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VET 433a - Small Animal Stream 1 > Infectious Dz > Flashcards

Infectious Dz Flashcards

Exam 3

1
Q

What are the 2 types of diagnostic tests?

A

antibody

organism

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2
Q

What are some advantages of organism testing?

A
  • positive implies presence of organism
  • can localize dz from sample
  • sensitive in immunocompromised
  • quantification may be possible
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3
Q

What are some disadvantages of organism testing?

A
  • dec. sensitivity for some inf. (chronic, smoldering inf)
  • false (+)s possible
  • positive test =/= disease
  • no sense of chronology
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4
Q

Culture (type, pros, cons)

A
  • organism detection
  • Pros: organism id + sensitivity testing
  • Cons:
  • -> false neg from low sample size
  • -> some org. un-culturable
  • -> transport and storage == death
  • -> can be expensive
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5
Q

Immunoassays for antigen (type, pros, cons)

A
  • organism detection
  • Pros: n for organism detection, fast and easy (SNAP tests)
  • Cons:
  • -> false (-) w/ low [antigen]
  • -> false (+) w/ cross reaction
  • -> variable sens. and specificity
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6
Q

End Point PCR

A
  • only gives + or -

- no level of quantification

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7
Q

Real Time PCR

A
  • quantitative measurement of [DNA] present in sample
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8
Q

Cons of Real Time PCR

A
  • false (-) w/ strain variation
  • inhibition of certain enzymes
  • potential for false (-) from degradation
  • false (+) from contamination
  • can detect dead/ inactive organisms
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9
Q

Antibody Detection (pros)

A
  • sensitive as a single test in immunocompetent host w/ chronic dz
  • paired serology (IgM/G) allows from chronology
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10
Q

Antibody Detection (cons)

A
  • neg early on acute disease
  • neg w/ URT infections
  • neg w/ immunocompromised patients
  • false (+) are problematic
  • poor indicators of treatment success
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11
Q

When do to antibody vs organism?

A

Organism : acute disease, immunocompromised

Antibody: chronic persistent infection, organisms undetectable

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12
Q

Actinomyces (epidemiology/ etiology)

A
  • does not exist freely in nature
  • n oropharyngeal and gi inhabitant
  • young adult to middle-aged large breed dogs/ usually immunocompetent
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13
Q

Actinomyces (pathogenesis)

A
  • grass awns in oropharynx penetrate and migrate
  • bite wound inoculation
  • CNS actinomycosis: hematogenous spread from thorax (abscess)
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14
Q

Diagnosis of Actinomyces or Nocardia

A
  • gram stain (thin, gram (+), filamentous bacteria)
  • H&E not effective stain
  • alert lab fro culture + mult samples
  • Nocardia is variably acid-fast (+) while Actinomyces is acid fast (-)
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15
Q

Treatment of Actinomyces or Nocardia

A
  • prolonged treatment w/ high dose abx to prevent relapse
  • drain abscesses or pyothorax first
  • Actinomyces: peneclillin is ideal
  • Nocardia: much worse prognosis, but TMS
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16
Q

Nocardia (etiology, epidemiology)

A
  • aerobe, ubiquitous soil saprophyte
  • 1/3-4 are immunosuppressed
  • much less common than actinomyces
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17
Q

Nocardia (pathogensis)

A
  • inhalation –> pulm nocardiosis –> pleural or systemic spread
  • hematogenous dissemination to other organs
  • skin involvement: firm to fluctuant SQ swellings containing serosanguinous –> purulent fluid
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18
Q

3 major groups of mycobacterium

A
  1. Tuberculosis mycobacteria (m. tuberculosis and m. bovis)
  2. Opportunistic mycobacteria (slow and fast growing)
  3. Lepromatous mycobacteria
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19
Q

Tuberculous Mycobacteria

A
  • m. tuberculosis and m. bovis
  • highly pathogenic
  • reverse zoonosis [m. tuberculosis is potentially zoonotic)
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20
Q

Opportunistic Mycobacteria

A
  • saprophytic, survive > 2 years in env.
  • slow-growing (m. avium complex)
  • rapid-growing (RGM)
  • not zoonotic
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21
Q

Pathogenesis of Opportunistic Mycobacteria (slow and RGM)

A
  • multiply intracellularly at inoculation site and local LN
  • Avium tend to be disseminated
  • Defective cell-mediated immunity –> allows for persistence or dissemination –> granuloma formation
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22
Q

