Viro - Swine 1

drraythe's version from 2015-08-30 22:34

Classical swine fever (CSF) aka Hog Cholera!!!

Question Answer
Etiological agent? DNA or RNA? Enveloped or Naked?Flaviviridae, RNA, enveloped (I like the FLAV of cauliflower)
What is the morbidity rate like? What is the mortality rate like?BOTH ARE HIGH!!! Super bad dz
Where does this dz occur geographically?Many other places but ERADICATED FROM THE US
What clinical sign is always present?LEUKOPENIA (bc its in lymphoid organs)
How often/what kinda death can occur from Hog Cholera? (Age related?)Very deadly in general! Can have sudden peracute death without CS in YOUNG swine, or older pigs may die within a week or later from 2° bacterial inxns
What are the INITIAL CS?High fever, depression, conjunctivitis, vomiting & diarrhea/or constipation & also opportunistic 2° bacterial pneumonia (lung & GI crap)
What CS do you see AFTER the initial signs?Paresis, paralysis, circling, tremors, occasional convulsions, hyperemia & purpura of abdomen & ears. (Results of the Encephalitis & the bleeding)(PURPURle cauliflower)
What are the CS like for pregnant sows & newborn piglets?Pregnant sows will get reabsorption of fetus, abortion, fetal mummification & stillbirths (all the things that can go wrong with a preg will). Newborns may die, or survive with tremors, runting & progressive dz causing death weeks or months after birth
How much does severity of dz vary? Explain.Subacute & chronic (following longer incubation), extended or intermittent clinical dz. Due to strains of MODERATE virulence (diff strains of diff severity)
What are the tissues/organs/cells that this virus likes to replicate in?ENDOthelial cells, lymphoid organs, bone marrow, leading to hemorrhages, profound leukopenia & thrombocytopenia
What signs do you see in the peracute dz?No CS & no gross changes at necropsy (the die too fast!)
Pathognomonic of Hog Cholera upon autopsy?Infarction of the spleen (cauliflower for your spleen (& LNs) is bad)
What pathology do you see in acute cases?Submucosal & subserosal petechial hemorrhages, congestion, infarction of the spleen (pathognomonic), liver, bone marrow & lungs. DIC, also ENCEPHALITIS (blood issues+Encephalitis → cauliflower in lymphoid system & in brain & its messing with the blood)
What pathology do you see in chronic cases?Chronic cases, Necrotic Ulceration of the mucosa of the large intestine & opportunistic 2° bacterial pneumonia & enteritis (takes a while for necrosis & 2° infections to happen)
WHAT IS THE MOST PROMINENT LESION IN HOG CHOLERA (not clinical sign)?General exhaustion of the lymphoid system (cauliflower replacing lymphnodes is a bad idea)
What should you know about the piglets birthed by an infected mother?Live-born piglets, healthy or not, are persistently infected, immunologically tolerant & life-long virus shedders (just like BVD, which was also Flaviviridae. Persistant cauliflower problems...couldn't it have at least been broccoli?)
What should you know about diagnosing Hog Cholera, in general?NOTIFIABLE DZ
How do you dx Hog Cholera?IF in tissues & AG ELISA (Ag detection bc urgent to dx). NOTIFIABLE! Need laboratory confirmation! Virus isolation & neutralization assays are also done
Transmission of Hog Cholera is?DIRECT or INDIRECT CONTACT → FOMITES play a big role, as well as introduction of an inapparently infected swine (horrible dz does all the things, of course)
Method of control for Hog Cholera?Test & slaughter (super severe dz, super severe control)

African swine fever (ASF)

