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 it is in the lymphoid organs)
how often/what kinda death can occur from hog cholera? (age related?)
Very deadly in general! can have sudden peracute death without clinical signs in YOUNG swine, or Older pigs may die within a week or later from secondary bacterial infections
what are the INITIAL clinical signs?
high fever, depression, conjunctivitis, vomiting and diarrhea/or constipation and also opportunistic 2* bacterial pneumonia (lung and GI crap)
what clinical signs do you see AFTER the initial signs?
Paresis, paralysis, circling tremors, occasional convulsions, hyperemia and purpura of abdomen and ears. (results of the encephalitis and the bleeding)(PURPURle cauliflower)
what are the clinical signs like for pregnant sows and newborn piglets?
Pregnant sows will get reabsorption, abortion, fetal mummification, and stillbirths (all the things that can go wrong with a preg will). Newborns may die, or or survive with tremors, runting, progressive disease causing death weeks or months after birth
how much does severity of dz vary? explain.
subacute and chronic (following longer incubation), extended or intermittent clinical dz. This is due to stains 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 and thrombocytopenia
what signs do you see in the peracute dz?
no clinical signs, and no gross changes at necropsy
pathognomonic of hog cholera upon autopsy
infarction of the spleen (cauliflower for your spleen (and LNs) is badddd)
what pathology do you see in acute cases?
there are submucosal and subserosal petechial hemorrhages, congestion, infarction of the spleen (pathognomonic), liver, bone marrow and lungs. DIC,also ENCEPHALITIS (blood issues+encephalitis-->cauliflower in lymphoid system, and in brain, and its messing with the blood)
what pathology do you see in chronic cases?
chronic cases, necrotic ulceration of the mucosa of the large intestine and opportunistic 2ry bacterial pneumonia and enteritis (takes a while for necrosis and secondary infections to happen, so, makes sense)
overall though, WHAT IS THE MOST PROMINENT LESION IN HOG CHOLERA? (not clinical sign)
general exhaustion of the lymphoid system (cauliflower replacing lymphnodes is a badddd idea)
what should you know about the piglets birthed by an infected mother?
Live-born piglets, healthy or not, are persistently infected, immunologically tolerant and life-long virus shedders (hey, 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?
how do you dx hog cholera?
need labratory confirmation! NOTIFIABLE! IF in tissues and ANTIGEN ELISA (Ag detection bc urgent to dx). Virus isolation and neutralization assays are also done. (YE BEWARE OF CAULIFLOWER)
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 and slaughter (super severe dz, super severe control)
etiological agent? DNA or RNA? Enveloped or naked?
Asfaviridae, DNA, enveloped (African, Ass. and remember on your ASfa is DNA)
microscopic give-aways 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 disease, and soft ticks are reservoirs and vectors
what are the two patterns of african swine fever?
Sylvatic cycle and epidemic / endemic cycles of domestic swine
what is the sylvantic cycle like?
between warthog and 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
clinical signs of african swine fever?
high fever, diarrhea, incoordination and postration. Also severe leukopenia, dyspnea, vomiting, nasal and conjunctival discharge, reddening or cianosis(she seemed to emphasize reddening) of the ears and snout, hemorrhages from nose and anus. ABORTION!
what is the mortality like for ASF?
The mortality can reach 100% in naïve populations but, once endemic, less severe disease and even suclinical and 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 and vascular systems. Will find petechia in the renal cortex!! (crystal african ass and ruby kidneys)
what clinical signs is the chronic disease characterized by?
Chronic disease is characterized by cutaneous ulcers, pneumonia, pericarditis, pleuritis and arthritis
how long does the disease last?
swine that manage to survive will be PERSISTENTLY INFECTED (persistently african crystal ass)
how do you diagnose african swine fever?
LABRATORY CONFIRMATION REQUIRED! detection of viral antigen (IF or ELISA) and virus isolation
what are 5 reasons why prevention and control of ASF are so difficult?
1) the lack of a vaccine 2) transmission through pork products 3) persistently infected pigs 4) tick involvement and 5) similarity to CSF(hog cholera) clinical signs (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 sylvantic cycle (warthog and ticks)
what is the main source of infection to domestic pigs?
other infected pigs, via direct contact or aerosols, and fomites
how is ASF transmitted?
direct contact, aerosols, fomites (fomites bc very stable in feces and blood etc), soft ticks!
why isnt there a vx/why are there problems developing a vx?
when vx, the pigs produce virus-specific antibodies but with no protective value (ASShole virus hides the important ags i think)
etiological agent of pseudorabies? DNA or RNA? Enveloped or naked?
herpesviridae, DNA, enveloped
microscopic give aways?
herpes=intranuclear inclusion bodies, BUT! THESE DONT ALWAYS SHOW UP IN THIS DZ!!!!!! Usually see microscopic lesions in CNS
how long does this dz last?
latency and 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 and nasal discharge, are NOT shed in feces or urine (doesnt 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 disease of swine but it can also infect a diverse range of secondary hosts (horses, cattle, sheep, goats, dogs, cats and many wild species but humans are refractory!
what are the clinical signs in pregnant sows?
ABORTIONS!!! before day 30, resorptions. after, abortions, and later in the preg there will be a mixture of mummified, macerated, stillborn, weak and normal piglets. Also, Pregnancy may be prolonged a couple of weeks (anything that can go wrong, will)
what are the clinical signs in piglets?
Maternal antibodies are protective and piglets suffer a much less severe disease and usually recover (lol go fig, the one little babies are fine in is the rabies one)
what are the clinical signs in weaned, growing, and mature swine?
sneezing, coughing and fever, constipation and occasional vomiting, then a few days later there is incoordination, muscle spasm, circling, intermittent convulsions and excess salivation. (mostly CNS and resp)
what is the mortality like?
mature swine mortality is low (2%) but they have significant weight loss and poor growth rates after recovery (fetii usually die, piglets usually fine)
how does a secondary host contract pseudorabies?
only when there is direct or indirect contact with swine
what are clinical signs like in secondary hosts? (cattle, dogs, cats were specified)
CATTLE: major sign is pruritus ("mad itch") and have progressive CNS involvement until death. DOGS: pruritus, paralysis of the jaws, drooling and 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!!!. they travel via axoplasm.
what are the gross lesions like in pseudorabies?
lack of gross lesions
how do you dx pseudorabies?
AB ELISA, IF, VIRUS ISOLATION and SERUM NEUTRALIZATION
how is pseudorabies transmitted? (in what, and how)
through nasal secretions and saliva (direct or indirect), and rats/raccoons(?) may contribute to farm to farm transmission
etiological agent? RNA or DNA? Enveloped or naked?
circoviridae, DNA, naked (vicious circle of MWMWMWMWMWMWMW)
where does this dz occur geographically?
N america and europe
what are the three forms of this disease?
(1) reproductive failure (2) respiratory dz in finishing pigs (aka adults) (3) porcine dermatitis and nephropathy syndrome
how is PMWS shed?
in the feces (my teat will only protect youfrom my shit for so long)
explain why this virus is called "postweaning"
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?
intranuclear inclusion bodies
how do you dx?
intranuclear inclusion bodies and 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 usful bc of the high prevelance of seropositives even without disease (vircious circo of dz means very common, serology wont help then)