Rapidly-growing Mycobacterium

A
  • inoculated into skin via trauma
  • enhance pathogenicity in adipose
  • most animals are immunocompetent
  • cats are most susceptible (especially female)
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23
Q

Clinical signs of RGM

A
  • cutaneous and subcutaneous granulomas (especially the inguinal area [mycobacterial panniculitis])
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24
Q

Diagnosis of RGM

A
  • Histopath –> pyogranulomatous inflammation
  • Isolation:
  • -> tuberculous can take 4-6 weeks to grow
  • -> RGM may take 3-5 days
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25
Q

Treatment of M. tuberculous

A
  • not recommended but has been successful

- prolonged treatment time (>6months)

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26
Q

What are the Canine Core Vaccines?

A
  • rabies
  • distemper (D)
  • adenovirus (A)
  • parvovirus (P)
  • lepto +/-
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27
Q

What are the feline Corse Vaccines?

A
  • Rabies
  • Feline Herpesvirus (FVR)
  • Feline Calicivirus (C)
  • Feline Panleukopenia (P)
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28
Q

Core Vaccine Protocol

A
  • 6-8 wks, then every 3-4 wks until 16 weeks for FVRCP or DAP
  • booster @ 6 months - 1 year then every 3 years except for: recombinant, lepto, lyme, bordatella
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29
Q

What is the Window of Susceptibility (for vaccination)?

A
  • the period of time between which:
  • -> the maternal antibodies are low enough to prevent disease
  • -> minimum titer to block vaccine
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30
Q

christina’s favorite food

A

dim sum

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31
Q

Canine Distemper

A
  • highly infectious
  • enveloped RNA virus (readily inactivated)
  • shep in resp secretions, feces, and urine for up to 3 months post infection
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32
Q

Canine Distemper Pathogenesis

A

Stage 1: Lymphoid Tissue
–> virus invades macrophages in URT –> lymphatic spread –> day 2-6 for systemic spread
–> fever, lymphopenia
Stage 2: epithelial and nervous tissue
–> day 8-9 –> epithelial and CNS invasion

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33
Q

Canine Distemper Clinical Signs

A

Early:
–> lethargy, inappetance, fever,
–> conjunctivitis, cough, serous ocular and nasal discharge
Progression:
–> obtundation, anorexia, comiting, diarrhea, –> moist cough, tachypnea
–> neuro signs

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34
Q

Canine Distemper Diagnosis

A
  • Clinical signs
  • CBC w/ viral inclusions
  • thoracic rads
  • CSF analysis
  • conjunctival scrapings for inclusions
  • RT-PCR
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35
Q

Infectious Canine Hepatitis (ICH)

A
  • usually young puppies
  • canine adenovirus-1 targets endothelial cells and hepatocytes
  • virtually extinct in USA
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36
Q

ICH Clinical Signs

A 
- most infections are sub-clinical
Acute form:
--> puppies age 6-10 wks
--> fever, anorexia, lethargy, tonsiliitis, cough, tachypnea, hepatomegaly, abd. apin, edema, ascites, CNS signs (hepatic encephalopathy)
--> corneal edema and anterior uveitis
Peracute --> death within a few days
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37
Q

Hallmark lesion of ICH

A
  • corneal edema and anterior uveitis

- type 3 hypersensitivity

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38
Q

ICH diagnosis

A
  • clinical signs
  • bloodwork abnormalities (liver signs)
  • PCR or histopath (of liver)
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39
Q

ICH prevention

A
  • vaccine for adenovirus-2 (protects for 1 & 2)

- do not use mucosal CAV-2 for CAV-1 prevention

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40
Q

Treatment of Canine Distemper Virus

A
  • supportive care only
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41
Q

Parvovirus

A
  • sever enteritis and leukopenia in dogs and cats
  • highly contagious, often fatal if untreated
  • feline panleuk is far less common than canine parvo
  • non-enveloped virus requiring rapidly dividing cells to replicate
  • shed for 4 wks post infection
  • resists disinfection and can survive up to a year on fomites
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42
Q

Parvovirus pathogenesis

A
  • oronasal exposure –> migration into local lymphoid tissues (viremia day 1-6) –> infection of gi, lymphoid, marrow tissues
  • -> sepsis, endotoxemia, and DIC
  • infections in utero or <8wks of age in cats causes cerebellar hypoplasia
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43
Q

