Bacteriology Exam 3

Front 1

name four different prions, the animals they infect, and the diseases they cause.

Back 1

1. PrP-SC; sheep/goats; transmissible spongiform encephalopathy, scrapie
2. PrP-BSE: cattle; BSE
3. PrP-VCJD: humans; variant Creutzfeld-Jacobs disease
4. PrP-CWD: cervids; chronic wasting disease (CWD)

Front 2

what is the term "prion" short for?

Back 2

protein infectious particle

Front 3

what are the two basic types of prion proteins?

Back 3

PrP-sen: protease sensitive
PrP-res: protease resistant

Front 4

in what two basic ways are protease resistant prion proteins (PrP-res) acquired?

Back 4

1. ingestion
2. PrP-sen conversion to PrP-res

Front 5

what are the two hypotheses about how protease sensitive prion proteins (PrP-sen) throughout the body can spontaneously convert to PrP-res proteins and cause disease?

Back 5

1. virino hypothesis: PrP-res may serve as receptor for a small nucleic acid
2. (most widely accepted) protein-only hypothesis: the PrP-res catalyzes the conversion to PrP-sen → PrP-res

Front 6

how is a prion disease diagnosed?

Back 6

- presumptive: clinical signs and ELISA from the retropharyngeal lymph nodes
- definitive: tissue of the obex of the brainstem is digested in protease and the residue is tested via immunohistochemistry or Western blot

Front 7

scrapie:
- causative agent
- species
- incubation time
- transmission
- clinical signs

Back 7

- PrP-SC
- sheep and goats
- 6-12 months
- ingestion of infected tissues; genetic predisposition
- pruritis/scraping (neurologic); hyperexcitability; ataxia; inappetance; death (starvation)

Front 8

BSE
- causative agent
- species
- incubation time
- transmission
- clinical signs

Back 8

- PrP-BSE ("mad cow disease")
- cattle
- 2-4 years
- ingestion of contaminated meat and bone meal
- aggressiveness, hyperexcitability, head rubbing, nose licking, ataxia, hypermetria (exaggerated gait), gradual weight loss despite normal appetite, unable to eat, death (starvation)

Front 9

Chronic Wasting Disease
- causative agent
- species
- incubation time
- transmission
- clinical signs

Back 9

- PrP-CWD
- deer and elk (cervids)
- 4-12 months
- horizontal transmission proposed
- ataxia, pacing, head tremors, salivation, weight loss, death

Front 10

what three genera of veterinary importance are in Family Anaplasmataceae?

Back 10

1. Neorickettsia
2. Anaplasma
3. Ehrlichia

Front 11

Family Anaplasmataceae:
- morphology
- motility
- staining

Back 11

- pleomorphic coccobacilli
- immotile
- too small for Gram stain; use Romanovsky stains

Front 12

name four Romanovsky stains?

Back 12

1. Diff-quik
2. Giemsa
3. Wright's
4. Gimenez

Front 13

Anaplasmataceae
- comment on the two forms of these bacteria
- how to they multiply
- what type of parasites are they and why?

Back 13

- morulae is the replicative form
- dense core is the infectious form
- the morulae divide inside the cell by binary fission, convert to dense cores, and lyse their cells
- they are obligate intracellular parasites because they are chemoheterotrophs, meaning they need some of the enzymes of the host to be able to divide

Front 14

what class of antibiotics is most useful in treating Anaplasmataceae, Chlamydiales, Rickettsiaceae, Coxiella, and Mycoplasmatales?

Back 14

tetracyclines

Front 15

fluke fever:
- causative agent
- species affected
- clinical signs
- how is it commonly acquired?

Back 15

- Neorickettsia helminthoeca
- dogs, other
- lymphadenopathy, GI
- consumption of raw fish, especially salmon

Front 16

Potomac horse fever
- causative agent
- old name of infectious agent
- clinical signs
- prevention

Back 16

- Neorickettsia risticii
- formerly Ehrlichia risticii
- primarily GI problems
- Ehrlichiosis bacterin vaccine

Front 17

Anaplasmosis
- causative agent
- species infected
- clinical signs
- prevention

Back 17

- Anaplasma marginale
- cattle
- anemia
- tick control, killed vaccine

Front 18

Equine granulocytic ehrlichiosis
- causative agent
- old name of infectious agent
- species affected
- clinical signs
- diagnosis
- prevention

Back 18

- Anaplasma phagocytophilum
- formerly Ehrlichia equi
- horses and dogs
- anemia, leukocytopenia, arteritis
- Dx: 4D SNAP test
- prevention: tick control

Front 19

Tropical Pancytopenia
- another name for this disease
- causative agent
- species affected
- clinical signs
- diagnosis

Back 19

- also called Canine ehrlichiosis
- Ehrlichia canis
- dogs
- epistaxis, hemorrhages, lymphadenopathy
- 3D or 4D SNAP test

Front 20

Heartwater
- causative agent
- old name for causative agent
- species affected
- clinical signs
- where is this disease found?
- control

Back 20

- Ehrlichia ruminatum
- formerly Cowdria ruminatum
- neurologic, lymphadenopathy, hemorrhages
- this is a foreign animal disease
- premunition is used to "vaccinate"

Front 21

what is premunition in terms of prevention of certain bacterial diseases? How does age play a factor in the procedure?

Back 21

- deliberately challenging the animal with attenuated organisms to build immunity.
- older animals have a risk of a carrier state, so this should be combined with tetracycline

Front 22

chronic respiratory disease in birds:
- another name for this disease
- causative agent

Back 22

- Mycoplasmosis; CRD
- Mycoplasma gallisepticum

Front 23

Mycoplasmosis in pigs
- causative agent
- clinical signs
- control

Back 23

- Mycoplasma hyopneumoniae
- respiratory, polyarthritis
- vaccine

Front 24

Contagious bovine pleuropneumonia
- causative agent
- clinical signs
- where is this disease found?

Back 24

- Mycoplasma mycoides ss mycoides
- pleuropneumonia
- foreign animal disease

Front 25

Mycoplasmosis in cattle
- causative agent
- clinical signs
- where is this disease found?

Back 25

- Mycoplasma bovis
- respiratory, mastitis
- usually found at large dairies

Front 26

Mycoplasmosis in goats
- causative agent
- clinical signs

Back 26

- Mycoplasma capricolum
- polyarthritis, conjunctivitis

Front 27

Mycoplasmosis in dogs
- causative agent
- clinical signs

Back 27

- Mycoplasma canis
- urogenital infection

Front 28

Mycoplasmosis in cats
- causative agent
- clinical signs
- differential diagnoses

Back 28

- Mycoplasma felis
- respiratory, conjunctivitis
- DDx: Chlamydiophila felis, feline calicivirus, feline rhinotracheitis virus

Front 29

Eperythrozoonosis
- causative agent
- old name for causative agent
- species affected
- clinical signs

Back 29

- Mycoplasma suis
- formerly Eperythrozooan sp.
- pigs
- anemia

Front 30

Hemobartenellosis in dogs
- causative agent
- old name for causative agent
- clinical signs
- control

Back 30

- Mycoplasma hemocanis
- formerly Hemobartonella canis
- anemia
- flea and tick control

Front 31

Hemobartenellosis in cats
- causative agent
- old name for causative agent
- clinical signs
- control

Back 31

- Mycoplasma hemofelis
- formerly Hemobartonella felis
- anemia
- flea and tick control

Front 32

Granular vulvitis/vaginitis
- causative agent
- species affected
- clinical signs

Back 32

- Ureaplasma diversum
- cattle
- urogenital infection

Front 33

what species in Family Mycoplasmatale commonly cause urinary tract infections in dogs and cats? Be specific as to which agent affects which host species

Back 33

1. Mycoplasma canis (dogs)
2. Ureaplasma canigenitalium (dogs)
3. Ureaplasma cati (cats)

Front 34

which species of Chlamydiophila have zoonotic potential? What are the animal hosts and clinical manifestations of these infections?

Back 34

1. Chlamydiophila psittaci in birds (especially psittacines); respiratory infection and polyserositis. Flu-like symptoms in humans.
2. Chlamydiophila abortus in sheep; causes abortion

Front 35

Psittacosis
- other names for this disease
- causative agent
- old name for causative agent
- species affected
- clinical signs

Back 35

- Chlamydiosis, Chlamydiophilosis
- Chlamydiophila psittaci
- formerly known as Chlamydia psittaci
- birds, humans (ZOONOTIC)
- birds: respiratory infection, polyserositis; humans: flu-like symptoms

Front 36

Feline conjunctivitis and rhinits
- causative agent
- old name for causative agent
- clinical signs
- differential diagnoses

Back 36

- Chlamydiophila felis
- formerly known as Chlamydia felis
- respiratory infection, conjunctivitis
- DDx: Mycoplasma felis, feline calicivirus, feline rhinotracheitis virus

Front 37

Enzootic abortion in ewes (EAE)
- causative agent
- old name for causative agent
- species infected
- clinical signs
- control

Back 37

- Chlamydiophila abortus
- formerly Chlamydia abortus
- sheep, humans (ZOONOTIC)
- abortion
- chemoprophylaxis with tetracycline during lambing season; vaccination; pregnant women should not handle infected sheep

Front 38

Ovine polyarthritis and conjunctivitis
- causative agent
- old name for causative agent
- species affected
- clinical signs
- when is this disease commonly seen?

Back 38

- Chlamydiophila pecorum
- formerly Chlamydia pecorum
- sheep, rarely cattle
- polyarthritis, conjunctivitis, (in cattle) neurologic
- epizootics associated with severe (cold) weather

Front 39

Rocky Mountain Spotted Fever
- causative agent
- species affected
- clinical signs
- control

Back 39

- Rickettsia rickettsii
- dogs, humans (ZOONOTIC)
- hemorrhages, anemia, vasculitis
- tick control

Front 40

Q fever
- causative agent
- species affected
- clinical signs

Back 40

- Coxiella burneti
- canids, felids, humans (ZOONOTIC)
- abortion; (in humans) flu-like symptoms and chronic disease

Front 41

Chlamydiales:
- atmospheric requirements
- comment on the two forms of this organism
- what type of parasite are they? why?

Back 41

- anaerobes
- elementary form is the non-replicating, infectious form; reticulate body is the intracellular, non-infectious, replicating form.
- they are obligate intracellular parasites because being chemoheterotrophic, they don't have all of the enzymes necessary to replicate outside the host cell

Front 42

describe the histological appearance of Cryptococcus

Back 42

- variably sized
- intra- or extra-cellular yeasts
- with thick, non-staining capsule
- and narrow-based budding

Front 43

what are two Cryptococcus species of veterinary importance? Comment on host immunity with regards to pathogenicity.

Back 43

1. Cryptococcus neoformans - compromised immunity required
2. Cryptococcus gatti - infects those with intact immunity

Front 44

Cryptococcus neoformans
- where is it found?
- host species
- route of infection

Back 44

- found worldwide
- cats, dogs <4 years of age, rarely in other species
- probably acquired bby inhaling basidospores or dried-up yeast cell

Front 45

what are three clinical signs of Neorickettsia helminthoeca and elokominca infection in dogs?

