AFIP Wednesday Slide Conference - No. 5
30 September 1998

Conference Moderator:
Dr. Terrance Wilson, Diplomate, ACVP
USDA Emergency Programs
Unit 41
4700 River Road
Riverdale, MD 20737-1231

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Case I - 96/1255 (AFIP 2550628);

one 2x2 histology color photo transparency
Case 5-1. Immunohistochemical stain for BVD virus structural & non-structural proteins
Note positive staining of blood vessel tunica media.
Signalment: A six-month-old, Brown Swiss calf was presented to the clinic with signs of respiratory distress.
History: Two calves from the same farm died a few days previously. Upon admission, the calf was in poor body condition, had a rectal temperature of 39.8°C, a heart rate of 60 beats per minute, and a respiratory rate of 60 breaths per minute. The animal coughed spontaneously. The clinicians detected loud respiratory signs in the ventral lung fields. The muzzle was dry, and the eyes were sunken. The calf was treated with NaCl-glucose, Clamoxylä, Flumilarä, and Ventipulminä. The calf's condition deteriorated over a five day period and was euthanized.
Gross Pathology: The calf was thin. There were multiple clumps of doughy, yellow, exudate in the tracheal lumen, and the tracheal mucosa was reddened. The cranial lung lobes were consolidated. On cut surface, a yellow-green, creamy mass was seen in the bronchi and bronchioli. The ventral portions of all left lung lobes were consolidated. All lung-associated lymph nodes were enlarged and edematous. The heart and other organs showed no macroscopic changes.
Laboratory Results:
Cytology Tracheobronchial wash:
Macrophages: +
Neutrophils: +++
Bacteria: ++
Cell detritus: +++
Bacteriology Tracheobronchial wash:
++/+++ Pasteurella haemolytica Biovar A
+ Leukocytes (microscopically)
Radiography: A peribronchial interstitial pattern could be seen in the dorsal areas of the lungs, and a bronchopneumonia was detected in the ventral areas of the lungs.
Parasitology: Eimeria, Trichostrongyles, and Strongylids were detected.
1. Hct: 20% (normal: 24-35%)
2. Hgb: 7.2 g/dl (normal: 8.3-11.7 g/dl)
3. Leukocytes: 2700/ml (normal: 4240-9090/ml)
4. Lymphocytes: 1782/ml (normal: 2192-5117/ml)
5. Fibrinogen: 16g/l (normal: 2-9 g/l)
Histology: The following organs were histologically examined: Lung; pulmonary lymph node; heart; liver; spleen; kidney; intestine; and brain.
Immunohistochemistry: Immunohistochemistry was performed on snap-frozen sections of skin, thyroid gland, tongue and abomasum collected at necropsy. Immunohistochemistry of the heart was performed on paraffin-embedded tissue. Four monoclonal antibodies against BVD-virus structural and non-structural proteins were applied using the LSAB-method. All organs examined were positively labeled. A positive control from a reference calf was run with each batch of monoclonal antibodies. A negative control with PBS (pH 8) was made with each slide.

Monoclonal Antibodies


 C42  15c5
 Skin  +  ++  +  ++
 Thyroid  + + + +
 Tongue  + + + +
 Abomasum  + + + +
 Heart  + nd ++ ++

(nd= not done)
Contributor's Diagnosis and Comments: Heart: Moderate subacute perivasculitis and vasculitis. Mild multifocal subacute myocarditis. Lung: Severe chronic bronchointerstitial pneumonia with bronchiectasia and bronchiolitis obliterans (not submitted).
The heart is submitted for Wednesday Slide Conference. The perivascular region and the vessel walls are infiltrated with mononuclear inflammatory cells. The endothelial cells are activated, and in some regions there is a hyaline degeneration of the vessel wall. This vasculitis was seen in the brain, intestine (vessels of the submucosa), and the heart.
The vasculitis is linked to a BVD-virus infection. It is known that infection with this pestivirus can induce perivasculitis and vasculitis with mononuclear inflammatory cells. These lesions can be found in the intestine, the brain, the heart, the adrenal cortices and other organs. Sometimes hyaline degeneration and fibrinoid necrosis of the vessel walls in the submucosa of the intestine and other organs can also be seen. Therefore, it is difficult to differentiate vasculitis due to BVD-virus from that seen in malignant catarrhal fever.
BVD-virus can induce immunotolerance, persistent infection, or mucosal disease. The course of the disease depends on the time of infection (prenatal or postnatal) and the viral strains involved. Due to BVD virus-induced immunosuppression, the calf became susceptible to respiratory infection.
Case 5-1. Immunohistochemical stain for BVD virus structural & non-structural proteins
Note positive staining of blood vessel tunica media.
20x obj.
Case 5-1. Heart: Note moderate influx of lymphocytes, few histiocytes, and rare neutrophils within and around the vessel wall.

