History
A dead 6-week-old black-and-white female piglet (Sus scofra domesticus) of unspecified breed was submitted to the Athens Diagnostic Laboratory for necropsy. The entire litter had a reported 2-week history of not doing well. The owner had treated the piglets with electrolyte solution and placed them in the shade, which resulted in transient improvement. One day after treatment, the piglet was found standing obtunded in the pasture. The animal was placed indoors, but subsequently developed seizures and died the following day. Piglets in the litter had no previous vaccinations, and the vaccination history, age, and previous reproductive history of the sow were unknown.
Gross Findings
At necropsy, the piglet was in good body condition (body condition score, 4/5). The integument was covered with numerous ectoparasites (lice and ticks). Copious white foam filled the trachea, and 20 mL of serosanguineous fluid was present within the thoracic cavity. All lung lobes were turgid and mottled dark red to tan with prominent interlobular septa and exuded moderate amounts of serosanguineous fluid on cut section, indicative of edema (Figure 1). The pericardial sac was mildly thickened and opaque and had multiple fibrinous adhesions along the epicardial surface. The left auricle and atrium were markedly dilated with multiple fibrous, corrugated and irregular, endocardial, plaque-like thickenings (jet lesions). Multiple yellow-red, proliferative, friable, cauliflower-like nodules covered most of the mitral valve leaflets and partially extended to the papillary muscle. Additionally, 60% of the capsular surface of the liver had white, firm, depressed foci that ranged from 0.6 to 1.0 cm in diameter. The small intestine, stomach, and esophagus contained numerous adult roundworms (consistent with Ascaris suum). Various tissue specimens were fixed in neutral-buffered 10% formalin, and fresh lesions from the mitral valve were submitted for bacterial culture.
Photographs of the thoracic and abdominal cavity (A) and heart (B) of a 6-week-old female piglet that died after a 2-week period of not doing well. A—Multifocally, depressed, white foci cover the hepatic capsule (arrows); the lungs did not deflate and all lung lobes are mottled tan and dark red (rectangle). Notice the diffuse expansion of interlobular septa with edema. B—Coalescing, irregular, yellow to red, proliferative nodules have effaced approximately 90% of the mitral valve leaflets (arrows). Also, fibrous endocardial thickening (jet lesions) in the left atrium (asterisks) is present.
Citation: Journal of the American Veterinary Medical Association 257, 9; 10.2460/javma.257.9.925
Photographs of the thoracic and abdominal cavity (A) and heart (B) of a 6-week-old female piglet that died after a 2-week period of not doing well. A—Multifocally, depressed, white foci cover the hepatic capsule (arrows); the lungs did not deflate and all lung lobes are mottled tan and dark red (rectangle). Notice the diffuse expansion of interlobular septa with edema. B—Coalescing, irregular, yellow to red, proliferative nodules have effaced approximately 90% of the mitral valve leaflets (arrows). Also, fibrous endocardial thickening (jet lesions) in the left atrium (asterisks) is present.
Citation: Journal of the American Veterinary Medical Association 257, 9; 10.2460/javma.257.9.925
Photographs of the thoracic and abdominal cavity (A) and heart (B) of a 6-week-old female piglet that died after a 2-week period of not doing well. A—Multifocally, depressed, white foci cover the hepatic capsule (arrows); the lungs did not deflate and all lung lobes are mottled tan and dark red (rectangle). Notice the diffuse expansion of interlobular septa with edema. B—Coalescing, irregular, yellow to red, proliferative nodules have effaced approximately 90% of the mitral valve leaflets (arrows). Also, fibrous endocardial thickening (jet lesions) in the left atrium (asterisks) is present.