Parvovirus Clinical Signs

A
  • incubation period (3-14 days canine, 2-10 days feline)
  • lethargy, fever –> vomiting and diarrhea
  • leukopenia
  • death in 1-2 days (peracute)
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44
Q

Parvovirus Diagnosis

A
  • CBC –> leukopenia
  • Fecal ELISA
  • fecal PCR
  • histopath –> gold-standard but on necropsy
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45
Q

Parvovirus Treatment

A
  • isolation
  • aggressive IV fluid therapy
  • broad-spectrum IV antimicrobials
  • IV dextrose
  • plasma for hypoalbuminemia
  • antiemetics
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46
Q

Parvovirus Prevention

A
  • vaccination (attenuated live)
  • vax to 16-18 wks of age
  • titers correlate w/ protection
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47
Q

Leptospirosis epidemiology

A
  • survives in stagnant or slow-moving warmer water, temp 0-25C
  • transmission via direct contact w/ contaminated urine, bite wounds, or ingestion of infected tissue
  • organisms penetrate intact mucous membranes or abraded skin
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48
Q

Leptospirosis Pathogenesis

A
  • actue kindey injury
  • +/- hepatic insufficiency
  • +/- hemorrhagic disease
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49
Q

Leptospirosis Cliinical Signs

A
  • fever, lethargy, inappetence
  • PUPD or anuria/ oliguria
  • abd. pain
  • mild peripheral lymphadenopathy
  • icterus
  • +/- uveitis
  • +/- tachypnea d/t pulm. hemorrhage
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50
Q

Leptospirosis Imaging findings

A
  • n thoracic rads

- abd. ultrasound –> hyperechoic renal cortices, perirenal fluid, renomegaly

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51
Q

Leptospirosis Diagnosis

A
  • antibody detection

- organisms detection –> kidney biopsy is less than ideal since there are low numbers of organisms

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52
Q

Leptospirosis Treatment

A
  • ampicillin or penicililin for comiting dogs
  • doxycyclin for 2wks post-vomiting
  • aggressive IV fluids
  • diuretics
  • antiemtetics
  • hemodialysis
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53
Q

Leptospirosis Prognosis

A
  • 85% survival rate w/ aggressive therapy
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54
Q

Hyperthermia

A
  • retained hypothalamic set-point
  • undesirable heat retention or heat overproduction
  • Cause: heat strokes, seizures, tetanus, adverse drug rxn, exercise
  • not responsive to anti-pyretics
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55
Q

Fever

A
  • exogenous pyrogens (LPS) stimulate release of endogenous pyrogens by macrophages –> IL1, 6, TNFa
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56
Q

2 Mechanisms of Fever

A
  1. Humoral mechanism: endogenous pyrogens activate arachidonic acid pathway in microglial cells; PGE2 raises set point in hypothalamus
    - -> sympathetic generation/ retention of heat (vasoconstriction, shivering)
  2. Neuronal hypothesis: C5a stimulates PGE2 production by liver; vagaly mediated neural response
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57
Q

What is a “drug fever”

A
  • elevated body temp d/t drug-induced alterations in muscle activity or sensitivity of hypthalamic neurons
  • actually a hyperthermia
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58
Q

What are 3 examples of “drug fever”s

A
  1. Malignant hyperthermia –> mutation in ryanodine receptor causes excessive influx of Ca and depletion of ATP
  2. Serotonin syndrome
  3. Opioid in cats: excitement, excessive sedation, staring, hyperthermia
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59
Q

Factors that modify a fever

A
  1. extremes of age
  2. renal failure (uremic acids are cryogenic)
  3. immunosuppression
  4. anti-inflammatory drugs
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60
Q

Fever Type

A
  1. Persistent: above n throughout day, but does not vary
  2. Remittent: above n throughout day, and does vary widely (eg. endocarditis)
  3. Intermittent or relapsing (cyclic neutropenia, borrelia)
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61
Q

Fever Magnitude

A
  1. Low grade (<104F)
    - fungal inf.
    - bartonellosis, lyme disease
    - mycobacterial/ mycoplasma inf.
  2. High grade (>104F)
    - viral or bacterial inf.
    - salmon poisoning
    - rocky mountain spotted fever
    - Plague and Tularemia
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62
Q

Fever of Unknown Origin (FUO)

A
  • prolonged fever >3wks duration ass. w/ vague, non-specific signs of illness
  • diagnosis uncertain after 1 wk of hospitalization involving thorough lab tests
  • ~20% of fever cases are of unknown origin
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63
Q

