Enteroviral Polioencephalomyelitis in Finishing-age
On a 300 sow, farrow-to-finish pork production facility
2 out of approximately 2500 (0.08%) 12 to 15-week old finishing
pigs were getting progressively ataxic and uncoordinated over
a period of one day. No other pigs in the finishing barn
were showing clinical signs and mortality in the nursery and
finishing barn for the past 6-9 months had averaged 1%. The
owner wanted to know what the problem was before a potentially
large outbreak occurred. What differentials should be considered?
Relatively Common Causes of CNS Disease in Finishing-age
1. Bacterial otitis media usually few pigs are affected
with head-tilt, a droopy ear, ataxia and/or recumbency.
2. Bacterial meningitis caused by S. suis or H.
parasuis although less common in finishing pigs
than in nursery-age pigs, limited sporadic outbreaks occur
in finishing pigs.
3. Pseudorabies virus although it is tempting to
eliminate this pathogen from consideration following eradication
efforts, it is better to be safe than sorry!
Clinical symptoms in finishing pigs include flu-like
pneumonia with coughing anddyspnea, tremors, circling, head
tilt, lateralrecumbency, opisthotonus, nystag-mus and convulsions.
4. Water deprivation/salt toxicity commonly caused
by human error, but may be due to faulty or poorly adjusted
equipment. Symptoms include irritability, convulsions and
Less Common Causes of CNS Disease in Finishing-age
1. Enteroviruses cause sporadic enceph-alomyelitis
manifested as tremors, convulsions, recumbency, ataxia,
posterior paresis and/or posterior paralysis.
2. PRRS virus although uncommon, some highly virulent
strains of PRRSV can cause cerebral vasculitis and encephalitis
that is fatal.
3. Rabies virus very uncommon in pigs due to husbandry
practices, but should be considered due to fatal zoonotic
4. Edema disease more common in nursery-age pigs,
but can occur sporadically in finishing pigs (known as cerebrospinalangiopathy).
Clinical symptoms include ataxia and convulsions.
5. Bacterial encephalitis caused by Salmonella cholerasuis.
Some strains of S. cholerasuis can cause cerebral
vasculitis and encephalitis as a component of septicemicsalmonellosis.
In these cases, the more common purple discoloration
of skin, ischemic necrosis of skin on the tips of the ears,
diarrhea and other well-known gross lesions are usually present
and help with a strong presumptive diagnosis.
6. Intoxications chlorinated hydrocarbon or organophosphate
pesticides are the most common toxic causes of tremors or
convulsions. Selenium intoxication due to feed mixing errors
causes ataxia and posterior paresis/paralysis. Inorganic
arsenicals cause paralysis.
Clinical Examinations: On arrival,
only the 2 reported finishing pigs were affected. They were
both in good flesh and had normal rectal temperatures. Pig
1 was alert, but severely ataxic. Pig 2 was mentally dull
and laying down. Attempts to get the pig up resulted in a
sitting position, with the pig soon opting to lay down.
Necropsy Examinations: In pig 1 the
lungs were diffusely gray and rubbery with petechia on the
pleural surface. Frothy white fluid oozed from the cut surface
of the lung. Interstitial pneumonia was suspected. In pig
2 there were no observed gross lesions.
Submission to a Diagnostic Laboratory
Tissues should be collected in 10% neutral buffered formalin
for histopathology and fresh/refrigerated for bacteriology,
virology, and toxicology.
- Meningeal swabs collected aseptically for bacterial culture.
Disarticulate the skull from the atlas, flame the foramen
magnum with a portable torch, carefully insert a culturetteTMtype
swab into the calvarium through the foramen magnum, swab
around the brain stem and cerebellum, withdraw and insert
into the plastic sheath- release the fluid to keep the swab
moist and refrigerate.
- Spinal cord. Due to the history of ataxia and
paresis, it is imperative to remove the spinal cord
for testing. It may be easier to anticipate the difficulty
and time required and, instead, submit the entire pig for
- Ileum or ileal mucosal swab for bacterial culture (E.
coli strains associated with edema disease; positive
for F18 or K88 fimbria and contain the gene for edema disease
toxin synonyms include SLTIIvariant, STX
toxin and shigatoxin E.
Results of Laboratory Testing
Brainstem: nonsuppurative encephalitis, multifocal,
moderate Spinal cord: nonsuppurative poliomyelitis, multifocal,
severe Lung: interstitial pneumonia, histiocytic, multifocal,
No significant or consistent bacterial isolates
Serum: PRRSV positive by virus isolation
Tonsil and brain; PRV negative by fluorescent antibody
Brain and spinal cord: Enterovirus, positive
by virus isolation test
Additional History and Comments
Five years ago this farm suffered high morbidity and financial
losses due to enteroviral poliomyelitis in finishing-age pigs.
The offending enterovirus was isolated and serotyped as a
type 6. As many as 50% of pigs in finishing barns became
ataxic and developed posterior paralysis necessitating euthanasia
or premature sale. For this reason, and due to concurrent
problems with PRRS, the farm was depopulated for one month,
the pits were emptied, all buildings including pits were cleaned
and disinfected and the farm was repopulated.
