Swine diseases
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Atrophic rhinitis: Bordetella bronchiseptica
and Pasteurella multocida (primarily type D)
Swine influenza: influenza virus
Mycoplasma pneumoniae: “enzootic
pneumonia,”
Actinobacillus pleuropneumoniae: Gramnegative
Pasteurella: Gram negative
Verminous pneumonia
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Bordatella bronchiseptica
◦ aerobic, Gram-negative rod
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Pasteurella multocida
◦ Gram negative
coccobacillus
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High ammonia
Restricted to swine (described in dog and
goat)
In the United States, AR is becoming a rare
disease as
◦ early weaning, age
segregation and/or vaccination.
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Hx: Described in 1830
and in US in 1944
Clinical signs: 1wk weaning
early stages: snuffling,
sneezing, snorting,
◦ Epiphora, +/- epistaxis
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which may progress:
atrophy and distortion
of the turbinates, nasal
and facial bones of
some affected pigs
 twisted snouts
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Dff: rhinitis: porcine reproductive and
respiratory syndrome virus (PRRS),
pseudorabies virus (PRV), inclusion body
rhinitis (cytomegalovirus), or excessive dust
or ammonia
Diagnosis
 Necropsy - 2nd premolar or 1st cheek tooth in pigs
less than 6 months of age
 Nasal culture for either organism
Toxigenic P. multocida produce a
potent toxin that causes a rhinitis with
progressive osteopathy of facial and
turbinate bones
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Treatment
 tetracyclines in the feed: farrowing/weaning
 LA200 to neonates
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Control or eradicate
◦ improvement of husbandry: management and
housing, including ventilation, all in all out, reduce
stress
◦ vaccination program for the breeding stock, pigs, or
both.
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Influenza virus: type A influenza
viruses
(family Orthomyxoviridae).
Zoonotic
Serologic surveys show that nearly
all of the herds in the Midwest
have antibodies to SIV
Outbreaks associated with
movement or extreme weather
changes
 up to 100% morbidity
 low mortality unless secondary
bacterial infection complicates things
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Swine influenza subtype H1N1:
◦ 1st appeared in western Illinois in 1918
◦ influenza pandemic that killed an
estimated 20 million people
worldwide
interspecies transmission:
among swine, chickens, ducks, turkeys, many wild birds
and people
2 or more strains of virus: potential for reassortment
(genetic “shift”).
H3N2 and H1N2 emerged during the 1990s: triple
reassortment” variants that are comprised of swine, human,
and avian viral genes
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inflammation with
widespread degeneration
and necrosis of cells lining
bronchi and bronchioles
Sudden: sudden onset of
fever, occulonasal
discharge, prostration and
weakness
Progression: paroxysmal
coughing over a relatively
short course of 5-7 days
low mortality
Both lungs are non-collapsed. There is diffuse tan
consolidation of cranial lobes, and multifocal lobular
consolidation of the caudal lobes, consistent with
bronchointerstitial pneumonia
Credit: Dr. B. Janke, Iowa State University, College of Veterinary
Medicine, Veterinary Diagnostic Laboratory
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Diagnosis
 Necropsy - cranioventral pneumonia:
 fluorescent antibody technique on fresh lung sections
 immunohistochemistry techniques on formalin-fixed lung
sections
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Treatment - supportive
Prevention
 closed herd
 control secondary infections
 keep away from humans
(no shows!)
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inactivated by many disinfectants (2 wks
environment)
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Enzootic pneumonia: acute and severe
disease, PRDC (porcine resp dz complex)
Weaned – grower/finisher
increases the severity of several other
infections: (PRRS) and influenza
Carrier swine
very costly, widespread disease of swine,
largely because of its negative effects on
growth rate and feed efficiency
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Transmission: direct,
aerosal, transplacental
Most common cause of
chronic pneumonia
◦ Chronic, non-productive
cough
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Low mortality
Secondary bacterial
complication
Dff
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Diagnosis
 Necropsy - “plum colored”or pale cranio-ventral
pneumonia
 Culture to rule out secondary bacteria
fluorescent antibody,
immunohistochemical,
or polymerase chain
reaction (PCR) techniques
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Treatment - Lincomycin in feed
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Prevention - improve management
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Gram-negative,
capsulated,
coccobacillary rod
Host specific
Intensive swine
operations
Inapparent carriers
Release toxins
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Peracute, acute,
and chronic forms
Clinical signs
 severe respiratory
distress
 death
marked dyspnea with mouth breathing
+/- bloody discharge from the mouth
and nose
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Risk factors:
◦ Overstocking, inadequate ventilation,
coinfection with other respiratory pathogen,
stress
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Diagnosis
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necropsy - fibrinous pleuropneumonia
often diaphragmatic lobes most severe
culture is difficult
complement fixation serology
Treatment
 ceftiofur (Naxcel) and procaine penicillin
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Control
 vaccination of young pigs
• Classic lung lesions caused by
Actinobacillus
pleuropneumoniae.
