Viro - Bovine 1

drraythe's version from 2015-08-30 22:30

*Foot & Mouth Dz (FMD) (FMD can be cutely remembered as fast moving dz)

Question Answer
Systemic or specific system dz?Systemic
Etiologic agent? (RNA or DNA? Naked or Enveloped?)Picornaviridae, ssRNA(+) Linear, NAKED → EXIT BY LYSIS (Pico-chu put his foot straight in his mouth & exploded)
Causes what (basic), who are the animals affected by FMD, & in what capacity are they affected?Causes vesicular mucosal lesions in RUMINANTS & SWINE. HORSES ARE REFRACTORY (refractory = wont get infected, not even subclinical infxn)
If an animal is "refractory" to FMD, what does this mean? Who fits this description?They won't get infected, not even a subclinical infxn. Horses are refractory to FMD.
Is FMD reportable? Is it zoonotic? Does it have economic impact? ElaborateREPORTABLE(she had notifiable). There are countries that have eradicated the dz, & there are TRADE BARRIERS between eradicated & non-eradicated countries. It can be ZOONOTIC but it is rare. (Economic loss due to slow recovery is more important than the acute dz itself)
What are the serotypes of FMD? & why do we care?7 serotypes are: A, O, C, SAT1, SAT2, SAT3, & Asia1. This is relevant bc ties in w/ the diagnosis & the vaccinations used. THERE ISNT CROSS PROTECTION. (I took the SAT 3 times before I decided to give up & move to ASIA w/ my Only Cow Avis )
Are there different kinds of FMD?YES! 7 diff serotypes w/ no cross protection. See "serotype" card for more.
What is the mortality like? The morbidity?Mortality is low but morbidity is extremely high (so don't usually die, but is hella contagious)
What is the most important loss related to FMD?The most important loss is due to the slow recovery after the dz than the acute dz itself (trade limitations/ loss of meat & milk product is a huge economic impact, whereas the dz is usually not fatal, so we actually care more about the economic losses)
What is viral shedding like in FMD?There is SHEDDING EVEN BEFORE CLINICAL SIGNS! Intermittent shedding AFTER infxn. (She had in another place: there is excretion of virus, 24hrs before the onset of clinical signs!!!)
Is there cross-protection between the 7 serotypes of FMD?NO!! so a new serotype will act as if it were a completely new dz epidemic
Is there a vx for FMD? How effective is it?Technically yes, however Vaccines are NOT very efficient bc of the continuous antigenic drift (not shift, drift bc 1-segment genome) & they are only type-specific (no cross protection)
What are the clinical signs in cattle/calves?Drop in milk production! (economic importance) there is drooling, & vesicles appear in tongue, gums, interdigital skin, coronary band & teats. Then the vesicles rupture & cause ulcerative lesions. In CALVES under 6mo, death can result from myocarditis. ABORTION can happen, but from the FEVER, not the dz itself!!!
Does FMD cause Abortion? Why or why not?It DOES, but not directly. The dz doesn't cause Abortion but the fever from the dz CAN cause the Abortion
What is recovery like for cattle w/ FMD? Notes about this?The animals are poor or non-productive for a LONG time after infxn (ECONOMIC IMPORTANCE). Also, they will intermittently shed!!!!
What are the clinical signs of FMD in pigs?LAMENESS, primarily. (Pigs say FMD is lame)
Describe the PERSISTENCE for FMD. How much, for who? Explain how shedding ties into thisCOWS & SHEEP will continue to shed FMD for a while, but FMD is NOT PERSISTENT IN SWINE!!!
How well does immunity help in protecting against FMD?Immunity is only short lived, & DOESN'T protect against the 6 other (7 total) serotypes that are out there
What should you know about the differential diagnoses for FMD, along w/ FMD?ALL OF THEM ARE REPORTABLE!
How do you test for FMD? How wouldn’t you test for FMD?Antigen ELISA s are commercially available to detect all types (you can also use RT-PCR). You would NOT use antibody ELISA bc it would take a while for Abs to form, & there is URGENCY FOR PROMPT DIAGNOSIS!
What is 1 of the reasons that FMD is so hard to control? What are routes of transmission of FMD?BC it can have LONG DISTANCE AIRBORNE TRANSMISSION!!!! so the WIND can carry it FARRRR away (other types of xmission are → Main route of infxn is inhalation of droplets but infected food, contaminated vaccines or semen & fomites have also been described)
When/how is there EXCRETION of the virus?If infected by respiratory route, the virus replicates in the pharynx & is followed by viremia, at this point there is excretion(droplets/milk) of virus, 24hrs before the onset of clinical signs!!!
How do you treat FMD?Most of the time, exposed animals are slaughtered, & there is an imposed quarantine & movement restriction
Ddx for FMD?Vesicular stomatitis, enterovirus, & vesicular dz in swine

