2-week-old, male, pig (Sus scrofa).The young pig was submitted for necropsy with a history of sudden death.
The coronary bands of all four feet were pale and blanched, but there were no vesicles.Â A pale,
sloughed, necrotic area measuring 1.5 cm in length and 1 cm in width was present on the dorsum of the tongue.
There was severe hydropericardium, with 5-6 ml of yellowish fluid with fibrin clots present in the pericardial sac.
The heart was diffusely involved, with pale streaks separated by darker areas noted on the epicardium and cut
surfaces of the heart.Â Fibrin strands were found in the abdominal cavity.
Heart: Severe diffuse myocardial necrosis.Â Necrotic cardiomyocytes were intensely
eosinophilic, fragmented, had lost their cross striations and had pyknotic nuclei.Â Moderate numbers of macrophages
and smaller numbers of lymphocytes and neutrophils were present in the necrotic areas.Â Similar inflammatory cells
were present on the epicardial surface.
Heart: Myocardial necrosis, acute, severe with histiolymphocytic
infiltrates, pig (Sus scrofa).Â The lesion is consistent with Foot and Mouth Disease.
Aetiologic diagnosis: Aphthovirus myocarditis
(clinical pathology, microbiology, PCR, ELISA, etc.): Heart, nail, tongue and pericardial fluid
samples were positive for Foot and Mouth Disease, Virus type O, by antigen capture ELISA.(1,2) Results were from
the World Foot and Mouth Disease Reference Laboratory at Pirbright.
Heart, nail, tongue and pericardial fluid samples were positive for FMDV, type O, Southeast Asia (SEA) topotype, Mya-98 lineage, by nucleotide sequencing.(10) Results were from the World Foot and Mouth Disease Reference Laboratory at Pirbright.
Foot and mouth disease
Foot and mouth disease (FMD) affects cloven hoofed animals, with the most dramatic
clinical infections of domestic swine and cattle.(7) It is caused by seven serologically distinct types (A, O, C, Asia 1,
Southern African Territories [SAT] 1, 2, and 3) of Foot and Mouth Virus (FMDV) in the genus Aphthovirus, family
Picornaviridae.(1) Type O and Asia 1 viruses are the most widespread viruses and are endemic in Asia.9 The SAT
type viruses have never been reported in Asia.
FMDV is a single stranded RNA virus with a protein capsid consisting of four viral proteins enumerated as VP1, VP2, VP3 and VP4.(1) Subtype-specific neutralization epitopes have been identified among the four capsid proteins, primarily within VP1.(6,8) The serotype prevalent in Hong Kong SAR has been and continues to be serotype O.(4) However, the topotype has recently changed from Cathay to the South East Asia topotype with a subsequent increase in clinical signs and mortalities.Â The Southeast Asia (SEA) topotype, Mya-98 lineage, has been confirmed by the World Foot and Mouth Disease Reference Laboratory at Pirbright.Â Similar topotypes have been identified in the Republic of Korea and Japan recently.Â This recent spread of FMD in the Far East indicates the possibility of disease spread both within and outside the region, as happened during the FMD O PanAsia pandemic of 1999-2001.(4,10)
In swine, vesicles often form on the rostrum of the snout and around the nares.Â Foot lesions, when present, frequently extend along the coronary bands and dewclaws, and in severe cases can cause sloughing of the claw. Tongue lesions tend to coalesce and ooze a serous fluid when ruptured, leaving behind a visible raw and denuded stratum germinativum.(6)
Mortality is not commonly seen in FMD cases unless young pigs are affected.Â Young pigs up to 14 weeks of age, but particularly those less than 8 weeks of age, may die without developing any clinical signs of FMD due to heart failure, which is characterized by acute myocarditis that at times may be seen macroscopically as whisps of blanched areas on the epicardium that extend into the endocardium, a consequence of the damage caused by viral replication to the developing myocardium.(3,9,11)
Heart: Myocarditis and epicarditis, necrotizing, subacute, diffuse, severe, with lymphohistiocytic
and neutrophilic interstitial inflammation and perivasculitis.
Conference discussion focused on the differential diagnosis for myocarditis in the pig.