Question Answer
Etiological agent? DNA or RNA? Enveloped or naked?Asfaviridae, DNA, enveloped (African, Ass. & remember on your ASfa is DNA)
Microscopic giveaways of ASF?Paracrystalline arrays in the cytoplasm (crystal African ass)
Why is it so difficult to eradicate ASF?Wild warthogs are asymptomatic but have the dz & soft ticks are reservoirs & vectors
What are the two patterns of African swine fever?Sylvatic cycle in wild warthogs & epidemic / endemic cycles of domestic swine
What is the sylvatic cycle like?Btwn warthog & tick - no domestic pigs involved
What is the epidemic/endemic cycle like?Occurs in domestic pigs. Tick can jump from warthog to pig. Then there can be direct pig to pig infection or infected meat
CS of African swine fever?High fever, diarrhea, incoordination & prostration. Also severe leukopenia, dyspnea, vomiting, nasal & conjunctival discharge, reddening or cyanosis (she seemed to emphasize reddening) of the ears & snout, hemorrhages from nose & anus. ABORTION! (very very similar to CSF!!)
What is the mortality like for ASF?The mortality can reach 100% in naïve populations but, once endemic, less severe dz & even subclinical & persistant infections occur
What/WHERE are the gross lesions associated with an acute infection of African swine fever?Gross lesions are most prominent in lymphatic & vascular systems. Will find petechia in the renal cortex!! (crystal African ass & ruby kidneys)
What CS is the chronic dz characterized by?Chronic dz is characterized by cutaneous ulcers, pneumonia, pericarditis, pleuritis & arthritis
How long does the dz last?Swine that manage to survive will be PERSISTENTLY INFECTED (persistently African crystal AS(f)shole dz)
How do you diagnose African swine fever?LABRATORY CONFIRMATION REQUIRED! Detection of viral antigen (IF or ELISA) & virus isolation. You must diff against CSF (Hog Cholera)
What are 5 reasons why prevention & control of ASF are so difficult?1) No vaccine
2) Transmission through pork products
3) Persistently infected pigs
4) Tick involvement
5) Similarity to CSF (Hog Cholera) CS (African crystal ass with ruby kidneys gives me persistant boners)
What is one way people try to control ASF?Surveillance in ASF-free countries
Why is eradication unlikely?Impossible to break sylvatic cycle (warthog & ticks)
What is the main source of infection to domestic pigs?Other infected pigs, via direct contact or aerosols & fomites
How is ASF transmitted?Direct contact, aerosols, fomites (fomites bc it's very stable in feces & blood etc) & soft ticks!
Why isnt there a vx/why are there problems developing a vx?When vxd, the pigs produce virus-specific antibodies but with no protective value (ASShole virus hides the important ags I think)

Pseudorabies (Aujeszky’s dz)

Question Answer
Etiological agent of Pseudorabies? DNA or RNA? Enveloped or naked?Herpesviridae, DNA, enveloped
Microscopic giveaways?Herpes = intranuclear inclusion bodies, BUT they are NOT diagnostic! THESE DONT ALWAYS SHOW UP IN THIS DZ!!!!!! Usually see microscopic lesions in CNS
How long does this dz last?Latency & persistent shedding are common (herpes)
What is shedding like? In what is the virus shed?Can be persistent (herpes) Recovered pigs can shed continuously in their nasal secretions. ARE shed in saliva & nasal discharge, are NOT shed in feces or urine (doesn’t go into blood, stays in the resp/CNS)
Where do you find this dz geographically?Endemic in most parts of the world
How much of a problem is Pseudorabies in the US?Has been eradicated from the domestic populations, BUT! Dz persists in WILD PIG POPULATION IN SOUTHERN US
Who does this dz effect?This is a dz of swine but it can also infect a diverse range of 2° hosts (horses, cattle, sheep, goats, dogs, cats & many wild species but humans are refractory!
What are the CS in pregnant sows?ABORTIONS!!! If before day 30, fetus will resorb. After, abortions & later in the preg there will be a mixture of mummified, macerated, stillborn, weak & normal piglets. Also, Pregnancy may be prolonged a couple of weeks (anything that can go wrong, will)
What are the CS in piglets?Maternal antibodies are protective & piglets suffer a much less severe dz & usually recover
What are the CS in weaned, growing & mature swine?Sneezing, coughing & fever, constipation & occasional vomiting, then a few days later there is incoordination, muscle spasm, circling, intermittent convulsions & excess salivation. (Mostly CNS & resp)
What is the mortality like?Mature swine mortality is low (2%) but they have significant weight loss & poor growth rates after recovery (fetii usually die, piglets usually fine)
How does a 2° host contract Pseudorabies?Only when there is direct or indirect contact with swine
What are CS like in 2° hosts? (Cattle, dogs, cats were specified)CATTLE: Major sign is pruritus ("mad itch") & have progressive CNS involvement until death
DOGS: Pruritus, paralysis of the jaws, drooling & howling but with NO tendency to attack
CATS: Super acute, basically die before signs
What is the pathogenesis/ how does the virus move in the body?NO VIREMIA!!! Travels via axoplasm (along nerves)
What are the gross lesions like in Pseudorabies?Lack of gross lesions
How is Pseudorabies transmitted? (In what & how)Through nasal secretions & saliva (direct or indirect) & rats/raccoons(?) may contribute to farm to farm transmission

Postweaning Multisystemic Wasting Syndrome (PMWS)

