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VET433A > Week 8 - Infectious > Flashcards

Week 8 - Infectious Flashcards

1
Q

Why do we perform diagnostic tests? (4)

A
  1. to rule out dz - dz presence or absence
  2. gauge severity
  3. monitor response to therapy - how well are you treating dz
  4. inform prognosis
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2
Q

What is sensitivity?

A

proportion of [dz positive] that actually [test positive]

TP/(TP+FN)

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3
Q

100 dogs have an infection and 90 test positive. What is the sensitivity?

A

90/100 = 90%

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4
Q

What is specificity?

A

proportion of [dz negative] that actually [test negative]

TN/(TN+FP)

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5
Q

100 dogs are NOT infected, 95 of those test negative. What is the specificity?

A

95/100 = 95%

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6
Q

What’s the pros to a highly (100%) sensitive test?

A

A highly sensitive test catches every animal with the disease, with some false positives. But if the test is negative, we can feel comfortable it is a TRUE negative.

If you test positive, it COULD be a false positive. (so they could actually be disease free)

You don’t get false negatives.

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7
Q

What’s the pros to a highly (100%) specific test?

A

A highly specific test catches every animal without the disease, with some false negatives. But if the test is positive, we can feel comfortable it is a TRUE positive.

If you test negative, it COULD be a false negative. (so they could actually have the disease)

You don’t get false positives.

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8
Q

What is a Positive Predictive Value?

A

Proportion of the test positives that actually have the disease

TP/all positives

all positives = true and false positives

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9
Q

What is a Negative Predictive Value?

A

Proportion of the test negatives that don’t actually have disease

TN/all negatives

all negatives = true and false negatives

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10
Q

What are the two major categories of diagnostic tests for infectious diseases?

A
  1. Organism Detection
  2. Antibody Detection
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11
Q

What are some examples of Organism Detection tests? Remember you can assess for:

whole organisms
antigen
nucleic acid (DNA or RNA)

A

Cytology and Histopathology
-can be insensitive

Culture and Identification
-culture allows for antimicrobial susceptibility testing
-false negatives with low speciment size or after abx
-some unculturable
-loss of viability with storage
-False positives from contamination by commensals
-expensive

Antigen Assays (ELISA)
-detect organic proteins
-False negatives with low antigen levels
-False positives from cross-reaction
-Variable sensitivity and specificity

Nucleic Acid Assays - PCR

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12
Q

What are some examples of Antibody Detection tests?

A

ELISA
Western Blot
Lateral flow assays
Indirect IFA
Agglutination tests
Gel immunodiffusion

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13
Q

Pros and cons to organism detection?

A

PROS
-Positive implies presence of organism
-Can localize the disease process
-Sensitive in the immunocompromised
-Quantification of organism numbers may be possible

CONS
-False positives possible
-Positive test doesn’t always imply disease
-No sense of chronology
-Low sensitivity for some infections

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14
Q

What are some examples of antigen detection assays?

A

FeLV SNAP test
Parvovirus fecal antigen SNAP test
Heartworm test (4DX)

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15
Q

When do we consider PCR for Organ Detection?

A

When it is difficult or dangerous to culture

Prior to robust antibody production (acute disease)

In animals that won’t mount a strong antibody response – immunocompromised

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16
Q

For Organism Detection via PCR – what are some PCR cons?

A

False negatives if insufficient sample type/size

False negative if there is strain variation

Inhibition of enzymes from some bodily fluids

False negative from degradation of nucleic acid – especially RNA

False positives from contamination

Can detect inactivated organisms if nucleic acid still present

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17
Q

What does antibody detection mean?

A

There is/was evidence of infection.

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18
Q

There are two types of antibody titers for antibody detection. What are they?

A
  1. Paired acute and convalescent antibody titers required to document infection for acute diseases
    - Leptospirosis, anaplasmosis
  2. Single antibody titers can be accurate for some chronic, persistent infections
    - Lyme disease, FIV
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19
Q

What are the cons to antibody detection?

A

Antibodies must be present to be detected!

  1. Negative early for acute diseases
    - Before a good Ab response
  2. Negative with localized disease
    - When you don’t get a good systemic response
  3. Negative in immunocompromised patients
    -When they can’t mount a good Ab response
  4. False positives are common
    - Previous exposure or infection
    - Cross-reactivity
    - After vaccination (except DIVA assays)
    DIVA = Discrimination of infected and vaccinated animals
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20
Q

What are some examples of antibody detection assays?

A

FIV test
Tick born disease on 4DX
Leptospirosis MAT

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21
Q

What is hyperthermia?

A

-Normal set point retained

-Body overheats due to undesirable heat retention or over-production of heat

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22
Q

What are examples of hyperthermia?

A

-Heat stroke, excitement, seizures, tetanus, adverse drug reactions, strenuous exercise

-Not responsive to anti-pyretics, can be severe and rapidly fatal

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23
Q

What is fever?

A
  • Exogenous pyrogens (eg. LPS) stimulate release of
    endogenous pyrogens by macrophages
  • Il-1, Il-6 and TNF-α
  • Alter hypothalamic set point
  • Humoral mechanism
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24
Q

What is “Drug Fever”?

A

-NOT fever
-technically hyperthermia

-Increased body temperature due to drug-induced alterations in muscle activity OR sensitivity of hypothalamic neurons to changes in body temperature

-

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25
Q

What types of “Drug Fever” are there?

A
  1. Malignant hyperthermia
    -Autosomal dominant mutation of the ryanodine (RYR1) receptor in dogs
  2. Serotonin syndrome in humans
  3. Opioids in cats
    -Excitement, excessive sedation, staring, hyperthermia
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26
Q

What factors modify fever?

A
  • Extremes of age
  • Renal failure
    -Uremic toxins are endogenous cryogens or
    antipyretics, or alter basal metabolic rate
    -Fever = > 101F
  • Immunosuppression
  • Anti-inflammatory drugs
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27
Q

There are 3 types of fevers, what are they?

A
  1. Persistent = above normal throughout day, does not
    vary more than 2 degrees F
  2. Remittent = above normal throughout day, varies more than 2 degrees F e.g. endocarditis
  3. Intermittent or relapsing e.g. Borrelia, cyclic neutropenia
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28
Q

What is a fever of unknown origin? FUO

A

-Prolonged fever of > 3 weeks duration associated with vague, nonspecific signs of illness

-Temperature > 1.5oF above normal on several occasions

-Diagnosis uncertain after 1 week of hospitalization involving repeated physical examination and routine laboratory tests

  • Three outpatient visits OR
  • Three days in the hospital without elucidation of a cause OR
  • One week of “intelligent and invasive” ambulatory (outpatient) investigation
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29
Q

Fever implies ____________

A

INFLAMMATION

not infection

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30
Q

Why do we vaccinate?

A
  1. To improve the specific immune response in an animal
    -provides protection against an infectious disease (or toxin exposure)
    -lowers the risk of developing signs of illness when naturally exposed or reduces the clinical signs associated with infection if contracted
  2. Less morbidity (animal and client suffering)
  3. Less mortality

4.Lower cost of pet care (illness $$$ > vaccine $)

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31
Q

FVRCP vaccines includes what?