FUO how to identify

A
  • look for Infectious, Neoplastic, or Immune- mediated cause

- Localize the lesion (eyes, skin, rectal, musculoskeletal)

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64
Q

Exam and Tests for FUO

A
  • CBC, Chem, UA –> rads, ultrasound
  • repeat your physical exam
  • Arthrocentesis (IMPA is a common cause of FUO), lymph nodes, blood culture, serology (tick borne, lepto, toxo, neospora, fungal)
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65
Q

Cause of FIP

A
  • feline enteric coronavirus
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66
Q

Pathogenesis of FIP

A
  • fecal-oral spread of avirulent form from another cat
  • lives in GI tract
  • mutates into virulent form (FIPV)
  • multiplication in macrophages
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67
Q

T/F: pure bred cats have higher incidence of FIP than non-pure bred

A

Yes

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68
Q

PE findings with FIP

A
  • fever
  • tachypnea
  • muffled heart sounds
  • icterus
  • organomegaly (liver, spleen, kdiney)
  • ant uveitis
  • ret. detachment, hemorrhage
  • neuro signs
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69
Q

Lab findings with FIP

A
  • NNN anemia
  • neutrophilia, leukopenia, thrombocytopenia
  • azotemia
  • elevated liver enzymes
  • high bilirubin
  • high globulins
  • low albumin
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70
Q

FIP Effusion

A
  • high protein
  • low cells
  • straw colored and viscous
  • modified transudate, most likely
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71
Q

FIP Diagnostic Testing

A

Serology (pos = exposure to any coronavirus)
RT-PCR (no specific mutation for FIP)
Biopsy and Cytology (ICC on effusion)(Biopsy/IHC –> fibrinous lymphadenitis)

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72
Q

FIP treatment

A
  • supportive only

- prednisolone, +/- antivirals

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73
Q

FIP prognosis

A
  • 1 day – 1 year (most 5-7 weeks)
74
Q

FIP neg pronostic indicators

A
  • wet/ effusive FIP
  • high bilirubin
  • lymphopenia
  • failure to respond within 3 days of treatment
75
Q

FIP prevention

A
  • selective breeding programs
  • inform breeder
  • decrease stress
  • don’t breed FIP + cats
76
Q

FIP Vaccination

A
  • temp-sensitive intranasal vax
  • adm. at 16 weeks
  • efficacy debated
77
Q

FeLV (general)

A
  • leading cause of feline mortality
78
Q

FeLV (Etiology)

A
  • enveloped RNA virus

- susceptible to desiccation heat, disinfections

79
Q

FeLV (Epidemiology)

A
  • transmission is in saliva (requires prolonged, close contact)
  • viremic cats can live months to years (max 4 years)
  • transmission via blood transfusion
80
Q

FeLV (Age-Related Resistance)

A
  • progressive dz incidence decrease as age increases

- uncommon to see it over 10 years

81
Q

FeLV (prevalence)

A
  • up to 30% of cats in cateries

- <3% of suburban and shelter cats (because of effective treatment and prevention protocols)

82
Q

FeLV (prognostic factors)

A
  • challenge dose
  • immune status
  • age
  • viral strain
83
Q

FeLV (Pathogenesis)

A
  • oronasal exposure –> oropharyngeal lymphoid tissue –> few peripheral mononuclear cells (ELISA +) –> spleen, LNs, epithelial tissues, marrow (ELISA +, IFA +) –> poor immune response === FeLV disease
84
Q

FeLV (regressive vs progressive)

A

Regressive:
- FeLV inserts itself into the genome, but is effectively silenced and will not replicate itself
Progressive:
- FeLV inserts itself into the genome and reproduces
- more common in younger animals

85
Q

What kinds of diseases do you see with FeLV infection?

A
  • Lymphoma : esp. mediastinal lymphoma causing a pleural effusion
  • Leukemia : pancytopenia w/ lethargy, sepsis, hemorrhage
  • Anemia : impaired red cell production w/ macrocytosis
86
Q

FeLV (Diagnosis)

A
  • Antigen-detection ELISA (screening) and IFA

- PCR (not recommended for screening) for both DNA (proviral) and RNA

87
Q

T/F: a regressor FeLV cat will be PCR (+) and RT-PCR (-) and ELISA (-)

A

T

88
Q

FeLV (Treatment)

A
  • chemo for lymphoma
  • transfusions for anemia
  • abx for 2* lesions
  • antivirals have not been effective
89
Q

