Swine diseases
Neonates 0-3 weeks (birth: 3-4 lbs)
<4 kg (8.8 lbs) Weanlings/nursery 3-10 weeks (~ 25 lbs)
4-25 kg (8.8 – 55 lbs) Growers/finisher 10-26 weeks (~ 50
lbs)
25-120 kg (55 – 264 lbs) Breeders/adults >6-8 months (~ 220 - 240 lbs)
>120 kg (> 264 lbs)
Multisystemic Diseases Respiratory Diseases Gastrointestinal Diseases Neurologic Diseases Musculoskeletal Diseases Reproductive Diseases Dermatology Miscellaneous
Nutritional◦ Vitamin E / selenium deficiency
Infectious◦ Erysipelas (Erysipelothrix rhusiopathiae): gram +
rod◦ Glasser’s disease (Haemophilus parasuis): gram -
coccobacillus◦ Salmonella: gram negative◦ PRRS (arterivirus)◦ Pseudorabies virus (herpes virus)
Erysipelothrix rhusiopathiae Gram positive rod
Environmental contaminant most herds have carriers
Septicemia diamond skin, arthritis, endocarditis, necrosis
acute septicemia ◦ fever, prostration,
anorexia, vomiting, reluctance to walk
◦ Hemorrhages may be present in multiple organs throughout the body.
◦ Mortality can be quite high.
chronic forms of infection include endocarditis and arthritis
"Diamond skin disease" erythematous skin lesions •These may be the classic diamond-shaped lesions or more diffuse edema and erythema. •The lesions are due to vasculitis and thromboembolism.
Treatment Penicillin Tetracyclins
Prevention and control Sanitation Vaccinate at weaning and
then q6 months Zoonotic: ‘erysipeloid’
occupational diseases for people such as veterinarians, abattoir workers and fisherman
Direct contact
Penicillin – first choice people and animals cephalosporins and clindamycin -people. Caution and hygiene are important to
prevent infection when working with potentially infected animals or in potentially contaminated environments
Haemophilus parasuis small, pleomorphic, and fastidious, Gram-negative
rod (coccobacillus) Endemic 3wk – 3 month (have no active/passive
immunity) initiated by stress
◦ weaning, changes in environment, commingling, or as coinfection with other disease agents
Also associated with PRRS or swine influenza
1931 an organism, presumably the same one, was isolated from swine with influenza and named Haemophilus influenzae suis.
1943 it was clear that the organism was a pathogen in its own right, not necessarily associated with swine influenza, and the name was shortened to Haemophilus suis.
1976, definitive taxonomic studies resulted in the present name, Haemophilus parasuis
Initially: fever, anorexia, depression Meningoencephalitis:
◦ tremors, incoordination, posterior paresis or lateral recumbency
Polyserositis Polyarthritis Mortality at any age Less common clinical signs:
◦ rhinitis, dyspnea, reddening of the conjunctiva, cyanosis of the extremities and edema of the eyelids or ears
Serosal surfaces: peritoneum, pleura, pericardium, joints, meninges
Polyserositis (serous membrane inflammation with effusion, fibrinous),
Pleuritis Pericarditis Peritonitis
Pig with Glässer’s disease. Noticeable presence of fibrin in the peritoneal cavity (fibrinous peritonitis) and pericardiac cavity (fibrinous pericarditis
red, multifocal, disseminated and suggestive of septicemia and hematogenous spread
Diagnosis Culture is difficult (but try it)
Brain, visceral pleura and other serosal exudates are preferred culture sites
Go with suspicion from gross lesions Molecular techniques for identifying H. parasuis
(research) Treatment: Antibiotics and sulphonamides
Penicillins Tetracyclins periodic evaluation of antibiograms is warranted. Mass: medicate, through the water (same age group)
Prevention and control Reduce stress Control of other diseases: PRRSV prophylactic antimicrobials Vaccine at weaning then again 3-4 weeks later
against one serovar of H. parasuis may not assure good protection against all serovars. (21 serovars)
2000 serotypes: small, hardy, ubiquitous, Gram-negative bacilli◦ Salmonella cholerasuis: mostly only in swine◦ Salmonella typhimurium
Zoonotic Contaminated pork products are not a primary
source of food-borne salmonellosis outbreaks in people but efforts to reduce salmonellae in the pork food chain are a high priority for the swine industry
disease in both people and swine include Salmonella serotypes typhimurium, enteritidis, agona and heidelberg
Microbiologist Brad Bearson analyzes cultures for the presence of Salmonella enterica serovar Typhimurium in swine feces.