Encephalomyocarditis virus (EMCV), a Cardiovirus of the Picornaviridae family, was the favored etiology by most
participants.Â Histologic findings are similar to those found in this case with diffuse myocardial necrosis, and the
inflammatory infiltrate with EMCV is typically mononuclear.Â Other viruses associated with myocarditis in the pig
include porcine parvovirus and porcine circovirus 2 associated with postweaning multisystemic wasting syndrome.(7)
Vitamin E/selenium deficiency causes myocardial necrosis; however, inflammation is minimal.Â Additionally,
several parasitic etiologies can cause myocarditis, including Toxoplasma gondii, Sarcocystis spp., Taenia spp.,
Trypanosoma spp.Â and Trichinella spiralis.(12)
The exact cause of death in myocarditis is unknown.Â Death could be due to the effects of the offending agent (e.g. viral damage to myocytes), the ensuing inflammatory response, or both.Â Infiltrating cytotoxic T lymphocytes can produce direct myocyte necrosis.Â Activated histiocytes and lymphocytes produce a cytokine milieu resulting in myocyte metabolic disturbances, reduced contractility, and dysrhythmia.Â Death during the acute phase of myocarditis is often attributed to dysrhythmias.(7) Animals surviving the acute phase begin resolution in which macrophages arrive to remove the necrotic debris.Â Due to the continuous contraction of cardiac myocytes, their regenerative capabilities are limited; therefore, healing most often occurs through fibrosis.(5)
1.Â Davies G.Â Foot and mouth disease.Â Res Vet Sci.Â 2002;73:195-199.
2.Â Hoffmann B, Beer M, Reid S, et al.Â A review of RT-PCR technologies used in veterinary virology and disease control: Sensitive and specific diagnosis of five livestock diseases notifiable to the World Organization for Animal Health.Â Vet Microbiol.Â 2009;139:1-23.
3.Â Kitching RP, Alexandersen S.Â Clinical variation in foot and mouth disease.Â Rev sci tech Off int Epiz.Â 2002;21(3): 513-518.
4.Â Knowles NJ, Samuel AR, Davies PR, Midgley RJ, Valarcher J-F.Â Pandemic strain of Foot-and-Mouth Disease Virus Serotype O.Â Emerg Infect Dis. 2005;11(12):1887-1893.
5.Â Kumar V, Abbas AK, Fausto N, Aster JC.Â The gastrointestinal tract.Â In: Kumar V, Abbas AK, Fausto N, Aster JC, eds.Â Robbins and Cotran Pathologic Basis of Disease. 8th ed.Â Philadelphia, PA: Elsevier Saunders; 2009:85-86.
6.Â Lubroth J.Â Foot and mouth disease: A review for the practitioner.Â Vet Clin Food Anim.Â 2002;18:475-499.
7.Â Maxie MG, Robinson WF.Â Cardiovascular system.Â In: Maxie MG, ed.Â Jubb, Kennedy and Palmers Pathology of Domestic Animals. 5th ed., vol.Â 3.Â Philadelphia, PA: Elsevier Ltd; 2007:41-43.
8.Â Meyer RF, Knudsen RC.Â Foot and mouth disease: a review of the virus and the symptoms. J Envir Health. 2001;64(4):21-23.
9.Â Oeem JK, Yeh MT, McKenna TS, et al.Â Pathogenic characteristics of the Korean 2002 isolate of Foot and Mouth Disease Virus serotype O in pigs and cattle.Â J Comp Path. 2008;138:204-214.
10.Paton DJ, King DP, Knowles NJ, Hammond J.Â Recent spread of foot-and-mouth disease in the Far East.Â Vet Rec. 2010;166:569-570.
11.Ryan E, Horsington J, Durand S, et al.Â Foot and mouth disease virus infection in young lambs: pathogenesis and tissue tropism.Â Vet Microbiol.Â 2008;127:258-274.
12.Van Vleet JF, Ferrans VJ.Â Cardiovascular system.Â In: McGavin MD, Zachary JF, eds.Â Pathologic Basis of Veterinary Disease.Â 4th ed.Â St.Â Louis, MO: Elsevier; 2007:563-564, 591-593.