer (>1:800) in unvaccinated dog is considered positive
- 4 fold rise in titer (2 weeks apart) indicative of acute infection

134
Q

general characteristics of Leptospirosis

A
  • spiral with hook-shaped ends, motile with endoflagella
  • gram (-), do not stain well with gram’s stain - requires silver staining, dark field
    >250 serovars
135
Q

Leptospirosis: Encounter

A
  • L. interrogans is an obligate pathogen
  • can survive for months in enviro (moist soil)
  • high temp or acidic pH is detrimental
  • ambient temp, neutral pH favors growth
136
Q

Leptospirosis: carrier animals

A

persist in renal tubules or genital tract
main source of infection
-infected animals SHED lepto through urine and contaminated enviro
-recovered dogs can shed for months

137
Q

Leptospirosis: direct transmission

A

from infected animal to healthy animal via contaminated urine, venereal or trans-placental transfer

138
Q

Leptospirosis: indirect transmission

A 
contaminated waters (ponds, river, moist soil)
contaminated environment
139
Q

Leptospirosis: maintenance host

A

animal species that become long term (asymptomatic) carriers and are main source of transmission

140
Q

leptospirosis: incidental host

A

animal species that acquire infection from carrier animals, leading to acute leptospirosis

141
Q

Leptospirosis: Entry and multiplication

A
  • penetrate through intact mucouc membranes of mouth, nose or eyes OR abraded, scratched or water softened skin
  • enter the blood vascular space (systemic circulation)
  • multiply rapidly and spread to many tissues (kidney, liver, spleen, lungs, eyes, genital tract, CNS
  • renal colonization in most infected animals (replicates and persists in renal epithelium)
142
Q

Leptospirosis virulence factors (2)

A

LPS: incites significant damage
Hemolysins: lysis of cells (also flagellum)

143
Q

Leptospirosis: clinical findings, Dog

A
  • uremic type (all serovars)

- icteric type (icterohemmorhagiae, pomona, grippotyphosa)

144
Q

uremic type Leptospirosis: clinical findings, dog

A
  • inappetance, lethargy, vomiting, polyuriaa, polydipsia, fever
  • oliguria, anuria, severe renal azotemia (90% cases)
  • UA: gluc, prot, active sediment, granular casts
145
Q

Icteric type Leptospirosis: clinical findings, dog

A
  • peak signs 6-8 days post onset
  • focal hepatic necrosis
  • icterus, mild-moderate hypoalbuminemia
  • chronic active hepatitis, fibrosis, failure
146
Q

Leptospirosis Clinical findings Cattle

A

(red water disease)
Abortion - L. hardjo
-abort from 4 months to term
- clinical signs in Dam (or not)
(icterus, hemoglobinuria, high fever, mastitis (thick ropy secretions) infertility>)
- Calves: immune-hemoglobinuria, mediated hemolytic anemia, acute renal failure

147
Q

Leptospirosis clinical findings horses

A 
(moon blindness)
recurrent uveitis
-up to 67% of cases
-organism need not be present to have chronic disease (autoantibodies)
acute renal failure in foals
148
Q

Leptospirosis: immunity

A

conferred via antibodies directed against LPS (adequate antibody response within 7 to 10 days PI)
-little corss protection across serovars, though sera with one serovar may have cross reactivity against other serovars

149
Q

cross reactivity vs cross protection

A

cross protection - Antibody protection for more infections
cross reaction = on a titer test ab bonds to 2 ag
in vitro vs in vivo

150
Q

Leptospirosis Diagnosis

A

culture is not useful diagnostically

clinical pathology :

 - U/A: hematuria, pyuria, proteinuria, glucosuria
 - Blood profile: increased BUN and creatinine, thrombocytopenia, increased serum bilirubin

bacteriology : (can be isolated first 7-10 days) avoid citrate anticoagulant
urine - pH 7 before transport, multiple samples (intermittent shedding) EMJH media
dark field microscopy

