Other coronoviruses including:

Porcine hemagluttingating encephalomyelitis virus 

Porcine epidemic diarrhea virus 

Respiratory variant of TGE - porcine resp coronavirus 

Fecal-oral transmission 

diarrhea within 24 hours, vomiting in less than 2 weeks 

younger pigs more effected than older (because enterocytes are slower to be replaced at a young age) 

Biosecurity - no wild animals 

hygiene 

increase lactogenic immunity - give vax to sow, expose her to virulent virus WT virus and older pigs will not contract clinical disease!

(vaccines not effective with piglets) 

Increase the immunity in infected sows - expose them to WT virus from herd (1-2 mon before parturition)

Clean and isolate sows, farrow and early wean the piglets.  

Monitor piglets for seroconversion - if titer is rising they would need to be eliminated 

BHV1 (pestivirus)

BVD (pestivirus)

Border Disease Virus (pestivirus of S & G)

Cache Valley fever virus (bunyviridae Sheep and goats, cattle too maybe but less important) 

Akabane (bunyviridae - NOT IN US)

Pseduorabies (feral swine contact, southern US) 

Porcine parvovirus 

PRRS

CSF virus 

What virus causes "hairy shaker" disease? 

And what is "hairy shaker" disease?

Border Disease Virus (Flaviviridae/pestivirus) 

causes abnormal coat and tremors in sheep 

Can cause abortion if infected in the first 90 days of gestation.

Congenital anomalies: Hairy shaker disease, arthogryposis, hydroencephaly

If infected between 70 - 80 days of gestation

Repro failure: 

Arthrogryposis 

Hydraencephaly 

When does reproductive failure occur if infection with Porcine Parvovirus occurs?

Why?

If infection occurs BEFORE mid-term of 56 days, 

this is because the virus takes 2 weeks to move from placenta to uterus.

If they are exposed when 70 days - the piglet can eliminate the virus 

Once the virus cross placenta and infects piglet - their growth stops.

The virus then spreads through the uterus to subsequent to piglets, but takes time so it allows them to gain in size.  There may be a range from mummified fetuses to normal piglets in a single litter. 

Expose naive gilts/sows to WT PPV PRIOR to breeding 

- use of killed vaccine 

Bovine Leukemia virus 

Maedi-Visna Virus 

Ovine pulmonary adenomatosis virus (jaagsiekte virus)

What is the mechanism of oncogenesis from bovine leukemia virus?

How does this differ from FeLV???

**************

Ovine pulmonary adenomatosis 

OPA vs OPP

(lets be honest OPP - gross)

Stillbirth

Mummified fetus

Embryonic

death 

Infertility 

Vesicular stomatitis 

contagious pustular dermatitis 

pseudocowpox and other poxviruses 

bovine mammallitis virus 

papillomaviruses 

FMDV

Vesicular stomatitis virus 

swinepox virus 

FMDV

swine calicivirus (vesicular exanthema) 

swine vesicular disease (picornaviridae and FAD) 

Mechanical transmission by fomites

and biting insects 

Virus can survive for a few days in the environment, especially if cool, moist and has organic material 

(MILKING MACHINES) 

Scarification in the axillary region 

this is when humans can get the infection

Clinical presentation of Cowpox virus is most severe in:

a) cows

b) rodents

c) cats 

d) humans

Answer: C) cats

it is severe in cats, starting as a single lesion that rapidly spreads.

Cowpox virus is a DNA virus but does not code for all their transcriptional proteins.

True or False?

FALSE 

the Cowpox virus genome codes for all of its own transcriptional and translational enzymes

Pox viruses are DNA viruses so they replicate in the cytoplasm and will have cytoplasmic inclusions.

True or False?

Respiratory infection: pneumonia

Encephalitis 

hyperkeratosis of the foot pads 

GI upset

systemic infection

Where in the cell would inclusion bodies of Canine distemper virus be when:

a) convunctival smear preformed

b) vaginal smear preformed

c) brain tissue cytology

Conjunctiva & vaginal = cytoplasmic inclusions

BRAIN = Nuclear inclusions

Which virus is herringbone shaped:

Canine distemper or Canine Adenovirus?

about 70 days

Canine Distemper Virus (CDV)

Canine Adenovirus 1 (CAV1)

Canine Parvovirus 2 (CPV2)

Feline Panleukapenia Virus (Parvo or feline distemper)

FIP

Highly virulent strains of calicivirus

Where does the Canine distemper virus replicate?

This virus replicates in lymphocytes and macrophages, thus causing immunosuppression. 

This will cause the clinical sign of leukopenia, but also weakened the defense against secondary bacterial infections. 

Infectious Canine Hepatitis 

generalized disease 

gastroenteritis 

Upper respiratory 

CNS

interstitial nephritis 

corneal edema - "blue eye"

"Blue Eye" or Corneal edema is seen in which virus?

Canine Adenovirus 1 

(infectious canine hepatitis virus) 

NOT CAV2 !!

WIDESPREAD VACCINATION!

although maternal antibody can interfere with immunization in both viruses

Which virus will survive longer in the environment:

Canine distemper virus or Canine adenovirus 1?

Canine adenovirus 1 - it is very stable in the environment and can survive for weeks. This allows for natural vaccination because recovered or vaccinated dogs shed virus in urine for 6 months. 