Back 45

- Fever
- Vomiting/Diarrhea
- Lymphadenopathy
(Mortality up to 90% if untreated)

Front 46

what is the pathology of disease and lesions caused by Neorickettsia helminthoeca and elokominca?

Back 46

- leukopenia progressing to leukocytosis associated with secondary infections
- lymphadenopathy (especially mesenteric) with lymphoid necrosis
- petechial hemorrhages in intestinal mucosa

Front 47

how are Neorickettsia helminthoeca and elokominca infections diagnosed?

Back 47

- serology: IFA
- cytology: LN aspirate, buffy-coat monocytes, macrophages
- fecal flotation for presence of fluke eggs

Front 48

Name six clinical signs of Neorickettsia risticii in horses

Back 48

1. Fever
2. +/- diarrhea
3. decreased gut sounds
4. painful abdomen
5. lameness
6. abortion

Front 49

What is the pathology and lesions caused by Neorickettsia risticii in horses

Back 49

- leukopenia with rebound leukocytosis
- anemia
- elevated PCV
- GI mucosal hyperemia/necrosis
- ulcerative gastroenteritis
- fluid-filled cecum/colon
- laminitis

Front 50

what diagnostic tests are used for definitive diagnosis of Neorickettsia risticii in horses?

Back 50

- serology: ELISA, IFA, Ab response detectible but not responsive
- Cytology/Histopathology
- Colonoscopy
- PCR

Front 51

how is Neorickettsia risticii controlled and prevented in horses?

Back 51

- vaccination - "Ehrhichiosis" bacterin with a booster
- if booster is not used, horses will become infected, but disease will be less severe
- vector control (snails)

Front 52

Anaplasma marginale
- species affected
- where is it prevalent?
- how is it transmitted?

Back 52

- cattle
- south-east, Gulf coast; worldwide
- Ticks, Tabanidae (horse flies), possible from needles

Front 53

Anaplasma marginale
- comment on age-related factors
- comment on carrier state factors with regards to disease manifestation
- five clinical signs

Back 53

- calves < 1 year are susceptible to infection, but refractory to disease; generally cows > 1 year old are affected with disease
- carriers can develop disease when stressed
1. fever
2. muscle weakness
3. icterus
4. abortion (due to fetal hypoxia)
5. mortality

Front 54

Anaplasma marginale infection in cattle histopathologic signs

Back 54

(note that this is a hemolytic disease)
- > 15% RBCs infected
- low PCV
- low RBC
- ↑bilirubin
- severe hemolytic anemia
- no hemoglobinurea (as opposed to Babesia)
- necropsy: thin, watery blood; icterus; hepatosplenomegaly; enlarged gallbladder

Front 55

how is Anaplasma marginale infection in cattle diagnosed?

Back 55

- serology: ELISA, IFA, CF
- cytology: Geimsa stain

Front 56

how is Anaplasma marginale infection in cattle controlled?

Back 56

- vaccination with correct killed whole-cell product - note different regions have different antigenic variants
- premunition in older animals + tetracycline in feed
- continuous feeding of tetracycline
- vector control (ticks, flies)

Front 57

what are two unique clinical signs of Anaplasma phagocytophilum in horses?

Back 57

1. limb edema
2. ataxia

Front 58

comment on the zoonoses of Anaplasma phagocytophilum

Back 58

possible cause of Human Granulocytic Ehrlichiosis (HGE)

Front 59

how do does become infected with Anaplasma platys? clinical signs? diagnosis?

Back 59

- Rhipicephalus sanguineus ticks
- fever
- depression, anroexia
- epistaxis, hemorrhages of mucous membranes
- lymphadeonpathy
- thrombocytopenia, mild regenerative anemia
- Dx: see organisms in platelets

Front 60

what causes Canine Ehrlichiosis?
- who gets the disease
- how is it acquired?
- phases of the disease

Back 60

- Ehrlichia canis
- usually puppies; German shepherds are predisposed
- transmitted from Rhipicephalus sanguineus ticks
- disease: acute phase; subclinical phase; chronic phase

Front 61

what are six clinical signs of Ehrlichia canis?

Back 61

1. recurrent fever
2. epistaxis due to lung and nasal mucosal hemorrhage (disease attacks platelets)
3. oculonasal discharge
4. SQ hemorrhage
5. lymphadenopathy
6. convulsions → death

Front 62

how does Ehrlichia canis cause acute disease in dogs?

Back 62

hemorrhages due to anti-platelet antibodies, preventing platelet aggregation

Front 63

what is the causative agent of Heartwater, species affected, and clinical signs?

Back 63

- Ehrlichia ruminatum
- cattle, sheep, goats, wild ruminants
- "Sick animal" signs
- acute form - fever, tachypnea, hyperasthesia, muscle twitching, paddling, opisthotonus, nystagnus, convulsions, death
- subacute form - fever, mild CNS signs
- there is a subclinical form

Front 64

what are the pathological lesions associated with Heartwater (Ehrlichia ruminatium) infection?

Back 64

- hydropericardium
- sub-epicardial/endocardial hemorrhages
- hydrothorax
- pulmonary edema
- ascites
- edema of LN and brain
- splenomegaly
- renal necrosis

Front 65

Family Rickettsiaceae
- type of parasite
- morphology
- staining

Back 65

- obligate intracellular parasite
- cocobacilli
- need a Romanovsky stain (Wright's, Giemsa)

Front 66

Coxiella
- morphology
- type of parasite
- staining

Back 66

- pleomorphic, but often rod-shaped
- obligate intracellular parasite
- Romanovsky stain or acid-fast

Front 67

Coxiella
- virulence factors
- how do they survive outside the host?

Back 67

- LPS, can undergo phase variation
- forms endospores that are environmentally resistant

Front 68

Mycoplasmatales
- morphology
- type of parasite
- staining

Back 68

- they have no cell wall and are pleomorphic
- chemoheterotrophs (compete with cells for nutrients)
- they are too fragile to stain

Front 69

Mycoplasmatales
- atmospheric requirements
- plasma membrane composition
- comment on size of the organisms and the genome

Back 69

- facultative anaerobe
- trilaminar cell membrane high in sterols
- they are the smallest and simplest prokaryotes with a small, circular genome

Front 70

What are two genera of veterinary importance in Order Mycoplasmatales

Back 70

1. Mycoplasma
2. Ureaplasma

Front 71

Chamydiales Elementary Body
- what does it do?
- morphology
- structure of the cell

Back 71

- this is the non-replicating, infectious form
- coccoid and smaller than reticulate body
- rigid walled, has a bilayer membrane, densely-packed cell

Front 72

Chlamydiales Reticulate Body
- what does it do?
- morphology
- structure of the cell

Back 72

- this is the replicating, non-infectious form
- spherical to ellipsoid and is 2-3x larger than the elementary body
- bilayer membrane enclosing reticulated cytoplasm; has ribosomes

Front 73

Chlamydiales
- type of parasite
- comment on its genome
- atmospheric requirements

Back 73

- obligate intracellular parasite
- contains both DNA and RNA
- anaerobic; has no cytochromes

Front 74

Chalmydiales
- why is it an obligate intracellular parasite?
- comment on environmental survival

Back 74

- it is a chemoheterotroph and needs ATP from host, as well as other metabolites
- the elementary body can survive a long time in soil, secretions, and feces

Front 75

Chlamydiophila psittaci in birds - 6 clinical signs

Back 75

1. sinusitis
2. conjunctivitis
3. airsacculitis
4. fibrinous pericarditis
5. perihepatitis
6. polyserositis

Front 76

Chlamydiophila psittaci in birds diagnosis

Back 76

- serology
- Kodak SureCell or Clearview Chlamydia
- stained impression smears
- PCR
- culture

Front 77

which Chlamydiophila species are zoonotic or potentially zoonotic? Reportable?

Back 77

1. Chlamydiophila psittaci - reportable
2. Chlamydiophila abortus
3. Chlamydiophila felis

Front 78

how is Chlamydiophila psittaci controlled and prevented?

Back 78

- no vaccine
- biosecurity
- quarantine with chlortetracycline in the feed

Front 79

Chlamydiophila abortus
- common species infected
- transmission
- clinical signs

Back 79

- sheep, but it is also zoonotic (pregnant women should not handle sheep)
- horizontal transmission from aborted fetuses and placentas
- abortion, stillbirths, weak lambs, placentitis

Front 80

Chlamydiophila abortus
- diagnosis
- control and prevention

Back 80

- Dx: serology, cytology, histopath
- inactivated vaccine prior to breeding with boosters
- tetracycline in feed 2 weeks prior to lambing and throughout lambing season

Front 81

Chlamydiophila pecorum
- species affected (diseases)
- transmission

Back 81

- sheep (ovine polyarthritis and conjunctivitis)
- cattle (sporadic bovine encephalomyelitis)
- transmission from aerosol or oral ingestion of infectious materials

Front 82

Chlamydiophila pecorum in sheep
- disease name
- predisposing factors
- clinical signs

Back 82

- ovine polyarthritis and conjunctivitis
- stress is needed such as overcrowding, high nutritional plane, inclement weather
- (typically mild) conjunctivitis with follicular hyperplasia, loss of body condition, polyarthritis

Front 83

Chlamydiophila pecorum in cattle
- disease name
- clinical signs

Back 83

- sporadic bovine encephalomyelitis
- (typically affects young), hypersalivation, peritonitis, anorexia, pneumonia, dyspnea, encephalitis, ataxia

Front 84

Chlamydiophila pecorum
- diagnosis
- control and prevention

Back 84

- cytology, Kodak SureCell, Clearview Chlamydia, culture
- no vaccine; add tetracyclines to feed in inclement weather

Front 85

Chlamydiales
- environmental stability
- how are they acquired
- what general clinical signs do they produce?
- how are they treated?
- public health concerns

Back 85

- environmentally stable
- transmitted through inhalation and/or ingestion
- conjunctivitis / URT infection / polyserositis, polyarthrtitis
- treated with tetracyclines
- persistent/latent infections that can be zoonotic

Front 86

Chlamydiophila felis
- what disease does it cause?
- how is it transmitted?

Back 86

- feline conjunctivitis and rhinitis (old name: feline pneumonitis)
- aerosol; contact with infectious agents

Front 87

what are five clinical signs of Chlamydiophila felis infection in cats?

Back 87

1. fever
2. URT
3. erythematous/swollen conjunctiva
4. follicular hyperplasia in the eye
5. chronically, weight loss

Front 88

Chlamydiophila felis
- diagnosis
- control and prevention

Back 88

- cytology: intracytoplasmic inclusions in Giemsa-stained conjunctival smears
- antigen detection tests
- culture
- control and prevention: vaccination with annual booster

Front 89

comment on the zoonosis of Chlamydiophila felis

Back 89

- conjunctivitis (most common)
- reports of endocardidits, glomerulonephritis, chronic cough, flu-like symptoms

Front 90

what is the Rickettsia species of veterinary importance and the major disease that is causes? species susceptible?