*Bovine Papillomatosis

Question Answer
What is the etiologic agent? DNA or RNA? Naked or enveloped?Papovaviridae, dsDNA, NAKED circular
Who gets BPV?All ages common in calves & yearlings
Are there various types of BP?YES! Don’t need to know specific types go w/which clinical signs tho. (See clinical sign card for more)
Why are there variations of the clinical signs of BP? What ARE the various clinical signs?There are different types associated w/ different lesions. This can mean they can look diff & end up in diff spots. (1)Can have a fibrous core covered w/ squamous cell epithelium w/ hyperkeratinization of the outer layers. Can vary from small & firm to large cauliflowers, & may be found in teats, udders, head, neck, omasum, vulva, penis, anus. Other types have (2) Cutaneous lesions w/o fibroblast proliferation, which tend to persist as flat w/ a broad base. There is also a type which can cause (3) GI & BLADDER(endemic hematuria), & in this case lesions & may progress to squamous cell carcinoma (usually warts are BENIGN so this is unique)
By which route is an animal infected w/ BP?Through ABRASIONS on the skin.
After gaining entry to the body, how/what does BP infect, w/ what result?Infxn of epithelial cells results in hyperplasia, degeneration & hyperkeratinization
How do you treat BP?SPONTANEOUS REGRESSION → gets better on its own after ~4-6 month
How do we control BP?Usually dz is SELF-LIMITING, but the duration varies, recombinant DNA vaccine is avail
Body system affected, or systemic?Skin dz
Is there a vx?Yes (no cross protection between types)

*Bovine Mammilitis

Question Answer
Etiologic agent? DNA or RNA? Enveloped or Naked?Bovine Herpesvirus 2 (BHV-2), Herpesviridae! DNA, ENVELOPED. (OMG TITTY HERPES, LULZx2)
Are there diff types of BM?YES! However, she only seemed to care about MAMMILLITIS(which is the condition formed in the udder). (The other form is Pseudo-Lumpyskin)
How do you diagnose Mammillitis? Things to note about the dx? How can you confirm the dx?Diagnosis is CHALLENGING, bc it looks SIMILAR to warts, Cowpox, Pseudocowpox, vesicular stomatitis & FMD (all of the ADVANCED LESIONS ARE VERY SIMILAR IN ALL OF THESE DZs, so EARLY EXAMINATION/EVALUATION of the herd is advisable. EM(electron microscopy) & virus isolation from scrapings or vesicular lesions can confirm the diagnosis
Describe the shedding of Bovine MammilitisHERPES = IS FOREVER latent, recrudescent, intermittent, or continuous shedding can occur
Clinical signs of BM?(Wasn't in red) is like Pseudolumpyskin but localized to the udder. Basically nodules on the mammary gland, ↓ milk production, maybe mastitis. Thing to note is that it looks a lot like vesicular stomatitis, FMD, Papillomatosis, Pseudocowpox etc.


Question Answer
Which is in North America(& worldwide), Cowpox or Pseudocowpox?Pseudo (Cowpox is only in Europe & Russia, no need to know tho)
Etiological agent of Pseudocowpox? DNA or RNA, naked or enveloped?Poxviridae, DNA, (some) enveloped, *DNA which replicates in the cytoplasm (has Pox in the name, GDI)
Is Pseudocowpox an acute or chronic dz?Chronic (Pseudo horse shoe stomping on udder feels like it lasts FOREVER for the cow)
What is a pathognomonic lesion of Pseudocowpox?HORSESHOE-SHAPED SCABS
Where do lesions of Pseudocowpox occur?MAINLY ON THE TEATS bc of this, can also be on the muzzles/mouths of suckling calves (a horse Pseudo-stomped on the cows tits)
What other dz should you think about when you think about Pseudocowpox dz, & why?You should think of Lumpyskin dz, BC they are ddx

*Bovine Viral Diarrhea (BVD)* very important.