A

FVR: feline herpes virus (feline viral rhinotracheitis)
C: calicivirus
P: Panleukopenia

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32
Q

Which are the core vaccines for cats?

A

FVRCP
FelV - sometimes
Rabies

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33
Q

Which are the core vaccines for dogs?

A

Rabies
Canine Distemper (D)
Canine adenovirus 2 (A)
Canine parvovirus (P)
Leptospira +/-

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34
Q

What are vaccine protocols?

A

▪6-8 weeks, then every 3-4 weeks until at least 16 weeks for FVRCP or DAP
-trying to aim for time where maternal antibodies aren’t enough to protect animal anymore

▪Booster within 1 year then every 1 or 3 years except for
-Leptospira and Borrelia (bacterins)
-Bordetella
-FHV1 and FCV in high-risk situations

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35
Q

What is Canine Distemper?

A

▪Enveloped RNA virus
▪Family Paramyxoviridae, Genus Morbillivirus
▪Readily inactivated in the environment
▪Disease in dogs, raccoons, ferrets, exotic felids
▪Strain virulence and neurotropism varies

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36
Q

How is Canine Distemper virus shed?

A

▪Shed in respiratory secretions, feces and urine (all body secretions) for up to 3 months after infection
▪Spread by direct contact, aerosol, or respiratory droplet exposure
▪Raccoons may be a source
▪Many infections subclinical
▪Infections often occur when maternal antibody wanes

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37
Q

What are the CS for Canine Distemper Virus?

A

Early signs:
▪Lethargy, inappetence, fever
▪Conjunctivitis, cough, serous ocular and nasal discharge

Progression to:
▪Obtundation, anorexia, vomiting, diarrhea
▪Mucopurulent ocular and nasal discharge
▪Moist cough, tachypnea
▪Neurologic signs

▪Nasal and footpad hyperkeratosis (‘hard pad’)
▪Optic neuritis and chorioretinitis (‘gold medallion lesions’)
▪ENAMEL HYPOPLASIA

Neuro signs:
▪May be delayed up to 12 weeks
▪Development unpredictable
▪Hyperesthesia
▪Ataxia, circling, head tilt, tremors
▪Paralysis
▪MYOCLONUS
▪Partial or generalized seizures

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38
Q

Describe the pathogenesis of Canine Distemper virus?

A

There are 2 stages

Stage 1: Lymphoid Tissue
-Virus inhaled, contacts upper resp tract epithelium
-Replication in local macrophages -> lymphatic spread
-Tonsils and bronchial nodes
-Systemic lymphoid tissue - GIT, spleen, MLN, Kupffer
cells
-results in FEVER LYMPHOPENIA

Stage 2: Epithelial and Nervous Tissue
-Once in the lymphoid tissue, it will spread to the blood
-It will go into epithelial tissue and CNS via hematogenous spread:
1. Good humoral and Cell Mediated response > virus eliminated
2. Intermediate response > Persistent infection (CNS, cutaneous, ocular signs)
3. Poor response > Fulminant epithelial infection (severe GI signs, pneumonia, +/- CNS signs)

▪Immunosuppression is a key feature (lymphocytolysis)
▪Race between virus and host
▪Opportunistic infections can occur

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39
Q

How do you DIAGNOSE Canine Distemper Virus?

A
  1. CBC
    ▪Lymphopenia
    ▪Distemper virus inclusions
  2. Conjunctival scrapings for inclusions
    ▪Fluorescent antibody
    ▪False positives and false negatives (more false
    neg)

3.RT-PCR
▪Respiratory secretions, CSF, feces, urine
▪False positive possible within 1-3 weeks of vaccination

  1. Thoracic radiographs
    ▪Bronchopneumonia
  2. NECROPSY AND HISTOPATHOLOGY are considered to be the gold standard
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40
Q

How do you TREAT Canine Distemper Virus?

A

Supportive care
▪Isolation
▪IV fluids
▪Parenteral antimicrobial drugs
▪Oxygen supplementation

Neurologic signs usually permanent
▪May or may not be compatible with life
▪Warn owners if not yet present

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41
Q

How do you PREVENT Canine Distemper Virus?

A

-vaccines! (Modified Live Vaccines)
-vax before shelter entry

-In shelter outbreaks, consider serological testing
▪Separate and vaccinate seronegative animals
▪Foster incoming seronegative animals until they seroconvert
▪Any positive titer is protective

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42
Q

If you’re seronegative that mean you do/don’t have antibodies.

A

If you’re SERONEGATIVE you DON’T have antibodies.

you are NOT protected

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43
Q

What is Infectious Canine Hepatitis? (ICH)

A

▪Caused by canine adenovirus-1 (CAV-1)
-related to CAV-2 (respiratory disease)

▪Systemic viral infection of dogs - usually young puppies

▪Targets endothelial cells and hepatocytes (liver issues)

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44
Q

How is Infectious Canine Hepatitis transmitted?

A

▪Oronasal exposure: animal-to-animal contact
or exposure to contaminated fomites

▪CAV-1 is shed in feces, urine, and saliva

▪Shedding of CAV-1 in the urine can last for
6-9 months.

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45
Q

What are the CS of Infectious Canine Hepatitis?

A

-mostly subclinical

Peracute form
▪Circulatory collapse
▪Death in 24-48 hours

Acute form
▪Puppies aged 6-10 weeks
▪Fever, anorexia, lethargy, tonsillitis
▪Cough, tachypnea
▪Hepatomegaly, abdominal pain, edema, ascites
▪Vomiting, diarrhea
▪Hemorrhages
▪CNS signs (hepatic encephalopathy, direct damage)

▪Fever common in early phase

▪Corneal edema (‘blue eye’) and anterior
uveitis
-Hallmark lesion
-Type III (immune complex) hypersensitivity
-May be the only sign
-Can be painful

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46
Q

How do you DIAGNOSE Infectious Canine Hepatitis?

A

Bloodwork
▪CBC: lymphopenia, neutropenia
▪Chemistry: Increased liver enzymes, hypoglycemia

UA: Bilirubinuria, proteinuria

Organism detection
▪PCR (e.g., on blood, respiratory secretions, urine)
▪Histopathology at necropsy
▪Intranuclear inclusions in Kupffer cells, hepatocytes,
glomeruli, blood vessels (meninges, renal tubular
vascular endothelium)

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47
Q

What is parvo?

A

-Panleukopenia in cats

▪Severe enteritis and leukopenia in dogs and cats

▪Highly contagious, often fatal if untreated

▪Parvovirus is is one of the world’s most common canine infectious diseases

-Panleuk does not infect dogs

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48
Q

What kind of virus is Parvovirus?

A

▪Tiny, non-enveloped viruses
▪Require rapidly dividing cells to replicate
▪Shed for max. 4 weeks after infection (rarely > 2 weeks)
▪Resist disinfection and survive > 1 year on fomites

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49
Q

What is the signalment of Parvovirus in dogs?