FeLV (Prevention)

A
  • killed or recombinant vax
  • 2 doses @ 9 wks then every year (recombinant) or every 2-3 years (killed)
  • only vax FeLV (-) cats
90
Q

FIV (general)

A
  • worldwide distribution

- chronic infection –> immunodeficiency

91
Q

FIV (Etiology)

A
  • enveloped RNA virus

- infection is for life

92
Q

FIV (Epidemiology)

A
  • prevalence in sick cats 13-15%
  • prevalence in healthy cats 2-3%
  • 2-3x greater incidence in males
  • mean age of 6-8 years
93
Q

FIV (Transmission)

A
  • saliva by biting
  • transplacental transmission depends on: strain or degree of maternal viremia
  • most kittens infected by saliva or milk
  • indoor housing decreases transmission rates
94
Q

FIV (Pathogenesis - target cells)

A
  • T helper (CD4+) and then later attack of CD8 and B cells

- tissue macrophages

95
Q

FIV (Pathogenesis results)

A
  • gradual destruction of immune system
  • promotion of neoplastic disease
  • neurological disease
96
Q

FIV (Clinical Findings)

A 
Transient Primary Illness
- transient lymphadenopathy, pyrexia, depression, anorexia, neutropenia, lymphopenia 
Subclinical Phase 
- hyperglobulinemia
Terminal Phase
- 2* infections = **stomatitis**, recurrent URTD, diarrhea, weight loss, chronic skin dz, opportunistic inf
- ocular dz
- eventual neuro signs
- chronic wasting
97
Q

FIV (diagnosis)

A
  • Antibody Testing (ELISA, Western Blott)
  • antigen levels are low in FIV
  • ELISA has potential for false(+) - maternal antibodies, retest
  • ELISA has potential for false(-) - cats w/ acute dz, end-stage dz
98
Q

FIV (Treatment)

A
  • antivirals (AZT –> improves stomatitis and CD4/8 ratios, protease inhibitors not useful, no effective treatment known)
  • keep cats indoors
  • identify and treat opportunistic infections
99
Q

FIV (prevention)

A
  • inactivated vaccine used to be available (interferes w/ snap idexx test)
100
Q

5 Ground Rules of Immunosuppressive therapy

A
  1. make sure that it’s immune-mediated disease prior to treatment
  2. warn o that neoplasia/ infection may go undetected despite best efforts
  3. think before you clip
  4. minimize excessive immunosuppression - never use more than 2 drugs at once
  5. maintain contact w/ your patient
101
Q

3 most common immune-mediated diseases

A
  1. IMHA
  2. ITP
  3. IMPA
102
Q

Glucocorticoids (drug examples)

A
  • prednisone/solone, dexamethasone
103
Q

Glucocorticoids (adverse effects)

A

Think Cushing’s like symptoms

  • PUPD, polyphagia
  • panting
  • muscle wasting
  • skin thinning, hair loss
  • hepatomegaly
  • calcinosis cutis
104
Q

T/F: it is ok to combine a glucocorticoid with an NSAID for increased effect.

A

False

105
Q

Azathioprine (moa)

A
  • competes with adenine, that prevents nucleic acid synthesis
106
Q

Azathioprine (general facts)

A
  • drug sparing effect for glucocorticoids
  • almost always given with a glucocorticoid
  • inexpensive drug, but monitoring costs money
107
Q

Azathioprine (adverse effects)

A 
Do not give to cats
Dogs:
- gi upset
- impaired hair growth
- bone marrow suppression
- hepatotoxicity
- pancreatitis
- profound weakness and tetraparesis
108
Q

Chlorambucil (species, disease uses, adverse effects)

A
  • alkylating agent
  • used most often in cats
  • IBD, Lymphoma, immune diseases
  • adverse effects uncommon
109
Q

Cyclosporine A (moa)

A
  • interacts w/ cyclophilins in lymphocytes, blocking formation of transcription factors needed for T cell activation and cytokine synthesis (mainly IL-2)
110
Q

Cyclosporin A (uses)

A
  • immune suppression

- atopic dermatitis

111
Q

Cyclosporin (adverse effects)

A
  • gi signs (most common)
  • gingival hyperplasia
  • hirstitism
  • nephrotoxicity
  • hepatotoxicity
  • neoplasia
112
Q

Ciclosporin (drugs)

A
  • neoral and atopica are much better formulations than generic d/t bioavailability difference
113
Q