AFIP Diagnosis: Heart, myocardium: Vasculitis and perivasculitis, lymphohistiocytic and plasmacytic, multifocal, moderate, with vascular fibrinoid necrosis, mild interstitial edema, and myocardial necrosis, Brown Swiss, bovine.
Conference Note: Sarcocysts are infrequently present in some sections. Multifocal myocardial degeneration is also present in some of the examined sections.
Most conference participants agreed that fibrinoid necrosis of vessels with perivascular distribution of inflammatory cells in the myocardium is an unusual feature of BVD-virus (BVDV) infection. Vasculitis has been frequently reported in arterioles of the mesentery and intestinal submucosa. It has also been reported in other organs, including the heart. A differential diagnosis for bovine viral myocarditis discussed by conference participants included malignant catarrhal fever (MCF) and rinderpest.
Bovine viral diarrhea virus is a pestivirus which occurs as cytopathogenic (cp) and noncytopathogenic (noncp) biotypes based on their effects on tissue culture cells. The cytopathogenic virus causes diarrhea in cattle exposed postnatally between six months and two years of age. Clinically, the virus usually causes a mild, acute, transient diarrhea with high morbidity. In some cases, new strains of cpBVDV have caused outbreaks with high mortality rates.
Mucosal disease occurs in cattle that become infected in utero with noncpBVDV. These animals develop a persistent infection with the subsequent development of immunotolerance. Mucosal disease, which is almost invariably fatal, generally develops in animals between six months and two years of age and occurs when the noncpBVDV is transformed to cpBVDV through RNA recombination. Superinfection of cpBVDV may cause mucosal disease in persistently infected animals if the cytopathogenic strain antigenically matches the noncytopathogenic strain. Antigenically different cpBVDV strains will not cause mucosal disease.
Pestiviruses are enveloped, RNA viruses that measure 40 to 70nm in diameter. The pestivirus genus in the family Flaviviridae also includes the viruses which cause hog cholera in swine and border disease in sheep. Swine may be infected with BVDV, but the virus does not cause clinical disease with the exception of pregnant sows in which fetal death and resorption may occur.
While the character and distribution of histologic lesions may suggest a specific etiology, ancillary diagnostic tests and procedures are often required to accurately diagnosis the various bovine viral gastrointestinal and vesicular diseases. Virus isolation requires labor intensive methods, prolonged periods of time, and may fail to detect infection in a significant number of animals. Recently developed immunohistochemical methods and polymerase chain reaction tests provide practical, rapid means to accurately confirm BVDV infection in animals.
Rinderpest, a morbillivirus of the family Paramyxoviridae, causes necrosis of intestinal glands and Peyer's patches reminiscent of the gastrointestinal lesions of BVD. Rinderpest may also cause a necrotizing vasculitis; however, syncytial cells with eosinophilic intracytoplasmic inclusions are often seen histologically in cattle infected with rinderpest, and when present, distinguish it from BVD and MCF. Intranuclear inclusions may also occur within the syncytial cells of rinderpest lesions.
MCF, caused by a lymphotrophic gammaherpesvirus, causes a marked perivascular and intramural infiltration of predominately large lymphocytes with large nuclei and prominent nucleoli. There is often an associated fibrinoid necrotizing vasculitis. The characteristic inflammatory infiltrates and vascular changes occur in almost all organs. Unlike rinderpest and BVD, the underlying lymphoproliferative nature of MCF often causes a prominent lymphocytic hyperplasia in multiple lymph nodes and prominent lymphoid follicles in the splenic white pulp. The vascular lesions are more consistently present and more severe in MCF than in BVD.
Contributor: Institute of Veterinary Pathology, University of Zurich, Winterthurerstr. 268, Zurich Switzerland 8057.
1. Kent TH, Moon HW: The comparative pathogenesis of some enteric diseases. Vet Path 10:414-469, 1973.
2. Jubb KVF, Kennedy PC, Palmer N: The alimentary system. In: Pathology of Domestic Animals, 4th ed., vol. 2, pp. 149-158, Academic Press Inc., 1993.
3. Baszler TV, Evermann J, Kaylor PS, Byington TC, Dilbeck PM: Diagnosis of naturally occurring bovine viral diarrhea virus infection in ruminants using monoclonal antibody-based immunohistochemistry. Vet Pathol 32: 609-628, 1995.
4. Thur B, Zlinsky K, Ehrensperger F: Immunohistochemical detection of bovine viral diarrhea virus in skin biopsies: A reliable and fast diagnostic tool. J Vet Med B43:163-166, 1996.
5. Jones TC, Hunt RD, King NW: Diseases caused by viruses. In: Veterinary Pathology, 6th ed. Williams and Wilkins. pp. 299-302, 1997.