A

▪Puppies and kittens 6 weeks to 6 months
▪Declining maternal antibody
▪Rapidly dividing cells
▪Concurrent viral, bacterial and parasitic infections
▪Rottweilers, Dobermans, Americans Pit Bull Terriers, GSDs, Chihuahuas?
▪Prevalence highest in summer (3 times more likely in July, August, and September)– flies?

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50
Q

What is the transmission of parvovirus?

A

▪Transmission by contact with feces, vomit, fomites

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51
Q

What is the pathogenesis of Parvovirus?

A

-Oronasal exposure
-Oropharyngeal lymphoid tissue
-GI epithelium, lymphoid tissue, marrow (also lungs, spleen, liver, kidney, heart)

Causes:
Intestinal crypt cell destruction >
-Neutrophil sequestration
-Impaired cell turnover
-Villous blunting
-Malabsorption
-Increased permeability
+/- Intussusception

Results in Bacterial translocation > SEPSIS, ENDOTOXEMIA, DIC

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52
Q

What can happen if Parvovirus infects in utero <2weeks of age?

A

▪Dam subclinical

▪Myocarditis and CHF (congestive heart failure) in puppies (rare due to maternal
antibody)

▪Cerebellar hypoplasia in kittens (and rarely dogs)
-Also optic nerve atrophy, retinopathies

▪Reproductive failure or fading puppies/kittens

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53
Q

Feline parvo/panleuk is associated with what congenital abnormality?

A

Cerebellar Hypoplasia

▪Infection in utero or at <~ 9 days
▪Ataxia, intention tremors, incoordination, broad-based stance
▪Clinical signs appear at 2-3 weeks
▪Mental status normal, acceptable pets
▪Other signs less common
-Seizures
-Behavioral changes
-Retinal degeneration, folding
-Optic nerve hypoplasia

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54
Q

What are the CS for parvovirus?

A

▪Incubation period
-3-14 days CPV-2
-2-10 days FPV

▪Lethargy, fever, then inappetence, vomiting and diarrhea
-Usually bile-stained vomit in cats
-Yellow-gray, blood-streaked, or dark red malodorous
diarrhea
-Abdominal pain, dehydration

▪Leukopenia

▪Peracture form: Death in 1-2 days
-Secondary to gram-negative bacterial sepsis, DIC

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55
Q

How do you DIAGNOSE parvo?

A

▪History, clinical signs

▪CBC
-Leukopenia (not always present, not specific)

▪Chemistry
-Electrolyte abnormalities
-Hypoglycemia
-Prerenal azotemia

▪Fecal antigen ELISA
-Approx. 50% sensitive
-Detects FPV
-May get false positive post recent (10 days) vaccine -
modified live virus

▪Fecal PCR
-Positive after vaccination

▪Serology
-Tests for protective antibody titers, not for infection

▪Histopathology
-Intestinal crypt necrosis
-Intra-nuclear inclusion bodies
-Immunohistochemistry

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56
Q

How do you TREAT Parvo?

A

▪Isolation
▪Aggressive IV fluid therapy
▪Broad-spectrum IV antimicrobials
-Cefazolin
-Enrofloxacin/ampicillin
▪Intravenous dextrose
▪Plasma for hypoalbuminemia
▪Antiemetics
▪Immune plasma?
-Need large doses parenterally (6.6 – 11 mL/kg)?
-Best after infection but before clinical signs

▪NPO or early enteral feeding via NE tube
▪Central parenteral nutrition
▪Gradual reintroduction of water then food
▪Treat parasites

▪Outpatient protocol – SC fluids, maropitant and cefovecin
-Not optimal

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57
Q

How do you PREVENT parvo?

A

▪Vaccination
-Attenuated live vaccines
-Avoid use in pregnancy, kittens and puppies < 4 weeks
-Immunosuppressed animals

▪Pregnant queens in shelters?

▪Vaccinate to 16-18 weeks

▪Titers correlate with protection
-ANY antibody titer = protection in dogs > 20 weeks
-Lack of antibody titer does not necessarily mean lack of protection

▪Hygiene and appropriate disinfection

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58
Q

What is canine enteric coronavirus?

A

▪Enveloped RNA virus, fecal-oral transmission
▪Infects villus tips
▪Susceptible to desiccation and disinfection
▪Many strains
▪Widespread subclinical infection
▪Disease in pups < 6 weeks, often with co-pathogens
-Short incubation period
-Shedding for 2 weeks
-Usually mild, self-limiting diarrhea

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59
Q

How do you diagnose canine enteric coronavirus?

A

▪RT-PCR (‘fecal PCR panels’)

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60
Q

How do you prevent canine enteric coronavirus?

A

-hygiene
-vaccines - unproven benefit

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61
Q

What is Leptospirosis?

A

▪Wild and domestic animal reservoir hosts
-Shed in urine
-Different serovars/genotypes adapted to different reservoir hosts

▪Widespread subclinical exposure

▪Young, lepto-unvaccinated adult dogs

▪Rare in cats

▪Survives in stagnant or slow-moving, warmer water

▪Temperatures 0 to 25 degrees C (32-68 degrees F)

▪Increased rainfall/flooding is a risk factor but not
required

▪Disease seen in small-breed dogs from urban areas

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62
Q

How is Lepto transmitted?

A

▪Direct contact with contaminated urine, bite wounds or ingestion of infected tissues

▪Indirect contact with urine- contaminated food, water, soil, bedding

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63
Q

What is the PATHOGENESIS of Lepto?

A

▪Organisms penetrate intact mucous membranes or abraded skin
-Bacteremia with spread to liver and kidney as well as other tissues (pancreas, lung, meninges, genital tract, eye etc)

▪Extent of disease depends on strain virulence and host susceptibility

▪Acute kidney injury, +/- hepatic insufficiency, +/- hemorrhagic disease (liver dz, NOT liver failure)

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64
Q

What are the CS of Lepto?

A

▪Fever, inappetence, vomiting, dehydration
▪Reluctance to move
▪PUPD or anuria/oliguria
▪Abdominal pain
▪Mild peripheral lymphadenomegaly
▪Icterus
▪+/- uveitis
▪+/- tachypnea due to pulmonary
hemorrhage

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65
Q

What are some Lepto lab findings?

A

CBC
▪leukocytosis
▪anemia
▪thrombocytopenia (50-60%)

Chemistry
▪azotemia
▪+/- elevated liver enzymes (ALP>ALT)
▪ normal cholesterol
▪normo- or hypokalemia
▪hypoalbuminemia
▪ high CK

▪UA: casts, glucosuria, organisms not seen

▪Significant proteinuria not a feature (interstitial
nephritis)

▪Differential diagnosis: other causes of AKI

thoracic Rads
▪Normal
▪Mild interstitial to patchy or diffuse alveolar pattern

US
▪Hyperechoic renal cortices
▪+/- perirenal fluid
▪Renomegaly

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66
Q

How do you DIAGNOSE Lepto?