Back 90

- Rickettsia rickettsii
- Rocky Mountain Spotted Fever
- dogs and humans

Front 91

Rickettsia rickettsii
- transmission
- reservoir hosts
- what age group of dogs is most commonly infected?

Back 91

- Dermacentor ticks
- reservoir: wild rodents, hares, rabbits
- dogs < 2 yr are most commonly infected

Front 92

what are six clinical signs of Rickettsia rickettsii infection in dogs?

Back 92

1. fever
2. abdominal pain
3. swelling in the extremeties, face, pinnae, genitals
4. mucous membrane hemorrhage
5. lymphadenopathy
6. polyarthritis

Front 93

how can Rickettsia rickettsii infection lead to death in dogs (pathogenesis)

Back 93

- thrombocytopenia, anemia and leukopenia → leukocytosis
- necrotizing vasculitis
- DIC

Front 94

how is Rickettsia rickettsii infection in dogs diagnosed?

Back 94

- serology: IFA, latex agglutination
- histopath/skin biopsy with Giemsa stain
- organism will appear in endothelial cells and vascular smooth muscle
- PCR of blood
- 4D SNAP test

Front 95

how is Rickettsia rickettsii infection in dogs treated and prevented?

Back 95

- Tx: doxycycline
- tick control

Front 96

what is the Coxiella species of veterinary importance? in what animals does it cause disease?

Back 96

- Coxiella burnetti
- cattle, sheep, goats, canidae, felidae, wild herbivores, humans

Front 97

Coxiella burnetti
- transmission
- environmental stability
- what are the main two clinical signs in animals?

Back 97

- transmitted by direct and/or indirect contact with infected tissues, aerosols, dust from dried tissues, insect vectors
- stable in the environment as endospores
- infertility and abortion are the main clinical signs

Front 98

comment on the pathology of Coxiella burnetti

Back 98

- multisystemic
- may localize in mammary tissue, lymph nodes, uterus, placenta
- infertility, abortion, ocassionally placentitis/endometritis

Front 99

Coxiella burnetti
- diagnosis
- control and prevention

Back 99

- serology, cytology with acid-fast or Giemsa (lives inside phagocytes)
- control: vaccine under development

Front 100

comment on the zoonoses of Coxiella burnetti:
- disease
- people at risk
- symptoms

Back 100

- Causes Q Fever in humans
- ranchers, veterinarians, slaughterhouse workers
- flu-like symptoms

Front 101

who first predicted antimicrobial resistance?

Back 101

Fleming

Front 102

what is the biggest problem facing antibiotics?

Back 102

resistance

Front 103

what are the four mechanisms for antimicrobial resistance?

Back 103

1. prevent entry of drug
2. pump out the drug
3. inactivate the drug
4. change target site for drug

Front 104

what is intrinsic antimicrobial resistance and give one important specific example

Back 104

- bacteria's "natural" ability to resist effects
- all bacteria of a certain type possess this property
- e.g. aminoglycosides and anaerobes

Front 105

what is acquired antimicrobial resistance?

Back 105

- obtains the ability to resist the drug and was previously susceptible
- found in certain strains/subtypes of a particular species (i.e. this is nit intrinsic to the species)

Front 106

what are the two types of antimicrobial resistance

Back 106

intrinsic and acquired

Front 107

what are the two major mechanisms for acquired microbial resistance?

Back 107

1. mutatons
2. aquisition of resistant genes

Front 108

by what two phenotypes does a mutation of genetic code confer antimicrobial resistance? give an example.

Back 108

1. change of a target site for a normal physiological process
2. change in cell structure
- example: Mycobacterium tubercuolsis has a mutant rpoB gene that still codes for the functional protein, but that does not bind to rifampin

Front 109

what are three ways that bacteria can acquire foreign genes that encode for antimicrobial resistance? give two important examples.

Back 109

1. transformation
2. transduction
3. conjugation
- MRSA
- β-lactam resistance

Front 110

Give an example of a specific and common dairy management practice to control scours, that may be contributing to antimicrobial resistance, why this is bad practice, and how this problem can be solved.

Back 110

- many dairies add low levels of antibiotics to milk replacers to prevent neonatal scours.
- neonatal scours has multiple etiologies, including non-bacterial infectious agents and antibiotic use is not very effective at treating scours
- improve husbandry practices (cleanliness, good colostrum, vaccination, etc.); provide fluid therapy as this is the most effective treatment for scours; only use antimicrobials when there are signs of systemic infection

Front 111

what are seven good husbandry practices to control neonatal scours?

Back 111

1. clean maternity pens
2. quality colostrum management
3. good milk replacer
4. individual isolated hutches
5. proper vaccination
6. biosecurity
7. isolation of new or sick animals

Front 112

Give three examples of how bacteriologists are worried about the cattle industry developing antimicrobial resistance

Back 112

1. Medicated milk replacers to prevent scours
2. Mastitis treatment
3. Treatment of shipping fever

Front 113

what is the most commonly prescribed type of antibiotic in small animal medicine?

Back 113

β-lactams

Front 114

explain how does previous exposure to antimicrobials correlate with antimicrobial resistance

Back 114

it was shown that dogs previously prescribed antimicrobials had a much greater risk of developing antimicrobial resistant strains of normal flora

Front 115

give some examples of how bacteriologists are worried about small animal practice developing antimicrobial resistance.

Back 115

- routine neutering with prophylactic penicillin
- treatment of FLUTD with a/b without testing to see if it is infectious
- canine (kennel cough) and feline URD: is it viral or bacterial? Kennel cough is self-limiting

Front 116

what are four circumstances in which antimicrobial susceptibility tests are indicated?

Back 116

1. young (neonates) or critically ill patients
2. infection in a normally sterile site, especially if it is difficult to treat (e.g. osteomyelitis) or has a significant impact on the health of the patient (e.g. septicemia)
3. pathogens with an unpredictable susceptibility pattern (e.g. S. aureus, Klebsiella, Enterobacter)
4. failure of presumptive or confirmed bacterial infection to respond to therapy

Front 117

what are five circumstances in which antimicrobial susceptibility testing is NOT indicated?

Back 117

1. if the bacteria are predictably sensititive (e.g. β-hemolytic Streptococcus)
2. high level of efficacy of empirical treatments (e.g. uncomplicated cystitis)
3. multiple bacteria isolated from abscesses or wounds
4. normal flora
5. anaerobes

Front 118

what are the two basic types of susceptibility testing and the most common type of test for each one?

Back 118

1. Agar Disk Diffusion (ADD) - Kirby Bauer modification
2. Broth Dilution tests - microdilution

Front 119

Mycoplasma gallisepticum
- species affected
- transmission

Back 119

- birds
- horizontal: aerosol, direct contact; vertical: hen-to-egg

Front 120

What are four clinical signs associated with Mycoplasma gallisepticum infection?

Back 120

1. upper respiratory signs
2. progressing to lower respiratory signs
3. joint swelling
4. reproductive problems

Front 121

how is Mycoplasma gallisepticum infection diagnosed?

Back 121

- serology: plate agglutination, hemagglutination inhibition, ELISA
- PCR
- histopath (plasmacytic/lymphocytic infiltrate)
- FA
- culture

Front 122

what is the gross pathology of Mycoplasma gallisepticum infection?

Back 122

- sinusitis
- caseous airsacculitis
- synovitis
- may progress to secondary colibacillosis with fibrinous polyserositis

Front 123

Mycoplasma gallisepticum
- control and prevention

Back 123

- cull
- vaccinate
- dip eggs from infected hens in Gentamycin solution
- destroy infected breeder flocks
- established Mycoplasma-free premises
- buy birds from National Poultry Improvement Program certified hatcheries and breeders

Front 124

what three antibiotics are generally used to treat Mycoplasma infection?

Back 124

1. Tylosin (50S drug)
2. Tetracyclines (30S drug)
3. Sulfa drugs (folate)

Front 125

Mycoplasma hyopneumoniae
- species infected
- transmission

Back 125

- swine
- horizontal: aerosol, direct contact, sows may shed to piglets at birth

Front 126

what are three clinical signs of Mycoplasma hyopneumoniae infection in pigs?

Back 126

1. URI
2. LRI
3. swollen joints

Front 127

what are three things can occur secondarily to Mycoplasma hyopneumoniae infection of the upper respiratory tract?

Back 127

- non-suppurative polyarthritis
- pneumonia
- predisposition to secondary bacterial infection

Front 128

how is Mycoplasma hyopneumoniae infection in pigs diagnosed

Back 128

- serology: ELISA, IFA
- PCR
- culture

Front 129

Mycoplasma mycoides ss mycoides
- species infected
- comment on the occurrence of this disease

Back 129

- cattle (contagious bovine pleuropneumonia)
- it is a foreign animal disease with no cure that has been eradicated from teh US, Europe, and Australia

Front 130

Mycoplasma bovis
- major diseases
- occurrence
- diagnosis

Back 130

- Mastitis, Pneumonia in Calves, genital infections, joint infections
- mainly a problem of large dairy herds
- Dx: PCR, culture

Front 131

Mycoplasma bovis
- Treatment
- Control and prevention

Back 131

- Tilmicosin, tylolsin, tetracyclines, florfenicol (for systemic)
- no cure for mastitis - cull
- don't feed mastitic milk to calves; quarantine and test replacement cows and heifers

Front 132

Mycoplasma capricolum
- species affected
- major diseases

Back 132

- sheep and goats
- LRT infections, joint swelling, ketaroconjunctivits

Front 133

Mycoplasma capricolum
- Diagnosis
- Treatment
- Control and prevention

Back 133

- Dx: culture
- Tx: antibiotics
- control and prevention: biosecurity, cull

Front 134

Mycoplasma canis
- clinical signs
- diagnosis
- treatment

Back 134

- pneumonia, urinary and repro tract infections
- culture
- doxycycline, fluoroquinolones

Front 135

Mycoplasma felis
- clinical signs
- diagnosis
- treatment

Back 135

- pneumonia, conjunctivitis
- culture
- doxycycline, fluoroquinolones

Front 136

which species of Order Mycoplasmatales are known for causing genitourinary infections (and possibly respiratory infections) in
- cattle?
- dogs?
- cats?

Back 136

- cattle: Ureaplasma diversum (urogenital only)
- dogs: Ureaplasma canigenitalium (urogenital only); Mycoplasma canis (urogenital and respiratory)
- cats: Ureaplasma cati (urogenital and respiratory)

Front 137

what are six general clinical signs that are associated with Mycoplasma infection?