• Focal areas of necrotizing
pneumonia isolated in the
dorsal and caudal portions of
the lungs is a diagnostic
feature.
• the entire lung lobe can also
be involved.
• fibrinous pleuritis is common
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Gram negative coccobacillus
Most common bacterial isolate from pig lungs
opportunistic pathogen
 mycoplasma, influenza, actinobacillus, stress
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clinical signs
 moist productive cough
 dyspnea
 some die
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Diagnosis
 necropsy - suppurative cranio-ventral
bronchopneumonia
 may be pleuritis similar to actinobacillus
 culture
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Treatment - penicillin, tetracyclines
Control
 look for underlying disease
 medicate feed and water (tetracyclines)
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Ascaris suum - direct life cycle
◦ pneumonia, hepatitis, and ill thrift
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Metastrongylus elongatus - earthworm intermediate
Problem with pasture pigs
Clinical signs
 poor doer
 respiratory distress
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Secondary bacterial infection
“Milk spots” liver, worms in the GI
Levamisole, ivermectin
• 15-40 cm long, thick bodied, round
worms
• Eggs persist in environment 15 yrs
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Stomach
 Ulcers
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Small intestine
 E. coli (piglets): Gram-negative, flagellated bacilli
 TGE (piglets): coronavirus
 Clostridium (piglets): large, anaerobic, Gram positive
bacillus
 Coccidiosis (>7 days): protozoa
 Rota virus (post weaning)
 Salmonella (any): Gram-negative bacilli
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Large intestine
 Swine dysentery (grower/finishers): Gram-negative,
anaerobic
 Proliferative enteropathy (grower/finishers)
 Hemorrhagic bowel syndrome
 Proliferative illeitis
 Whipworms (growers)
 Salmonella (any): Gram-negative bacilli
Infection with and/or agent
Unweaned
piglets
Nursery pigs
Grow/finish pigs
Enterotoxigenic E. coli
++++
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+ (early grower)
Rotaviral infection
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+ (early grower)
Transmissible gastroenteritis virus
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(TGE)
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Adults
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Clostridium difficile
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Clostridium perfringens Type A
++++
Clostridium perfringens Type C
++++
+ (rare)
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Coccidiosis
Isospora suis
Salmonellosis
Swine dysentery
Brachyspira hyodysenteriae
Proliferative enteropathies
Lawsonia intracellularis
Porcine epidemic diarrhea virus
(exotic)
Whipworm infection
Trichuris suis
+++
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Almost always the pars esophagea (nonglandular stomach)
Non-specific lesions
Can lead to “bleed-out”
Predisposing factors...
 Finely ground feed
 Stress
 Vit E/Selenium def
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Weaning onwards
Melena, ulceration of squamous
portion of stomach, anorexia
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E. coli: Gram-negative, flagellated bacilli
Most impt cause of diarrhea in piglets <5
days old!!!
O157:H7, does not appear
to cause disease in swine
Toxins
Clinical signs
 clear watery to pasty brown feces
 dehydration and depression
 death losses higher in younger pigs
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Diagnosis
 ph of feces (>8)
 culture of organism (large number)
 necropsy - dilated gas filled small intestine
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Treatment
 Ampicillin, tetracyclin, gentamicin, fluids
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Control
 sanitation, vaccination of sow
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Coronavirus (similar to FIP)
Epidemic form (all ages)
Endemic form (1-8 weeks old)
WINTER disease
Clinical signs
 Neonates (1-8 days)– watery diarrhea with
undigested milk, vomiting and high mortality rates
in piglets
 Growers, finishers - diarrhea recovers <7days
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Morbidity and mortality high in pigs
<2weeks old
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Diagnosis
 ELISA, immunoflourescence of gut contents
 Necropsy
 undigested milk in small intestine
 thin walled, transparent small intestine
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Treatment - supportive
Control
 isolate new additions for 2 weeks, keep dogs and
bird away (carriers)
 Immunization of sows or piglets
 Grind up piglet guts and feed to pregnant sows
Distended intestine with fluid ingesta
thin translucent intestinal wall
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Clostridium perfringens type C
sudden death in 1-2 day old piglets
Clinical signs
 BLOODY DIARRHEA
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Diagnosis
 Necropsy - blood in jejunum with flecks of mucosa,
necrosis of small intestine
 Clinical signs
 Histopathology - large gram positive rods
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Treatment
 usually die too quickly
 type C antitoxin
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Control
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Sanitation
Type C antitoxin within minutes of birth
Vaccination of sow
Prophylactic bacitracin or penicillin to piglets
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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
http://www.cfsph.iastate.edu/DiseaseInfo/dis
ease.php?name=influenza&lang=en
http://microgen.ouhsc.edu/a_pleuro/a_pleur
o_home.htm