A
  1. History, clinical signs, laboratory findings
  2. Antibody-detection tests
    ▪Microscopic agglutination test, paired titers (interval 2-4 weeks)
    ▪Initial titers often negative
    ▪Positive titers from subclinical exposure and vaccination (up to 1:6400)
    ▪Fourfold rise in titer required over >2 weeks
    ▪Positive titers to multiple serovars due to cross-reactivity
    ▪Highest titer is NOT predictably the infecting serovar
  3. SNAP Lepto
  4. WITNESS Lepto (Zoetis) - IgM based
  5. Darkfield microscopy of urine: insensitive
  6. Culture: special media, 4-6 weeks, not done
  7. PCR
  8. Kidney biopsy
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67
Q

How do you TREAT Lepto?

A

▪Ampicillin or penicillin for vomiting dogs
▪Doxycycline for 2 weeks after vomiting stops (d/c penicillin)
▪Aggressive IV fluid therapy
▪Diuretics
▪Antiemetics
▪Hemodialysis – the sooner the better if rehydrated and oliguric (low urine output)

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68
Q

Lepto prognosis

A

Good - 85% survival rate with aggressive therapy

CKD could be sequela

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69
Q

How do you PREVENT Lepto?

A

▪Treat co-exposed household dogs
▪Restriction of access to wildlife/rodents
▪Vaccination
-Shift to ‘core’
-annual vaccine

▪No need to place in isolation

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70
Q

What are vector borne diseases?

A

-Diseases (infections) transmitted by blood-feeding
arthropods (mosquitoes, ticks, fleas)

-can be viral, bacterial, protozoal, parasitic

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71
Q

What are some tick vectors in the US?

A
  1. IXODES
    Ixodes pacficus
    Ixodes scapularis (deer tick - black legged tick)
  2. RHIPICEPHALUS
    Rhipicephalus sanguineus (brown dog tick)
  3. DERMACENTOR
    Dermacentor Andersoni (rocky mountain wood tick)
    Dermacentor variabillis (american dog tick)
  4. AMBLYOMMA
    Amblyomma aermicanum (lone star tick)
    Ambylomma maculatum (gulf coast tick)
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72
Q

What is rickettsiae/rickettsial organisms? (big group of bacteria)

A

-Arthropod-transmitted
-Gram-negative pleomorphic BACTERIA - coccobacilli
-Obligately intracellular, may form morulae

-seen with bacteria: Ehrlichia spp., Anaplasma spp., Rickettsia spp., Neorickettsia spp.

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73
Q

The bacteria rickettsiae responds to which abx?

A

Doxycylcine!

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74
Q

The dz of Erlichia and Anaplasma affect monocytes, granulocytes and platelets. Which bacterias affect which cells?

A

Monocytes:
-Ehrlichia canis

Granulocytes (neutrophils and eosinophils)
-Ehrlichia ewingii, Anaplasma phagocytophilum

Platelets
-Anaplasma platys

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75
Q

What dz can the bacteria Ehrlichia canis cause?

A

Canine Monocytic Ehrlichiosis

attacks monocytes

mainly in SE/SW states, warmer climates
rare in cats

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76
Q

Canine Monocytic Ehrlichiosis – caused by bacteria Ehlrichia Canis – is transmitted by which vector?

A

Rhipicephalus sanguineus - dog brown tick

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77
Q

Explain the transmission of Ehrlichia Canis and its role in the pathogenesis of Canine Monocytic Ehrlichiosis

A

-no transovarial transmission - Transstadial
–larvae acquire pathogen by feeding off animal/canids

-Incubation period 8-20 days

-Acute phase (first 2-4 weeks)
–Multiplies in monocytes with splenomegaly, lymphadenopathy
–Infected cells adhere to endothelium in lungs, meninges and kidneys – can cause systemic vasculitis-like signs
–Thrombocytopenia, +/- mild leukopenia, anemia

78
Q

What is Transovarial transmission?

A

Pathogen transmitted through successive generations of ticks

Pathogens are present in eggs laid by ticks, when eggs hatch, larvae are infected

79
Q

What is Transstadial Transmission?

A

Pathogen is transmitted from one life stage of the tick to another

Larvae are hatched uninfected – must acquire infection later in life

80
Q

CS of Canine Monocytic Ehrlichiosis - Ehrlichia canis

A

-Lymphadenopathy, splenomegaly
-Pallor, bleeding tendencies (thrombocytopathia)
-Weight loss, debilitation
-Anterior uveitis, retinal hemorrhage
- +/- Neurologic signs
-secondary infections

81
Q

How do you diagnose Canine Monocytic Ehrlichiosis - Ehrlichia canis?

A

-Variable anemia, pancytopenia, lymphocytosis, thrombocytopenia
-Morulae (mostly only acute)
-Hyperplastic (acute/chronic) or hypoplastic (chronic) marrow
-Polyclonal or rarely monoclonal gammopathy
- +/- protein-losing nephropathy

-Organism Detection Tests: Morulae, PCR panels - best for acute

-Antibody detection tests: Lack sensitivity early, Cross-reactivity among Ehrlichia species
–SNAP 4Dx Plus ELISA
–Quantitative serology (IFA)

82
Q

How do you TREAT Ehrlichia canis?

A

-Persistent infection = prolonged treatment
-Doxycycline 5 mg/kg PO q12h 6-8 weeks
-Prognosis good for acute ehrlichiosis
-Poorer for chronic ehrlichiosis

82
Q

Which bacteria causes Canine Granulocytic Anaplasmosis? Which vectors carry it?

A

Bacteria: Anaplasma phagocytophilum

in Upper Midwest, northeast, CA, OR and Europe

-Ixodes scapularis in the midwest
-Ixodes pacificus in northern CA

-Same vectors as Borrelia burgdorferi, often
co-transmitted

83
Q

What is Canine Granulocytic Anaplasmosis? Some lab findings?

A

-Widespread subclinical infection

-Fever, lethargy, lymphadenopathy, SPLENOMEGALY, scleral injection

-Thrombocytopenia, mild anemia, neutropenia/neutrophilia, lymphopenia, hypoalbuminemia, elevated ALP

84
Q

How do you DIAGNOSE Canine Granulocytic Anaplasmosis?

A

Organism detection tests
-Morulae within granulocytes (look like Ehrlichia ewingii but different geographic distribution)
-PCR – best test

Antibody detection tests - usually negative initially
-Not really useful for diagnosis
-IDEXX SNAP 4Dx Plus, Accuplex
-Acute and convalescent phase serology

85
Q

How do you TREAT Canine Granulocytic Anaplasmosis?

A

DOXY!

86
Q

Granulocytic anaplasmosis look a lot like which other bacteria/disease?

A

Ehrlichia ewingii ehrlichiosis

Ehrlich ewingii’s vector is Amblyomma americanum

87
Q

What is Rocky Mountain Spotted Fever caused by? What is its vectors?

A

-Bacteria: Rickettsia rickettsii

-Vector: Dermacentor spp. and Rhipicephalus sanguineus (brown dog tick)

88
Q

What the Pathogenesis of Rocky Mountain Spotted Fever?

A

-Most cases March-October

-Ticks attach for 5 to 20h

-transstadial transmission (tick acquires bacteria from a host)

-Rickettsiae infect ENDOTHELIAL CELLS of
small blood vessels
–Vasculitis, necrosis, increased vascular permeability
–Edema, hemorrhage, hypotensis, shock

89
Q

What are the CS of Rocky Mountain Spotted Fever?