Serology: microscopic agglutination test (MAT)
- preferred: rising antibody titer (4 fold rise in 2-4 weeks)

other tests: FAT, ELISA, PCR

151
Q

Leptospirosis Treatment

A

animicrobials

  • reduce fever and bacteremia in a few hours
  • eliminate carrier state at 2 weeks (must continue Ab for 2 weeks)

treat systemic complications (renal, electrolyte, hemostatic)

bacterins (tetravalent, bivalent)

vaccinate - 2-3 injections, 2-3 weeks apart, boost 6-8 months, only effective if serovars in enviro are represented

152
Q

leptospirosis antimicrobial for Dogs and other animals

A

dogs - PenicillinG/ampicillin/ doxycycline

want drugs that accumulate in renal tissue

153
Q

Mycoplasma general characteristics

A
  • smallest self-replicating bacteria
  • No cell wall (no peptidoglycan layer, no LPS (endotoxin), highly flexible)
  • do not stain by grams method (Giemsa)
  • resistant to antibiotics which interfere with cell wall function
  • extremely fragile (susceptible to desiccation, heat, detergents, disinfectants)
  • fastidious bacteria (need special media) - facultative anaerobe
  • obligate parasites
  • endogenous or exogenous in origin
154
Q

Mycoplasma - Exogenous

A
  • typically introduced into a group by addition of clinically healthy carrier animal
  • infection spread direct/droplet contact with oral, ocular, genital secretions, iatrogenic, via tick bites
155
Q

Mycoplasma - Endogenous

A

some ar enormal flora

  • chronic or low grade infections
  • various stress conditions may predispose to infection
    • concurrent bacterial or viral infection
    • transportation stress
156
Q

Mycoplasma - virulence factors

A
  • Adhesins: surface structure used for binding bacteria to host cells
  • Capsules: aid formation fo biofilm, impede host defense, improves persistence in enviro
  • Hydrogen peroxide: affects ciliary movement in trachea and induces hemolysis
  • Biofilm: increase resistance to desiccation, heat and complement mediated lysis
157
Q

2 major forms of mycoplasma infections

A
  1. Localized infection - mycoplasma usually remain localized to one or more organs
  2. Invasive blood borne infections - invasive mycoplasmas penetrate epithelial barriers and enter blood stream
158
Q

Mycoplasma localized infections

A

“chronic respiratory disease” caused by M. gallisepticum in chickens, turkeys, game birds

159
Q

Mycoplasma localized infection encounter/entry

A
  • infection via respiratory route
  • infection is exogenous in origin (in mycoplasma free flocks)
    -can also be transmitted vertically and enter flock thru infected eggs
    asymptomatic carriers become sick/shed organisms in respiratory aerosols if stressed (endogenous)
160
Q

Mycoplasma localized infection: multiplication and spread

A

-M gallisepticum attaches ciliated epithelium of trachea via ADHESIN and multiplies

161
Q

Mycoplasma localized infection: damage

A

M. gallisepticum destroys cilia

lesions include sinusitis, tracheitis, airsacculitis

162
Q

Mycoplasma localized infection: symptoms

A

coughin, sneezing, nasal discharge, difficulty breathing, reduced growth, decreased egg production
-high morbibity, mortality low

163
Q

Mycoplasma localized infection: diagnosis

A

culture
FA
PCR from exudate & tissue
ELISA on serum

164
Q

Mycoplasma localized infection: Treatment and control

A

antibiotics (tylosin, tiamulin, chloretracycline, lincomycin)

  • depopulation and disinfection if wish to eradicate
  • live vaccine is available
165
Q

Mycoplasma Invasive infection

A

can be endogenous or exogenous

  • penetrate epithelial barriers and enter blood stream
  • generalized infection & acute septicemia leading to fever and sudden death
  • inapparent mycoplasmemia leads to localization in serosal cavities adn joints

-ex. M hyosynoviae - commensals URT and causes of arthritis in pigs

166
Q

Feline hemotrophic mycoplasmosis

A
  • aka feline hemobartonellosis
  • hemolytic anemia in cats
    3 distint hemotrophic mycoplasma in cats
    1. M. hemofelis (most common)
    2. M. hemominutum
    3. M. turicensis
167
Q

