Case Study:

Enteroviral Polioencephalomyelitis in Finishing-age Pigs 

History

  On a 300 sow, farrow-to-finish pork production facility in Indiana, 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 Pig

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 lateral recumbency.

Less Common Causes of CNS Disease in Finishing-age Pigs

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  implications.

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.

On-Farm Examination

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  culturette^TM–type 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.

- Brain

- 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 necropsy.

- 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   SLTII_variant, STX toxin and shigatoxin E.

- Tonsil

-  Spleen

-  Lung

-  Serum

Results of Laboratory Testing

Histopathology:

  Brainstem: nonsuppurative encephalitis,  multifocal, moderate  Spinal cord: nonsuppurative poliomyelitis,   multifocal, severe  Lung: interstitial pneumonia, histiocytic,  multifocal, moderate

Bacteriology:   

  No significant or consistent bacterial  isolates 

Virology

   Serum: PRRSV positive by virus isolation

   Tonsil and brain; PRV negative by  fluorescent antibody test

   Brain and spinal cord: Enterovirus,   positive by virus isolation test

Final Diagnosis

            PRRS  Entoviralpolioencephalomyelitis

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 and myocarditis.

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 litters.

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 at IowaStateUniversity has just recently developed an Rt-PCR test for porcine enteroviruses.  The sensitivity is not well characterized, but should exceed that of virus isolation.

Treatment: None

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

 Medicine  Resident

-edited by Greg Stevenson, DVM, PhD,

  ADDL Pathologist

References

Derbyshire, JB. Enterovirus In: Straw B,  D’Allaire S, Mengeling WL, Taylor DJ, eds. Diseases of Swine 8^th ed. Ames, Iowa, Iowa State University Press; 1999:145-150

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.