Ciclosporin (metabolism)

A
  • p450 metabolism

- binds p-glycoprotein (may predispose to ivermectin toxicity)

114
Q

Mycophenolate mofetil

A
  • inhibits purine synthesis
  • glomerulonephritis
  • will cause gi toxicity
115
Q

IMHA

A 
- type 2 hypersensitivity (antibody mediated)
Prognostic factors:
- intravascular hemolysis
- absence of regeneration
- auto-agglutination
- thrombocytopenia
- hyperbilirubinemia
116
Q

IMPA

A
  • Type 3 hypersensitivity reaction
  • common in dogs, uncommon in cats
  • may be 2* to infection, drugs, neoplasia
117
Q

IMPA (treatment)

A
  • azothioprine (number 1 choice), ciclosprin (good #2)

- -> no NSAIDs w/ pred

118
Q

IMPA (clinical signs)

A
  • stiffness, reluctant to rise, shifting leg lameness
  • fever +/- joint signs
  • peripheral lymphadenomegaly
  • swollen, painful, warm joints
119
Q

IMPA (diagnosis)

A
  • cbc, chem, ua
  • rads
  • +/- joint radiographs (n in acute disease)
  • arthrocentesis (minimum 3 joints)(ideal)
120
Q

Rickettsia (general)

A
  • arthropod transmitted
  • obligate intracellular
  • gram (-) bacteria
121
Q

Rocky Mountain Spotted Fever (epidemiology)

A
  • most cases march-october
122
Q

Rocky Mountain Spotted Fever (pathogenesis)

A
  • ticks must attach for 5-20 hours
  • infects endothelial cells of small vessels –> vasculitis
  • see a vasculitis, necrosis, increased vasc permeability
  • edema, hemorrhage, hypotension, shock
123
Q

Rocky Mountain Spotted Fever (clinical signs)

A
  • ADR (fever, anorexia, depression)
  • edema, hyperemia, necrosis of extremities
  • mucopurulent ocular discharge
  • joint pain/ swelling/ myocarditis
124
Q

Rocky Mountain Spotted Fever (Diagnosis considerations)

A
  • indistinguishable from acute ehrlychiosis but much shorter course (<2wks)
  • very lethal disease
125
Q

Rocky Mountain Spotted Fever (Diagnosis)

A
  • Serology (IFA, ELISA)
  • 4x increase in titers
  • PCR
  • Direct FA of biospy samples (75% positive by day 3-4)
126
Q

Rocky Mountain Spotted Fever (Treatment)

A
  • doxycycline for 2 weeks
127
Q

Rocky Mountain Spotted Fever (Prevention)

A
  • lifelong immunity following infection

- no vaccine

128
Q

Canine Monocytic Ehrlichiosis (3 Pathogenic Phases)

A

Acute Phase (first 2-4 weeks):
–> multiplies in monocytes w/ splenomegaly and lymphadenopathy
–> infected cells adhere to lungs, kidney, meninges
–> thrombocytopenia, +/- leukopenia, anemia
Subclinical Phase (weeks 6-9)
–> no signs
Chronic Phase
–> impaired bone marrow fxn

129
Q

Canine Monocytic Ehrlichiosis (Clinical Signs)

A

Acute: ADR, oculonasal discharge, edema of limbs and scrotum
Chronic: pallor, bleeding tendencies despite good platelet count, ant. uveitis, hemorrhage

130
Q

Canine Monocytic Ehrlichiosis (Diagosis)

A
  • pancytopenia, lymphocytosis, thrombocytopenia
  • +/- coombs (+) anemia
  • id of morula on blood smear (within monocytes)
  • Serology: 4DX snap test
  • IgG between 7-28 days post-inf
131
Q

Canine Monocytic Ehrlichiosis (Treatment)

A
  • Doxycycline for 6-8 weeks

- prognosis is good for acute ehrlichiosis

132
Q

Canine Granulocytic Anaplasmosis (Pathogenesis)

A
  • subclinical infeciton in many dogs

- fever, lethargy, lymphaneopathy, splenomegaly, scleral injection

133
Q

Canine Granulocytic Anaplasmosis (Diagnosis)

A
  • morulae w/in the granulocytes

- Serology: SNAP vs IFA

134
Q

Canine Granulocytic Anaplasmosis (Treatment)

A
  • doxycycline
135
Q

Salmon Poisoning (etiology)

A
  • neorickettsia helminthoeca

- transmitted via ingestion of a fish containing trematode/ fluke: nanophyetus salmincola