A

-Incubation period 2-14 days
-Fever, anorexia, depression
-Edema, hyperemia and necrosis of extremities
-Mucopurulent ocular discharge
-Vomiting, diarrhea
-Neurologic signs
-Respiratory signs
-Joint pain and swelling, muscle pain
-Cardiac arrhythmias
-Bleeding/thrombosis
-Permanent cardiovascular, renal and neurologic damage possible

90
Q

What are some lab findings with Rocky Mountain Spotted Fever?

A

-Leukopenia/leukocytosis, anemia,
thrombocytopenia**, rarely DIC

-Hypoalbuminemia, elevated liver enzymes

91
Q

How do you DIAGNOSE Rocky Mountain Spotted Fever/Rickettsia ricketsii?

A

-an ACUTE disease

-Indistinguishable from acute ehrlichiosis but SHORT
course
-Dead or better in 2 weeks
- +/- tick infestation, season, travel history
-Acute and convalescent phase titers
-IFA (eg. Protatek) – but no point-of-care tests
-Cross-reactivity with other SFG rickettsiae
-Organism detection tests?

92
Q

How do you TREAT Rocky Mountain Spotted Fever?
How can you prevent it?

A
  • Doxycycline - 5 mg/kg q12h 2 weeks
  • Improvement in 24-48 h
  • Use fluids with caution - bc of vasculitis, so can easily fluid overload
  • Lifelong immunity following natural infection
  • Effective vaccination not available
  • Tick prevention
  • Dogs a sentinel for human disease
93
Q

Which bacteria is involved with Salmon poisoning disease?

A

-Bacteria: Neorickettsia helminthoeca

-bacteria lives in a fluke!
-Fluke/trematode: Nanophyetus salmincola

fluke wil penetrate salmon
dog eats salmon

affects dogs, NOT cats

94
Q

What is the PATHOGENESIS of Salmon poisoning disease?

A

-Mature flukes in intestine release rickettsiae into
intestinal epithelial cells
-Spread to rest of body via lymphatics
-Ulcerohemorrhagic enteritis
-Lymphoid tissue invasion by macrophages and plasma cells

-Trematode eggs are in the feces 5-8 days after fish
ingested; shed for 60-250 days

95
Q

What are the CS for Salmon Poisoning disease?

A

-incubation period 5-8 d (up to 33 d)

-Fever, anorexia, vomiting, diarrhea, profound weight
loss, lymphadenopathy, splenomegaly, DEATH in 7-10
days if untreated

96
Q

How do you DIAGNOSE Salmon Poisoning disease?

A

-History of fish exposure in 50% of cases

-CBC: lymphopenia, thrombocytopenia (90%)
-Chem: hypoalbuminemia and ­ALP

-Trematode eggs best identified by combining flotation and sedimentation
- > 80% of cases
- Inclusions in macrophages in LN aspirates
- PCR on feces or LN aspirates

97
Q

How do you TREAT Salmon Poisoning disease?

A
  • Tetracyclines for 2 weeks
  • Doxycycline
  • Parenteral oxytetracycline if vomiting
  • Praziquantel for the fluke infestation
  • IV fluids +/- blood products
  • Dogs should not eat raw fish!
98
Q

Where is Lyme dz mainly found in the US?

A

Northeast - 90% of cases

99
Q

Which tick carries Lyme dz?

A

Ixodes scapularis (deer tick - brown legged tick)

100
Q

What is the life cycle of Lyme dz?

A

-Ixodes scapularis ticks are usually infected after feeding on the white-footed mouse

-Nymphs most likely to transmit infection
–Small
–Engorge quickly
–Most prevalent in spring, summer

-transtaddial – need to feed off of rodents - white footed mouse/grey squirrel/birds

101
Q

The Ixodes Scapularis carries what bacteria to cause Lyme dz?

A

Borrelia burgdorferi

102
Q

What is the pathogenesis of Lyme dz/Borrelia?

A

-tick (Ixodes scapularis) takes up blood meal
-tick gets infected by spirochetes
-spirochetes attach to tick midgut using outer surface protein called OspA
-OspA adheres to TrospA on midgut

-now the infected tick will take another blood meal on a different animal
-the spirochetes will travel from midgut to the salivary glands > infect animal

-saliva can surround spirochete and prevent it from being detected by animal’s immune system - saliva associated transmission
–Inhibits CD4+ cell activation, proinflammatory cytokine production

103
Q

Borrellia is mainly found in connective tissue/blood?

A

Borellia migrates through connective tissue. NOT in blood.

104
Q

What is Erythema Migrans?

A

-lesion of Lyme dz
-big rash - target lesion

dogs don’t get this – humans do
dogs can get rash, just not erythema migrans

105
Q

CS of Lyme Dz

A
  • No signs
    – 95% of infected dogs
  • Neutrophilic polyarthritis – Thrombocytopenia, arthritis
    – 2-5 months after infection
  • Protein-losing nephropathy (Lyme nephritis)
    – Sterile immune-complex disease?
    – Retriever breeds – Thrombocytopenia
    – Sterile immune-complex disease
106
Q

How do you DIAGNOSE Lyme dz?

A

CS

Organism detection tests not really useful
-Blood?
-Skin biopsies?
-Synovial fluid?

Serology

107
Q

How do you serologically diagnose Lyme Dz?

A

Outer surface proteins of borellia:
-OspA - helps spirochete to adhere, down regulated when tick feeds on host, briefly expressed, also vaccine antigen -> when taken up in blood meal, antibodies work in tick and kills spirochete
-OspC - starts to be expressed when spirochete migrates to salivary gland of tick, expressed in salivary gland, lots of variants - leads to reinfection
-C6/VSLE - only expressed during natural infection, diagnostic antigen
-OspF - light outer surface protein, immune response would mean chronic infection

C6 peptide
-SNAP 4Dx® Plus, IDEXX
-Quant C6® ELISA, IDEXX
-Antech Accuplex

Multi-target antibody assays
-Western blotting
-Cornell bead: OspA, OspC, and OspF
-Zoetis VETSCANTM: VlsE, OspC, flagellin (single line)
–Canine Flex4 Rapid (includes Anaplasma, Ehrlichia, HW Ag)
–Lyme Rapid

108
Q

With acute lyme disease, you can get false positives with testing. Why?

A

Dogs w lyme dz will NOT get negative results

-Incubation period 2 to 5 months
-IgM/IgG not useful
-Antibody negative Lyme rare in dogs

109
Q

How do we TREAT Lyme dz?

A

-monitor

-Doxycycline 4 weeks for sick dogs
–Amoxicillin
–Cefovecin 8 mg/kg SC, 2 doses, 14 days apart

-Organism elimination?

-Monitoring with quantC6?
–Reinfections may occur
-Immunosuppressive drugs for Lyme nephropathy
–Mycophenolate

-Healthy seropositive dogs
–Emphasize ectoparasite control
–Consider vaccination

110
Q

What is FeLV?

