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CASE I – 00N 392 (AFIP 2741081)
Signalment: 5-year-old, female, Angus-cross cow, bovine
History: Chronic weight loss and poor-doer with diarrhea for two months. Four other herd mates have died with similar clinical signs. Two hundred head were purchased the first week of January 2000. They were vaccinated with IBR-BVD-PI3-BRSV, Lepto 5-way, Clostridium 7-way, and dewormed. This cow was dewormed again one month prior to death.
Gross Pathology: Angus-cross bovine in poor nutrition. The mucosa throughout the small intestinal tract is severely thickened with prominent corrugated mucosal folds. The mesenteric lymph nodes are markedly enlarged and firm.
Laboratory Results: None requested.
Contributor’s Diagnoses and Comment: 1. Intestine, enteritis, granulomatous, diffuse, severe.
2. Mesenteric lymph nodes, lymphadenitis, granulomatous, diffuse, severe (mesenteric lymph node is not included on microslides).
The gross and microscopic changes are diagnostic of Mycobacterium paratuberculosis infection.
AFIP Diagnosis: Small intestine: Enteritis, granulomatous, diffuse, severe, with myriad intrahistiocytic bacilli, Angus-cross cow, bovine.
Conference Comment: The pathogenesis of Mycobacterium avium paratuberculosis infection (Johne’s disease) is best understood in cattle, although the disease also occurs in sheep, goats, pigs, and equidae, and has been implicated in some cases of Crohn’s disease in humans. The classic intestinal change of thick small intestinal mucosa folded into transverse rugae is caused by granulomatous mucosal and submucosal inflammation, edema and villus atrophy. Malabsorption and filtration secretion of electrolytes, fluids and plasma proteins overwhelm the resorption capacity of the colon.
Hypoproteinemia and emaciation progressively develop with profuse diarrhea, despite a retained appetite. In advanced cases, aortic subintimal fibrosis and mineralization may be present. Ileocecal lymphadenopathy and lymphangitis of serosal and mesenteric lymphatic vessels may be the only recognizable gross lesions. There is no correlation between the severity of clinical disease and microscopic lesions. Animals that appear relatively healthy can have severe histologic lesions, while animals that have died from Johne’s disease can have gross and histologic changes that are difficult to detect.
Culture of M. paratuberculosis can take 2-4 months and requires mycobactin as a source of iron.
Contributor: Louisiana State University, School of Veterinary Medicine, Department of Veterinary Pathology, Baton Rouge, LA 70803
Reference: Barker IK, van Dreumel AA, Palmer N: The alimentary system. In: Pathology of Domestic Animals, ed. Jubb KVF, Kennedy PC, Palmer N, 4th ed., vol. 2, pp. 247-252. Academic Press Inc., San Diego, CA, 1993
CASE II – S99-1994 (AFIP 2743652)
Signalment: 12-week-old, male-castrated, Landrace, domestic pig
History: Four out of ten pigs had diarrhea. The next day they showed symptoms like tonoclonic convulsions, seizures and head trembling. Then they became cyanotic and dyspneic. The treatment with penicillin and colistine was unsuccessful. Death occurred shortly after appearance of clinical signs.
They were fed with hotel meal waste plus supplement. They did not have free access to water.
Two pigs were presented for necropsy.
Gross Pathology: No significant changes were identified at necropsy. The stomach was moderately filled with yellow to brownish fluid. The content of small and large intestine was normal. The subcutis was dry.
Laboratory Results: Instestinal bacterial cultures were positive for hemolyzing Escherichia coli of serotype 0:101 (Moon 431).
Contributor’s Diagnoses and Comment: 1. Brain, cerebrum: Cerebrocortical necrosis, laminar, subacute, severe with dystrophic mineralization.
2. Meningoencephalitis, non-suppurative and eosinophilic, multifocal, subacute, moderate to severe, perivascular.
Etiology: Subacute salt poisoning.
The pathologic alterations were limited to the brain and are typical for subacute salt poisoning. There is a marked edema of the cerebral cortex with laminar degeneration and necrosis of neurons. There is moderate to severe inflammation in the meninges and perivascularly in the cerebrum with variable numbers of macrophages, lymphocytes, plasma cells and eosinophils. The presence of eosinophils was confirmed by special stain (Lendrum).
Salt poisoning, water deprivation, or sodium ion toxicosis is very common in swine and poultry. It is caused by the ingestion of large quantities of sodium chloride combined with an inadequate water supply, as in this case, or by a totally lacking water supply, e.g., by blockage of water pipes or freezing of troughs. The likelihood of salt poisoning is increased with too much dietary salt as is found in meal waste. The pathogenesis remains unclear as to how and why sodium induces a meningocerebral eosinophilia. Elevated CNS salt level presumably incites cerebral edema.
