History
A 6-week-old female mixed-breed piglet with a history of respiratory tract disease died unexpectedly after a short period of dyspnea and was submitted for necropsy. The piglet was part of a small group of piglets raised for research purposes and was the only one that developed clinical signs.
Photograph of the abdominal and thoracic cavities (A) and heart (B) of a piglet that died with dyspnea of short duration. Pale yellow strands of fibrin cover the hepatic capsular surface, intestinal serosa, and pulmonary pleural surface. The pericardial sac is distended as a result of fluid and fibrin accumulation. In panel B, the pericardial and epicardial surfaces are thickened by accumulations of fibrin admixed with blood.
Citation: Journal of the American Veterinary Medical Association 249, 6; 10.2460/javma.249.6.603
Necropsy Findings
Given the piglet's sudden death, no antemortem physical examination was performed. On necropsy, the carcass was in good body condition. Approximately 50 mL of turbid yellow fluid with numerous free-floating strands of fibrin was located within the abdominal cavity. The hepatic and splenic capsular surfaces as well as the gastric and intestinal serosal surfaces were covered by thick, pale yellow strands of fibrin (Figure 1). Moderate amounts of fibrin were also covering the visceral pleura. The lungs were diffusely atelectatic, dark red, heavy, and firm. The trachea, bronchi, and lower airways contained moderate amounts of pink foam. The pericardial sac was markedly distended by approximately 30 mL of redtinged fluid, and the cardiac epicardial surface was diffusely covered by thick layers of fibrin admixed with blood. Bronchial, mediastinal, and mesenteric lymph nodes were swollen and mottled red to tan. No other gross changes were observed. Samples of lung tissue and abdominal fluid were submitted for aerobic bacterial culture.
Formulate differential diagnoses from the history, clinical findings, and Figure 1—then turn the page→
Histopathologic and Microbiological Findings
Tissue samples from the stomach, intestines, liver, spleen, kidneys, heart, lungs, lymph nodes, and brain were examined histologically. Histologic examination of liver, spleen, and kidney tissues revealed scattered neutrophils admixed with fibrin and edema fluid expanding the hepatic, splenic, and renal capsular surfaces. A similar inflammatory infiltrate was observed expanding the gastric and intestinal serosal surfaces and adjacent mesentery. Mesothelial cells in all affected abdominal organs (stomach, intestines, liver, spleen, and kidneys) were reactive, with plump cytoplasm and prominent nuclei. The pericardial sac was diffusely expanded by dense layers of fibrin, hemorrhage, and cell debris admixed with large numbers of neutrophils and macrophages and fewer lymphocytes and plasma cells (Figure 2). Additionally, plump fibroblasts and newly formed capillaries with areas of hemorrhage overlaid the inflammatory infiltrate. Scattered neutrophils and fibrovascular tissue extended into the underlying superficial myocardium. In the lung tissue, alveolar septa were diffusely expanded by moderate numbers of macrophages and fewer neutrophils admixed with fibrin, edema fluid, and areas of hemorrhage. Bronchial and bronchiolar lumina occasionally contained small amounts of mucus and neutrophils. Interlobular septa and pleura were variably expanded by scattered macrophages and neutrophils with fewer lymphocytes and plasma cells admixed with edema fluid and hemorrhage. Lymphoid follicles of the bronchial and mesenteric lymph nodes were often poorly distinct, and the lymphatic tissue throughout the cortex and medulla was multifocally replaced by abundant suppurative inflammation. Sections of heart, lung, and brain were stained with Gram special stain and did not reveal any intralesional bacteria. Aerobic bacterial culture of lung tissue yielded heavy growth of Streptococcus suis and light growth of Trueperella pyogenes. Streptococcus suis serotyping identified the organisms as either type 1 or type 2. There was no bacterial growth from the abdominal fluid sample.
Photomicrograph of a section from the heart of the piglet in Figure 1. Notice that the epicardial surface is diffusely expanded by an outer layer of fibrin admixed with neutrophils, cell debris, and hemorrhage (asterisk) underlined by an inner layer of edematous fibrovascular tissue and scattered inflammatory cells (thick arrow). Inflammation multifocally extends into the underlying myocardium (thin arrow). H&E stain; bar = 1 mm.
Citation: Journal of the American Veterinary Medical Association 249, 6; 10.2460/javma.249.6.603
Morphologic Diagnosis and Case Summary
Morphologic diagnosis: diffuse, fibrinous, and fibrosing polyserositis (abdominal and thoracic cavity) with suppurative lymphadenitis (bronchial and mesenteric lymph nodes) and diffuse interstitial pneumonia.
Case summary: fibrinous polyserositis caused by S suis in a piglet.
