Reoviridae, RNA, naked (same as Rota- your tongue would have to be dead & blue for you to want to lick Milk Scours off a calf)
What is important to know about this virus (the virus itself not the dz) (2)
SEGMENTED (so fast reassortment) & is an ARBOVIRUS (MIDGES)
Where is this virus geographically prevalent?
Nowadays present in all countries in the tropics & subtropics (think of drinking fancy blue drinks on a tropical beach & that’s why your tongue is blue)
Which animals does Bluetongue effect?
MAINLY sheep, but can also occur in cattle & goats (subclinically)
Why is knowing about this dz important?
Although there is death & loss of conditioning, main problem is its a MAJOR TRADE BARRIER
What are the clinical signs of Bluetongue?
Nasal discharge, cyanotic tongue (no duh), edema of head & neck, Coronitis (inflammation of coronary band), ABORTIONS!!! & congenital abnormalities. Some strains in North America can cause peracute fatal Hemorrhagic Dz
In what way might a strain of Bluetongue in N. America might differ in its clinical signs?
Some N. American strains can cause peracute fatal Hemorrhagic Dz
What is the shedding of Bluetongue virus like?
There are NO lifelong shedders or tolerogenic infxns that being said, when the animal is infected, they are viremic & can shed for quite a while
How easy is it to isolate the virus?
DIFFICULT TO DO
How do you dx virus?
Can isolate, but DIFFICULT TO DO. Can use SEROLOGY → Ab ELISA (used to have crossrxn but now more specific test), & RT-PCR can be used
What are the 2 syndromes caused by CAE? (Include when these occur)
(1) ENCEPHALITIS occurs in KIDS, 2-4mo old (2) More commonly, ARTHRITIS in goats older than 1 year
What are the clinical signs of CAE?
Progressive Leukoencephalomyelitis, lameness (from the arthritis → joints are swollen & painful, the movement t is restricted, & they can have flexion contractures), wasting, trembling, their hair coat is dull. Interstitial mastitis & interstitial pneumonia. In the TERMINAL STAGES, you will see paralysis, abnormal position of head & paddling (will "paddle themselves to death"). HOWEVER, IMPORTANT TO NOTE → they remain afebrile, alert & w/ good appetite & sight (when not in terminal stages)
Unique things to know about clinical signs?
They remain afebrile, alert & w/ good appetite & sight!!!! This hasnt been the case w/ any other virus!!!
How does this virus damage the CNS?
Focal malacia (tissue softening) in the white matter (NOTE: Prions affect the GREY matter!) & this histologically is characterized by cell inflammation & demyelination
Explain how the joints are affected in this dz
Lameness often occurs bc of the arthritis. Joints are swollen & painful, movement is restricted, & they can have flexion contractures. The lesions are of proliferative synovitis. The dz overall leads to degenerative changes
2 weird clinical signs which you wouldnt think would occur w/ CAE?
Interstitial mastitis & interstitial pneumonia
How do you dx CAE?
RETROVIRUS = SEROLOGY!!!!!!!! (Ab detection)
Is there a vx?
No! It's a Retrovirus!
How is CAE usually transmitted?
Usually transmitted "vertically" through colostrum & milk! (NOOOOOOOO dangerous goatcheese!!!!)
What is the best way to control CAE?
Since xmission is usually through milk/colostrum, you can heat it at 56°C for 1 hr, feed pasteurized goat or cow’s milk & raise them in isolation from infected animals (keep them away from milk & mom & they're good)
Etiological agent? DNA or RNA? Enveloped or Naked?
IT IS A PRION!!!
How does Scrapie affect a herd?
Only a few sheep in a flock are sick at a time but losses are significant over the years (so no obvious outbreaks!)
What sp does Scrapie effect? Any breed diffs?
SHEEP. There are more susceptible breeds → SUFFOLK & Hampshire (technically goats can be affected, but only after exposure to infected sheep/pasture, & we didn't need to know this)
What is the incubation time of Scrapie?
What are the clinical signs? (Onset? length of course of dz before death?)
Onset is insidious (gradual) & sheep become excitable, w/ tremors in the head & neck. Then there is intense pruritus → wool loss & raw skin. There is progressive deterioration over 1-6 months w/ emaciation, ataxia, paralysis & death
Where are the lesions, & what do they look like?