Back 137

1. conjunctivitis
2. upper respiratory tract infection
3. pneumonia
4. genital and repro tract infection
5. mastitis
6. polyarthritis

Front 138

Name three hemotrophic species of Mycoplasmas and the species that they infect

Back 138

1. Mycoplasma suis - pigs
2. Mycoplasma haemocanis - dogs
3. Mycoplasma maemofelis - cats

Front 139

what are the three basic physical parameters (not anatomical) of skin that act as defense mechanisms?

Back 139

1. dryness
2. pH (usually acidic)
3. low temperature"

Front 140

how does the skin physically (not chemically) get rid of transient bacteria?

Back 140

sloughing of keratinized cells

Front 141

what three basic ways do skin secretions resist colonization of transient microorganisms?

Back 141

i. Holocrine sebaceous glands secrete long chain FAs, which inhibit bacterial growth
ii. Holocrine and apocrine sweat glands contribute to intercellular seal in superficial epidermal layers, limiting microbial access
iii. Self-sterilization

Front 142

what chemicals does the skin secrete to self-sterilize?

Back 142

1. Sweat glands secrete lactate, propionate, acetate, caprylate, and high concentrations of NaCl
2. Interferon, lysozyme, transferrin, and Igs

Front 143

where do the resident microflora live on the skin?

Back 143

1. Surface of epidermal layers (stratum corneum)
2. Distal parts of sweat glands and hair follicles

Front 144

what parts of the body have skin that contains the highest amount of normal flora? How does these numbers compare to mucus membranes?

Back 144

(Numbers highest in moist, protected areas)
- Axilla, inguinal, interdigital spaces, and skin folds
- lower numbers than mucus membranes (10^2 – 10^6 per cm^2)

Front 145

what are the two basic ways that resident microflora of the skin prevent non-normal flora from colonizing?

Back 145

1. Exclude intruders by excreting inhibitory metabolites (VFAs, antibiotics), bacteriocins
2. Prevent other bacteria from attaching (occupy available niches)

Front 146

what types of organisms are considered to be normal flora of the skin?

Back 146

1. Mostly G+
2. Few G-
3. Lipophilic yeasts in low numbers – Malassezia pachydermatis

Front 147

name four species of GRAM-POSITIVE bacteria that are common transient microflora of the skin

Back 147

a. S. intermedius/pesudintermedius (dogs)
b. S. aureus (other spp.)
c. β-hemolytic Streptococci
d. Enterococcus spp.

Front 148

name three species of GRAM-NEGATIVE bacteria that are common transient microflora of the skin. Also, name one common general source of mixed bacteria and the common location on the body

Back 148

a. E. coli
b. Pseudomonas aeruginosa
c. Proteus spp.
d. Fecal bacteria – feet (farm)

Front 149

where on the skin contains the very largest populations of normal flora and how are other parts of the body thought to acquire these bacteria?

Back 149

- Greatest numbers at mucocutaneous junctions (oral, nasal, anal)
- Seeded to other areas of skin by grooming

Front 150

skin immune system (SIS):
- what triggers a response?
- from where do these immune cells take their origin
- what specific types of cells are in the SIS?

Back 150

i. Responds to local antigenic stimuli
ii. Cells and their functions correspond to those in the other mucosal surfaces (e.g. GALT)
iii. Prominent cell = Langerhans and dendritic cells

Front 151

describe the action and lifetime of the skin immune system cells (Langerhans, dendritic)

Back 151

1. Non-phagocytic
2. Antigen-presenting
3. Long term residents

Front 152

what are 8 predisposing factors to skin infections?

Back 152

1. Anatomic defects – skin folds
2. atopy (allergens: inhaled, food, contact; breed predilection)
3. ectoparasites
4. endocrine disorders (Cushings, hypothyroidism)
5. defects in cornification (seborrhea)
6. nutritional deficiencies (zinc)
7. immunologic disorders (immunosuppression, autoimune dzs)
8. iatrogenic (drug eruptions, excess or inappropriate a/b or corticosteroid use)

Front 153

comment on the bacteria involved in pyoderma in dogs.
- most common species
- others
- otitis externa
- deep pyoderma
- what is required for development of pyoderma

Back 153

1. >90% of cases involve S. intermedius/pseudintermedius
2. Occasionally S. aureus or rarely S. hyicus
3. Otitis externa – S. Schleiferi & others
4. Deep pyoderma may involve other bacteria
5. Pyoderma is considered to be a secondary skin disease - need host compromise

Front 154

what are the three main classifications of pyoderma?

Back 154

1. surface pyoderma
2. superficial pyoderma
3. deep pyoderma

Front 155

what three diseases are associated with surface pyoderma and what are their clinical signs?

Back 155

i. Pyotraumatic dermatitis - Hotspots/Acute moist dermatitis/Moist eczema
ii. Skin fold pyoderma (intertrigo) -. Lip, nasal, tail, or vulval folds (Shar-pei)
iii. Mucocutaneous pyoderma - Mainly lips and perioral skin; Also eyelids, nares, vulva, prepuce, or anus

Front 156

what is another name for skin fold pyoderma? what classification of pyoderma is this? what bacteria cause this infection?

Back 156

- intertrigo
- surface pyoderma
- Caused by coagulase +’ve Staph infections

Front 157

what two diseases are associated with superficial pyoderma?

Back 157

1. impetigo (puppy pyoderma)
2. superficial bacterial folliculitis

Front 158

impetigo
- who is affected
- what type of disease is it?
- scientific name for this disease
- where on the body is it found?

Back 158

- puppies ("puppy pyoderma")
- superficial pyoderma
- Superficial pustular dermatitis
- Hairless areas of skin, especially in the inguinal and axillary regions

Front 159

superficial bacterial folliculiltis
- what type of disease is it?
- causative agent
- pathogenesis
- where on the body are lesions present?

Back 159

- superficial pyoderma
- Caused by coagulase +’ve Staph infections
- Infection begins in the hair follicle → papule → pustule → epidermal collarette → crust
- Commonly affects groin, axilla, and interdigital skin; may become generalized

Front 160

what are four lesions associated with deep pyoderma?

Back 160

1. Deep folliculitis and furunculosis
2. Pyotraumatic folliculitis
3. Folliculitis (muzzle, pedal, callus, etc.)
4. Cellulitis secondary to parasites, etc.

Front 161

what bacteria commonly cause deep pyoderma?

Back 161

May be mixed: S. intermedius complex + E. coli, Proteus spp., P. aeruginosa, etc.

Front 162

Diamond skin disease:
- cause
- source
- transmission

Back 162

i. Cause: Erysipelothrix rhusiopathiae
ii. Source: Carrier animals, fomites (scabs)
iii. Transmission: Damaged skin (rain)

Front 163

Anthrax:
- cause
- source
- transmission

Back 163

i. Cause: Bacillus anthracis
ii. Source: Spores in the environment; Infected carcass
iii. Transmission: Inoculate bacteria; Ingest/inhale spores

Front 164

Bumble foot:
- cause
- source
- transmission

Back 164

i. Cause: Staphylococcus aureus
ii. Source: Normal flora
iii. Transmission: opportunistic

Front 165

Dermatophytosis:
- cause
- source
- transmission

Back 165

i. Cause: Dermatophytes (Microsporum, Trichophyton, Epidermophyton)
ii. Source: Carrier animals; fomites
iii. Transmission: Contact with arthrospores

Front 166

Ringworm:
- cause
- source
- transmission

Back 166

i. Cause: Dermatophytes
ii. Source: Carrier animals; fomites
iii. Transmission: Contact with arthrospores

Front 167

Fungal Dermatitis:
- cause
- source
- transmission

Back 167

i. Cause: Malassezia
ii. Source: Normal flora
iii. Transmission: opportunistic

Front 168

what is the scientific name for an abscess?

Back 168

mycetoma

Front 169

what are seven bacteria that cause skin nodules and draining abscesses (bacterial pseudomycetoma)?

Back 169

1. Mycobacteria spp.
2. Nocardia spp.
3. Actinomyces spp.
4. Dermatophilus congolensis
5. Rhodococcus equi
6. Corynebacteria spp.
7. Arcanobacterium pyogenes

Front 170

what is dermatophytic pseudomycetoma?

Back 170

"ringworm gone bad" - skin nodules with draining tracts and abscesses

Front 171

what two fungal infections that cause eumycotic pseudomycetoma?

Back 171

1. Phaeohyphomycosis
2. Zygomycoses

Front 172

what are five types of fungal infections that can cause skin nodules and draining abscesses?

Back 172

1. Dermatophytes (Dermatophytic pseudomycetoma)
2. Phaeohyphomycosis (Eumycotic mycetoma)
3. Zygomycoses (Eumycotic mycetoma)
4. Cryptococcosis
5. Sporotrichosis

Front 173

what are four basic diagnostic tests used for skin infections?

Back 173

1. skin scrapings
2. cytology
3. c/s testing
4. biopsy

Front 174

what are two common ways that skin scrapings are used to diagnose skin infections?

Back 174

i. Superficial scrapings/plucked hairs in 10% KOH to look for arthrospores of dermatophytes
ii. Deep scrapings to look for mites

Front 175

how is cytology performed on the skin? what should you look for to diagnose a skin infection?

Back 175

- Direct impression smears or sticky tape preparations
- Look for overgrowth: Many cocci, Many PMNs, Many yeast

Front 176

comment on the indications of culture/susceptibility for surface pyoderma.

Back 176

1. Don’t culture surface infections
2. Topical antibiotics efficaciously cannot be measured by Kirby Bauer tests

Front 177

comment on the indications of culture/susceptibility for superficial pyoderma.

Back 177

1. c/s testing rarely indicated for superficial infections
2. if animal is non-responsive to therapy, may do c/s: sample pustule, nodule, etc.

Front 178

comment on the indications of culture/susceptibility for deep pyoderma.

Back 178

1. may do c/s for deep, mixed infections
2. do not sample draining tracts

Front 179

what is the 5-step process for sampling a pustule?

Back 179

1. Pick an intact pustule
2. Clean skin surface over pustule with alcohol and allow to dry
3. Open pustule with fine needle
4. Use swab to collect pus
5. Place in transport media and send to diagnostic laboratory

Front 180

when are skin biopsies indicated for diagnosis of a potential skin infection?

Back 180

i. Useful with open wounds with deeper infections
ii. Useful in atypical or severe cases, e.g. deep pyoderma to differentiate between bacterial infections, mycoses, neoplasia, immune-mediated diseases

Front 181

how do you treat surface pyoderma?

Back 181

Topical therapy (e.g. antibacterial shampoos) are frequently all that is required

Front 182

how do you treat superficial pyoderma?
- specific antibiotics
- routes of administration
- time

Back 182

- SYSTEMIC anti-staphylococcal antibiotics: Cephalosporins, lincosamides, macrolides, potentiated ampicillin
- Long treatment times (30-60 days)
- Also use topical antibacterial shampoos

Front 183

how do you treat deep pyoderma?