Feline hemotrophic mycoplasmosis: encounter and entry

A
  • not known
  • male, non-predigreed outdoor cats are highly susceptible
  • predisposing factors: stress, FIV/FeLV, abscesses, corticosteroids

-can be endogenous /exogenous in origin

168
Q

Feline hemotrophic mycoplasmosis: endogenous vs exogenous

A

endogenous: low grade/inapparant infection are common

exogenous:
- arthropod vectors
- biting and fighting
disease transmitted from queen to new borne
- blood transfusion

169
Q

Feline hemotrophic mycoplasmosis: multiplication and spread (4 phases)

A
  1. Preparasitemic phase
    • 1-3 weeks PI, bacteria replicating but not present in detectable levels in blood, mild reduction in HCT
  2. Acute phase
    • 30 days or more, high number of bacteria in blood, peak over 1-5 days and rapidly decline, death of massive bacteremia, parasitic RBC are sequestered in spleen, rapid decrease in HCT, without treatment 1/3 cats die of anemia
  3. Recovery phase
    • time from last major bacteremia until HCT has stabalized close to reference range, regenerative bone marrow response will compensate for the erythrocyte destruction (~1 months)
  4. Chronic/carrier phase
    • recover from acute infection then chronically infected for months or years, carrier cats are balanced state in which multiplication is balanced by phagocytosis and removal of organism
170
Q

Feline hemotrophic mycoplasmosis: Damage

A

regenerative anemia with polychromasia and reticulocytosis

-precipitous drop in HCT

171
Q

Feline hemotrophic mycoplasmosis: clinical signs

A
  • Acute disease: fever, marked mental depression, tachypnea, weakness, anorexia, weight loss, pale mucous membranes, dehydration
  • Chronic Disease: mild anemia, generally remains bright and alert
172
Q

Feline hemotrophic mycoplasmosis: diagnosis

A

M. hemofilis cannot be cultured in lab
blood smear:
- organisms usually present in RBC, false negatives (organisms detected 50% of time),
-false positives: accurate discrimination from false positives
- prepare smear from fresh blood (organisms may detach in EDTA)
- Antibiotics reduces number of organims

PCR:

  • highly sensitive
  • as low as 50 M. hemofelis can be detected in blood
  • PCR positive 4-15 days PI
  • PCR negative during therapy
  • carrier stages are common so PCR/blood smear should be correlated with clinical findings
173
Q

Feline hemotrophic mycoplasmosis: treatment and prevention

A
  • blood transfusion
  • glucocorticoids (reduce erythrocyte phagocytosis)
  • antibiotics (tetracycline/doxycycline (3 weeks) does not clear infection
174
Q

Mycobacterial infections

A
  • aerobic, non-spore forming, non-motile “gram-positive rods”
  • Acid-Fast bacilli (AFB)
    • cell wall structure (mycolic acids &lipids, protect against phagocytosis, extreme pH and enviro stresses)
  • Can NOT be stained with gram staining - need Zheil-Neelsen method
  • slow growing
  • complex egg-basd media for growth -must tell lab
  • facultative intracellular pathogens of macrophages (inhibit fusion of phagosome and lysocome, cause granulomatous infections)
  • disease chronic and progressive
  • 7 genus includes diverse species (some are obligate pathogens, some are saprophytes)
175
Q

mechanism of granuloma formation

A

mycobacteria live inside macs, bacilli released from dead macs, engulfed by new one. T-cells surround macs to induce macrophages to kill bacteria.
cytokines increase macs to area, gradual accumulation of macs leads to granuloma consisting of peripheral zone of T-lymphocytes, macs, fibroblasts and giant cells, with central caseous necrosis

176
Q

Mycobacterium obligate pathogens

A

M Bovis or M tuberculosis

  • grow slow
  • must cause disease for efficient transmission
  • survive in the environment for long time
177
Q