Case II - 96/558/4 (AFIP 2641092)

Signalment: An adult horse.
History: A horse was inoculated orally with 50,000 TCID50 equine morbillivirus/Hendra virus (EMV/HeV). Seven days post inoculation, it developed tachycardia, anorexia, lethargy, and increased respiratory rate. The horse deteriorated over the next 24 hours and was euthanized.
Gross Pathology: At necropsy there was marked pulmonary edema with marked dilatation of lymphatics over the pleural surface of the lung. All lymph nodes were congested. There were no other gross post mortem lesions.
Laboratory Results: Virus was isolated from the lung, kidney, spleen, and urine. Lung, kidney, and many other tissues were positive by indirect immunoperoxidase test using a rabbit polyclonal serum to inactivated EMV/HeV.
Contributor's Diagnosis and Comments:
1. Lungs: Edema, subacute (severe interlobular) and vasculopathy with endothelial syncytia.
2. Kidneys: Vasculopathy with endothelial syncytia.
The presence of syncytial endothelial cells in small and medium-sized vessels in many organs is a diagnostic feature of this disease, and in some lung sections in this case, is associated with mural necrosis and lymphoid cell infiltration. Laboratory methods demonstrated that viral antigen was confined to vascular tissue and was readily identified in the tunica intima of arteries and veins. The tunica media had positive immunostaining in a smaller number of blood vessels. Positive immunostaining has been observed in syncytial endothelial cells which are characteristic of this infection.

In September 1994 in Hendra, a suburb of Brisbane, Australia, infection with a previously undescribed member of the Paramyxoviridae family resulted in the deaths of 13 horses and one human (the adult male horse trainer) from an acute respiratory disease. The virus was provisionally designated as equine morbillivirus, but subsequent studies [3,4]; indicated the virus cannot be easily classified in any of the existing genera in the family Paramyxoviridae. Consequently, the virus has been renamed Hendra virus (HeV) [3,4,5].
In October 1995, a farmer developed fatal encephalitis as a result of HeV infection which was attributed to exposure to two HeV infected horses that had died more than one year earlier [7]. Extensive serological surveys throughout Queensland have found no further evidence of HeV infection in horses or humans [8,9]. However, fruit bats (flying foxes, Pteropus sp.) were found to have a high prevalence of serological reactors to HeV indicating they may be a wildlife reservoir of the virus [10]. Serological evidence of HeV infection has not been found in any animal species other than fruit bats. In experimental studies, guinea pigs and cats have been found to be susceptible to HeV infection [11,12]. The lesions of HeV infection in horses have been described by Hooper et al [13].
10x obj
Case 5- 2. Lung. The pleura and interlobular septa are markedly expanded by clear space (edema) and scattered lymphocytes an plasma cells. A pleural arteriole has fibrinoid degeneration and necrosis of its walls with infiltrating and adjacent lymphocytes and plasma cells.
20x obj.40x obj
Case 5- 2. Lung. Attached to the wall of this pulmonary artery there are 3 endothelial syncytial cells. A 40x objective view illustrates an eosinophilic intracytoplasmic inclusion body separating the several of the nuclei of this cell.
20x obj
Case 5- 2. Kidney. Note the syncytial endothelial cell expanding the wall of a small arteriole adjacent to the glomerulus.