A

Feline Leukemia Virus

-Leading cause of feline mortality
-Immunosuppression, bone marrow disorders,
hemopoietic neoplasia

-enveloped RNA virus - retrovirus > goes into genome
-Susceptible to dessication, heat and disinfectants

111
Q

How is FelV transmitted?

A

-Transmission difficult: requires close contact
-Shed in saliva
-Transmission via blood transfusion - so SCREEN donor cats

112
Q

What does it mean that FelV has an age-related resistance?

A

-in this case, FelV is very rare to be found in cats more then 10 years of age - only young to middle aged cats
-however, can be more common if immune-suppressed

113
Q

What are the regressive and progressive forms of FelV?

A

Regressive: cat becomes infected, virus is a part of genome, but silent. Not making virus. Possibly affect oncogenes, etc.

Progressive: progress into felv associated dz

Progressive disease (persistent viremia) occurs in
-70-100% of neonates without maternal antibody
-30-50% of 8-12 week old kittens
-< 10-20% of adult cats after prolonged exposure

114
Q

What factors affect the outcome with Felv?

A

-Challenge dose - how much of virus
-Viral strain
-Immune status
-Age

115
Q

What is the PATHOGENESIS of Felv?

A

-Most persistently viremic cats die in 4 years

-Malignant transformation results from
proviral integration into the genome near a
cellular oncogene

116
Q

After initial infection, what are the 4 outcomes a cat can have with Felv?

A
  1. Abortive infection
  2. Primary Viremia
    2a. Regressive Infection
    2b. Progressive Infection
117
Q

What would the antigen, RNA, DNA, and antibody statues be for an Abortive Infection for Felv?

A

Antigen negative
RNA negative
DNA negative
Antibody positive

118
Q

What would the antigen, RNA, DNA, and antibody statues be for a Primary Viremia for Felv?

A

Antigen positive
RNA positive (by 1 week)
DNA positive/negative
Antibody positive

119
Q

What would the antigen, RNA, DNA, and antibody statues be for a Regressive Infection for Felv?

A

Antigen negative
RNA negative
DNA positive
Antibody positive

120
Q

What would the antigen, RNA, DNA, and antibody statues be for a Progressive Infection for Felv?

A

Antigen positive
RNA positive
DNA positive
Antibody positive

121
Q

What are some Felv-associated diseases?

A

-lymphoma
-leukemia
-Myelodysplasia
-Myelofibrosis
-Anemia
-Immunosuppression
-Immune Complex Diseases
-Reproductive Diseases
-Peripheral lymphadenopathy
-Enteritis
-Neurologic Disease

-Multiple cartilagenous exostoses
-Olfactory neuroblastoma
-Keratin horns

122
Q

What’s a common lymphoma for Felv+ cats?

A

mediastinal lymphoma

-80% are FeLV +
-Pleural effusion containing lymphoblasts
-Dyspnea, regurgitation, Horner’s syndrome, decreased chest compressibility

123
Q

What other lymphoma can Felv+ cats get?

A
  1. Multicentric lymphoma
    -Multiple site involvement
  2. Renal lymphoma

GI lymphoma is usually FeLV negative!!!
-most common lymphoma in cats
-usually in 8+ year olds

124
Q

What type of leukemia can felv+ cats get?

A

-Acute granulocytic, erythroid, lymphoid or
megakaryocytic

-Pancytopenia with lethargy, bacterial infections,
sepsis, hemorrhage

125
Q

What kind of anemia can felv+ cats get?

A

Anemia through multiple mechanisms
1. Impaired erythroid production
-Nonregenerative anemia
–Isolated and severe = pure red cell aplasia
–With leuko- and/or thrombocytopenia = aplastic anemia
-Macrocytosis without regeneration

  1. immune-mediated destruction
  2. Anemia of inflammatory disease
126
Q

How does felv+ cats have immunosuppression?

A

-Mechanism poorly understood

-Impaired T cell and neutrophil function

-Predisposes to:
–Bacterial infections
–Viral infections eg. FIP, URTD
–Protozoal infections
–Fungal infections eg. cryptococcosis

127
Q

How do you DIAGNOSE Felv?

A
  1. Antigen-detection ELISA and IFA
    -Detect p27 core antigen
    -ELISA first choice for screening and diagnosis
    –Cheaper and more sensitive than IFA
    –Sensitivity and specificity 98%
    –False positives more likely when incidence is low**
    –50% chance of a false positive when used for screening
    –Retest using diagnostic lab or another test kit
  2. PCR
    -proviral DNA
    -blood screening

Verify progressive infection
-Retest ELISA+ cats 3 months later OR
-Do an IFA test OR
-Do a quantitative PCR assay

128
Q

How do you TREAT Felv in cats?

A

-Chemotherapy for lymphoma
-Blood transfusions, erythropoieitin/darbepoietin
-Glucocorticoids for immune-mediated disease with some cases
-Antimicrobials for secondary infections
-Antivirals (AZT, raltegravir) have shown some clinical
activity but have significant drawbacks

129
Q

What to tell owners of healthy viremic cats with felv?

A

-Retest first
-Some may develop regressive infection
-Other cats in the household may be infected or immune
-House all cats indoors
-Vaccinate FeLV+ cats as necessary
-FVRCP as normal

130
Q

How do we PREVENT felv?

A

Vaccines!
-Whole inactivated (killed) vaccines
-Nonadjuvanted recombinant canarypox vaccine (BI)

-Two doses SC, from 9 weeks of age then annually (recombinant) or every 3 years

-core in kittens, then based on risk

-Test first, vaccinate only FeLV negative
cats

-vaccination does not interfere with testing

131
Q

What is FIV?

A

Feline Immunodeficiency Virus

-Enveloped, single-stranded RNA virus

-Infection is for life
-Antibody positivity = current infection

-Prevalence 2-3 times greater in males
–More profound than for FeLV

-retrovirus

132
Q

What is the signalment for FIV?

A

Prevalence 2-3 times greater in males
-More profound than for FeLV

Free-roaming and feral cats

Mean age 6-8 years
-80% of cats are over 2 years
-Disease mostly in adult/geriatric cats

133
Q

How is FIV transmitted?

A

Saliva by biting

Transplacental transmission depends on:
-Strain
-Degree of maternal viremia
-Most kittens probably infected via saliva or milk

Indoor housing DECREASES transmission

134
Q

What is the PATHOGENESIS of FIV?

A

Targets:
-T helper (CD4+) lymphocytes
-Later CD8+ cells and B cells
-Tissue macrophages
-For some strains, other cells such as astrocytes

Results in
-Gradual destruction of the immune system
-Promotion of neoplastic disease (less than FeLV)
-Neurologic disease

135
Q

Where does FIV start in the body?