Citation: Journal of the American Veterinary Medical Association 257, 9; 10.2460/javma.257.9.925
Formulate differential diagnoses from the history, clinical findings, and Figure 1—then turn the page→
Histopathologic Findings
Sections of mitral valve, heart, lungs, liver, spleen, kidneys, brain, and portions of the gastrointestinal tract were processed routinely for histologic examination. The mitral valve leaflets were markedly thickened and irregular with multifocal bulbous projections composed of mucinous degeneration, streaming fibroblasts, large numbers of macrophages, and scant neutrophils (Figure 2). The surface of the thickened valve contained myriad bacterial colonies composed of gram-positive rods that were embedded in foci of necrosis and fibrin (Figure 3). Multifocally, myocardial fibers were necrotic with loss of striations, sarcoplasmic hyalinization, and nuclear pyknosis. Additionally, small infiltrates of neutrophils, macrophages, and lymphocytes were present in the adjacent myocardium of the papillary muscle. Within the lungs, alveolar septa were diffusely thickened, the alveoli contained numerous foamy alveolar macrophages with scant amounts of hemosiderin and proteinaceous edema fluid, and there were multifocal areas of hemorrhage and fibrinous exudation. In the liver, diffuse, moderate centrilobular congestion with very mild attenuation of hepatic cords was present. No notable findings were observed in the examined sections of brain, spleen, kidneys, and portions of the gastrointestinal tract. Aerobic bacterial culture from sections of mitral valve and lungs yielded heavy and light growth of Erysipelothrix rhusiopathiae, respectively.
Photomicrograph of a section of mitral valve with vegetative lesions from the piglet in Figure 1. Notice the markedly thickened and irregular valve leaflet with multifocal bulbous projections and mucinous degeneration. H&E stain; bar = 2 mm. Inset—Higher-magnification view of the area outlined by the rectangle in the main image. Streaming fibroblasts with prominent nuclei are embedded in moderate amorphous amphophilic matrix. H&E stain; bar = 100 mm.
Citation: Journal of the American Veterinary Medical Association 257, 9; 10.2460/javma.257.9.925
Photomicrograph of a section of mitral valve with vegetative lesions from the piglet in Figure 1. Notice the markedly thickened and irregular valve leaflet with multifocal bulbous projections and mucinous degeneration. H&E stain; bar = 2 mm. Inset—Higher-magnification view of the area outlined by the rectangle in the main image. Streaming fibroblasts with prominent nuclei are embedded in moderate amorphous amphophilic matrix. H&E stain; bar = 100 mm.
Citation: Journal of the American Veterinary Medical Association 257, 9; 10.2460/javma.257.9.925
Photomicrograph of a section of mitral valve with vegetative lesions from the piglet in Figure 1. Notice the markedly thickened and irregular valve leaflet with multifocal bulbous projections and mucinous degeneration. H&E stain; bar = 2 mm. Inset—Higher-magnification view of the area outlined by the rectangle in the main image. Streaming fibroblasts with prominent nuclei are embedded in moderate amorphous amphophilic matrix. H&E stain; bar = 100 mm.
Citation: Journal of the American Veterinary Medical Association 257, 9; 10.2460/javma.257.9.925
Photomicrograph of a section of a vegetative lesion on the mitral valve. Notice the streaming fibroblasts, large numbers of macrophages, and scant numbers of neutrophils. H&E stain; bar = 200 mm. Inset—Multiple bacterial colonies composed of gram-positive rods are embedded in foci of necrosis and fibrin. Gram stain; bar = 20 mm.
Citation: Journal of the American Veterinary Medical Association 257, 9; 10.2460/javma.257.9.925
Photomicrograph of a section of a vegetative lesion on the mitral valve. Notice the streaming fibroblasts, large numbers of macrophages, and scant numbers of neutrophils. H&E stain; bar = 200 mm. Inset—Multiple bacterial colonies composed of gram-positive rods are embedded in foci of necrosis and fibrin. Gram stain; bar = 20 mm.
Citation: Journal of the American Veterinary Medical Association 257, 9; 10.2460/javma.257.9.925
Photomicrograph of a section of a vegetative lesion on the mitral valve. Notice the streaming fibroblasts, large numbers of macrophages, and scant numbers of neutrophils. H&E stain; bar = 200 mm. Inset—Multiple bacterial colonies composed of gram-positive rods are embedded in foci of necrosis and fibrin. Gram stain; bar = 20 mm.