Question Answer
Etiologic agent of BVD? DNA or RNA? Enveloped or naked?Flaviviridae, RNA, enveloped. (Diarrhea has such a good flavor, they should pack it in envelopes & sell it)
Does BVD occur in the USA?Yes!
What are the 2 dzs associated w/ this? (Diff dz syndromes by same etiological agent)(1) BVD
(2) Mucosal dz (chronic & acute)
What are the clinical signs of BVD (NOT MD) in postnatal infxn of non-pregnant cattle?Panleukopenia, diarrhea, erosive stomatitis, drop in milk yield, Bc of the immunosuppression it is not uncommon to see 2⁰ respiratory & GI bacterial infxns
What are the clinical signs of BVD (NOT MD) in infxn of pregnant cows? (I.e., what happens to the fetus) (3 situations)Transplacental spread occurs frequently The outcome depends on the AGE OF THE FETUS!!!
(1) infxn at < 80 days(less than a little over 2mo), fetus will die & be resorbed
(2) infxn at 80-125 days(a little over 2mo to ~4mo), (immune system starts to develop but fetus is not immunologically competent) the fetus/calf will be IMMUNOTOLERANT to the BVDV*(more on this later)
(3) infxn after 125 days(4mo) → Bovine fetal immunologic competence is reached! Abortions, weak calf syndrome or congenital defects (CNS, retina) may occur. The most common defect is cerebellar hypoplasia!!(Think: ataxia). [Note: this can be asked in months OR days, she said]
Explain the CP vs the NCP strains of BVD in the diagram (more detail later)CP = cytopathic. The cytopathic strain stays in GI, does not usually cause persistent viremia, so doesn't usually go transplacental, so usually just has adult diarrhea effects, etc. NON-cytopathic will infect other tissues, can cause persistent viremia & avoid immune system, CAN get into fetus transplacentally
Explain the immunotolerant calf (when does this happen, how, what is the result of this, what should you know as a vet?)If fetus is infected between days 80 & 125, it is not immunologically competent, & it's body recognizes the virus as "self" instead of foreign. This is "immunotolerance" & then the animal is PERSISTENTLY INFECTED (so they are often called PI's). The PIs are the 1s that will develop mucosal dz, bc MD only occurs in PERSISTENTLY INFECTED ANIMALS (they are also the major spreaders of the dz)
WHEN/WHO gets the mucosal dz? (Triggers?)Occurs in calves 6-18 months of age (0.5-1.5yr) that are PI (were infected from 80-125days while not immunocompetent) & are therefore immunotolerant to noncytopathic (ncp) BVDV. They appear clinically normal until 3 possible triggers to have them develop ACUTE or CHRONIC MD
(1) Superinfxn w/ a homologous BVDV
(2) Mutation of the ncp to cytopathic (cp) variant
(3) Vaccination w/ MLV(modified live vx) of BVDV
What are the clinical signs of the ACUTE form of MUCOSAL DZ?Ttachycardia, polypnea, watery diarrhea, Feces may contain blood & have foul odor, Erosions & ulcers may be present on the tongue, palate, & gingiva while epithelial erosions may be pronounced in the interdigital regions, coronary bands, teats, vulva, & prepuce. Also corneal opacity, ↓ rumination, & bloat
How do you tell the difference between FMD & acute mucosal dz, which have very similar symptoms?If you see just 1 or 2 case of these symptoms, it is probably MD, but if there are lots of cases, it is more likely to be FMD
What is the prognosis like for acute mucosal dz? What is life like for those after acute MD?VERY HIGH MORTALITY RATE (approaching 100%). For those who manage to survive, they are prone to develop the chronic form of MD
What is chronic mucosal dz? What are the clinical signs? Prognosis?Follows the acute MD. Have intermittent diarrhea, chronic bloat, & Nasal-ocular discharge is commonly seen. They usually die, if they arent euthanized first.
What industry-relevant place can BVDV replicate?The seminal vesicles & the prostate gland, which means there can be venereal transmission! ALWAYS buy semen from reputable sources.
Where does non-cpBVDV like to replicate? What immune response does it provoke?All throughout the host (leukocytes, lymphoid tissue, the proximal colon & the respiratory tract, seminal vesicles & prostate) & can cause a persistent VIREMA which is why it is able to move transplacentally & affect a fetus. non-cpBVDV will stimulate a HUMORAL immune response (Abs & shit) bc it is everywhere & in the blood
Where does cpBVDV like to replicate? What immune response does it provoke?Replicates in the GI only! So it doesnt cause persistent viremia, so it doesn't infect fetuses. Also, since it only stays in the GI, it usually provokes a local, CELL-MEDIATED immune response
What is the best way to diagnose BVD? What other way can you use, but what is the risk?Best way = Viral antigen detection in tissues (IHC). You could also use serology, but interpretation of seronegative result must be made considering immunological tolerant state of some animals!!!!!
How can BVD be spread? Most efficient spread?MOST EFFICIENT SPREAD is from PI to other individuals. It can also be spread via fomites. (Feces, urine, oral or nasal secretion & amniotic fluid or semen from infected animals)
Explain 2 different situations of an animal (PI or naive) being introduced to an unaffected or infected herdIn herds where the virus has been present only sporadic losses occur when a naïve animal is introduced as the rest have immunity. In a virus free herd, the introduction of a PI animal will result in dramatic losses
What is the MOST IMPORTANT thing to do to control BVD?Most important for control is to detect the PI animals & eliminate them. QUARANTINE new animals, or only allow mature immune animals into the herd!
Is there a vx? What to know?YES, there is an attenuated vx, but they can cause PI animals to develop mucosal dz & cause Abortions, stillbirths & birth defects
Body system involved, or systemic?Systemic
GOLD STANDARD for dx BVD?Cell culture/isolation

BVD *Know this Diagram*