The clinical signs of salt poisoning include loss of appetite, thirst, salivation, diarrhea and neurological disorders such as characteristic tonoclonic convulsions with opisthotonus. Affected animals wander aimlessly, appear to be blind and deaf, become comatose and recumbent with paddling of the limbs. Animals with clinical signs have a poor prognosis with most dying within a few days. As in this case, some pigs that appear to be unaffected may succumb later to a subacute polioencephalomalacia. If pigs live several days, the eosinophils may disappear to be replaced by mononuclear cells.
The postmortem macroscopic lesions are not specific; there may be mild to moderate cerebral edema, as well as a mild gastritis, gastric ulcers or enteritis. The contents of the large intestine may be abnormally dry and adherent to the mucosa.
The isolation of hemolyzing E. coli serotype 0:101 is only of importance in suckling piglets in the first two weeks, thus this animal was only a carrier.
AFIP Diagnosis: Brain, cerebral cortex: Necrosis, laminar, with edema, lymphoplasmacytic and eosinophilic encephalitis, and mineralization, Landrace, porcine.
Conference Comment: The pathophysiology of excessive dietary sodium intake without access to adequate free water is well documented in pigs. With developing hypernatremia, brain cells have a compensatory mechanism of rapidly accumulating electrolytes (sodium, potassium and chloride) to prevent the movement of intracellular fluid into the hyperosmolar cerebrospinal fluid and plasma. This mechanism prevents intracellular water from following concentration gradients that would cause cellular dehydration and, consequently, brain shrinkage. Such a situation could lead to disruption of cerebral blood supply in the calvarium and cerebral infarction, inhibition of energy pathways, or cerebral edema.
When pigs are allowed access to water again, they often overindulge and sodium concentration in extracellular fluid is lowered rapidly through dilution effect. Intracellular osmolarity is now greater and water moves into neurons along a concentration gradient. Cerebral edema and the clinical signs of salt toxicity, or water deprivation syndrome, are then manifested. In known cases of water deprivation, access to water or the replacement with intravenous fluids should be gradual. Despite these measures, the prognosis is generally poor.
Contributor: University of Zurich, Institute of Veterinary Pathology, Winterthurerstrasse 268, CH-8057 Zurich, Switzerland
References: 1. Angelos SM, Van Metre DC: Treatment of sodium balance disorders: water intoxication and salt toxicity. Vet Clin North Am: Food Anim Pract 15(3):587-607, 1999
2. Clarke EGC, Clarke ML: Mineral or inorganic substances. In: Veterinary Toxicology, 1st ed., pp. 50-52. The Williams & Wilkins Co., Baltimore, MD, 1975
3. Marks SL, Carr J: Water deprivation in weaned pigs. Vet Rec 125(18):460, 1989
4. Straw BE, D’Allaire S, Mengeling WL, Taylor DJ. Diseases of Swine, 8th ed., pp. 747, 792, 870, Iowa State University Press, Ames, IA, 1999
5. Summers BA, Cummings JF, de Lahunta A: Degenerative diseases of the central nervous system. In: Veterinary Neuropathology, 1st ed., pp. 254-255. Mosby-Year Book, New York, NY, 1995
CASE III – 00R27 II (AFIP 2739558)
Signalment: 5-week-old, mixed breed, porcine, (Sus scrofa domestica).
History: This tissue is from one of 42 pigs experimentally inoculated with Shiga toxin 2e-producing Escherichia coli strain (serotype O139, producing F18ab fimbriae and heat stable enterotoxin B). Pigs were orally challenged 1 day after weaning at age of 2 weeks. This pig remained free of clinical signs indicative of edema disease (edema and neurologic impairment such as head tilt, circling, incoordination, ataxia, and recumbency) or any other disease for the length of experiment. It was euthanized with barbiturates 3 weeks after the challenge. At necropsy, sections of ileum (1 m proximal from ileocecal junction) and brain stem (medulla) were collected in 10% neutral buffered formalin.
Gross Pathology: No gross lesions noted.
Laboratory Results: Stx2e was detected in Vero cell assay of fecal samples collected during the 2-week period after inoculation (titers peaked at 32,000 – 65,000).
Contributor’s Diagnosis and Comment: Ileum: Vasculitis, necrotizing, multifocal, subacute, moderate to severe with fibrinoid, perivascular edema and perivasculitis, mixed breed, porcine.