136
Q

Salmon Poisoning (Pathogenesis)

A
  • mature fluke in intestine release rickettsia into intestinal epithelium
  • spreads systemically via lymph
  • ulcerohemorrhage enteritis
  • lymphoid tissue invasion by macs and plamsa cells
137
Q

Salmon Poisoning (Clinical Signs)

A
  • vomiting, hemorrhagic diarrhea
138
Q

Salmon Poisoning (diagnosis)

A
  • hx of fish exposure
  • thrombocytopenia (in 90% of cases)
  • id of eggs (>80% of cases)
  • inclusions of macs in LN aspirates
139
Q

Salmon Poisoning (treatment)

A
  • tetracyclines for 2 weeks (doxycycline)
  • praziquantil for fluke infestation
  • IV fluids +/- blood products if needed
140
Q

Borrelia burgdorferi (Pathogenesis)

A
  • must be attached for 48 hours
  • trans. via tick saliva
  • replicates and migrates through connective tissue
141
Q

Borrelia burgdorferi (Clinical Sings)

A
  • arthritis, fever, lymphadenopathy, anorexia for 2-5 months after tick bite
  • protein-losing nephropathy (IHC of renal biopsy)
142
Q

Borrelia burgdorferi ( Diagnosis)

A
  • non-specific signs
  • joint taps (neutrophilic mono/polyarthritis)
  • organism tests available but not sensitive
  • Serology (+) result = exposure at some point
143
Q

Borrelia burgdorferi (treatment)

A
  • doxycycline for 4 weeks (1st choice)
144
Q

Borrelia burgdorferi (prevention)

A
  • tick inspection after outdoor activity
  • topical ectoparasitides
  • prophylactic abx not recommended
  • vaccines (efficacious but controversial d/t high adverse effects and yearly dose rate)
145
Q

Canine Bebesiosis (etiology)

A
  • rbc parasite
  • tick-borne disease
  • can be trans. through blood transfusions
146
Q

Large Babesia

A
  • singly or paired in RBCs
  • B. vogeli and B. canis (least pathogenic organisms)
  • higher prevalence in kennels, adults, greyhounds
147
Q

Large Babesia (clinical signs)

A
  • hemolysis
  • anemia, fever, hypotensive shock
  • sometimes: icterus, splenomegaly, IMT
148
Q

Babesia gibsoni

A
  • small babesia
  • found singly in RBCs
  • mostly in pits/ staffies
149
Q

Babesia gibsoni (clinical signs)

A
  • fever, anorexia, weakness
  • anemia, thrombocytopenia
  • HCT may normalize 2-3 months post infection
150
Q

Babesia conradae

A
  • medium-size organism

- very similar to B. gibsoni

151
Q

Canine Babesiosis (Diagnosis)

A
  • CBC (low thomb, +/- regen anemia
  • Detection of organisms of blood smear
  • serology
  • PCR - current test of choice
152
Q

Canine Babesiosis (Treatment)

A
  • blood transfusions
  • fluids
  • antibabesial drugs (imodocarb proprionate for large)(atovaquone and azithromycin for medium/small)
153
Q

Canine Babesiosis (Prevention)

A
  • tick control
  • avoid splenectomy and immunosuppression in chronicity infected dogs
  • screen blood donors serologically
154
Q

Feline Cytauxzoonosis (etiology)

A
  • usually fatal, tick borne dz of cats
  • outdoor cats
  • bobcat reservoir
  • southern/ southereastern US
155
Q

Feline Cytauxzoonosis (Pathogenesis)

A
  1. Shizogonous phase: infected mononuclear cells rupture and release organisms leading to DIC and shock
  2. Intraerythrocitic phase: 1-3 days after shizonts appear, hemolytic anemia w/ high fever, ring-shaped org in RBCs
156
Q

Feline Cytauxzoonosis (Clinical Signs)

A
  • usually rapidly fatal: dark urine, dehydration, icterus, pallow, prolonged CRT, hypothermia
  • death w/in 5 days
157
Q

Feline Cytauxzoonosis (Diagnosis)

A
  • anemia, leukopenia, thrombocytopenia, hyperbilirubinemia
158
Q

Feline Cytauxzoonosis (Treatment)

A
  • high mortality despite treatment
  • supportive care
  • rare cats survive w/out treatment
159
Q

Leishmaniosis (Etiology)