“But S. Typhimurium’s success in swine isn’t just due to its increased motility when norepinephrine levels increase. It also has a mechanism for acquiring iron from its host to support its own growth and replication” 7/2009
In 1886 the organism now known as Salmonella serotype choleraesuis was erroneously reported to cause hog cholera
weaned or growing/finishing pigs
Low-level endemnicity, carriers
Septicemia pyrexia, anorexia purple discoloration of
the ears (infarction) Small or large intestinal
diarrhea (button ulcers) Pneumonia Rectal strictures
Pig, intestine. The intestinal lumen has reddened erosions and a fibrinonecrotic exudate. Credit: Dr. B. Inskeep, AFIP
Diagnosis Aerobic culture
Treatment Neomycin in the feed/water
for whole group Naxcel (ceftiofur) for
individual Prevention and control
Sanitation: inactivated by chlorine, iodine and phenol-based disinfectants
All in - all out operation Various vaccines (live
avirulent)Pig, mesenteric lymph node. The mesenteric lymph node is enlarged and edematous. This lymph node is good for obtaining cultures.Credit: Dr. B. Inskeep, AFIP
Porcine reproduction (sows and gilts) and respiratory syndrome (young growing pigs but also occurs in naïve finishing pigs and breeding stock)
Most important economic disease in USA (after eradication of classical swine fever)
Arterivirus: SS enveloped RNA Virus (high mutation rates)
persist in long-term carrier pigs (greater than 200 days) in reality stop shedding 60 days later
1987-88 in North Carolina, Iowa and Minnesota 1989 – 90: Several outbreaks in Indiana were reported During the subsequent decade, PRRS spread rapidly, both
in Europe and North America By the end of 1992 the disease was reported in Canada,
Great Britain and several European countries. Two distinct strains of virus, one in Europe and one in the
United States, were characterized as genetically different but are clinically similar in most respects. Both are now in the United States, along with a multitude of viral variants.
Old name: swine infertility and respiratory syndrome (SIRS)
Transmission: direct contact (very infectious): It is present in nasal secretions, urine, semen, mammary secretions and
feces. Clinical signs – neonates pulmonary intravascular macrophages (PIM) and
pulmonary alveolar macrophages (PAM); anorexia, lethargy, fever cyanosis of the ears, respiratory distress secondary bacterial pneumonia delayed or abnormal estrus cycle with increased
numbers of stillborns/mummies (3rd trimester)
Abortions, mummies and weak pigs
Lung affected with interstitial pneumonia of a pig with PMWS and co-infected with porcine reproductive and respiratory syndrome virus (PRRSV). This “infectious combination” is relatively frequent at field level; macroscopically it is not possible to distinguish between these two infections, so laboratory studies are required to confirm the etiologic diagnosis.
Diagnosis virus isolation (VI), detection of PRRS antigen by
fluorescent antibody tests (FAT) or immunohistochemistry (IHC), or detection of PRRS virus genome by polymerase chain reaction (PCR) and be coupled with presence of typical lesions.
serology provides indirect evidence of infection but does not determine if there is actual disease caused by PRRS virus.
Supportive care, treat secondary bacteria moderately resistant to environmental degradation,
the virus is easily inactivated by phenol, formaldehyde, and most common disinfectants
closed herds: ◦ replacements do not enter male or female replacements from
PRRSv positive herds outside the pyramid◦ Enter only PRRSv free replacement seedstock into a
production pyramid. semen:
◦ Do not use PRRSv positive semen from a stud outside the pyramid.