A

Lymphoid tissues
Salivary glands

transient primary illness (acute phase)

heads to mononuclear cells lungs, kidneys, GIT

leads to subclinical carrier phase:
decreased CD4+/CD8+ ratio
decreased CMI and humoral immunity
decreased memory responses
decreased mitogen responsiveness
decreased Il-12 and Il-2 production
decreased MHC-II expression
decreased neutrophil function

136
Q

CS of the transient primary illness/acute phase of FIV

A

-3-6 months, often unrecognized
-Transient lymphadenopathy, pyrexia, depression, anorexia
-Transient neutropenia and lymphopenia
-Sometimes URTD, enteritis and stomatitis
-Occasionally neurologic signs
-Behavior changes
-Partial or generalized seizures, paresis, anisocoria, motor abnormalities

137
Q

CS of the subclinical phase of FIV

A

-hyperglobulinemia

138
Q

CS of the terminal phase of FIV

A

Secondary infections:
-STOMATITIS, recurrent URTD
-Diarrhea, weight loss
-Chronic skin disease
–Dermatophytosis, mites, bacterial infections
-Other opportunistic infections
–eg. cryptococcosis, toxoplasmosis, mycobacteriosis
-Hyperglobulinemia

Ocular disease
-anterior uveitis, conjunctivitis, glaucoma
Eventually neurologic signs
-opportunistic infections, neoplasia, direct damage
Chronic wasting
Azotemia due to interstitial nephritis
Wasting, neurologic disease and tumors are the most common reasons for euthanasia

139
Q

How do you DIAGNOSE FIV?

A

Antibody testing

PCR is not helpful/organism detection tests are not helpful bc it’s low levels of virus (except terminal phase)

140
Q

How do you interpret FIV test results?

A

Maternal antibody up to and including 6 months of age
-Retest after 6 months

Antibody from previous FIV vaccination (no longer available, but can last 7+ years)

Retest adult SNAP ELISA+ cats?
-Low risk populations
-Western blotting
-Not a DIVA: Antigen and Witness vs IDEXX

Positive test results may be irrelevant to clinical problem

Negative results may occur in
-Cats in the acute stage (rarely recognized)
-Cats with end-stage disease (test with PCR)

141
Q

How do you TREAT FIV?

A
  • No good antivirals
  • Keep cats indoors
  • Identify and treat opportunistic infections
  • Manage stomatitis
  • Vaccinate for other pathogens (FVRCP)
142
Q

Hyperglobulinemia is a sign of

A

CHRONIC INFECTION

143
Q

What does a monogammopathy suggest?

A

neoplasia

144
Q

What does polyclonal gammopathy suggest?

A

inflammatory process, chronic stimulation

145
Q

What’s the signalment for FIP Cats?

A

young - 3mo to 3years
purebred

146
Q

How is FIP acquired?

A

– Fecal-oral spread of feline enteric (avirulent) coronavirus
– Acquired from another cat
– Mutation to virulent FIPV (‘internal mutation hypothesis’)
■ Multiplication in macrophages
– Strains vary in virulence
– Genetic susceptibility

147
Q

What are some differentials for fever + hyperglobulinemia?

A

Infectious:

FIP (viral)
bacterial/atypical bacteria (bartonella)
protozoal (Toxo)
fungal (histoplasma)
parasitic

148
Q

Feline Coronavirus is high with:

A

– Single cat vs. multicat household
– Infection, shedding, recovery
– Persistently-infected cats

149
Q

Virulent FCoV/FIP does/does not replicate in GI tract

A

DOES NOT

you don’t transmit FIP, you transmit feline coronavirus

150
Q

Feline coronavirus targets which cells?

A

Enterocytes > mild to inapparent enteritis

151
Q

FIP targets which cells?

A

Macrophages > fulminant dz

152
Q

What other abnormal PE findings can be found in cats with FIP?

A

■ Tachypnea
■ Muffled heart sounds
■ Icterus
■ Hepatomegaly
■ Splenomegaly
■ Irregular renomegaly
■ Abdominal masses
■ Anterior uveitis
■ Retinal detachment,
hemorrhage
■ Neurologic signs (seizure, vestibular)

153
Q

What lab abnormalities can be seen in cats with FIP?

A

■ NNN anemia
■ Neutrophilia
■ Lymphopenia
■ Thrombocytopenia
■ Azotemia
■ Elevated liver enzymes
■ Hyperbilirubinemia
■ Hypoalbuminemia
■ Hyperglobulinemia
– >50% effusive
– >70% noneffusive

154
Q

What sort of effusion is expected in cats with FIP?

A

FIP has it own type of effusion:

– Relatively low cellularity (2-5k)
– Proteinaceous/high protein
– Straw colored & viscous

155
Q

What does positive serology of FCoV mean?

A

■ Positive serology = exposure to any coronavirus (CCV, TGEV, FCoV)
■ Does not predict FIP
– Titers > 1:1600 may be suggestive
■ 98% specific, 67% sensitive in cats with compatible clinical signs
■ High titers useful for cats from households with 1 or 2 cats
■ Ensure go to endpoint
■ Titer results VARY between laboratories
– Some cats with end-stage FIP lack antibodies
■ Does not predict shedding
■ Does not indicate immunity to FIP
■ Paired titers are NOT helpful for diagnosis

156
Q

How do you DIAGNOSE FIP?

A
  1. RT-PCR
    – No specific mutation distinguishes virulent from nonvirulent strains
    ■ Some genes important (eg. 3c, 7b, spike protein genes)
    – IDEXX FIP RealPCR detects mutations in spike protein gene associated with virulence
    – False negatives with degradation, strain variability
    – Avirulent coronavirus strains can be found at any site in healthy and sick cats
    ■ Testing tissues and effusion not helpful alone
  2. Biopsy
  3. Cytology
  4. Immunohistochemistry - gold standard
157
Q

How do you TREAT FIP?

A

– Supportive care (fluids, nutrition, fluid removal)
– Anti-inflammatory and immunosuppressive drugs
– Novel antiviral medications

Nucleoside analogs: Inhibition of coronavirus RDRP (NSP12)

Protease inhibitor: Inhibition of coronavirus protease (NSP5)

158
Q

What is the prognosis for FIP?

A

■ What is the prognosis for a cat with FIP?
– Without treatment: Days to > 1 year (most 5 – 7 weeks)
– With treatment: good to excellent

■ Negative prognostic factors
– CNS involvement
– Prognosis dismal for cats that fail to respond beyond 3
days

159
Q

What is a Canine Babesiosis

A

-RBC parasites - intracellular PROTOZOAL parasites!
* Feline babesiosis not documented in US

160
Q

How is canine babesiosis transmitted?

A
  • Tick-borne (potentially)
  • Blood transfusions
  • Transplacental transmission (vertical transmission)
  • Direct transmission
161
Q

What are the vectors for Babesia vogeli, canis and rossi?

A
  • Large piriform organisms
  • Singly or paired in RBCs
  • B. vogeli: Rhipicephalus sanguineus (Cosmopolitan)
  • B. canis: Dermacentor spp (Europe, Africa, Asia)
  • B. rossi: Haemaphysalis leachi (South Africa)
162
Q

Which is the most common Babesia in the US?

A

Babesia Vogeli

least pathogenic

higher rates in
* Kenneled dogs
* Adults
* Greyhounds - they’re just more exposed due to geographic location, not that they’re genetically predisposed

163
Q

What is the vector for Babesia gibsoni?

A
  • Vector: Haemaphysalis spp.