Lesions are in the GREY MATTER (neuronal bodies, outside portion of brain) & there is NO INFLAMMATION OR IMMUNE RESPONSE (BC IT IS A PRION, NOT A VIRUS, BODY WONT REACT TO A PROTEIN LIKE THAT)
Would serology be useful in dx?
NO. NO IMMUNE RESPONSE. IS A PRION.
How do you diagnose Scrapie?
Usually look at histopathologic lesions in the brain (grey matter). IHC (on brain sections) & Western Blot (from CSF)
Etiological agent? (DNA or RNA? Naked or Enveloped?)
Retroviridae, RNA, enveloped
Is Maedi zoonotic?
No evidence of transmission to humans
What is the incubation time of Maedi?
What is Maedi aka?
Ovine Progressive Pneumonia
How would you describe the onset of Maedi? What are the clinical signs?
Insidious (slow) onset. It is PROGRESSIVE PNEUMONIA! There will be jerking of the head w/ each inspiration, & flared nostrils. There also might be nasal discharge & cough. Pregnant ewes might abort (ma-day went downhill when I aborted)
Maedi affects what animals?
Where are gross lesions found in Maedi, & what are they?
Only in lungs & associated lymphnodes. Lungs appear homogenously consolidated (HARD TO THE TOUCH), & DO NOT COLLAPSE WHEN THORACIC CAVITY IS OPENED
What is the immune system doing in Maedi?
There is immunopathology → therapeutic immunosuppression delays progress of degenerative changes (but it's gonna die anyway...so, is kinda worse)
How can you diagnose Maedi?
Antibody ELISA (SEROLOGY!!!! RETRO = SEROLOGY EVERY TIME), & WB (Western Blot) can be used to confirm diagnosis. Also antigen ELISA s can be used. Virus isolation can ALSO be used (need to stim cells w/ IL2 before the virus can grow in them tho)
How is Maedi transmitted?
Usually direct by droplet through blood, semen, bronchial secretions, saliva & milk. However, indirect transmission can occur (water, feces, etc)
Do asymptomatic sheep transmit the dz?
Usually not (rarely), HOWEVER, an asymptomatic ewe can xmit to her lamb through milk
What are 2 common mechanical vectors of Maedi?
Biting arthropods & surgical equipment
Is there a vx?
No → Retrovirus!
How do you control Maedi?
No vx, only control is in test & removal programs of already infected sheep, & avoiding transmission for uninfected
Contagious Ecthyma & also contagious Pustular dermatitis
Systemic or body system affected?
Etiological agent? DNA or RNA? Enveloped or naked?
Poxviridae, DNA, enveloped (Pox replicates in the cytoplasm)
Is Orf zoonotic?
Yes! Humans can get infected, but only when in close contact w/ sheep (occupational hazard)
What are the clinical signs? (Location of lesion, appearance?)
Usually involves the muzzle & lips, but can be w/in the mouth (esp. in lambs). Rarely lesions on eyelids, feet & teats. The lesions themselves usually progress from papules to pustules then to thick crusts (why condition is often called "scabby mouth")
What problems can the lesions cause, aside from them being lesions w/in themselves?
Having pustules/papules/crusts on the mouth means that it might prevent lambs from suckling, causing them to lose weight. Having open sores may lead to 2° infxns
How do you diagnose Orf?
Usually clinical diagnosis is enough (is there a scabby mouth?) (You can use EM to confirm tho)
Is Orf acute? Chronic? Is it a permanent infxn or are they immune after?
Orf can cause reinfxns OR chronic infxns (Orfs, like orcs, are very annoying)
How resistant is Orf in the enviro?
VERY, BC although it's enveloped, it is able to stay in SCABS (along w/ the fact that reinfxn & chronic infxns can occur) & so it is VERY hard to eradicate
How is Orf transmitted?
Can be direct or indirect through feed or fomites
Is there a vx?
How do you control Orf?
The EWE is vx BEFORE lambing, using a non-attenuated vx. Vx is applied by SCARIFIED SKIN, AXILLA which generates a short-lived immunity (passes maternal antibodies in colostrum this reduces the risk of the ewe transmitting ORF to the lamb)