AFIP Diagnosis:
1. Lung: Vasculopathy, characterized by endothelial syncytia, mural necrosis, fibrinoid change, subacute perivasculitis, and moderate interstitial edema, breed unspecified, equine.
2. Kidney, interstitial and glomerular blood vessels: Vasculopathy, characterized by endothelial syncytia, mural necrosis, and fibrinoid change.
Conference Note: In some sections of lung and kidney, rare eosinophilic intracytoplasmic inclusions are present within endothelial syncytia. Mild degenerative changes of glomeruli and tubular dilatation were also noted by some conference participants.
The two recent outbreaks of a previously unrecognized equine and human viral disease in Australia have sparked an intense research effort to determine the pathogenesis, species susceptibility, and reservoir of the virus. The disease in naturally infected horses is characterized by an acute onset of respiratory distress, anorexia, fever, depression, ataxia, and high mortality. As indicated by the contributor, this is a zoonotic disease. The virus has caused illness in three humans with two fatalities. Because of the uncertain classification of this newly recognized virus, it will be referred to in this text as equine morbillivirus/Hendra virus (EMV/HeV).
Experimentally, EMV/HeV causes lethal disease in horses, cats, and guinea pigs, while dogs, mice, rats, chickens and rabbits are refractory to infection. The lesion leading to death in experimentally infected horses and cats is interstitial pneumonia with pulmonary edema and accumulation of alveolar macrophages which develops subsequent to virus-induced vascular changes. Intramural edema, fibrinoid necrosis, endothelial syncytia, and perivascular mononuclear cell inflammatory infiltrates characterize the vascular changes. In horses, parenchymal lesions secondary to the vascular changes more commonly occur in the kidney and brain, while in cats, histologic changes in the gastrointestinal tract are more frequently observed. (The authors of the initial experimental investigation of EMV/HeV speculate that the variations in the distribution of lesions may be due to limited sampling of the equine gut. The urgency to establish the cause of the disease preempted an in-depth systematic study of the virus in horses).
The most significant gross lesion observed in experimentally infected horses is pulmonary edema with subpleural lymphangiectasis. The abundant frothy discharge present in the upper respiratory tract in naturally infected horses did not occur in experimentally infected horses; this may be due to environmental factors, various treatments applied to field cases, and increased time of lesion development in natural infections. In experimentally infected cats, hydrothorax and pulmonary edema are the prominent gross lesions with varying amounts of congestion and pulmonary hemorrhage.
In guinea pigs the fundamental histopathologic finding is fibrinoid degeneration/necrosis of small blood vessels surrounded by a mononuclear inflammatory cell infiltrate, similar to horses and cats. Additionally, the presence of endothelial syncytia is common to all three of the susceptible species. Unlike horses and cats, however, immunohistochemistry demonstrates that the virus preferentially affects the larger vessels in guinea pigs rather than the smaller vessels. This finding may explain the lack of severe pulmonary edema in infected guinea pigs, the fatal lesion of cats and horses. EMV/HeV does cause widespread vascular disease in guinea pigs and is responsible for lesions in a variety of organs. Cyanosis is observed grossly in infected guinea pigs and is thought to be caused by myocardial insufficiency, failure of the intercostal musculature, and/or failure of the lungs, rather than pulmonary edema.