CDV is quite labile and is only infective for a few hours.  

How does natural vaccination occur with

canine adenovirus 1?

HEMORRHAGIC GASTROENTERITIS 

myocarditis 

pulmonary edema 

generalized disease in young dog with no maternal antibody

FPLV

(Even though it is called feline distemper, it is in the Parvoviridae not the paramyxoviridae)

Paravovirus effects what cells of the GI tract?

How does this correlate to clinical signs?

CRYPT cells - which are rapidly dividing to replace absorptive enterocytes.  

this causes MALABSORPTIVE diarrhea

The VILLUS tips (mature enterocytes)

these are not dividing cells. 

The following viruses are spread fecal-orally, but which spreads to the site of repication hematogenously?

a) Rotavirus

b) Parvovirus 

c) Coronavirus

b) Parvovirus 

spreads through the blood to divide in the crypt cells of the intestine, which are rapidly dividing, then they cannot replace the enterocytes that are normally being lost.

What cell types does Feline Distemper virus replicate in?

How does this effect clinical presentation of the disease?

RAPIDLY DIVIDING CELLS

Crypt cells: hemorrhagic gastroenteritis

Neonatal cerebellar cells: cerebellar hypoplasia

Bone marrow: Panleukopenia

Post natal: most severe in kittens - GI and panleukopenia

Fetal form: cerebellar hypoplasia

Which characteristics describe feline parvovirus:

a) labile in environment 

b) highly contagious

c) high mortality 

d) transmitted by close contact

e) A and B

f) B and C

g) all of the above

ANSWER: F) 

it is quite stable in environment

is highly contagious

does cause high mortality

and is transmitted fecal-oral

(i should write his questions for him)

WET: More common (70%) effusive- high protein yellow fluid in abdomen and pleural cavities 

DRY: Less common, Non effusive - pyogranulomatous lesions of organs, body cavities, CNS, gut, eye

What virus did FIP emerge from?

What caused the difference in virulence?

enteric feline coronavirus - 

caused by macrophage tropic mutants (which increases virulence and causes clinical signs)

Coronaviruses like FCoV survive best is what type of conditions:

Dry or Moist?

MOIST = 24-36 hours

dry = less than 24 hours

In FIP, what events happen as the animal gets closer to death (can be more than one):

increased complement components 

increased body temp

increased antibody titer

increased immune complexes

Only the last two

When FIP infected cats get closer to death:

- body temp decreases

- complement components decrease 

- antibody titer increases

- ciculating immune complexes increase

FCoV specific cell mediated immunity

expression of IL10

NO ANTIBODY PROTECTION

(may even cause antibody enhancement)

possible Co-infection with FeLV

FeLV

This causes suppression of the immune system enough to not build an adequate CMI response 

-Immunoflourescent Assay test: high with dry form, low with wet form.

-Viral antigen in tissues

*diagnosis presumptive by clinical presentation - 

NO single DEFINITIVE TEST**

Influenza

PI5 

CAV1

CAV2

CHV1

Canine distemper virus 

FCV 

FHV1

Influenza 

Canine influenza originated from an equine strain, both have a2-3 and a2-6 linkages, but have 5 amino acids different. 

True or false?

True 

I couldnt make that up if I tried

mild upper respiratory disease 

but can have pneumonia 

Dogs are susceptible to horse strains of influenza but are resistant to avian strains.

True or False?

FALSE

Dogs are susceptible to both Equine (H3N8) AND 

Avian (H3N2 and H5N1)

H5N1 

Avian strain that can infect cats and dogs 

RT-PC: using M protein as target 

AG capture ELISA (using M protein) - not as reliable

Viral isolation - egg innoculation or MDCK with protease

Serology - hi titers by 8-10 day post infection

(6-8 days after onset of symptoms)

Young dogs: generalizaed hemorrhagic disease (kidney, lungs, liver)

Older dogs: genital vesicular lesions, vaginitis, balanoposthitis

Canine adenovirus 2

PI5 

Canine Herpesvirus 1

Bordetella bronchiseptica

strep equi zooepidemicus

Ulcers of the tongue are more common with which virus?

FCV

FHV1

FIP

Answer: FCV 

although feline herpesvirus can cause tongue ulcers, it is more common in calicivirus and also often more severe.

Feline caliciviruses are very resistant and can cause persistantly infected patients, who shed the virus for months to years.

true or false?

TRUE 

Viral isolation 

RT-PCR of nasal/conjunctival samples 

IFA of Antigen in conjunctiva

Feline herpes virus 1

feline calicivirus 

chlamydophila felis

(then comes bordetella bronchiseptica)

Rhinits

sinutitis

conjunctivitis 

tongue and oral ulcers 

corneal ulcers

"fading kitten syndrome"

FHV1

(FCV is more likely to cause tongue ulcers than FHV1 though)

FeLV (gammaretroviridae)

FIV (lentiretroviridae)

Canine parvovirus 1

canine rotavirus 

canine caronavirus 

Canine adenovirus 1 

Canine distemper 

feline rotavirus 

feline reovirus 

feline astrovirus 

toro-virus like (coronavirus)

felinepanleukopenia virus 

Cheetah 

high mortality