Back 183

i. Systemic antibiotics needed
ii. May need to do c/s testing if suspect mixed infection (e.g. based on cytology)

Front 184

immunomodulatory therapy for pyoderma
- indications
- precautions before administration of this therapy
- efficacy
- example of a drug

Back 184

i. Indications: Recurrent, idiopathic pyoderma that was responsive to antibiotics
ii. Rule out all underlying causes, e.g Demodicosis, flea allergy dermatitis, food allergy, and hypothyroidism
iii. Efficacy: questionable; Primarily used to prevent recurrence; Most important predictor is the selection of appropriate cases
iv. Example: Staphylococcus aureus Phage Lysate

Front 185

when are extended regimens of antibiotics indicated for pyoderma?

Back 185

Last resort in the management of recurrent bacterial pyoderma if all underlying causes have been ruled out.

Front 186

comment on particle size with regards to pulmonary defense mechanisms

Back 186

i. Non-respirable particles >/= 5 μm: These larger particles are deposited predominately in the pharynx or at the bifurcation of the airways through INERTIAL IMPACTION. They are consequently cleared from the upper airways and never reach the lower airways
ii. Respirable particles </= 5 μm: These particles are inhaled into the smaller airways. These are cleared by non-immunological and immunological mechanisms
iii. Key point: bacteria, some fungi, and viruses are all small enough to be inhaled

Front 187

what are the four main non-immunological pulmonary defense mechanisms?

Back 187

1. anatomy of the site (i.e. intertial impaction)
2. coughing
3. mucociliary clearance
4. pulmonary alveolar macrophages

Front 188

how does the position of a horse's head affect the particles that it inhales into its lungs?

Back 188

- vertical position (head down) = inertial impaction
- horizontal position (head forward when running or in a trailer) = increased entry into local airways

Front 189

where are the main locations of cough receptors?

Back 189

in the URT and at the tracheal bifurcation

Front 190

what are the three basic immunological defense mechanisms of the airways?

Back 190

1. pulmonary alveolar macrophages
2. neutrophils + macrophages, after opsonization
3. bronchiolole associated lymphoid tissue (BALT)

Front 191

what are the three basic functions of pulmonary alveolar macrophages?

Back 191

1. phagocytosis
2. antigen presentation
3. secretion of cytokines

Front 192

what types of immune cells make up BALT (and their basic function)?

Back 192

1. B-cells + plasma cells (antibody – IgA)
2. T cells (help and cytotoxicity)

Front 193

what are five common risk factors for respiratory infections?

Back 193

1. transportation
2. exercise-induced pulmonary hemorrhage
3. commingling and age
4. viral infections
5. housing conditions

Front 194

why does transportation increase the risk of a respiratory infection? How long does this process take?

Back 194

- Lower effectiveness of mucociliary clearance due to postural changes: cannot clear accumulated bacteria
- Start to get increased numbers of bacteria and PMNs by 4-6 hours

Front 195

what are the two common physical factors of housing (e.g. stabling, barns, sheds) that pose a risk for respiratory infection?

Back 195

i. Dusty feeds and bedding
ii. Decreased air quality

Front 196

normal flora of the URT:
- where are they found?
- what is the most distal part of the URT they are normally found?

Back 196

- Nasal cavity, oropharynx, nasopharynx
- Stop at the larynx

Front 197

in a healthy animal, comment on the bacteria that reach the LRT:
- numbers
- time
- type of bacteria

Back 197

- Low numbers
- Transitory (rapidly cleared)
- Includes non-pathogens

Front 198

what are three bacteria that are pathogenic, NORMAL flora in the HORSE that can cause RESPIRATORY infection?

Back 198

1. β-Streptococci
2. Pasteurellaceae
3. NSF anaerobes

Front 199

what are three bacteria that are pathogenic, NON-NORMAL flora in the HORSE that can cause RESPIRATORY infection?

Back 199

1. Bordetella bronchiseptica
2. Enterobacteriaceae
3. Rhodococcus equi

Front 200

what are five bacteria that are pathogenic, NORMAL flora in CATTLE that can cause RESPIRATORY infection?

Back 200

(Pasteurellaceae:)
1. Pasteurella multocida
2. Mannheimia haemolytica
3. Histophilus somni

4. Mycoplasma spp.
5. β-Streptococci

Front 201

what are three bacteria that are pathogenic, NON-NORMAL flora in CATTLE that can cause RESPIRATORY infection?

Back 201

1. Mycobacterium spp.
2. E. coli
3. Klebsiella pneumoniae

Front 202

what are five bacteria that are pathogenic, NORMAL flora in the PIG that can cause RESPIRATORY infection?

Back 202

(Pasteurellaceae)
1. Pasteurella multocida
2. Actinobacillus pleuropneumoniae
3. Actinobacillus suis
4. Haemophilus parasuis
5. Mycoplasma hyopneumoniae

Front 203

what are two bacteria that are pathogenic, NON-NORMAL flora in the PIG that can cause RESPIRATORY infection?

Back 203

1. E. coli
2. Klebsiella pneumoniae

Front 204

what are five bacteria that are pathogenic, NORMAL flora in the DOG that can cause RESPIRATORY infection?

Back 204

1. Pasteurella
2. β-Streptococci
3. Mycoplasma
4. Anaerobes
5. Actinomyces (pyothorax)

Front 205

what are five bacteria that are pathogenic, NON-NORMAL flora in the DOG that can cause RESPIRATORY infection?

Back 205

1. Bordatella bronchiseptica
2. E. coli
3. Klebsiella pneumoniae
4. Mycobacteria
5. Nocardia

Front 206

what are two genera of fungi that very commonly cause respiratory infection in dogs

Back 206

i. Blastomyces
ii. Histoplasma
(and others)

Front 207

what are the three basic mechanisms in which bacteria cause respiratory disease

Back 207

1. get there in high numbers
2. compromised host
3. virulence factors

Front 208

what are three common ways in which a host can acquire large numbers of bacteria in the lower respiratory tract?

Back 208

1. Transportation
2. Aspiration of oropharyngeal organisms
3. Change in anatomical structures (e.g. tie back in horses)

Front 209

why do large numbers of bacteria cause respiratory disease?

Back 209

Massive challenge can overwhelm pulmonary disease mechanisms

Front 210

what are three mechanisms by which virulence factors contribute to respiratory infection?

Back 210

i. Attach: pili (e.g. Bordatella bronchiseptica)
ii. Avoid phagocytosis: capsule/slime/O-side chains (e.g. Streptococcus spp., Klebsiella pneumoniae)
iii. Cause damage: endotoxin (e.g. E. coli); cytotoxins (e.g. Pasteurella spp., Bordatella bronchiseptica, β-Streptococci)

Front 211

what is the 6-step process for definitely diagnosing a bacterial infection in a normally "sterile" site?

Back 211

1. localize the site of infection
2. collect a sterile sample
3. assess the sample for inflammation
4. assess the sample for bacteria
5. culture/susceptibility testing
6. Interpret cultivation based on knowledge of possible causative agents and cytological results

Front 212

in what three basic ways can you localize the site of a respiratory infection?

Back 212

i. Clinical signs (Nasal discharge, Increased respiratory rate or dyspnea)
ii. Physical examination (Auscultation +/- rebreathing bag)
iii. Other diagnostic tests (Ultrasound, radiology, etc.)

Front 213

what are the three common ways that the lower respiratory tract is sampled?

Back 213

1. tracheal wash
2. bronchoalveolar lavage (BAL)
3. thoracocentesis

Front 214

contrast tracheal wash with BAL in frequency that these techniques are performed and their usefulness

Back 214

1. Tracheal wash: Most often used; collects from the cranioventral lung lobes – the correct site
2. Bronchoalveolar lavage: Rarely indicated; collects from the caudodorsal lung lubes - does not usually collect sample at the correct site

Front 215

thoracocentesis for diagnosis of respiratory infection
- indications
- minimum amount of samples needed for a proper technique

Back 215

- indicated for pleuritis or pleuropneumonia
- at least two samples: need at least one sample from each side of the chest

Front 216

what does a normal cytology of pleural fluid contain?

Back 216

a. high % neutrophils
b. few mesothelial cells
c. low total number of cells

Front 217

what does a normal cytology of a tracheal wash look like?

Back 217

a. Many ciliated columnar epithelial cells
b. High % macrophages, few neutrophils

Front 218

what does an abnormal cytology of pleural fluid look like?

Back 218

a. High number of PMNs
b. High protein
c. +/- intracellular bacteria

Front 219

what does an abnormal cytology of a tracheal wash look like?

Back 219

a. High percentage of PMN
b. +/- presence of intracellular bacteria

Front 220

when is culture/susceptibility testing indicated for a respiratory infection?

Back 220

i. Only if evidence of inflammation +/- bacteria
ii. Interpret in light of known pathogens
iii. Do susceptibility testing only if indicated

Front 221

when is aggressive antibiotic therapy indicated for respiratory infections?

Back 221

More likely for LRT infections, as they may be life threatening

Front 222

what two basic types of antibiotic therapy are commonly employed for respiratory infections?

Back 222

1. systemic therapy
2. topical therapy (nebulization)

Front 223

systemic therapy for respiratory infection:
- procedure
- why is systemic better than topical?

Back 223

- Empirical and then changed based on culture/susceptibility testing
- Better penetration of antibiotics into consolidated lung tissue if given systemically rather than topically

Front 224

what are the three very basic ways in which respiratory infections are treated?

Back 224

1. antibiotics
2. hydration
3. supportive care

Front 225

what are the two ways in which hydration is used to treat respiratory infection and why?

Back 225

i. Systemic hydration: Aid mucociliary clearance and secretion mobilization
ii. Airway hydration: aerosol therapy may help to mobilize secretions (e.g. nebulizer)

Front 226

what are three types of supportive care that can be given to animals with a respiratory infection?

Back 226

1. Oxygen
2. Drainage and lavage if possible (pleuropneumonia)
3. +/- NSAIDs

Front 227

what three types of drugs are contraindicated in bacterial pneumonia and why?

Back 227

Antitussives, diuretics, antihistamines for bacterial pneumonia as they inhibit mucokinesis and exudate removal

Front 228

what is the first step in a bacteria causing GIT disease and how do the microflora prevent this?

Back 228

1. To produce disease, potentially pathogenic bacteria must first adhere to target cells
2. If target cell is already occupied by resident flora (niche), they cannot adhere → colonization resistance
3. If the bacteria cannot adhere, it cannot cause disease

Front 229

what are five ways that normal flora of the GIT colonize a niche and fend off potential pathogens?

Back 229

i. Fimbriae for attachment
ii. Surface carbohydrates specific for host cell receptors
iii. Production of bacteriocins/microsins to kill other bacteria
iv. Compete better to acquire nutrients (starve the pathogens)
v. Fatty acid secretion by obligate anaerobes

Front 230

what are two proposed ways that fatty acid secretion by obligate anaerobes is protective to the GIT from disease?

Back 230

1. Regulates number and types of facultative bacteria (including potential pathogens)
2. Potentially toxic to members of Enterobacteriaceae

Front 231

what are three properties of the host's GIT that defend against pathogens and allow for normal flora?