Morbilliviruses are relatively large (150-250 nm), enveloped, and contain single-stranded RNA. Examples of other morbilliviral diseases include canine distemper, peste des petits ruminants, phocine distemper, dolphin morbilliviral disease, and measles. While interstitial pneumonia with syncytial cells is commonly seen in morbilliviral infections, EMV/HeV is unique in that it demonstrates a greater affinity for vascular tissues than the other morbilliviruses. The other morbilliviruses, such as measles and canine distemper, may infect endothelium but do not cause the vascular lesions observed in EMV/HeV. This vascular tropism occurs in both intravenously inoculated horses and subcutaneously inoculated cats and guinea pigs, suggesting that this affinity for blood vessels is real rather than a function of the route of inoculation.
Histologically, the vascular degeneration of EMV/HeV infection resembles the changes observed in equine viral arteritis. Grossly, African horse sickness causes pulmonary edema very similar to that of EMV/HeV and should be considered in the differential diagnosis.
While investigators of the experimental equine cases noted a histological absence of intracytoplasmic and intranuclear inclusions within syncytia, a few conference participants identified rare eosinophilic intracytoplasmic inclusions within endothelial syncytia, especially within the renal vasculature. This histologic finding is consistent with other morbilliviral infections.
Contributor: Australian Animal Health Laboratory, Ryrie Street, Geelong, Victoria, Australia 3219.
1. Murray PK, Selleck PW, Hooper PT et al.: A morbillivirus that caused fatal disease in horses and humans. Science 268:94-96, 1995.
2. Selvey LA, Wells RM, McCormack JG et al.: Infections of humans and horses by a newly described morbillivirus. Med J Aust 162:642-645, 1995.
3. Wang LF, Michalski W, Yy M, Pritchard LI, Crameri G, Shiell B, Eaton BT: Novel P/V/C gene in a new Paramyxoviridae virus which causes lethal infection in humans, horses and other animals. J Virol 72:1482-1490, 1998.
4. Yu M, Hannsson E, Shiell B, Michalski W, Eaton BT, Wang LF: Sequence analysis of the Hendra virus nucleoprotein gene: Comparison with other members of the subfamily Paramyxovirinae. J Gen Virol (in press).
5. Murray PK, Eaton B, Hooper P, et al.: Flying foxes, horses and humans: A zoonosis caused by a new member of the Paramyxoviridae. In: Emerging Infections 1, pp. 43-58, ASM Press, Washington D.C., 1998.
6. O'Sullivan JD, Allworth AM, Paterson DL et al.: Fatal encephalitis due to novel paramyxovirus transmitted from horses. Lancet 349:93-95, 1997.
7. Hooper PT, Gould AR, Russell GM, Kattenbelt JA, Mitchell G: The retrospective diagnosis of a second outbreak of equine morbillivirus infection. Aust Vet J 74: 244-245, 1996.
8. Selvey L, Taylor R, Arklay A, Gerrard J: Screening of bat carriers for antibodies to equine morbillivirus. Comm Dis Intell 20:477-478, 1996.
9. Ward MP, Black PF, Childs AJ, et al.: Negative findings from serological studies of equine morbillivirus in the Queensland horse population. Aust Vet J 74:241-243, 1996.
10. Young PL, Halpin K, Selleck P et al.: Serological evidence for the presence in pteropus bats of a paramyxovirus related to equine morbillivirus. Emerg Infect Dis 2:239-240, 1996.
11. Westbury HA, Hooper PT, Selleck PW, Murray PK: Equine morbillivirus pneumonia: Susceptibility of laboratory animals to the virus. Aust Vet J 72:278-279, 1995.
12. Hooper PT, Ketterer PJ, Hyatt AD, Russell GM: Lesions of experimental equine morbillivirus pneumonia in horses. Vet Pathol 34:312-322, 1997.
13. Hooper PT, Westbury HA, Russell GM: The lesions of experimental equine morbillivirus disease in cats and guinea pigs. Vet Pathol 34323-329, 1997.