In the Purdue Animal Disease Diagnostic Laboratory, we
typically diagnose 3-5 cases of polioencephalomyelitis due
to porcine enteroviruses per year. Most cases involve either
nursery- or finishing-age pigs. Usually, few animals are
affected and the disease is quickly self-limiting. However,
in the past 5 years, we have seen 2 outbreaks on unrelated
geographically distant farms that were very severe and that
continued despite various attempts to prevent the disease
through management changes. It is unclear whether these severe
outbreaks are due to unusually virulent viral strains, introduction
of new viral strains onto farms with immunologically naïve
pigs, changes in modern swine rearing practices that create
subpopulations of pigs that are more susceptible to endemic
enteroviruses or other factors.
Porcine Enteroviruses and Disease
Etiology: Family Picornaviridae, virions
are spherical, 25-31nm, nonenveloped, single stranded RNA
virus. They are stable when treated with lipid solvents and
heat. The virions are resistant to pH values from 2 to 9
and are resistant to various disinfectants. Only sodium hypochlorite
and 70% ethanol inactivate enteroviruses. The virus survives
in the environment for more than 168 days at 150C
and can also survive in liquid manure for long periods of
time. Manure aeration, ionizing radiation of liquid manure
and anaerobic digestion can inactivate the virus.
Epidemiology: Transmission of porcine enterovirus
is by the fecal-oral route and transmission by mechanical
vectors is likely. There are at least 11 serotypes of enteroviruses
in swine, based on virus neutralization tests. The degree
of cross-protection between serotypes is unknown. Teschen
disease, a severe encephalomyelitic disease, is caused by
highly virulent serotype 1 strains not found in North
America. Less virulent serotype 1 strains cause
a milder form of polioencephalomyelitis known as Talfan disease
or enzootic paresis. These Talfan strains, as well as strains
of all other serotypes, are found in North America.
Endemic infection with porcine enteroviruses is common. In
fact, nearly all swine herds are endemically infected with
multiple serotypes of porcine enterovirus. Infection is likely
maintained in susceptible weaned pigs following decay of maternal
antibody. Factors that cause periodic limited or less common
severe outbreaks of disease are poorly understood.
Clinical signs: Most infections with
porcine enteroviruses are asymptomatic; i.e., endemic infection
of most swine herds is completely without clinical disease.
The best characterized and most financially significant clinical
syndromes caused by porcine enteroviruses include nervouse
disease (polioencephalomyelitis) and reproductive failure
(SMEDI syndrome). Enteroviruses have also been suggested
as possible causes of mild diarrhea, pneumonia, pericarditis
Polioencephalomyelitis Teschen disease, caused
by highly virulent serotype 1 strains, is characterized by
high morbidity and mortality in all ages of pigs. Polioencephalomyelitis
manifests clinically first with fever, anorexia and ataxia
and later with opisthotonus, convulsions, nystagmus, paralysis,
coma and death within 3-4 days. Talfan disease is less severe
with lower morbidity and mortality and usually occurs in nursery-
or finishing-age pigs.
Reproductive failure The constellation of symptoms
associated with enteroviral reproductive failure is known
by the acronym SMEDI which stands for stillbirth,
mummified fetuses, embryonic death and infertility. Pregnant
females show no clinical symptoms and overt abortions are
not common so disease is manifested as an increase in not-in-pig
or NIP sows that once tested positive for pregnancy as well
as an increase in stillborn and mummified pigs in newborn
Diagnosis: Enteroviral disease is confirmed
by demonstrating appropriate clinical symptoms, gross lesions
(reproductive disease) or microscopic lesions (polioencephalomyelitis)
and the presence of enterovirus in fetuses (reproductive disease)
or central nervous tissue (polio -encephalomyelitis). Because
of the ubiquitous nature of porcine enteroviruses, demonstration
of virus in tissues other than nervous tissue in pigs with
nervous disease does not constitute a diagnosis. Virus isolation
is the method commonly employed to detect enteroviruses; however,
the test has only moderate sensitivity in nervous tissues
from pigs with nervous disease and very low sensitivity in
degenerate tissues from stillborn and mummified fetuses.
Recently, an nRt-PCR test was described, but the test is not
generally available. The veterinary diagnostic laboratory
has just recently developed an Rt-PCR test for porcine enteroviruses.
The sensitivity is not well characterized, but should exceed
that of virus isolation.
Prevention: Modified live and inactivated
vaccines are described in the literature and have been used
for Teschen disease in Europe; however,
there are no commercial vaccines available in the United
States. Vaccines would likely
be serotype-specific with little cross protection between
serotypes. Due to the large number of serotypes in the U.S.
and the infrequency of enteroviral disease in swine, development
of a commercial vaccine is unlikely. Other methods of prevention
or control of disease are not described.
-by Roberta Alvarez, DVM, Production
-edited by Greg Stevenson, DVM, PhD,
Derbyshire, JB. Enterovirus In: Straw B, DAllaire
S, Mengeling WL, Taylor DJ, eds. Diseases of Swine
8th ed. Ames, Iowa, Iowa State University Press;
Zell, R., Krumbholz, A., Henke, A, Birsch-Hirschfeld E. et
al. Detection of porcine enterovirus by nRt-PCR: differentiation
of CPE groups I-III with specific primer sets. Journal of
Virological Methods, 2000; 88:205-218.