Back 231

i. Receptors for fimbriae and carbohydrates
ii. Small intestine: Peristalsis to sweep non-adherent bacteria away
iii. Large intestine: Physicochemical properties – low redox potential, fatty acids, and pH

Front 232

what is the main immunological defense system in the GIT?

Back 232

Gut associated lymphoid tissue (GALT)

Front 233

what is the most important risk factor for acquiring a GIT infection?

Back 233

use of antimicrobial drugs

Front 234

what are two major ways in which antimicrobial use decreases colonization resistance in the GIT?

Back 234

1. Many antibiotics decrease Streptococcal species in the mouth. This allows repopulation with antibiotic resistant Enterobacteriaceae and environmental bacteria (e.g. Pseudomonas)
2. Also affect obligate anaerobes in the mouth and large intestine. This causes a decrease in fatty acids and therefore a proliferation of Enterobacteriaceae (e.g. Salmonella)

Front 235

what are seven general risk factors for GIT infection?

Back 235

1. antimicrobial use
2. immunosuppressive drug therapy
3. GIT stasis/decreased motility
4. young age
5. "stress"
6. change in diet
7. preceding or concomitant viral infection

Front 236

what are four common causes of GIT stasis/decreased mobility that may predispose an animal to GIT infection?

Back 236

1. Change in diet
2. Cold weather
3. Intestinal obstruction
4. Pain/colic

Front 237

what are four common conditions that make young animals more susceptible to GIT infection?

Back 237

i. Immuno-naïve
ii. Failure of passive transfer (lack of protective antibody)
iii. Devoid of normal flora (Less colonization resistance)
iv. Receptors for pathogens may be present

Front 238

what are two ways in which change in diet may predispose an animal to a GIT infection?

Back 238

i. May cause change in bacterial flora as they compete for nutrients
ii. May also change gut motility

Front 239

how can a rotavirus infection predispose an animal to a GIT infection?

Back 239

Rotavirus infection causes re-expression of receptors on enterocytes, allowing ETEC to bind to enteric epithelium in older calves

Front 240

name four bacteria that cause GIT disease in PUPPIES.

Back 240

a. E. coli (ETEC?, EPEC, EHEC)
b. Salmonella
c. Campylobacter spp.
d. Clostridium perfringens

Front 241

name four bacteria that cause GIT disease in ADULT DOGS.

Back 241

a. Clostridium spp.
b. Salmonella
c. Campylobacter?
d. E. coli (EHEC)?

Front 242

name five bacteria that cause GIT disease in FOALS.

Back 242

a. E. coli (?)
b. Salmonella
c. Clostridium spp.
d. Rhodococcus equi
e. Lawsonia intracellularis

Front 243

name four bacteria that cause GIT disease in ADULT HORSES.

Back 243

a. Clostridium perfringens
b. Clostridium difficile
c. Salmonella
d. Neorickettsia risticii (Potomac Horse Fever)

Front 244

name three bacteria that cause GIT disease in CALVES.

Back 244

a. E. coli
b. Salmonella
c. Clostridium perfringens

Front 245

name three bacteria that cause GIT disease in ADULT CATTLE.

Back 245

a. Salmonella
b. Clostridium spp.
c. Mycobacterium avium ss paratuberculosis

Front 246

name two bacteria that cause GIT disease in PIGLETS.

Back 246

a. E. coli (ETEC)
b. Clostridium perfringens

Front 247

name five bacteria that cause GIT disease in ADULT PIGS.

Back 247

a. E. coli (EPEC, EHEC)
b. Salmonella
c. Lawsonia intracellularis
d. Brachyspira hyodysenteriae
e. Brachyspira pilosicoli

Front 248

what are two ways in which a host can acquire a GIT infection?

Back 248

May arrive by feco-oral route or ascend from lower tract

Front 249

what are three types of virulence factors that can affect a GIT infection?

Back 249

i. Pili/adhesins (e.g. E. coli) help attachment (selective adsorption)
ii. Exotoxins and endotoxin: enterotoxin – disruption of fluid and electrolyte regulation of target cell; Cytotoxins – damage and kill target cells (associated with invasion)
iii. Invasion: Localized; Systemic

Front 250

The passage of viable bacteria from the GIT to extra-intestinal sites, such as the mesenteric lymph nodes, liver, spleen, kidney, and blood

Back 250

Bacterial translocation

Front 251

what are three common factors that promote bacterial translocation?

Back 251

1. Overgrowth with Gram-negative enteric bacilli
2. Impaired host immune defenses
3. Injury to the intestinal mucosa resulting in increased intestinal permeability

Front 252

what is the appropriate technique to collect a fecal sample?

Back 252

1. Multiple samples (3-5)
2. Large volumes (~5 grams) – if large animals
3. Put in transport media (e.g. Cary Blair medium)
4. Culture and/or detect specific toxins/pili

Front 253

what clinical sign is considered evidence of GIT inflammation?

Back 253

diarrhea

Front 254

what are three advantages/disadvantages of fecal smears with regards to bacterial GIT infection?

Back 254

1. Don’t see inflammatory cells
2. Some value for diagnosing Campylobacter
3. Little value for diagnosing Clostridium spp.

Front 255

when is culture of fecal samples indicated and how is this properly done?

Back 255

i. Culture feces only if looking for specific bacteria
ii. Must use specialized media
iii. Interpret in light of known pathogens

Front 256

what are five types of modern diagnostic tests that can be done to definitively diagnose GIT infections?

Back 256

i. ELISA – to detect specific E. coli pili
ii. Serology (e.g. Lawsonia intracellularis)
iii. Toxin detection (e.g. Clostridium perfringens or E. coli enterotoxin)
iv. γ-IFN (e.g. Mycobacterium paratuberculosis)
v. PCR (e.g. M. paratuberculosis, L. intracellularis)

Front 257

when is topical treatment of GIT bacterial infection indicated?

Back 257

never

Front 258

when is systemic antibiotic therapy for GIT infections indicated? when is it not indicated?

Back 258

1. Selective cases
2. Indications of fever, depression, shock
3. Low WBC counts (or marked left shift and toxic changes)
4. Not indicated in uncomplicated GIT infections

Front 259

what are three supportive/adjunctive therapies for GIT infections?

Back 259

1. fluid therapy - most important; usually also requires electrolytes
2. anti-motility agents - contraindicated for infectious diarrhea
3. protectants/absorbants - some value in some cases

Front 260

what are four aspects of normal micturition that provide defense to bacterial infection?

Back 260

i. Frequency
ii. Volume
iii. Direction (out of the body)
iv. Diluting effect

Front 261

what are four aspects of the normal urethra that provide defense to upper URT infection?

Back 261

1. High-pressure zone
2. Contraction and peristalsis between voiding
3. Length of urethra (longer in males)
4. Decreased epithelial receptors proximally

Front 262

what are two aspects of the normal bladder that provide defense to bacterial infection?

Back 262

1. Phagocytic ability of cells in the transitional epithelium
2. Surface glycosaminoglycans

Front 263

what are two aspects of the normal ureters that provide defense to bacterial infection?

Back 263

1. Vesicoureteral valve
2. Contractions and peristalsis

Front 264

what are six aspects of the urogenital mucosal barrier that provide defense to bacterial infection?

Back 264

1. Normal flora (bacterial interference)
2. Epithelial desquamation
3. Rapid PMN response
4. Antibody (IgA, also IgG, IgM)
5. Mucoproteins/glycoprotein (slime)
6. Lysozyme

Front 265

what are three aspects of normal urine that provide defense to bacterial infection?

Back 265

1. High concentration/osmolality
2. High urea
3. Acidic pH

Front 266

what are 9 predisposing factors for a urinary tract infection? (yes, 9!)

Back 266

1. Age – young animals
2. Female – short urethra
3. Concurrent crystals or calculi (trauma)
4. Disorders of growth – polyps/hyperplasia/neoplasia
5. Endocrine disorders: hyperadrenocorticism - ↑cortisol; diabetes mellitus – glucosuria
6. Renal failure
7. Immunosuppressive therapy: Corticosteroids; Cancer chemotherapy
8. Difficult parturition (cows and sows)
9. Spinal injury or peripheral nerve damage: Interference with free flow of urine and compete emptying of the bladder, leading to urinary stasis

Front 267

what are four predisposing factors for genital tract infection of the mare?

Back 267

(usually due to abnormal clearance of post-mating endometritis)
a. conformation defects that increase vaginal pooling of bacteria
b. ↓myometrial activity/ability in older and multiparous mares
c. ↓PMN activity/ability to clear bacteria in older mares
d. Trauma during mating

Front 268

normal flora of the urogenital tract:
- locations of normal flora
- where proximally does normal flora stop?

Back 268

- prepuce, penis, distal urethra, vagina
- normal flora stops basically at mid-urethra and external cervix

Front 269

what are four aspects of bacteria that reach the upper urogenital tract in a normal, healthy animal?

Back 269

1. Low numbers
2. Transitorily – rapidly cleared
3. Included non-pathogens
4. They do not induce inflammation

Front 270

which eight bacteria cause urinary tract infections in DOGS?

Back 270

1. E. coli (40%)
2. Proteus
3. Klebsiella
4. β-Streptococci and Enterococci
5. Staphylococcus intermedius/pseudintermedius complex
6. Pseudomonas aeruginosa (<5%)
7. 20% mixed
8. Leptospira – nephritis

Front 271

which three bacteria cause genital tract infections in DOGS?

Back 271

1. E. coli
2. Anaerobes
3. Brucella canis

Front 272

which bacteria cause urinary tract infections in HORSES?

Back 272

none!

Front 273

which seven bacteria cause genital tract infections in HORSES?

Back 273

1. β-Streptococci
2. Klebsiella pneumoniae
3. E. coli
4. Pseudomonas aeruginosa
5. Taylorella equigenitalis (CEM)
6. Leptospira
7. Salmonella abortus-equi

Front 274

which two bacteria cause urinary tract infections in CATTLE?

Back 274

1. Corynebacterium renale (+ other spp.)
2. Leptospira

Front 275

which seven bacteria cause genital tract infections in CATTLE?

Back 275

1. Brucella abortus
2. Leptospira
3. Campylobacter spp.
4. Listeria spp.
5. Histophilus somni
6. Mycoplasma
7. Arcanobacterium pyogenes

Front 276

which three bacteria cause urinary tract infections in PIGS?

Back 276

1. Leptospira
2. Actinobaculum suis
3. E. coli, etc.

Front 277

which two bacteria cause genital tract infections in PIGS?

Back 277

1. Brucella suis
2. Leptospira

Front 278

what are five types of virulence factors that bacteria can use to cause urogenital tract infections

Back 278

i. Pili/adhesins (e.g. E. coli) help attachment
ii. Capsule (e.g. Klebsiella) help prevent phagocytosis
iii. O-side chains (e.g. E. coli) decrease smooth muscle contractility
iv. Cytotoxins (e.g. hemolysins) cause damage and increase invasiveness
v. Flagella (e.g. Proteus) – motility helps invasion

Front 279

in what three ways would you specifically localize the site of infection for a urogenital infection?