Question Answer
Etiological agent? RNA or DNA? Enveloped or naked?Circoviridae, DNA, naked (vicious circle of MWMWMWMWMWMWMW)
Where does this dz occur geographically?N America & Europe
What are the three forms of this dz?(1) Reproductive failure
(2) Respiratory dz in finishing pigs (aka adults)
(3) Porcine Dermatitis & Nephropathy Syndrome
How is PMWS shed?In the feces (my teat will only protect you from shit for so long)
Explain why this virus is called "post weaning"Passive immunity protects from systemic infection until 6-9 weeks of age, when maternal antibodies decline viral spread is observed (post weaning 69? oh my)
Is there a vx?Yes!
Microscopic giveaways?Intranuclear inclusion bodies
How do you dx?Intranuclear inclusion bodies & DEMONSTRATION OF THE VIRUS IN THE LESION. NEED CONFIRMATION BY VIRUS ISOLATION OR PCR (confirm the presence of the virus but not the etiology of the dz). Serology is not useful bc of the high prevalence of seropositives even without dz (vircious circo of dz means very common, serology won’t help then)

Porcine Parvovirus

Question Answer
Etiological agent? DNA or RNA? Enveloped or naked?Parvoviridae, DNA, naked
Microscopic giveaways?Intranuclear inclusion bodies IN DIVIDING CELLS (repro & GI cells)
How resistant?PARVO → Premises may remain infected for months even when hygiene appears satisfactory
What is SMEDI?Stillbirth, Mummified, Embryonic Death, Infertility
Does parvovirus cause abortions?Not causes SMEDI
What is the most important impact of porcine parvo?REPRO FAILURE
CS before 30 daysEmbryonic Death (& resorption) & infertility (EDI)
30-70 daysSM (Stillbirth, Mummification)
After 70 daysThere is immune-competence & there are developing lesions but they are affected less severely
What kind of signs do you see in sows which might make you think there is porcine parvo happening?Sows return to estrus prematurely. Some sows stay "endocrinogically pregnant"
If a sow is able to go to full term, but was infected with parvo, what would the litter look like?Smaller than normal litters & mummified fetuses
How is the blood affected?Leukopenia (its parvo, lulz)
How are boars affected?Low fertility
How does the dz differ in endemic areas?It is the Naive populations which have the most severe acute dz. once endemic, suclinical & persistent infxns occur
What is the shedding like?Swine parvovirus causes persistant infxn w/ chronic shedding
How long does the dz last?Swine parvovirus causes persistant infxn with chronic shedding (OPPOSITE OF DOG ONE)
How do you diagnose porcine parvovirus?IF OF FETAL TISSUES (got a bunch of dead babies, might as well use them)
What is a major factor of spreading parvovirus?Boars play a significant role in disseminating the virus that they shed in their semen for protracted periods (penis parvo)
Are there immunotolerant carriers?Maybe, BUT HASNT BEEN PROVEN!!
Is there a vx?YES (brief window of opportunity to vx gilts before they are bred)

Transmissible Gastroenteritis (TGE)

Question Answer
Etiological agent? DNA or RNA? Enveloped or naked?Coronaviridae, RNA, enveloped
What are the 4 diff dz patterns of corona virus?(1) Transmissible Gastroenteritis
(2) Vomiting & Wasting dz
(3) Porcine Epidemic Diarrhea
(4) Respiratory dz
Which age are most severely infected?Neonates
What are the CS (in babies)Vomiting & profuse yellow diarrhea (Yellow TGE instead of orange), weight loss, death w/in 1 wk
What part of the body is most affected & in what way?Small intestine villi are blunted
How fast is recovery from TGE?Usually rapid bc crypt cells not affected (Not Parvo! Corona affects the tips → like a crown, just on top)
Where do you see gross lesions?Usually limited to the GI
Do maternal Abs help?Colostral IgA is helpful, systemic IgG is not (A is A HELPER)
How do you diagnose TGE?Mucosal impression smears, IF, virus isolation
Does TGE have a vaccine?Yes, but it is not very affective in direct vax
How have we been using the vax to control TGE?Good protection has been achieved by giving virulent strains to pregnant sows, boosting lactogenic immunity in piglets

Swine Vesicular Dz

Question Answer
Etiological agent? DNA or RNA? Enveloped or naked?Picornaviridae, RNA, naked
What do you really need to know about swine vesicular dz?NOTIFIABLE!! & CONTROLLED!! bc Ddx are FMD (& vesicular stomatitis)
Who else does swine vesicular dz affect?HUMANS! ZOONOTIC! Cause influenza like symptoms
CS?Vesicles btwn the heel & the coronary band & btwn the digits & 10% of cases there are also vesicles in snout, lips and tongue
How/what is swine vesicular dz shed in?Feces (PICOchu crap dz makes even swine & humans sick)
What do we need to know about dx?DO IT FAST & REPORT if you see vesicular lesions!!
How to Dx?Ag ELISA, RT-PCR, Viral isolation in cell culture
How well does this Virus do out in the environment?Resistant in the environment (NAKED) (resists low pH & ambient temperatures)
How is it spread?Easily transmitted in infected meat (for months or years)