◦ Assure any outside semen is from a stud that is confirmed PRRSv free before entering it into a production pyramid.
commercial modified live vaccines◦ Live vaccines pose a dilemma as vaccine virus may act as a
foreign introduction Change feed with mycotoxins
Aujesky’s disease Type 1 Herpes virus: alphavirus The disease was eradicated from the US
commercial pig industry in 2004 but remains in some localized feral swine populations
Species: cattle, sheep, dogs, cats, and goats but not horses AND rats, mice, raccoons, opossums, rabbits, and several fur-bearing mammals◦ Close contact with infected swine
central nervous system (CNS), respiratory system or reproductive system
Not humans!
The disease is named after the Hungarian veterinarian Dr. Aladár Aujeszky who linked the disease in cattle, dogs, and cats in 1902.
Pseudorabies was not identified as a viral disease in swine until 1909
Prior to 1960, the disease in swine was important in Eastern Europe but major outbreaks did not occur in the US until the mid-1970s
In 1989, the US embarked on a 5-stage Federal/State/Industry program for eradication of PRV in swine; eradication of PRV from the commercial industry was achieved in 2004
Baby piglets up to 100% mortality high fever, depression, anorexia, tremors,
incoordination, dog-sitting position, vomiting, foaming at the mouth, blindness, paddling, coma and convulsions
Weanling/growers up to 60% mortality in weanlings, 0-15% in finishers pneumonia impt, neurologic dz, vomiting, extreme
pyrexia Adults - often inapparent
can cause stillbirth/abortion
Dead pigs (and a cat), a result of PseudorabiesMummified pigs, a
symptom of Pseudorabies
Lesions on post-mortemed lung
Lesions on nose of piglet
Reportable disease! Diagnosis
Necropsy - histologic lesions in brain, ulcers in gi tract
Serum neutralization is standard test ELISA can be used as a screening test
Treatment - none Prevention
closed herd! quarantine! restrict wildlife The virus can be destroyed by many disinfectants,
including orthophenylphenol, quarternary ammonium or iodine compounds, and 5% sodium hydroxide
vaccination
Regulation◦ use of vaccine regulated by states◦ federal regulations for monitoring
all animals over 6mo old must be tested 25% of herd tested q3months or... 10% of herd tested q1month
Nursery or grower pigs (few weeks – 4 months)
Vitamin E / Selenium deficiency Feeds high in the concentration of polyunsaturated
fatty acids, copper, vitamin A or mycotoxins can either destroy vitamin E or make it less bioavailable
Grains from soils deficient (midwest) in selenium, or selenium antagonists in mixed feeds, can result in feeds low in selenium.
Both vitamin E and selenium work as antioxidants.
Clinical signs acute death (mulberry heart disease) muscle weakness (white muscle disease)
more common in lambs, calves and chickens rather than swine
Diagnosis Necropsy - hydropericardium, fibrinous epicarditis,
myocardial hemorrhage Diffuse hepatic necrosis - hepatosis dietetica Liver selenium < 0.5 ug/g
The condition was named after the mottled appearance of the heart muscle in affected pigs. Typically, there are alternating areas of necrosis and hemorrhage throughout the myocardium.
Hepatosis dietetica consists in a degenerative lesion caused by vitamin E and selenium insufficiency.
prevention or treatment of a deficiency, pigs can be injected with vitamin E and/or selenium and tissue levels will be increased rapidly.
supplementation of feed or drinking water Sows injected in late gestation give birth to
pigs with increased levels of both compounds.
MHD is more responsive to vitamin E; HD more so to selenium
http://www.aphis.usda.gov/animal_health/animal_dis_spec/swine/
http://www.ncsu.edu/project/swine_extension/ncporkconf/2002/roberts.htm
http://www.vetmed.wisc.edu/pbs/zoonoses/Erysipelas/erysipelasindex.html
http://vetmed.iastate.edu/vdpam/new-vdpam-employees/food-supply-veterinary-medicine/swine/swine-diseases/haemophilus-parasuis-
http://vetpath.wordpress.com/category/necropsy-cases/
http://www.fmv.utl.pt/atlas/figado/pages_us/figad015_ing.htm