Signalment:  

9-day-old piglet, Sus scrofa domesticusThis piglet is from a unit with ongoing diarrhea problems.

Gross Description:  

The carcasses were thin and rough-haired. One of two pigs had milk in the stomach. The small intestines were thin-walled and fluid-filled. Spiral colons contained watery feces.

Histopathologic Description:

Jejunum and ileum have severe atrophic enteritis. There is villus fusion and epithelial attenuation.

Morphologic Diagnosis:  

Severe atrophic enteritis with villus fusion and epithelial attenuation. 

Lab Results:  

Porcine epidemic diarrhea virus, confirmed with PCR. Immunohistochemistry stains are positive also.

Condition:  

Porcine epidemic diarrhea virus

Contributor Comment:  

Porcine epidemic diarrhea virus (PEDV) was first identified in England in 1971 and was then confirmed in the United States in the spring of 2013.(2) As of the summer of 2014, the virus has spread to 30 states and has resulted in the loss of millions of pigs. The disease causes severe diarrhea and vomiting in all ages of pigs with mortality in suckling pigs of 90-95%. The original US isolates were nearly identical to Chinese isolates from 2012. It is not known how PEDV arrived in the US. PEDV is a member of the genus Alphacoronavirus together with transmissible gastroenteritis virus (TGEV). 

The pathology of PEDV has been described in gnotobiotic pigs.(3) The lesions were similar to those observed in conventional pigs infected with PEDV.

JPC Diagnosis:  

Small intestine: Enteritis, necrotizing, with villous blunting and fusion, and crypt hyperplasia. 

Conference Comment:  

For an industry that excels in implementing biosecurity practices, the rapid spread of porcine epidemic diarrhea virus proves a major source of concern for our ability to control infectious diseases. In April 2013, hog confinement facilities with closed-herd strategies and shower-in, shower-out facilities broke out with explosive diarrhea and vomiting in suckling pigs. This led to a mortality rate approaching a staggering 95% within 3 days of the onset of clinical signs. Multiple facilities separated by hundreds of miles began to experience the same symptoms and a diarrhea epidemic ensued. Within months, the majority of states in the continental U.S. were reporting cases of PEDV.(2)

PEDV is an Alphacoronavirus that contains an enveloped, single-stranded positive-sense RNA genome.(2) It was first discovered in the UK in 1971 and continued to cause sporadic outbreaks in Europe and Asia for decades.(2) Though it is similar in structure and pathogenesis as TGE, its genome is more closely related to bat Alphacoronaviruses.(8) The virus targets intestinal epithelial cells of nursing pigs; however, infection of alveolar macrophages has also been demonstrated.(7) Typical microscopic findings include severe atrophic enteritis throughout the small intestine and viral shedding can precede and continue beyond the observation of clinical signs.(5) In this case, slides from multiple blocks were submitted and among them, the lesions varied from mild blunting and fusion of villi with moderate crypt hyperplasia to severe necrosis. There are also sections with mild loss of lymphocytes in Peyer's patches. Syncytial cell formation was evident throughout the more severely affected lesions. 

There has been much attention on the possible mechanisms of virus transmission. Transportation equipment and contaminated feedstuffs are the most often cited culprits, as this may explain the sporadic, simultaneous outbreaks in facilities separated by hundreds of miles.(3) Transmission between animals is largely fecal-oral, but airborne transmission is also suspected.(1)

PEDV contains a transmembrane envelope glycoprotein virulence factor called spike, which is responsible for binding and fusion to host epithelial cells and macrophages. Spike contains two domains, S1 and S2, and the S1 domain is the primary target of vaccines due to its specific high-affinity binding to cell receptors.(6) The first licensed vaccine for PEDV was released in the U.S. in 2014, and now there are several on the market. Incidence rate has been dropping recently and, while the disease has killed over seven million pigs in just the last year, it appears the peak of this devastating epidemic has already passed.

References:

1. Alonso C, Goede DP, Morrison RB, et al. Evidence of infectivity of airborne porcine epidemic diarrhea virus and detection of airborne viral RNA at long distances from infected herds. Vet Res. 2014;45:73.

2. Stevenson GW, et al. Emergence of porcine epidemic diarrhea virus in the United States: clinical signs, lesions, and viral genomic sequences. J of Vet Diagn Invest. 2013;25(5):649654. 

3. Jung K, et al. Pathology of US porcine epidemic diarrhea virus strain PC21A in gnotobiotic pigs. Emerg Infect Dis. 2014;20(4):662-665.

4. Lowe J, Gauger P Harmon K, et al. Role of transportation in spread of porcine epidemic diarrhea virus infection, United States. Emerg Infect Dis. 2014;20(5):872-874.

5. Madson DM, Magstadt DR, Arruda PH, et al. Pathogenesis of porcine epidemic diarrhea virus isolate (US/Iowa/18984/2013) in 3-week-old weaned pigs. Vet Microbiol. 2014 Sep 22. pii: S0378-1135(14)00425-8. [Epub ahead of print]

6. Oh J, Lee KW, Choi HW, Lee C. Immunogenicity and protective efficacy of recombinant S1 domain of the porcine epidemic diarrhea virus spike protein. Arch Virol. 2014;159(11):2977-2987.

7. Park JE, Shin HJ. Porcine epidemic diarrhea virus infects and replicates in porcine alveolar macrophages. Virus Res. 2014;191:143-152.

8. Vlasova AN, Marthaler D, Wang Q, et al. Distinct characteristics and complex evolution of PEDV strains, North America, May 2013-February 2014. Emerg Infect Dis. 2014;20(10):1620-1628.

Click the slide to view.

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4-1. Jejunum

4-2. Jejunum

4-3. Jejunum

4-4. 

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