Case III - 96-9621 (AFIP 2639838)

Signalment: A seven-week-old, crossbred pig.
History: This pig, from a multisource nursery facility of about 700 animals, spontaneously developed an unusual dermatitis. Two other pigs in this group developed similar lesions.
Gross Pathology: Round to irregular, red to purple macules and papules, often coalescing to form large irregular patches and plaques, were present on the perineal area of the hindquarters, limbs, ears, and ventral abdomen. There was subcutaneous edema of the dependent sites.
Laboratory Results: Bacterial cultures were negative. Porcine respiratory and reproductive syndrome virus (PRRSV) was detected in tissue homogenate samples by PCR and virus isolation. Fluorescent antibody test was positive for porcine IgM and C3 within dermal blood vessels.
Contributor's Diagnosis and Comments: Cutaneous vasculitis, necrotizing and neutrophilic, with leucocytoclasia, thrombosis, dermal hemorrhages and focal coagulative epidermal necrosis.
Haired skin from the perineal area and from an ear are submitted. A severe necrotizing vasculitis affecting small-caliber vessels is characterized by infiltration of the vascular wall by neutrophils, leucocytoclasia, fibrin exudation, and thromboses with reactive-hypertrophied endothelial cells. In some sections these changes are best observed in the deeper dermis and panniculus. Other cutaneous changes include severe dermal hemorrhages, perivascular infiltration of mononuclear cells and eosinophils, and coagulative necrosis of the epidermis. Lesions found in other organs included bronchointerstitial pneumonia, generalized reactive lymphadenopathy, and perivascular cuffing of mononuclear cells in various tissues including skin.
The cutaneous lesions in this case are part of a porcine systemic vascular disease first recognized in the United Kingdom [1,2], and subsequently in several countries including Canada [3,4] and the United States [5]. Because of the frequent involvement of the skin and kidneys among organs affected with the vascular lesions, the disease was originally called porcine dermatitis/nephropathy syndrome [1]. The disease affects mainly grower pigs and has a low prevalence in swine herds. The prognosis of the condition in affected pigs is dependent on the extent and the severity of the vascular lesions found in internal organs, particularly within the kidneys in which a severe exudative and necrotizing glomerulonephritis may develop. The gross appearance and the distribution of the cutaneous lesions in this animal are characteristic of the disease in its acute stage.
This vascular disease mainly involves small-caliber blood vessels and appears to be immune-mediated [4,6]. The cause of the condition is still undetermined, but it has been suggested that PRRSV infection may play a role in the pathogenesis of this systemic vascular disease of swine [4,7].
20x obj.
Case 5-3. Dermis. There is a brisk infiltrate of neutrophils and eosinophils around, infiltrating, and effacing the necrotic walls of two parallel arterioles.
AFIP Diagnosis: Haired skin: Vasculitis and perivasculitis, necrotizing, neutrophilic and eosinophilic, acute, with multifocally extensive dermal and subcutaneous hemorrhage, multifocal epidermal necrosis, and mild epidermal hyperplasia, cross-bred pig, porcine.
Conference Note: Porcine reproductive and respiratory syndrome (PRRS) is a disease of pigs caused by an arterivirus that commonly manifests as reproductive failure in sows, pneumonia in young swine, and increased preweaning mortality. Additionally, immunohistochemical studies suggest an association between PRRS virus and a recently recognized systemic vasculitis primarily affecting the skin and kidneys in young growing pigs, initially termed dermatitis/nephropathy syndrome. In pigs with skin and kidney lesions typical of the disease, viral antigen has been detected in macrophages surrounding affected vessels. Through the use of reverse transcription-polymerase chain reaction, PRRS viral RNA has been detected in the lung and spleen of these animals.
In addition to the gross lesions in the skin, the kidneys may occasionally be swollen, pale, and contain numerous cortical petechial hemorrhages, the result of an underlying necrotizing vasculitis which occurs in the small and medium-sized vessels. Pneumonia with generalized lymphadenopathy is usually observed as well. The distribution of the cutaneous lesions described by the contributor is typical for this entity. The acute cutaneous lesions are hemorrhages due to necrotizing vasculitis, while chronic lesions are brown crusts that cover ulcerated or excoriated areas of skin.
This systemic vascular disease of swine shares several similarities with some of the human cutaneous vasculitides; leukocytoclastic vasculitis in people occurs as hemorrhagic coalescing papules and plaques often on dependent sites of the body such as the legs and arms. Cutaneous necrotizing vasculitis often accompanies systemic disease. While the skin may be the only organ affected, other internal organs including the kidneys, central nervous system, gastrointestinal tract, and joints, are often involved. This is true in both pigs and humans. Systemic vasculitis may occur from direct injury to vessels by infectious agents or by immune-mediated mechanisms; most cutaneous vasculitides are thought to be immune-mediated. Immune-mediated vascular damage may occur through one of several mechanisms including formation or deposition of immune complexes in vessels followed by cell-mediated or cytotoxic antibody attack of vessels.