A
  • important human dz
  • mediterranian, central and south america
  • sandfly vector
160
Q

Leishmaniosis (Clinical Signs)

A
  • hyperkeratosis and intradermal nodules

- splenomegaly, lymphadenopathy, polyarthritis, glomerulonephritis, uveitis, rhinitis

161
Q

Leishmaniosis (Diagnosis)

A
  • visualization of amastigotes in biopsies or aspirates
162
Q

Leishmaniosis (Treatment)

A
  • controversial
163
Q

Hepatozoonosis (Epidemiology)

A
  • H. americanum infects dogs in the southeastern US
164
Q

Hepatozoonosis (Life cycle)

A
  • dog eats tick
  • cysts containing merozoites form in tissues
  • pyogranulomatous inflammation
165
Q

Hepatozoonosis (Clinical Signs)

A
  • wasting disease/ myositits
  • pain, gait abn
  • glomerulonephritis
166
Q

Hepatozoonosis (Diagnosis)

A
  • marked luekocytosis
  • hypoglycemia
  • skeletal radiographs
  • PCR of muscle biopsy is the gold standard
167
Q

Hepatozoonosis ( treatment)

A
  • longterm adminstration of decoquinate for remission, no cure
168
Q

Neospora (Etiology)

A
  • life cycle resembles that of toxoplasma w/ dog as definitive host
  • transplacental transmission following ingestion of tissue cysts by carnivores or oocytes by herbivores
169
Q

Neospora ( Clinical signs)

A

Herbivores: abortion
Carnivores: neuromuscular abnormalities, ascending paralysis and muscle atrophy and stiffness in dogs less than 6 months of age

170
Q

Neospora (tranmission)

A
  • ingestion of cysts will infect

- most are transplacental d/t reactivation of bradyzoite cysts during pregnancy

171
Q

Toxoplasma (Etiology)

A
  • toxoplasma gondii

- cats are definitive host

172
Q

Toxoplasma (Epidemiology/ Cycles)

A
  • sexual reproduction (enteroepithelial cycle) occurs only within the gi tract of the cat and sheds out oocysts
  • asexual reproduction (extraintestinal cycle) occurs in all other species but does not result in shedding
173
Q

Toxoplasma (Reactivation of bradyzoites)

A
  • sever immune suppression from high steroids, HIV, chemotherapy, anti-organ-rejection
174
Q

Toxoplasma (Transplacental Infection)

A
  • naive humans and animals infected just prior to pregnancy
  • placentitis and spread of tachyzoites to fetus
  • pregnancy =/= reactivation
175
Q

Toxoplasma (route of infection)

A
  • transplacental
  • bradyzoite cyst ingestion
  • occyst-contaminated food, water, soil
176
Q

Toxoplasma (Diagnosis)

A
  • Cytology –> tachy rarely seen
  • Radiology –> diffuse interstitial to alveolar patter/ pleural effusion; hepatomegaly, peritoneal effusion
  • Fecal exam –> cats are rarely shedding
  • Serology –> IgM >64 or 4x rise in titers
  • Org. Detection –> histopath detection of tachyzoites aided by IHC (not bradyzoites)
177
Q

Toxoplasma ( treatment)

A
  • supportive therapy

- clindamycin

178
Q

Toxoplasma (Risk of cat ownership)

A
  • 30% of dogs and cats are seropositive
  • Pet cats are of little risk
  • seronegative cats at greatest risk to seronegative women
179
Q

Toxoplasma ( Cat Clinical Signs)

A
  • enteroepithelial cycle usually subclinical
  • extraintestinal cycle:
  • -> stillbirth, neonatal death
  • -> anorexia, fever, CNS, dyspnea, coughing, comiting, diarrhea
  • -> uveitis, chorioretinitis
180
Q

Toxoplasma (Dogs clinical signs)

A
  • similar to cats
  • ocular disease less common
  • chrnoic neuromuscular disaese
181
Q

Toxoplasma ( Humans)

A
  • immunocompetent –> flu-like symptoms
  • AIDS and transplant patients:
  • -> 95% of cases d/t bradyzoite cyst reactivation
  • -> encephalitis, chorioretinitis, occasional pneumonia
182
Q

Toxoplasma (Epidemiology - humans)

A
  • 25-50% of humans seropositive
  • cysts present in lamb, pork
  • reduction of bradyzoite cyst levels (cook, salt, cure foods)(microwave doesn’t work)

VET 433a - Small Animal Stream 1 (10 decks)

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