Mycobacterium - saprophytes

A

non-tuberculous mycobacteria (NTM) capable of causing opportunistic infection

  • unpredictable susceptibility to antibiotics (culture and senstitivity are important)
  • can cause skin infections in dogs, cats, other animals due to wound contamination
  • inhalation: pneumonia
  • ingestion: GI infection including lymph nodes
  • immunosuppression: disseminated systemic disease
178
Q

diagnosis of NTMs (mycobacteria)

A

histology:
-pyogramulomatous inflammation, filamentous bacteria, ZN stain: filamentous “acid fast bacilli)

PCR:
on tissue sections or culture

Culture and sensitivity

179
Q

Major pathogenic mycobacteria

A

M. Bovis -aka bovine tuberculosis (wide host range)
- primarily cattle. also others, except chickens are resistant

M. tuberculosis
-primarily human, but dogs, rodents, swine also

M avian subspecies avium
-primarily poultry, also pigs, horses, wild birds

M avian subspecies paratuberculosis (Johne’s disease)
- Cattle, sheep, goats, deer

180
Q

M. bovis (Bovine tuberculosis) : encounter

A

infected animals are the source

  • bacteria in exhaled respiratory droplets, sputum, milk, feces, urine, vaginal discharge (10 bacteria are enough to cause infection via AEROSOL but need 10^7 for oral infection)
  • survives in enviro for 4 days (summer), 28 days (winter)
  • survives longer in organic material
  • crowded/enclosed conditions aid transmission
181
Q

M. bovis (Bovine tuberculosis) : Entry, multiplication, spread

A
  • bacteria inhaled or ingested and are taken up by macrophages
  • multiply intracellularly and travel inside macs to regional lymph nodes (2 wks)
  • spread through lymphatics and blood, disseminate widely (liver, spleen, lungs, brain, bone) (3-4 wks)
182
Q

M. bovis (Bovine tuberculosis): 2 outcomes

A

adequate cell mediated immunity controls infection (latency)

unchecked multiplication of bacteria leads to tuberculosis (systemic granulomas)

183
Q

M. bovis (Bovine tuberculosis) : clinical signs

A
  • maybe no sings
  • signs depend on organs involved
  • respiratory signs - moist cough, dyspnea, weight loss
  • rarely mastitis
  • enlarged bronchial, mediastinal, mesenteric notes at necropsy
184
Q

M. bovis (Bovine tuberculosis) : Diagnosis: caudal fold test

A

Caudal fold test (intradermal skin test)

  • measuring delayed type hypersensitivity to intradermally injected tuberculin (PPD - purified protein derivative) of M. bovis
  • swelling at 48-72 hours (cows become test positive 3-6 wks PI) (false negs)
  • must be confirmed by comparative cervical test- reaction to M. bovis, not M. avium considered positive
185
Q

M. bovis (Bovine tuberculosis) : diagnosis

A
  • Caudal fold test
  • lesions at necropsy (acid fast bacteria microscopically, lok for granulomas)
  • culture (requires special media and lab, definitive diagnosis possible)
  • PCR (definitive diagnosis, rapid and sensitive)
186
Q

M. bovis (Bovine tuberculosis) :treatment and control

A
  • no treatment recommended (slaughter)
  • test newly introduced animals (test before purchase, isolate and retest 60 days after purchase)
  • mostly eliminated from commercial US herds
  • threat: wildlife (deer)
  • no vaccine
187
Q

Johne’s Disease (Bovine paratuberculosis)

A

caused by M. avium subsp. paratuberculosis (MAP)

188
Q

Johne’s Disease (Bovine paratuberculosis) : Encounter

A
  • environment w/ fecal material from infected animals
  • organism replicates only inside host but can survive in enviro in soil and water >1 yr
  • very slow-growing: >8 weeks to get colony in lab
  • USDA est. 70% of US dairy herds infected
189
Q

Johne’s Disease (Bovine paratuberculosis) : Entry, multiplication, spread

A
  • fecal-oral infection
  • exposed shortly after birth by ingestion of manure, contaminated feed/water or by acquisition of organisms in udder or milk
  • organisms ingested by macs in peyers pathces of ileum
  • bacterial multiply intracellularly, kills macs, spreads to adjacent cells
  • to control, more immune cells recruited to intestine, large amounts of cytokines released -> thickening of intestine and loss of absorptive funcion
190
Q