Comments
In the case described in the present report, gross and histologic findings were consistent with porcine polyserositis1–6 and the etiologic diagnosis was confirmed by results of aerobic bacterial culture of samples of fresh lung tissue. Bacterial etiologic agents associated with porcine polyserositis include S suis type 2, Haemophilus parasuis (Glasser disease), Mycoplasma hyorhinis, and Escherichia coli.4,5 The light growth of T pyogenes from the lung tissue in this case was attributed to the chronicity of the disseminated S suis infection.
Streptococcus suis are gram-positive cocci that can normally inhabit the respiratory, intestinal, and genital tracts of healthy pigs.2,3,5 Strains of S suis are serotyped according to their polysaccharide capsular antigens.2,3 Currently there are 35 identified serotypes of S suis, but because clinical disease in pigs in the United States has been mainly associated with S suis type 2 infection,2,3,5 this serotype will be the focus of discussion. Streptococcus suis infection is not exclusive to pigs and the organism has been isolated from multiple species including ruminants, horses, deer, cats, dogs, and humans with clinical signs of pneumonia, meningitis, arthritis, and endocarditis.1,3,5 Human cases have nearly exclusively involved individuals who live and work in close contact with pigs.3–5 Transmission of S suis type 2 among pigs occurs primarily via aerosol through the respiratory system, but infection can also be acquired via fomites because the bacteria can be relatively long lasting in the environment when protected in organic material such as feces or carcasses.5 Infection is typically spread to naïve animals via contact with healthy carrier pigs. Weanlings and grower pigs are particularly susceptible to infection, and pigs between 5 and 10 weeks of age are mostly affected.5
In pigs, the initial clinical sign associated with S suis type 2 infection is typically an increase in body temperature that corresponds with the initial bacteremia. Other clinical signs include anorexia, signs of depression, and shifting lameness.5 Clinical signs may be absent in animals with acute infection, and affected pigs may die suddenly. Meningitis may be a feature of S suis type 2 infection in some pigs.5 Therefore, neurologic signs such as incoordination and abnormal stance progressing to inability to stand, paddling, convulsions, and nystagmus may develop.5 Streptococcus suis infection can also cause septicemic disease or be associated with other clinical syndromes, such as polyarthritis, pneumonia, and, less commonly, endocarditis, rhinitis, vaginitis, and abortion.3,5
At necropsy, pigs with acute infection may lack detectable gross lesions.3,4 However, when lesions are present, they usually reflect their septicemic nature. Similar to what was observed in the piglet of the present report, S suis infection–associated pathological changes include fibrin exudation on the surface of multiple organs and lymphadenomegaly.3,4 Other conditions that may develop include pneumonia, cardiac valvular endocarditis, necrotizing myocarditis, and fibrinous arthritis.3 Histopathologic findings are typically characterized by disseminated fibrinous and suppurative inflammation and fibrinous bronchopneumonia.3,5 Interstitial pneumonia can develop secondary to septicemia,5 as it did in the piglet of the present report. Although gross and histologic findings are often strongly suggestive of a diagnosis of porcine polyserositis, isolation of S suis from affected organs is a definitive finding.5 Similar to the results in the case described in the present report, detection of S suis in the lungs is often accompanied by isolation of other microbial agents such as Pasteurella multocida, Actinobacillus pleuropneumoniae, and T pyogenes.5
Treatment of porcine polyserositis is based on administration of antimicrobials, and penicillin has been reported as very effective.3,5 Prevention of clinical disease should primarily focus on husbandry issues, such as reducing overcrowding, improving ventilation, avoiding excessive temperature fluctuations, and housing pigs in similarly aged cohorts.3,5 Prevention of possible concurrent diseases may also decrease the likelihood of development of S suis infection.3,5,6 Commercial vaccines against S suis are available, but with regard to disease prevention, vaccination results are inconsistent.3
References
1. Gottschalk M, Higgins R, Jacques M, et al. Description of 14 new capsular types of Streptococcus suis. J Clin Microbiol 1989;27:2633–2636.
2. Huh HJ, Park KJ, Jang JH, et al. Streptococcus suis meningitis with bilateral sensorineural hearing loss. Korean J Lab Med 2011;31:205–211.
3. Staats JJ, Feder I, Okwumabua O, et al. Streptococcus suis: past and present. Vet Res Commun 1997;21:381–407.
4. St. John VS, Wilcock B, Kierstead M. Streptococcus suis type 2 infection in swine in Ontario: a review of clinical and pathological presentations. Can Vet J 1982;23:95–97.
5. Straw BE, Zimmerman JJ, D'Allaire S, et al. Chapter 14: streptococcal diseases. In: Diseases of swine. 9th ed. Ames, Iowa: Blackwell, 2006; 769–777.
6. Thanawongnuwech R, Brown GB, Halbur PG, et al. Pathogenesis of porcine reproductive and respiratory syndrome virus-induced increase in susceptibility to Streptococcus suis infection. Vet Pathol 2000;37:143–152.