Several etiologies should be considered for erythema or skin discoloration in pigs. Erysipelothrix rhusiopathiae, or swine erysipelas, causes characteristic rhomboid or "diamond skin" lesions acutely in pigs; the causative agent is a small, pleomorphic, gram-positive bacterial rod that is sensitive to penicillin. Bacterial septicemia caused by a variety of agents (Streptococcus suis, Actinobacillus suis, A. pleuropneumoniae) may cause transitory reddish discoloration of the skin. Additionally, salmonellosis, Hemophilus parasuis, A. suis, and swine erysipelas may cause cyanosis and congestion of the extremities with petechiation and congestion in several organs. Porcine stress syndrome, associated with handling or similar stresses in genetically predisposed animals, may cause generalized blotchy blue or red discoloration of the skin; usually there is also associated skeletal or myocardial necrosis.
Contributor: Department of Pathology and Microbiology, Faculty of Veterinary Medicine, University of Montreal, C.P. 5000 St-Hyacinthe, P.Q. Canada J2S 7C6.
1. Smith WJ, Thomson JR, Done S: Dermatitis/nephropathy syndrome of pigs. Vet Rec 132:47, 1993.
2. White M, Higgins RJ: Dermatitis/nephropathy syndrome of pigs. Vet Rec 132:199, 1993.
3. Hélie P, Drolet R, Germain M-C, Bourgault A: Systemic necrotizing vasculitis and glomerulonephritis in grower pigs in southwestern Quebec. Can Vet J 36:50-154, 1995.
4. Thibault S, Drolet R, Germain M-C, D'Allaire S, et al.: Cutaneous and systemic necrotizing vasculitis in swine. Vet Pathol 35:108-116, 1998.
5. Duran CO, Ramos-Varas JA, Render JA: Porcine dermatitis and nephropathy syndrome : A new condition to include in the differential diagnosis list for skin discoloration in swine. Swine Health Prod 5:241-245, 1997.
6. Sierra MA, de las Mulas JM, Molenbeek RF, van Maanen C et al.: Porcine immune complex glomerulonephritis dermatitis (PIGD) syndrome. Europ J Vet Pathol 3:63-70, 1997.
7. Segales J, Piella J, Marco E, Mateu-de-Antonio EM, et al.: Porcine dermatitis and nephropathy syndrome in Spain. Vet Rec 142:483-486, 1998.

Case IV - A44522 (AFIP 2638306)

