Food Ani. Med- Swine- Other Swine Dzs

drraythe's version from 2016-04-29 15:28


Question Answer
what is morbidity and mortality of hog cholera like? Classical swine fever is a highly contagious, viral disease of swine that in its most virulent form causes morbidity and mortality approaching 100%
where geographically is hog cholera? Classical swine fever is currently found in Central and South America, Caribbean, Europe & Asia
what is the etiological agent of classical swine fever/hog cholera? Pestivirus (family Togaviridae) related to BVD and BD
what is virulence of HC like? Virulence increases within a single passage through pigs
how labile is the pestivirus in the environment? (what temps is it resistant to? what CAN disinfect it?)Moderate resistance to environmental influences: Persist for days to weeks in feces and bedding, Survives for months to years in chilled and frozen pork, Inactivated by 2% sodium hydroxide or lipid solvents
explain the pathogenesis of HC (how does it enter the body/where does it go/where does it replicate?) Ingestion -->Tonsils --> Lymph nodes (REPLICATION takes place in lymphoid tissues)--> Viremia --> Epithelial cells --> Shed in many secretions and excretions
how do swine shed the HC virus (pestivirus) Within three to four days, virus spreads to many epithelial-type cells and is present in excretions and secretions
what are clinical signs of HC like?Nonspecific in acute outbreaks: Depression (a hunched posture with drooping head and a straight-hanging tail), anorexia, high fevers (106)--> piling up, +/- Diarrhea or constipation, and CNS SIGNS: Reeling when forced to walk, Hindquarter paresis or paralysis, convulsions
what are some CNS SIGNS pigs with HC might getReeling when forced to walk, Hindquarter paresis or paralysis, convulsions
if you see this pig, what are you thinking?depressed pig (hunched posture with drooping head and a straight-hanging tail)
If you suspect hog cholera, what should you do?REPORT********~
(said dont need to know dx but this is reportable so read over) 3 lab procedures used to dx(1) Immunoflorescence of viral Ag on frozen tissue ( Tonsil, Pharyngeal lymph nodes, Spleen, Kidney and Distal ileum) (2) VI on cell culture + ID viral antigen via FA (3) ID AB virus neutralization tests
is there vx for HC?yes, attenuated
what are some management things you should do to make sure pigs dont get infected with HC? Ban the feeding of raw garbage to pigs, Prohibits the dumping of trash by ships in port


Question Answer
what other dz does ASF's signs and lesions look like?classical swine fever (Depression (a hunched posture with drooping head and a straight-hanging tail), anorexia, high fevers (106)--> piling up, +/- Diarrhea or constipation, and CNS SIGNS: Reeling when forced to walk, Hindquarter paresis or paralysis, convulsions )
what is the most common way pigs get ASF? Commonly introduced by feeding uncooked garbage
etiological agent of ASF?virus
should you worry about pork products if your herd gets ASF?ASF virus persists in pork for long periods of time
most common way ASF transmits from pig to pig?oronasal secretions
how is ASF transmitted?DIRECT OR INDIRECT! (1) can be from Infected animals (Direct transmission usually is through oronasal secretions) (2) fomites (3) Tick vectors: Several species of soft ticks-- In Africa, a cycle of inapparent infection is established between ticks and wild boars, warthogs and bush pigs (ASF virus is passed transovarially in some ticks)
which insect vector spreads ASF?ticks
explain the pathogensis of ASF (where does it enter the body, where does it replicate, etc)eaten--> Infection of tonsils and mandibular lymph nodes --> lymph & blood --> 2* replication sites (bone marrow, lung, spleen and kidney) --> persistent viremia (~1 wk post infection)
The main target cells of the virus include? what are the results of this targeted tropism? Monocytes, Macrophages, RE cells, Endothelial cells, & platelets (so blood and lymphatic stuff). Destruction of APC’s (antigen presenting cells) interferes with formation of protective antibodies, and Destruction of endothelial cells and vascular --> hemorrhages, edema and transudate formation.
why might ASF cause swine to become ataxic? May also lead to meningoencephalitis responsible for ataxia
what are the CSs of an ACUTE outbreak of ASF? Anorexia, High fever, Listlessness, Incoordination, Leukopenia, Cutaneous hyperemia, Skin hemorrhages and Hyperpnea... Vomiting, diarrhea, dehydration and ocular discharge are possible...
what is morbidity and mortality like for ASF?(acute) Morbidity and mortality can approach 100% with death in four to seven days (chronic has low mortality)
what are the CSs in subacute or chronic cases of ASF?abnormal respiration, abortion and low mortality
(dont need to know) dx of ASF?Detection of Virus, Viral Antigen, or Antibodies: Hemadsorption test= Virus ID, Direct Immunofluorescence= ID Ag in frozen sections, Several Techniques= ID virus in paraffin-embedded tissue sections, Indirect immunofluorescence, ELISA, CF, Immunoblotting, & Radioimmunoassay= ID Antibodies, Sensitive Dot Immunobinding Assay for field Dx
is there a vx for ASF?VX DO NOT WORK!!!
if there is a US outbreak what must you do?Slaughter --> burial or cremation. This is done to Infected pigs and any with possible direct or indirect contact