-small babesia

-In the US most cases of B. gibsoni are diagnosed in Pitbull and Staffordshire bull terriers

-Some coinfected with Babesia vulpes

164
Q

Where is Babesia Conrade found?

A
  • California and other southern states
  • Medium-sized organism
  • Initially misidentified as B. gibsoni
  • Coyotes
165
Q

CS of Babesia vogeli

A
  • Incubation period 10-21 days
  • Anemia, fever, hypotensive shock in peracute/acute cases
  • Sometimes icterus, splenomegaly and immune-
    mediated thrombocytopenia
  • Chronic carrier state - usually subclinical

-less pathogenic
-clinically well

166
Q

CS of Babesia gibsoni/conrade

A
  • Incubation period 1-2 weeks
  • Fever, anorexia, weakness
  • Anemia, thrombocytopenia
  • Splenomegaly, lymphadenopathy
  • Icterus rare
167
Q

How do you DIAGNOSE Babesia?

A
  1. Bloodwork
    * Thrombocytopenia, increased MPV
    * Anemia (+/-) regeneration
    * Leukopenia
    * Hypoalbuminemia, hyperglobulinemia
  2. Detection of organisms on blood smears
    -Degree of parasitemia varies
  3. PCR – current test of choice
    -Not all assays detect all species
  4. Serology
    -Indirect IFA or ELISA
    -Titers > 1:80 positive
    -False negatives common
    -Cross-reactions occur unreliably
168
Q

How do we TREAT Babesia?

A
  • Blood transfusions
  • Fluids
  • Antibabesial drugs
    -Imidocarb diproprionate > clears large species
    -Atovaquone and azithromycin for B. gibsoni and B. conradae
  • Steroids used with care - bc may look like IMHA
169
Q

How do you prevent Babesia?

A
  • Tick control
  • Avoid splenectomy and immunosuppression in chronically infected dogs – spleen plays a big role in clearing out bad RBCs
  • Screen blood donors serologically
170
Q

What clinical features would make you suspect tick-borne/vector borne/Babesia?

A

fever, thrombocytopenia, hemolytic anemia (+/- regenerative anemia)

171
Q

What does Babesia look like/what other differential may you have?

A

IMHA
any other vector-borne dz
zinc
toxins - onion/garlic
hyperphosphatemia

172
Q

What is Feline Cytauxzoonosis? It’s a protozoal dz.

A
  • Usually (not always!) fatal, tick-borne disease of cats
  • Cytauxzoon felis - PROTOZA
  • Southern and SE US (Missouri, Arkansas, Oklahoma, Texas, Mississippi, Louisiana, Florida)
  • April to September
  • Outdoor cats - 80% of outdoor cats have it, just not clinical
  • Bobcat reservoir
173
Q

Which tick carries Cytauxzoon felis?

A

Amblyomma americanum - lodestar tick

174
Q

What is the pathogenesis of the protozoa Cytauxzoon felis?

A

rapidly fatal

Schizogonous phase
* Infected mononuclear phagocytes/macrophages obstruct veins in spleen, liver, lung, lymph nodes
* Rupture and release organisms
* Leads to DIC, shock

Intraerythrocytic phase
* 1-3 days after schizonts appear
* Hemolytic anemia, high fever
* Ring-shaped organisms in RBCs

175
Q

What are the CS of Feline Cytauxzoonosis?

A
  • Usually rapidly fatal
  • Anorexia, lethargy
  • High fever
  • Dark urine, dehydration, icterus, pallor, prolonged CRT, hypothermia
  • Death within 5 days
  • Attenuated strains have been found
  • Mild or no signs
176
Q

How do you DIAGNOSE Feline Cytauxzoonosis?

A

Bloodwork
* CBC: Nonregenerative anemia, leukopenia, thrombocytopenia
* Chemistry: hyperbilirubinemia,
hyperglycemia, hypoalbuminemia, elevated ALT
* Prolonged coagulation times

Organism detection
* Blood smear
* PCR

serology is not helpful bc it is an acute dz, so no antibodies would be made

177
Q

How do you TREAT Feline Cytauxzoonosis

A
  • High mortality despite treatment
  • Atovaquone and azithromycin - antiprotozoals
  • Supportive care, heparin?
  • Some cats have survived without
    treatment
178
Q

What is Leishmaniosis?

A

-caused by PROTOZOA - Leishmania
-public health concern bc zoonosis
-Dogs and rodents (cats?) reservoirs for human infection

179
Q

What is Leishmoaniosis vector?

A

Sandfly

180
Q

What is the pathogenesis of Leishmaniosis?

A
  • Flagellated promastigotes injected into vertebrate host,
    engulfed by macrophages
  • Transform into amastigotes, which replicate and infect new cells
  • Sandfly ingests amastigotes
181
Q

What are the CS for Leishmaniosis?

A

Cutaneous - Derm Issues
* Cutaneous lesions form in 90% of infected dogs 1 month to 7 years post infection
* Hyperkeratosis and intradermal nodules

Visceral
* Splenomegaly
* Lymphadenopathy
* Polyarthritis
* Glomerulonephritis
* Uveitis
* Rhinitis
* Icterus
* Thrombocytopenia
* poly- and monoclonal gammopathies

182
Q

How do you DIAGNOSE Leishmaniosis?

A
  • Visualization of amastigotes in biopsies or aspirates
  • PCR - GOLD STANDARD
  • Serology - could mean exposure, just not infection
183
Q

How do you TREAT Leishmaniosis?

A
  • Meglumine antimonate, sodium stibogluconate, amphotericin B, allopurinol
184
Q

What’s the prognosis for Leishmaniosis?

A
  • Prognosis variable, most recur
  • Treatment of dogs in the US controversial - bc of resistance. Don’t want resistance to treatment in humans.
185
Q

What is Hepatozoonosis?

A

Hepatozoon canis - PROTOZOA - infects dogs and cats in Africa, the southern US, southern Europe and Asia

Hepatozoon americanum - dogs and coyotes in southern US

186
Q

What is the vector for Hepatozoon canis? How about Hepatozoon americanum?

A

Canis: Rhipicephalus sanguineus - brown dog tick

Americanum: Amblyomma maculatum (Gulf coast tick)

187
Q

What’s different about the life cycle/transmission of Hepatozoonosis?

A

the entire tick is swallowed, not just blood meal of spirochetes in saliva of tick

188
Q

CS of Hepatozoonosis?

A
  • Incubation period 1 month
  • WASTING DISEASE
  • Fever, mucopurulent ocular discharge
  • Pain, gait abnormalities
  • Glomerulonephritis, amyloidosis
189
Q

How do you DIAGNOSE Hepatozoonosis?

A
  1. Bloodwork
    * Marked leukocytosis
    * Nonregenerative anemia
    * Hypoglycemia
    * Elevated ALP
    * Hypoalbuminem
  2. Skeletal radiographs
    -myositis - periosteal rxn on appendicualr skeleton
  3. Clear ovoid gamonts in PMNs on a blood smear
  4. Muscle biopsy to detect cysts or pyogranulomas is more sensitive
  5. ELISA for H. americanum antibodies
  6. Tests for H. canis are not useful

VET433A (8 decks)

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