Citation: Journal of the American Veterinary Medical Association 257, 9; 10.2460/javma.257.9.925
Morphologic Diagnosis and Case Summary
Morphologic diagnosis: severe, chronic, multifocal to coalescing, vegetative valvular endocarditis (mitral valve) with intralesional gram-positive bacterial rods consistent with E rhusiopathiae; moderate, chronic, multifocal pulmonary congestion and hemorrhage; and moderate, chronic, multifocal, hepatic capsular fibrosis with mild centrilobular congestion.
Case summary: vegetative valvular endocarditis attributable to E rhusiopathiae infection with valvular insufficiency, left atrial enlargement, and heart failure along with incidental hepatic capsular fibrosis associated with A suum larval migration in a piglet.
Comments
The piglet of the present report had vegetative, valvular endocarditis as a result of infection with E rhusiopathiae, which led to valvular insufficiency, left atrial enlargement, and heart failure. The pulmonary changes were associated with congestive heart failure. Additionally, the mild hepatic congestion indicated that there was progression to biventricular failure. The white, depressed foci on the capsular surface of the liver are commonly referred to as milk spots. These lesions are regions of fibrosis caused by migration of the larval forms of the nematode A suum from the intestines through the hepatic portal circulation.1
Erysipelothrix rhusiopathiae is a ubiquitous pathogen and a common cause of economic loss within the swine industry.2 The organism is suspected to be endemic in intensive swine production areas with up to 50% of pigs being colonized with E rhusiopathiae.3 Reports of erysipelas frequently involve growing and adult swine; however, infection can develop in turkeys, chickens, sheep, dogs, and various aquatic life.2–4 In humans who have high exposure to animals, E rhusiopathiae can cause an occupational disease, erysipeloid.2
Erysipelothrix rhusiopathiae is a facultative, non–spore-forming, pleomorphic, gram-positive bacillus.2 The organism is commonly spread in the feces and oronasal secretions of carrier swine, which can appear healthy. Erysipelothrix rhusiopathiae can remain in the soil for up to 35 days.2,4 Several bacterial virulence factors, including neuraminidase, hyaluronidase, and adherence surface proteins (RspA and RspB), are associated with the spread and entry of E rhusiopathiae into the host tissues.2,5 Affected valve leaflets become roughened and nodular as a result of fibrin deposition and bacteria colonization admixed with platelets and erythrocytes.6,7 Dissemination of vegetative bacterial emboli can cause sudden death in affected animals with no prior evidence of clinical signs.3
Clinical signs of erysipelas vary from characteristic skin lesions to sudden death, depending on the clinical form of disease. Acutely infected swine may have signs of depression and be febrile, anorexic, dehydrated, or reluctant to stand or move.3,6 Sudden death is often associated with severe, acute septicemia or occlusion of valvular orifices.7 Although not evident in the case described in the present report, a very common subacute to chronic form of erysipelas known as diamond skin disease is characterized by pink or purple, erythematous, diamond-shaped cutaneous infarcts covering the body, which develop secondary to vasculitis.2,6 Chronic forms of the disease are most commonly associated with vegetative valvular endocarditis, as seen in the piglet of the present report, as well as nonsuppurative arthritis, decreased growth rate, or large areas of necrotic, sloughed skin.2,3,6
Diagnosis of erysipelas is based on a combination of clinical signs, gross lesions, response to treatment, and isolation of the bacteria in culture of appropriate specimens. Characteristic rhomboid skin lesions with lameness or a rapid response to penicillin support a diagnosis of subacute to chronic erysipelas; however, a definitive diagnosis requires growth of E rhusiopathiae in aerobic bacterial culture or detection of E rhusiopathiae DNA in PCR assays.3,5,6