Question Answer
what is circovirus like?Small, DNA virus with a circular genome
how labile is circovirus? how can you disinfect it?Hardy in the environment, sensitive to most disinfectants. ( Chlorhexidine, ethanol, and iodine are less effective<--lol like all the common things??)
what are the two types of PCV? PCV1= nonpathogenic, PCV2= PCVAD & PCVD
which PCV is pathogenic?PCV2 which is PCVAD (Porcine circovirus associated disease) and PCVD
So PCV1 is non-pathogenic-- is this useful?lol Antibodies between the two types (PCV1 & PCV2) have low cross-reactivity, so not really helpful for developing vx
which herds are more likely to experience an outbreak of PCVAD (Porcine circovirus associated disease)? Herds that are endemically infected with other significant pathogens or management problems. And the outbreak will be more severe
what is morbidity and mortality like?Nearly all US swine herds are seropositive . Morbidity varies 2% - 30% Case fatality can reach 80%
two risk factors to pigs developing PCV?Co-infection with other viruses, vaccination (<--weird)
what is the pathogenesis of PCV? (where does it replicate, what kinda inflammation does it cause?)Viremia of variable duration--> Replication in macrophages and monocytes ("PCV pipe in your ONE (mono) CELL). CAuses Chronic lymphohistocytic to granulomatous inflammation
Mechanisms of immunity and expression of Dz are unknown...but what seems to be required for PCVAD to happen? Macrophage activation prior to PCV2 infection appears to be required for PCVAD
what are PCVAD (porcine circovirus associated dz ) Clinical Signs? Gradual wasting, Unthriftiness with a rough hair coat, Polypnea (panting), Dyspnea, Pallor, Diarrhea, Occasional icterus
what are PDNS (porcine dermatopathy and nephropathy syndrome ) clinical signs? (WHAT AGE?) Pigs 8-18 weeksof age, you will see red-purple blotches on the skin which are Sometimes slightly raised, most obvious on the hind legs and perineum, however can extend over the abdomen eventually covering the whole body. Most pigs with PDNS eventually die
DX (dont need to know)PCVAD Virus inclusion bodies in lymph organs by microscopy (IHC In situ hybridization to confirm Dz & PCV2 association, PCR to confirm virus not Dz, VI not useful, Serological tests confirm infection with PCV2= Most herds are positive. Virus is not always demonstrated in PDNS. IHC will demonstrate PCV2 on routine abortion panel
how do you tx PCV/PCVAD?No specific treatment for pigs with PCVAD (Anti-inflammatory agents and/or antimicrobials are sometimes used with success )
is there a vx for PCV?yes
what should you know about the PCV vx (important)Timing is extremely important.!!! 3 weeks b/f PCV exposure. (usually affected at 2-4mo)
will abx help PCV?well its a virus, but it can help with Control of other infections (PRRSV, parvovirus, etc)-- put the abx in the food/water
PDNS (porcine dermatopathy and nephropathy syndrome) kinda has similar presentation to...?PMWS= Post Weaning Multisystemic Wasting Syndrome
what age do pigs get PMWS (Post Weaning Multisystemic Wasting Syndrome)? When do they get PDNS? How do they look diff?PMWS= 10-20wk. PDNS= 8-18wk. (hence some confusion) The diff in looks:


Question Answer
what is the etiological agent of ERYSIPELAS?Erysipelothrix rhusiopathiae-- Gram +, aerobic, bent, thin bacillus
how labile is erysipelas? what can you use to disinfect it?Resistant to many environmental influences. Survives for long periods of time in pork meats, contaminated fish meal and decaying animal carcasses. Destroyed by many disinfectants (Caustic Soda and Hypochlorite)
which abx is erysipelas sensitive to? what is it resistant to?Sensitive to penicillin (it's G+!!) and +/- tetracycline... Resistant to may antibiotics including sulfonamides
who(age) is affected by E?Infectious Dz of grower & adult swine
who can be a carrier of E?Spread by carrier pigs & other animals (Birds, Pets, Wild Mammals) ( Flies and ticks are able to spread the Dz)
where is E shed from? Carriers and affected pigs shed bact. In feces and oronsal secretions
who (species) is affected by E? Occurs in swine, lambs, Turkeys, Localized skin lesions in people ***ZOONOTIC**
is there a seasonality of E? Can occur anytime of year (most prominent in late summer)
what do skin lesions of E look like?Although often occur this way, don't necessarily need to look like a diamond or rhomboid pattern
explain pathogenesis of E-- how does it get into body? where does it go? • Ingestion (or through skin wound) --> Tonsils --> Other lymph tissues -->Bacteremia
Question Answer
they are unsure, but what is the possible mechanism which causes the skin lesions and such? Produces Neuraminidase (cleaves MPS(matrix polysaccharides) of cell wall) --> Vascular damage --> Thrombosis + Chronic Arthritis+ VVE
which pigs are susceptible to E? Susceptibility to infection is poorly understood -- Not all infected pigs get the Dz
most common CS of CHRONIC E?Enlarged joints are most common
what is a bolded CS of acute E he mentioned?**Very High Rectal Temps (104 – 108 o F)
clinical signs of ACUTE E? Sudden Death, **Very High Rectal Temps (104 – 108 o F), Cyanosis of skin +/- diamond skin lesions, Very reluctant to move (stiff, +/- joint enlargement), abortion
clinical signs of CHRONIC E?Enlarged joints are most common, Low mortality, Sloughing of tips of ears and tails
what are the two DDX for dzs which can cause similar skin lesions?Actinobacillus suis and PCV can develop similar skin lesions
Acute Outbreaks respond well to..? (2) pen G and antiserum
where does he recc putting abx?drinking water
is there a vx for E?yes
When do you wanna vx? how do you vx? types of vx?Vaccination in the face of an outbreak is warranted. (1) Attenuated vaccines – injection or water (2) Bacterins - injection ( 2 doses will protect until market in most cases, Booster 1 – 2 times a year in breeding stock)


Question Answer
what causes FMD? how contageous is it?Highly contagious viral disease of many wild and domestic cloven-footed mammal
in swine what characterizes the dz?characterized by vesicles on the feet, snout, and in the mouth
who is resistant to FMD?Horses are resistant
what kind of hosts are swine with FMD? (they play a special role) Swine are “amplifier hosts” for FMD virus
4 ways FMD can be transmitted(1) Direct and indirect contact with infected animals & aerosolized respiratory secretions. Aerosol transmission can occur over distances as great as 30 miles <--wtf (2) FMD virus can be spread in pork (3) Contaminated biologics, including vaccines (4) People can carry & transmit the virus for a short time
if an animal recovers from FMD, what is the new problem?Some species of animals recover from FMD and remain carriers for weeks, months, or years
what is the pathogenesis of FMD? (where does it enter, where does it replicate, how does it continue its lifecycle) FMD enters via the respiratory tract --> Mucosal adherence --> Macrophages --> 2 o sites --> Replication --> Viremia --> More epithelial infection --> Vesicles --> Rupture --> Release of virus
Common vesicle sites of swine (4)?Snout, Mouth, Tongue, Esp. Feet
where is another place cows can get FMD which pigs MIGHT get?Cattle can get infection of mammary epithelium ( May also occur in swine)
what might lead to CHRONIC lameness associated with FMD?2 o infections are common esp. on feet --> chronic lameness
what additional problem might happen with neonates and young pigs? Myocardial necrosis in neonatal & young pigs (and sudden death in neonates)
what do lesions of FMD look like?
what are the progressing CSs you see with FMD? Lameness is the first sign noted in most cases. High temps, Slobbering and chomping, Abortion or stillborn infected pigs, Sudden death in neonates, Cutaneous vesicles
what is morbidity and mortality like in FMD?High morbidity and low (<5%) mortality except in neonatal pigs
if you think you have FMD on your hands what should you do?REPORTABLE!!! STATE WILL DX **FMD must be differentiated from other Dz that cause vesicles and erosive/ulcerative lesions
how is FMD controlled? U.S. relies on regulating importation of animals and animal products. Regulations on cooking and dumping of waste food. Early detection is left upon veterinary practitioners
is there a vx for FMD?Vaccine is used in some countries where the Dz has been eradicated
what is the 3 parts of the US control plan?(1) Quarantine and restrictions to movement (2) Slaughter, burial, incineration (3) Eradication is considered less costly than living with Dz