Back 279

i. Clinical signs
ii. Palpation (including rectal)
iii. Diagnostic tests

Front 280

what are four basic diagnostic tests that can be performed to localize the site of infection for a urogenital infection?

Back 280

1. Urinalysis
2. Uterine cytology
3. Ultrasound
4. radiology

Front 281

what are the three types of urine collection and the bacterial counts that must be exceeded to be considered significant?

Back 281

1. Free catch (voided, mid-stream); >10^5 significant
2. Catheterization; >10^4 significant
3. Cystocentesis; >10^3 significant

Front 282

what are five sterile sampling techniques used for a suspected genital infection?

Back 282

1. Clitoral swab for specific bacteria (e.g. Taylorella equigenitalis)
2. Guarded swab (e.g. equine endometritis)
3. Blood culture (e.g. Brucella spp.)
4. Fine-needle aspirate (uterus/testes)
5. Blood (serology, e.g. Leptospira spp.)

Front 283

what are two aspects that complicate the relevance of susceptibility testing of urogenital infections?

Back 283

1. Much higher concentrations of some (polar) antibiotics can be achieved in the urine (tetracycline); therefore, Kirby-Bauer underestimates true susceptibility
2. much lower concentrations of some antibiotics can be achieved at some sites (e.g. the prostate may have poor drug penetration)

Front 284

for bacterial prostatitis, what aspects ar considered when selecting an appropriate antibiotic?

Back 284

- the prostate may have poor drug penetration
- Treating chronic prostatitis requires a drug with high lipid solubility and a weak base that will be in the the ionized form in the prostatic fluid (pH 6.4)

Front 285

when is antimicrobial susceptibility testing not indicated and indicated for a urogenital infection?

Back 285

- Antimicrobial susceptibility testing NOT indicated for uncomplicated UTI
- Antimicrobial testing IS indicated for non-responsive UTI, prostatitis, orchitis, endometritis, and pyometra

Front 286

give a specific example of when topical therapy may be useful for a urogenital bacterial infection.

Back 286

may be helpful for endometritis in the mare

Front 287

what are three examples of supportive or adjunctive therapies for urogenital infections?

Back 287

i. Spay or neuter (pyometra, prostatitis)
ii. Drainage and lavage if possible (e.g. prostatic abscess)
iii. Some specific anti-testosterone drugs for prostatitis

Front 288

Dermatophytosis in humans:
- source
- epidemiology
- transmission
- clinical signs

Back 288

- Source: humans, animals, environment (anthrophilic, zoophilic, geophilic)
- 15% of human cases are Microsporum canis and up to 50% of cases are transmitted from animal to human
- Transmitted by direct contact or fomites
- Clinical signs are the same in humans and animals

Front 289

Sporotrichosis in humans:
- source
- transmission
- clinical signs

Back 289

("Rose Gardener's Disease")
- Source: soil, rarely infected animals (cats, horses)
- Transmission: through breaks in the skin or bites/scratches by cats
- Clinical signs: Same as in animals (cutaneous ulcerative lesions; non-healing and don’t respond to antibiotics; may have discharge);
- May also get systemic infection

Front 290

Bartonella henselae in humans:
- source
- transmission
- epidemiology
- clinical signs

Back 290

("Cat Scratch Fever")
- Source: cats (source for cats: fleas)
- Transmission: cat scratches or bites
- >22,000 cases reported per year in the US (mostly children); Cats rarely show clinical signs and 40% of cats are infected at some stage of their life.
- Clinical signs: Swollen lymph nodes = Parinaud’s Syndrome

Front 291

MRSA in humans:
- source
- epidemiology
- transmission
- clinical signs

Back 291

- Source: horse, pig, dog, cat, etc.
- These animals might have acquired MRSA from humans
- Transmission: most endogenous or from other infected humans (direct contact or fomites). Transmission from animals is rare, but has been reported
- Clinical signs: pyoderma, other body systems

Front 292

Leprosy in humans:
- source
- causative agent

Back 292

- 9-banded armadillo; non-human primates
- Mycobacterium leprae

Front 293

Blastomycosis in humans:
- clinical signs

Back 293

- same lesion in humans and animals (respiratory, myalgia, lymphadenopathy, uveitis, anemia)

Front 294

how is zoonotic dermatophytosis in humans controlled/prevented?

Back 294

1. Wash hand after contact (especially with young animals)
2. Correctly diagnose animals with lesions (may wish to isolate)
3. Clean/disinfect where animals live (dilute bleach)
4. Can be a bigger problem for immunocompromised people

Front 295

how is zoonotic sporotrichosis in humans controlled/prevented?

Back 295

1. Wear gloves when gardening (“Rose Gardener’s Disease”)
2. Recognize possible lesions and wear gloves when handling animal (cats, horses) – especially any discharges
3. Wash hands after glove removal

Front 296

how is zoonotic bartonellosis ("Cat Scratch Fever") in humans controlled/prevented?

Back 296

1. Flea control for your cat
2. Avoid “rough play” with your cats and wash any scratches/bites
3. Don’t let cats lick open wounds

Front 297

how is MRSA in humans controlled/prevented?

Back 297

1. Wash hand ans use alcohol based sanitizers
2. Keep open cuts/wounds clean and covered until healed
3. Avoid contact with lesions in animals and other people’s wounds

Front 298

comment on the role of dogs and cats in zoonotic MRSA infections:
- comment on them as a source
- prophylactic treatment of pets
- interspecies transmission

Back 298

a. Dogs and cats are likely colonized with human strains of MRSA
b. These are transient infections, so you don’t need to “decolonize pets”
c. Some evidence for interspecies transmission, though rare

Front 299

comment on the role of horses and pigs in zoonotic MRSA infections:
- comment on them as a source
- interspecies transmission
- prevalence in vetmed

Back 299

a. They have higher colonization rates with MRSA than dogs and cats, but these are usually non-human strains
b. Inter-species transmission has been reported, but rare
c. Study out of Australia – prevalence in humans is higher in equine vets

Front 300

comment on antibiotics with regards to the emergence of MRSA.

Back 300

Role of antibiotic misuse in food animals and companion animals (e.g. fluoroquinolones, 3rd generation cephalosporins, aminoglycosides) is associated with the emergence of MRSA

Front 301

Zoonotic GIT infections. Comment on the PERCEIVED importance of animals versus the ACTUAL importance.

Back 301

i. This is the single biggest thing people worry about when buying food
ii. Main importance of domestic animals (for human health) is that they act as reservoirs with subsequent contamination of the environment

Front 302

what are three main ways in which zoonotic GIT bacteria are transmitted to humans?

Back 302

i. Food contamination (most common)
ii. Contaminated water (“Montezuma’s Revenge”)
iii. Direct contact with infected animals is rare, but important

Front 303

name six zoonotic bacteria of the GIT.

Back 303

i. Campylobacter jejuni/coli
ii. Salmonella
iii. E. coli (e.g. O157:H7)
iv. Yersinia spp.
v. Brachyspira hyodysenteriae
vi. Helicobacter pylori

Front 304

what are the two most common genera of bacteria that infect the GIT of immunocompromised persons?

Back 304

Campylobacter and Salmonella

Front 305

name four bacteria involved in zoonotic systemic diseases

Back 305

1. Brucella
2. Leptospira
3. Yersinia pestis
4. Coxiella burnetti ("Q fever")

Front 306

what four species of Brucella are zoonotic?

Back 306

1. B. abortus
2. B. suis
3. B. melitensis
4. B. canis

Front 307

Zoonotic Brucella infection:
- source
- transmission
- clinical signs

Back 307

- Source: infected animals and their excretions (e.g. aborted fetus, blood, milk, etc.)
- Transmission: direct contact or aerosolization of bodily fluids of infected animals (especially vets); drinking raw milk or eating infected (undercooked) meat
- Clinical signs – different than animals: “flu-like” symptoms

Front 308

how are zoonotic Brucella infections controlled and prevented?

Back 308

1. Don’t drink raw milk or eat unpasteurized dairy products
2. Wear protective clothing when handling reproductive tract tissues and wash your hands
3. Be careful when practicing in other countries

Front 309

Zoonotic Leptospira infection:
- source
- transmission
- clinical signs

Back 309

- Source: infected animals and their excretions: Urine, aborted fetus, blood, milk, etc.; Contaminated water or soil (fomites)
- Transmission: direct contact/inhalation/ingestion of contaminated water, soil, or body fluids of infected animals (especially urine)
iii. Clinical signs - Same in humans; “flu-like” symptoms; Well’s disease

Front 310

how are zoonotic Leptospira infections controlled and prevented?

Back 310

1. Vaccinate animals
2. If diagnosed animals, don’t handle urine, blood, or tissues
3. Wear protective clothing
4. Wash hands, especially if contacted urine

Front 311

Zoonotic Yersinia pestis infection:
- source
- transmission
- clinical signs

Back 311

- Source: fleas, infected animals (e.g. cats, rodents)
- Transmission: Flea bites (most common); Direct contact with infected animals; Inhalation from animals with pneumonic form
- Clinical signs: the three forms of Plague: pneumonic, septicemia, bubonic

Front 312

how are zoonotic Yersinia pestis infections controlled and prevented?

Back 312

1. Flea control in pets
2. Correct diagnosis of infected animals (the “4-Corner States”) and avoidance of excretions
3. Rodent control and don’t allow cats to roam in endemic areas

Front 313

Zoonotic Coxiella burnetti infection:
- source
- transmission
- clinical signs

Back 313

- Source: infected animals giving birth, ticks
- Transmission: Aerosol of contaminated area (e.g. barnyard); Direct contact with birthing fluids; Tick bites (rare)
iii. Clinical signs – Q Fever: “flu-like” symptoms

Front 314

how are zoonotic Coxiella burnetti infections controlled and prevented?

Back 314

1. Wear protective clothing if in contact with placenta, birth tissue, fetal membranes, etc., of sheep, goats
2. Vaccination if you are in Australia

Front 315

Animal bites to humans:
- sources
- major bacteria
- other bacteria/fungi

Back 315

- Source: dogs, cats, rodents
- Major bacteria: P. multocida, Streps, Staphs, NSF anaerobes
- Others: Lepto, CSD, sporotrichosis, blastomycosis, plague, tularemia

Front 316

why is it important to discuss zoonotic diseases with clients versus just sending them to the doctor?

Back 316

i. Discussion of zoonosis is frequently not performed or inadequately performed
ii. Doctors give misinformation about zoonotic diseases, especially to immunocompromised people

Front 317

what are seven pieces of advice that you can give to (non-immunocompromised) clients about minimizing the risk of zoonotic disease?