Case 5-4. Gross. Overlying the muscle fascia there are two yellowish-tan serpentine parasites with a bulbous end and a slender body.
Signalment: Tissues from adult feral hogs, Sus scrofa.
History: The submitted tissues are from Florida feral hogs that were trapped by local hunters in the Lake Okeechobee and Placid area. After being transported to a Texas slaughter establishment, they were slaughtered under United States Department of Agriculture (USDA) inspection for human consumption. In April, 1998, while performing routine postmortem inspection of these animals, the USDA veterinarian identified 1-3 cm, white to tan-yellow lesions on the surfaces of the thoracic, thigh, and triceps musculature. Some of the lesions and associated muscle were collected and fixed in 10% neutral buffered formalin for histologic examination.
Gross Pathology: Distributed on the surfaces of muscles (abdominal, shoulder, thigh), and sometimes within the musculature itself, were 1-3 cm, white to tan-yellow nodules. The nodules were composed of a thin outer layer of connective tissue and fat. Upon incision, the nodules contained a coiled, flat, slender, white parasite, approximately 1 mm wide and up to 25 cm long. The anterior end had a bulbous enlargement (2X3 mm) with a central dimple or groove on the anterior aspect.
Laboratory Results: None.
Contributor's Diagnosis and Comments: Mild, multifocal lymphoplasmacytic eosinophilic fasciitis with intralesional cestode larvae, consistent with a pseudophyllidean plerocercoid.
Histologically, there is a cystic space in the epimysial connective tissue and fat. The space is surrounded by mild multifocal infiltrates of eosinophils, lymphocytes, plasma cells, and macrophages. The space contains single to multiple, closely bundled longitudinal sections of a parasite. The parasite has irregular folds of pseudosegmentation that is formed by a thick eosinophilic integument with inconspicuous microvilli. There is an intervening layer of subintegumentary cells that blend into a loose mesenchymal stroma that contains calcareous corpuscles, longitudinal strips of smooth muscle, and thin-walled excretory ducts.
Sparganosis is an infection of tissues by the plerocercoid stage of certain pseudophyllidean tapeworms. The plerocercoid was originally called Sparganum, before the relationship to the adult parasite was known. Adult stages of the parasite are typically found in the intestine of domestic, feral, or wild canids and felids, and eggs, rather than segments, are usually passed in the feces. Water is required for maturation and development of the ciliated coracidia from the egg, which is then followed by ingestion of the coracidium by a copepod crustacean where it develops into a procercoid. Due to this close relationship to a water environment, common hosts for the final intermediate plerocercoid stage include snakes and frogs. However, spargana may develop in the tissues of essentially all vertebrates with the exception of fish, by either ingestion of the procercoid or plerocercoid stage.
The importance of this infection lies in the serial transmission of the plerocercoid in paratenic hosts, which may include food animals and man. Spargana do not have distinct morphologic features, and therefore they must be fed to a definitive host before taxonomic separation into Spirometra and Diphyllobothrium species may be attempted. Sparganosis, caused by Spirometra erinacei, is a well-defined entity among local populations of feral hogs in Australia, where expanded inspection procedures have been adopted when the parasite is detected among animals slaughtered for human consumption. The parasites are typically found in the connective tissues under the peritoneum of the abdominal cavity, under the flare fat, between abdominal muscles, under the skin of the inner aspect of the hind legs, between the muscles of the hind legs, and under the peritoneal lining of the abdominal organs and mesentery. In contrast, report of infection of feral pigs in the United States is rare.
Grossly, the parasite may be mistaken for a small nerve or blood vessel, and it may be easily overlooked unless the individual is familiar with the disease and morphology of the parasite. Consumption of undercooked or raw meat and the use of fresh tissues as a poultice from an infected intermediate host have resulted in human infections.
2x obj.
Case 5-4. Muscle. Within the loose fibroadipose tissue adjacent to skeletal muscle, there are multiple profiles of an immature tapeworm (pleurocercoid), composed of loose mesenchyme bearing abundant oval shaped calcified bodies (calcarious corpuscles).
AFIP Diagnosis: Skeletal muscle and fibroadipose tissue: Plerocercoid (sparganum), with multifocal chronic-active and eosinophilic myositis and steatitis, feral hog (Sus scrofa), porcine.
Conference Note: As noted by the contributor, sparganosis may be acquired by humans through the ingestion of undercooked pork, in which the plerocercoid larvae remain alive, and through the application of infected fresh animal tissue poultices, as is practiced in some cultures. Frogs are most commonly used in this practice. The sparganum invades the human tissue where the poultice is applied, most often the eye. Additionally, humans may contract the disease through drinking water contaminated with infected copepods.
A rare form of human sparganosis has been described in which the infective plerocercoids proliferate and invade every tissue except bone. Only nine human cases of this proliferating sparganosis have been reported in which extensive invasion of the larvae into lymphatics produces pronounced edema and an elephantiasis-like syndrome. No confirmed animal cases of this atypical form of infection have been reported. The underlying cause of this variant of sparganosis is unknown but is believed to be aberrant forms of spirometrids. In general, sparganosis is a relatively benign human and animal disease; it may be more prevalent than reported due to this benign nature.
Contributor: United States Department of Agriculture, Food Safety and Inspection Service, Office of Public Health and Safety, P.O. Box 6085, Athens, GA 30604.
1. Daly JJ: Sparganosis. In: CRC Handbook Series on Zoonoses. Section C, Vol. 1, pp. 293-312, CRC Press, Boca Raton, FL, 1982.
2. Dunn AM: Veterinary Helminthology, 2nd ed., pp. 129-291, YearBook Medical Publishers, Inc., Chicago, IL, 1978.
3. Mueller JF: The biology of Spirometra. J Parasitol 60:3-13, 1974.
4. Appleton PL, Norton JH: Sparganosis: A parasitic problem in feral pigs. Queensland Ag J 102:339-343, 1976.
5. Smith HM, Davidson WR, Nettles VF, Gerrish RR: Parasitisms among wild swine in southeastern United States. J Am Vet Med Assoc 181:1281-1284, 1982.
International Veterinary Pathology Slide Bank:
Laser disc frame #3629
Ed Stevens, DVM
Captain, United States Army
Registry of Veterinary Pathology*
Department of Veterinary Pathology
Armed Forces Institute of Pathology
(202)782-2615; DSN: 662-2615
* The American Veterinary Medical Association and the American College of Veterinary Pathologists are co-sponsors of the Registry of Veterinary Pathology. The C.L. Davis Foundation also provides substantial support for the Registry.

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