Treatment of erysipelas is best achieved by administration of appropriate antimicrobials. Erysipelothrix rhusiopathiae is very susceptible to penicillin, which is often the best and most economic treatment choice; other effective treatment options for affected pigs in the United States include administration of ampicillin and cephalosporin and tetracycline classes of antimicrobials.3 Vaccination is the most effective intervention to prevent erysipelas outbreaks. Attenuated live or killed vaccines are available and should be given to piglets near the time of weaning or within several weeks thereafter.3,6 New additions to a herd should be vaccinated prior to entering the facility and should receive a booster vaccination 3 to 5 weeks later.3 Annual or semiannual booster vaccination is recommended for all breeding stock.3,6 Sows that are considered at high risk of infection can be vaccinated at 2 to 3 weeks prior to farrowing to confer protective immunity to piglets for up to 10 weeks after weaning. Additionally, piglets that are considered at high risk of infection can be vaccinated at 6 weeks of age.3,6,8 On some farms on which E rhusiopathiae is endemic, lactating sows can provide passive immunity to nursing piglets through maternal antibodies in milk, which can help to suppress clinical disease.3 Other protective measures that can be implemented to prevent outbreaks of E rhusiopathiae infection include proper sanitation and hygiene on premises and elimination of infected animals or those with clinical signs of disease from herds. Additional measures include controlling other carriers such as birds and rodents, especially in farms’ feed storage areas.3,8
Although reports of E rhusiopathiae infection in the United States are not very common because of effective vaccination protocols, good sanitation, and proper quarantine protocols, the potential for infection should be considered where there are sudden deaths among swine that had few to no clinical signs. Erysipelas should be a top differential diagnosis for swine with vegetative valvular endocarditis; however, Streptococcus suis can also cause vegetative lesions and therefore should be ruled out as a possible causative agent.6–9 Sporadic cases of vegetative endocarditis attributable to infection with Trueperella pyogenes, Staphylococcus aureus, Escherichia coli, Pasteurella multocida, Listeria monocytogenes, or Actinobacillus equuli have also been reported.9 Although the method of transmission of E rhusiopathiae was not ascertained in the case described in the present report, it was quite likely that there were carrier pigs present on the farm and that this piglet (and presumably other piglets) became susceptible to infection during or shortly after weaning because of the loss of protective passive immunity and lack of vaccination.2,3
References
1. Brown DL, Van Wettere AJ, Cullen JM. Hepatobiliary system and exocrine pancreas. In: Zachary JF, McGavin MD, eds. Pathologic basis of veterinary disease. 6th ed. St Louis: Elsevier, 2017;445.
2. Wang Q, Chang BJ, Riley TV. Erysipelothrix rhusiopathiae. Vet Microbiol 2010;140:405–417.
3. Forde T. Erysipelothrix rhusiopathiae infection in animals. Available at: www.merckvetmanual.com/generalized-conditions/erysipelothrix-rhusiopathiae-infection/erysipelothrix-rhusiopathiae-infection-in-animals. Accessed Jun 13, 2020.
4. Shimoji Y. Pathogenicity of Erysipelothrix rhusiopathiae: virulence factors and protective immunity. Microbes Infect 2000;2:965–972.
5. Brooke CJ, Riley TV. Erysipelothrix rhusiopathiae: bacteriology, epidemiology and clinical manifestations of an occupational pathogen. J Med Microbiol 1999;48:789–799.
6. Opriessnig T, Wood RL. Erysipelas. In: Zimmerman JJ, Karriker LA, Ramirez A, et al, eds. Diseases of swine. 10th ed. Hoboken, NJ: Wiley-Blackwell, 2012;750–759.
7. Robinson WF, Robinson NA. Cardiovascular system. In: Grant Maxie M, ed. Jubb, Kennedy, and Palmer's pathology of domestic animals. Vol 3. 6th ed. St Louis: Elsevier, 2016;30–33.
8. National Animal Disease Information Service. Erysipelas. Available at: www.nadis.org.uk/disease-a-z/pigs/erysipelas/. Accessed Sep 22, 2018.
9. Jensen HE, Gyllensten J, Hofman C, et al. Histologic and bacteriologic findings in valvular endocarditis of slaughter-age pigs. J Vet Diagn Invest 2010;22:921–927.
