Transcript swine - Dr. Brahmbhatt`s Class Handouts

Swine diseases
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Neonates
0-3 weeks
(birth: 3-4 lbs)
 <4 kg (8.8 lbs)
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Weanlings/nursery
3-10 weeks
(~ 25 lbs)
 4-25 kg (8.8 – 55 lbs)
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Growers/finisher
10-26 weeks
(~ 50 lbs)
 25-120 kg (55 – 264 lbs)
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Breeders/adults
 >120 kg (> 264 lbs)
>6-8 months
(~ 220 - 240 lbs)
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Multisystemic Diseases
Respiratory Diseases
Gastrointestinal Diseases
Neurologic Diseases
Musculoskeletal Diseases
Reproductive Diseases
Dermatology
Miscellaneous
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Nutritional
◦ Vitamin E / selenium deficiency
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Infectious
◦ Erysipelas (Erysipelothrix rhusiopathiae): gram +
rod
◦ Glasser’s disease (Haemophilus parasuis): gram coccobacillus
◦ Salmonella: gram negative
◦ PRRS (arterivirus)
◦ Pseudorabies virus (herpes virus)
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Erysipelothrix rhusiopathiae
 Gram positive rod
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Environmental contaminant
 most herds have carriers
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Septicemia
 diamond skin, arthritis, endocarditis, necrosis
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acute septicemia
◦ fever, prostration,
anorexia, vomiting,
reluctance to walk
◦ Hemorrhages may be
present in multiple
organs throughout
the body.
◦ Mortality can be quite
high.
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chronic forms of
infection include
endocarditis and
arthritis
"Diamond skin disease"
erythematous skin
lesions
• These may be the
classic diamondshaped lesions or
more diffuse edema
and erythema.
• The lesions are due
to vasculitis and
thromboembolism.
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Treatment
 Penicillin
 Tetracyclins
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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
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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
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Haemophilus parasuis
 small, pleomorphic, and fastidious, Gram-negative rod
(coccobacillus)
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Endemic
3wk – 3 month (have no active/passive
immunity)
initiated by stress
◦ weaning, changes in environment, commingling, or
as coinfection with other disease agents
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Also associated with PRRS or swine influenza
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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
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Initially: fever, anorexia, depression
Meningoencephalitis:
◦ tremors, incoordination, posterior paresis or lateral
recumbency
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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
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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
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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)
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Treatment: Antibiotics and sulphonamides
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Penicillins
Tetracyclins
periodic evaluation of antibiograms is warranted.
Mass: medicate, through the water (same age
group)
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Prevention and control
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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)
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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
“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
Microbiologist Brad Bearson analyzes
cultures for the presence of Salmonella
enterica serovar Typhimurium in swine
feces.
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In 1886 the organism now known as
Salmonella serotype choleraesuis was
erroneously reported to cause hog cholera
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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)
Pig, intestine. The intestinal lumen has
 Pneumonia
reddened erosions and a fibrinonecrotic
 Rectal strictures
exudate.
Credit: Dr. B. Inskeep, AFIP
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Diagnosis
 Aerobic culture
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Treatment
 Neomycin in the
feed/water for whole
group
 Naxcel (ceftiofur) for
individual
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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
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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
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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)
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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.
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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
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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.
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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.
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commercial modified live vaccines
◦ Live vaccines pose a dilemma as vaccine virus may act as a
foreign introduction
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Change feed with mycotoxins
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Aujesky’s disease
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Type 1 Herpes virus: alphavirus
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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
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central nervous system (CNS), respiratory system or
reproductive system
Not humans!
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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
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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
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Weanling/growers
 up to 60% mortality in weanlings, 0-15% in finishers
 pneumonia impt, neurologic dz, vomiting, extreme
pyrexia
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Adults - often inapparent
 can cause stillbirth/abortion
Dead pigs (and a cat), a result of
Pseudorabies
Mummified pigs, a
symptom of
Pseudorabies
Lesions on postmortemed lung
Lesions on nose of piglet
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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
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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
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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.
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Both vitamin E and selenium work as
antioxidants.
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Clinical signs
 acute death (mulberry heart disease)
 muscle weakness (white muscle disease)
 more common in lambs, calves and chickens rather than
swine
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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.
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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
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http://www.aphis.usda.gov/animal_health/an
imal_dis_spec/swine/
http://www.ncsu.edu/project/swine_extensio
n/ncporkconf/2002/roberts.htm
http://www.vetmed.wisc.edu/pbs/zoonoses/
Erysipelas/erysipelasindex.html
http://vetmed.iastate.edu/vdpam/newvdpam-employees/food-supply-veterinarymedicine/swine/swinediseases/haemophilus-parasuishttp://vetpath.wordpress.com/category/necr
opsy-cases/
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http://www.fmv.utl.pt/atlas/figado/pages_us
/figad015_ing.htm