Back 317

1. Keep pets healthy – vaccinate
2. Wash your hands
3. Clean wounds, bites, scratches, and keep covered
4. Keep animal areas clean and disinfected
5. Empty cat litter box daily (wear gloves)
6. Cook food appropriately and don’t feed raw meat/eggs to animals
7. Keep pets away from toilets, garbage, or feces from other animals and wildlife

Front 318

what types of pets should immunocompromised people not own?

Back 318

reptiles, amphibians, wild animals/birds, non-human primates, and YOUNG animals

Front 319

Blastomyces dermatidis
- where found
- major species infected
- clinical signs
- virulence factor
- cytology

Back 319

- saprophyte; SE and South-central river valleys
- dogs near water with moist conditions
- shifting leg lameness, respiratory, lymphadenopathy, uveitis, bone infection, anemia
- BAD-1 → anti TNF-α
- basophilic, broad-based budding

Front 320

Histoplasma capsulatum
- where found
- major species affected
- clinical signs
- radiograph interpretation
- cytology

Back 320

- bird/bat droppings; demolition sites; river valleys east, mid-west
- dogs < 4yr; cats
- cat: non-specific systemic infection
- dog: weight loss, anorexia, dyspnea, cough, GI (LBD, tenesmus, blood/mucus), anemia
- miliary/diffuse intersititial; bone marrow
- basophilic, eosinophilic center

Front 321

Coccidiodes immitis
- where found
- how infection happens
- development inside host
- clinical signs
- diagnosis
- cytology

Back 321

- SW US desert (after rains)
- inhale arthroconidia
- respiratory infection, disseminated
- Hx, clinical signs, cytology
- "half-empty/half-full" appearance (pink/blue)

Front 322

Cryptococcus
- 2 species of fungi
- where found
- major species affected
- how acquired
- clinical signs
- cytology

Back 322

- C. neoformans & C. gatti
- cats >> dogs (< 4 yr) > horse, cow
- inhalation: C. neoformans: immunocompromised; C. gatti: normal immunity
- "Roman Nose"; nasal discharge; meningoencephalitis
- dogs also: optic neuritis; retinal hemorrhage; GI; lymph nodes
- cow: mastitis
- horse: nasal granuloma
- cytology: basophilic, thick capsule → India ink

Front 323

Aspergillus
- horse
- dog
- cattle
- cats
- birds

Back 323

- horse: guttural pouch mycosis, mycotic keratitis, GI in foals
- dog: nasal aspergillosis, disseminated (↓ immunity)
- cattle: mastitis, abortion, pneumonia and GI in calves
- cats: rare
- birds: brooder pneumonia (hatchlings)

Front 324

Candida albicans
- where found
- neonates
- dogs
- cows
- cat
- diagnosis

Back 324

- commensal, found in environment
- neonates: mycotic stomatitis, G-E ulcers, rumenitis
- dogs: UTI, enteritis, cutaneous lesions, aspiration pneumonia
- cows: mastitis, abortion, ↓fertility
- cat: UTI
- diagnosis: visulization (yeast with pseudohyphae), culture

Front 325

Zygomyces & Phaeohyphomyces
- where found
- animals most susceptible
- clinical signs
- diagnosis
- risk factors

Back 325

- zygo: normal rumen flora; phaeo: saprophytes
- feedlot steer
- clinical signs: granulomatous lymphadenitis
- diagnosis: cytology, histology, Phaeo: culture
- risk factor: overcrowding

Front 326

Pneumocystis jirovecti
- susceptible animals
- clinical signs
- treatment

Back 326

- Miniature dachshund, Cavalier King Charles Spaniel
- cough, dyspnea
- Tx: sulfonamides

Front 327

Prototheca
- where located
- animals most susceptible
- clinical signs

Back 327

- Gulf coast; saprophyte; waste water?
- dogs and cats
- dogs: GI, colitis, bloody diarrhea, ocular
- cats: cutaneous lesions
- note: similar to green algae; poor prognisis

Front 328

Rhinosporidium seeberi
- where found
- clinical signs
- diagnosis

Back 328

- aquatic environments; emerging pathogen
- granulomatous rhinitis, nasal polyps
- diagnosis: visualize

Front 329

Dermatophytosis
- 3 fungal genera
- 3 classifications based on where they are found
- clinical signs
- how infection occurs
- diagnosis

Back 329

- Microsporum, Trichophyton, Epidermophyton
- geophilic, zoophilic, anthrophilic
- "ring worm"; hair loss, scaling, crusting, papules; lung cysts
- carrier animals; fomites; contact with arthrospores
- Dx: Wood's lamp (40% of infections, M. Canis); culture (test medium turns red); histopath/cytology (wet mount in KOH)

Front 330

Malasezzia pachydermatitis
- where found
- species affected
- clinical signs
- risk factors
- diagnosis

Back 330

- commensal yeast on skin
- dogs
- otitis externa; dermatitis (oily, smelly, alopecia, lichenification)
- risk factors: atopy, food allergy, ear conformation, mite infection
- diagnosis: diagnosis: visualize footprint-shaped/bottle-shaped yeast

Front 331

Sporothrix shenckii
- species commonly affected
- lesions
- diagnosis

Back 331

- horse, cat, dog
- cutaneous ulcerative lesions, non-healing and don’t respond to antibiotics, may have discharge
- diagnosis: cytology

Front 332

Phythium insidosum
- where found
- most common animals affected
- clinical signs
- diagnosis
- difference from Lagenidiosis

Back 332

- Gulf coast states, sporadically elsewhere
- dogs (large, working) and horses
- cutaneous: non-healing wounds and invasive masses that contain ulcerated nodules and draining tracts
- GI: weight loss; vomiting; diarrhea; thickening of stomach, SI, colon; mesenteric lymphadenopathy
- diagnosis: flagellated zoospores
- vs. Lagenidium: infection is uaually confined

Front 333

Lagenidium
- where found
- species mainly affected
- lesions
- difference from Phythiosis

Back 333

- (similar to Phythiosis); Gulf coast, moist areas
- dogs that swim
- cutaneous/subcutaneous lesions on extremities, mammary region, perineum, or trunk, with ulcerations
- vs. Phythiosis, this is an invasive infection

Front 334

what type of medium is used for a Kirby-Bauer agar disk diffusion test?

Back 334

Mueller-Hinton

Front 335

the circular area of clearance around an disk in a Kirby-Bauer is called what?

Back 335

zone of inhibition

Front 336

what measurement does a Kirby-Bauer agar disk diffusion test give you?

Back 336

a zone of inhibition, which is used to determine a breakpoint value

Front 337

what measurement does a dilution susceptibility test give you?

Back 337

minimum inhibitory concentration (MIC)

Front 338

what is the definition of the minimum inhibitory concentration (MIC)?

Back 338

the lowest concentration of an antimicrobial agent that completely inhibits the growth of a microorganism, as determined visually in a dilution susceptibility test

Front 339

In the following dilution susceptibility test, what is the MIC for the antibiotic being tested?

Back 339

1 μg/mL

Front 340

what are advantages and disadvantages of dilution susceptibility and agar disk diffusion tests?

Back 340

ADVANTAGES
- MIC can be determined
- may be used to optimize antimicrobial therapy by application of pharmacokinetic and pharmacodynamic principles

DISADVANTAGES
- interpretive criteria for susceptibility breakpoints is available for only a small number of drugs IN ANIMALS
- the rest of the data is extrapolated from human data

Front 341

since dilution tests are in vitro, what does the MIC actually mean? How does this translate to how the drug will work in vivo?

Back 341

- dilution tests detect the lowest concentration of an antimicrobial required to macroscopically inhibit the growth of a microorganism in the test medium
- this in vitro-derived concentration is ASSUMED to be the concentration of the infectious agent required in vivo to kill the organism by the drug, the immune system, innate clearance mechanisms of the body, or a combination of the above.

Front 342

based on the breakpoint value, what are the three possible outcomes that a lab will typically report with respect to a specific antibiotic and bacteria?

Back 342

- susceptible
- resistant
- intermediate

Front 343

from what are the majority of breakpoint values determined?

Back 343

from human clinical trials

Front 344

in a Kirby-Bauer, what is required of the test for a bacteria to be determined "susceptible?"

Back 344

the zone of inhibition must be equal to or greater than the susceptible breakpoint value

Front 345

in a Kirby-Bauer, what is required of the test for a bacteria to be determined "susceptible?"

Back 345

the zone of inhibition must be equal to or less than the resistant breakpoint value

Front 346

in a Kirby-Bauer, what is required of the test for a bacteria to be determined "intermediate?"

Back 346

the zone of inhibition must be greater than the resistant breakpoint value, but less than the susceptible breakpoint value.

Front 347

Practically, what does a "susceptible" result of a Kirby-Bauer test mean with regards to treating a patient with the antimicrobial in question?

Back 347

Treatment with this antimicrobial drug using standard label or recommended doses should produce a cure unless there are other factors independent of the drug's activity present.

Front 348

Practically, what does a "resistant" result of a Kirby-Bauer test mean with regards to treating a patient with the antimicrobial in question?

Back 348

Treatment with the antimicrobial drug in question will be ineffective, regardless of the dose administered or the location of the infection.

Front 349

Practically, what does a "intermediate" result of a Kirby-Bauer test mean with regards to treating a patient with the antimicrobial in question?

Back 349

The bacteria will be resistant to the drug in question unless dosing modifications are to be used (e.g. higher concentrations)

Front 350

when comparing an MIC by dilution to a breakpoint value, how must the values relate if
- it will produce a cure?
- it will be resistant?

Back 350

- cure: the MIC must be equal to or below the susceptible breakpoint concentration
- resistant: the MIC must be equal to or above the resistant breakpoint concentration

Front 351

what property of a drug that we were supposed to learn in pharmacology class is most affected when interpreting the results (e.g. breakpoint value) of an antimicrobial whose values were extrapolated from human clinical trial results?

Back 351

pharmacokinetics (e.g. absorption, drug distribution, metabolism, clearance)

Front 352

generally, what aspect of a site of infection would have a susceptibility testing result that underestimates true susceptibility?

Back 352

places where the penetration of the drug is higher (e.g. bladder, topical preps in the eye and ear), because much higher drug concentrations can be achieved at these sites.

Front 353

why is antimicrobial susceptibility not usually indicated in uncomplicated otitis externa?

Back 353

because very high concentrations of antimicrobial can be achieved through topical preparations

Front 354

what are some examples of pathological conditions that would change the penetration of an antimicrobial into a site (i.e. MIC was underestimated)

Back 354

- necrotic tissue
- pus
- tissue pH
- high bacterial concentrations
- biofilms
- intracellular survival

Front 355

what are four "body compartments" that can have limited antimicrobial penetration?

Back 355

1. CNS
2. eye
3. mammary tissue
4. prostate

Front 356

generally, when do susceptibility tests overestimate true susceptibility?

Back 356

in areas where there is lower penetration of the antimicrobial

Front 357

what aspect of bacterial growth is required for a susceptibility test to be valid

Back 357

they must be rapidly growing (vs. fastidious organisms such as anaerobes and Nocardia)