Feline calicivirus clinical signs for virulent systemic form
-mild upper respiratory signs
-conjunctivitis
-severe respiratory signs
-anorexia
-drooling
-diarrhea
-death
Feline calicivirus post mortem findings for virulent systemic form
- Cutaneous ulceration on the ears, face
- Subcutaneous edema of the face and limbs
Oral cavity:
* Erosion and ulceration of the tongue and hard palate
Thorax:
* Bronchointerstitial pneumonia
how does the virulent systemic form of feline calicivirus arise? who can it target?
- Rare manifestation, results from viral mutation, pathogenesis is poorly understood
- Highly contagious, rapidly fatal, affects juvenile and adult populations both vaccinated and unvaccinated
what samples should we send to the lab to test for calicivirus antemortem?
○ Swabs: nasal, conjunctival, pharyngeal
best testing modality for feline calicivirus
○ PCR most common for antigen detection*
What are the three possible causes for antibody to be present?
- Current active infection
- Previous infection
- Previous vaccination
Can any test differentiate between typical calicivirus infection and atypical virulent systemic calicivirus?
No
differential diagnoses for respiratory illness in cats (viral)
- Feline calicivirus*
- Feline herpesvirus 1 / feline viral rhinotracheitis
- Feline panleukopenia
- SARS Co-V-2
Suggestions to a shelter to control/prevent viral calicivirus (and other viral diseases)
- Quarantine new arrivals
- Vaccinate upon arrival
- Reduce stocking density if possible
- Improve hygiene → Recovered cats can shed for a long time and can be spread by BOTH aerosol transmission or fomites
- Isolate/quarantine sick animals
challenges with vaccinations for feline calicivirus
- Like many RNA viruses, there is variation between strains of feline calicivirus
- Creates a challenge with vaccination
- Vaccines are either single or dual strain
- Vaccination does not prevent infection, prevent carrier state, or protect against virulent strains
SCENARIO:
● 400 sow farrow-to-finish farm operation
● Began six weeks ago, some pigs went off feed, elevated temperatures which lasted seven to ten days
● More recently, a few pigs are coughing with increased respiratory rates
○ Pigs of all ages affected
○ Non-responsive to a course of antibiotics
○ Pigs were previously vaccinated against Mycoplasma hyopneumoniae
There has also been reproductive failure
1. Premature farrowing of live piglets(early deliveries)
2. Late term abortion
3. Stillborn and weak piglets causing increased pre-weaning mortality
4. Failure to conceive and maintain pregnancy (early pregnancy loss)
> > Piglets are coughing, farmer describes a “thumping” sound
> > 2 affected pigs have recently died
What are your differentials?
- PRRSV*
- Swine parvovirus
- Porcine circovirus 2
- inclusion body rhinitis
- swine influenza
Symptoms of porcine reproductive and respiratory syndrome virus (PRRSV)
● Stillbirths, mummified fetuses, premature farrowing,
● Respiratory thumping, anorexia
most economically important disease affecting swine producers:
PRRSV
how does PRRSV spread through a herd? what changes this? how is the virus maintained in the herd?
○ In a naive herd: infection spreads slowly throughout herd causing clinical picture as in this case with variable degrees of disease and death
○ In an endemically infected herd: infection is often subclinical
○ Virus is maintained in a population indefinitely by asymptomatic swine who shed the virus for up to 3-5 months
what does PRRSV predispose infected animals to?
Virus destroys pulmonary alveolar macrophages → risk of secondary bacterial pneumonia
what herds are most at risk for losses from PRRSV?
Greatest losses are seen in herds experiencing other concurrent infections
how is PRRSV transmitted?
● Virus transmission is by direct contact, airborne and via semen
can PRRSV spread in the winter?
Virus survives at low temperatures, so epidemic spread is quite efficient in the winter months
what does PRRSV look like on post mortem?
Lungs: Red, rubbery, do not collapse→ consistent with interstitial pneumonia
How should we test for PRRSV antemortem?
○ PCR on serum, oral fluids, semen
○ Testing of aborted fetuses is of less diagnostic utility
How should we test for PRRSV post mortem?
○ PCR on lung and/or lymphoid tissue
○ Immunohistochemistry on FFPE tissue:
low specificity and need to submit multiple pieces of lung
How does PRRS infection persist on an individual farm?
- Persistent infection of individual animals (specific numbers NOT important)
- Continual outside additions to farm population
What are the long-term consequences for a herd infected with PRRSV?
● Severity of PRRS within a herd long term is variable: no clinical disease, continued clinical disease and production losses
● Secondary opportunistic infections:
* e.g. bacteria like Hemophilus parasuis, Streptococcus suis, Mycoplasma hyponeumoniae
● Coinfection with PCV-2 can cause more severe lesions
* More severe clinical presentations and pulmonary lesions compared to either infection alone
Control of PRRS; what can we try, and how can we create a PRRS stable farm?
● No single effective control strategy
● Often goal is to create a “PRRS stable” farm through intentional exposure of entire stock (before breeding)
● Vaccination
● Elimination on individual farm very difficult
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2.1 Red Blood Cells47
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2.2 anemia39
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Non-regenerative Anemia / Polycythemia30
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hemostasis63
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white blood cells61
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Cytology44
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3.1 viruses and detection15
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3.2 viruses as pathogens46
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3.3 DNA viruses 143
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3.4 DNA viruses 283
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3.5 RNA viruses 152
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3.6 RNA viruses 249
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3.7 RNA viruses 353
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3.8 Retroviruses and Prions52
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Lab 3.1: Detection of Disease43
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Lab 3.1 Only17
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Lab 3.2, 3.3, 3.426
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Lab 3.519
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Lab 3.626
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Lab 3.724
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Lab 3.822