Johne’s Disease (Bovine paratuberculosis) : clinical signs

A
  • infection occurs in perinatal period, but signs rarely develop before 2 years of age
  • reduced milk production, diarrhea, weight loss, normal appetite
  • contagious, chronic debilitating enteritis with emaciation
  • shedders often not clinically ill
191
Q

Johne’s Disease (Bovine paratuberculosis): diagnosis

A

direct microscopy

  • DNA based PCR - sensitive
  • Sserological tests - low sensitivity (elisa)
  • Culture - from manure or ileal node, takes 3-4 months
  • intermittently shed in feces so fecal culture may be neg despite active infection
  • Johnin test
192
Q

Johne’s Disease (Bovine paratuberculosis) : treatment and control

A
  • no satisfactory treatment
  • eliminate infected animals
  • control: MAP enters herd thru introduction of infected healthy animals
    • test herds, babies born in clean enviro, avoid manure contamination of water/beed, identify infected animals and isolate or cull
193
Q

UTI definition

A

refers to microbial colonization of URINE or any urinary tract organ, except distal urethra (has normal flora)

194
Q

UTI clinical significance in canine and frequently isolated pathogens

A
  • Lower UTI (cyctitis) most common
  • E. coli, Proteus, Klebsiella (>75%)
  • staph, strep (<25%)
  • fungi (Candida)
195
Q

UTI common pathogens Feline

A

E. coli, proteus, staph, pasteurella

196
Q

UTI encounter

A
  • usually normal flora of lower UT

- opportunistic infections

197
Q

UTI entry

A
  • bacteria ascend through urethra into normally sterile bladder
  • colonization due to bacterial virulence factors (infection)
198
Q

Urinary tract defenses

A

flushing of urine - URINE FLOW

- anti-adherence mechanisms (epithelial cell exfoliation, urine osmolatiy, urinary oligosaccharides)

199
Q

causes of UTI

A

a) urinary stasis
b) mechanical impediment to flow
c) damage to epithelium
d) late gestation (pressure from uterus)
e) virulence factors (fimbriae)

200
Q

pyelonephritis

A

ascend through ureters to renal pelvis, much less common but much more serious than lower UTI

201
Q

UTI clinical signs

A

Dysuria

a) pollakiuria (increased freq)
b) oliguria - (reduction in output)
c) stranguria (straining)
d) HEMATURIA (blood in urinee)
e) painful bladder, small , firm

202
Q

recurrent cyctitis can lead to ?

A

pyelonephritis

prostatitis

203
Q

UTI - urinalysis

A
  • red/brown -> blood
  • transparency: turbid with pyuria, bacteriuria, crystaluria
  • foul smell
  • isosthenuric USG (with renal failure/metabolic dz)

2) dipstick - protein, occult blood, pH
3) micro exam - epithelial cells, erythrocytes, crystals, bacteria

204
Q

acid, rod (UTI)

A

E. coli

205
Q

acid, cocci (UTI)

A

step, enterococcus

206
Q

alkaline, rods (UTI)

A

proteus

207
Q

alkaline, cocci

A

staph

208
Q

Source of urine for diagnosis of UTI

A

cystocentesis - any positive culture is signficant

catheterization - < 10^3 = contamination
10^3-10^5 = questionable
>10^5 = significant

209
Q

antibiotic selection (UTI)

A

ampicillin concentrated >35 fold

  • need it to concentrate in urine not blood
  • administer for 10-14 days
  • aminoglycosides may be nephrotoxic
210
Q

UTI - treatment failures

A

underlying cause

  • relapse
  • reinfection
211
Q

relapse (UTI)

A

infection with same organism (not cleared by treatment)

212
Q

reinfection (UTI)

A

infection with a new organism (did not remove urolith)

213
Q

chronig UTI treatment

A

antibiotics for 4-6 weeks

-reculture at 48 hours after every month for 6 months

Bacteriology (2 decks)

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