Etiology: Shiga toxin 2e-producing E. coli (STEC)
Disease: Edema disease
In the ileum, numerous arterioles within submucosa and, to a lesser extent, deep layers of lamina propria are necrotic, with thickened walls (edema) that contain mixed inflammatory infiltrates composed of moderate numbers of neutrophils and lesser numbers of macrophages and lymphocytes. Arteriolar lesions are more severe, and more vessels are affected, in the submucosa away from Peyer’s patches. The inner layers of arteriolar tunica media are effaced by hypereosinophilic segmental or circumferential bands (fibrinoid necrosis). There are few to multiple foci of karyorrhectic and pyknotic nuclear debris in the wall of numerous arterioles. Neutrophils (often degenerate), macrophages and lymphocytes are present in aggregates around the areas of fibrinoid necrosis and individually throughout vascular walls. Around some vessels there is marked proliferation of mesenchymal cells (pericytes and fibroblasts). The submucosa is multifocally thickened and pale (edema) and contains moderate numbers of eosinophils, lymphocytes, and plasma cells. Submucosal lymphatics are moderately distended.
Histologic sections of medulla (brain stem) were also evaluated. Numerous arterioles were necrotic. In contrast to the fibrinoid necrosis seen in the ileum, the arteriolar lesions in brain stem were limited to individual foci of necrotic myocytes with hypereosinophilic cytoplasm and karyorrhectic and pyknotic nuclear debris.
Edema disease is caused by host adapted E. coli strains that possess F18 fimbriae and produce Shiga toxin 2e. The susceptibility to disease is determined by the presence of F18 receptors; the development of which coincides with weaning (change of diet and microflora and decrease of maternal immunity). Susceptibility to edema disease is linked to a genetic locus that encodes enzyme fucosyltransferase. Resistance to edema disease is a recessive trait.
Stx2e is the main virulence factor. Intravenous injection of purified Stx2e in pigs reproduces clinical signs and lesions of edema disease. Toxin binds to the crypt enterocytes, is absorbed into blood, and binds to susceptible vasculature in various organs. Receptors for Stx2e are glycolipids (Gb4, globotetraosyl-ceramide) expressed in organs commonly affected by Stx2e. Tissue damage tends to correlate with the blood flow for a particular organ. In in vitro tissue sections, Stx2e binds to both endothelium and media of arterioles. In naturally and experimentally infected pigs, microscopic lesions of edema disease are characterized predominantly by segmental necrosis that is limited to individual myocytes within tunica media. Lesions are most commonly found in brain stem, submucosa of gastrointestinal tract and mesocolon.
Mortality due to edema disease in experimental settings varies markedly between 10 to 50%. Those pigs that develop clinical disease tend to attain higher Stx2e titers in their intestine. In individual pigs, however, fecal Stx2e titers are not predictive for disease outcome. Microscopic lesions can be detected in infected pigs regardless of the clinical status. Microscopic lesions tend to be more severe in those pigs that remain asymptomatic for the duration of the experiment (2-3 weeks after inoculation) or in pigs with chronic edema disease in field conditions. In chronically infected pigs, often there is fibrinoid degeneration in addition to segmental necrosis within tunica media. Proliferative mesenchymal elements are also seen in the tunica media and tunica adventitia in more advanced (chronic) cases. Reduced weight gain is associated with asymptomatic STEC infection in pigs 2-3 weeks after weaning but this weight loss is compensated in the grow-finish period.
Shiga toxin 1 (Stx1) and Shiga toxin 2 (Stx2) are toxins homologous to Stx2e. They are produced by pathogenic E. coli strains that cause hemorrhagic colitis and hemolytic uremic syndrome in humans. Stx2e is about 50% and 89% homologous to Stx1 and Stx2, respectively, based on their amino acid sequence. All Shiga toxins are A-B type toxins composed of a single, enzymatically active A unit and a pentameric, receptor-binding B unit composed of 5 homologous subunits. After binding to a sensitive cell, A unit is transported to the rough endoplasmic reticulum where it binds ribosome, cleaving off a specific adenine residue and, thus, inhibiting protein synthesis.
Tissues were contributed by the Iowa State University Veterinary Medical Research Institute and Department of Veterinary Pathology.
AFIP Diagnosis: Small intestine: Vasculitis, necrotizing, fibrinoid, multifocal, moderate, with transmural edema, mixed-breed pig (Sus scrofa domestica), porcine.
Conference Comment: Edema disease must be differentiated from porcine herpesvirus-1 (pseudorabies), Salmonella meningoencephalitis, Streptococcus suis, Haemophilus parasuis (Glässer’s disease), and water deprivation/salt toxicosis.
Contributor: Iowa State University, College of Veterinary Medicine, Department of Veterinary Pathology, Ames, IA 50011
References: , 1996
CASE IV – 00-15328-1 (AFIP 2739179)
Signalment: Adult (age not specified), female, White Rock chicken.
History: A Salmonella pullorum reactor bird was submitted by the Illinois Department of Agriculture for confirmation of disease. The hen was clinically normal. The hen had been recently purchased and placed into a new flock.
Gross Pathology: The abdominal contents were loosely matted together by fibrin admixed with yolk material. The ovarian cluster contained follicles of varying sizes, shapes, and colors ranging from small, firm and grayish-black to essentially normal. Several of the follicles were misshapen and few were atrophic. The follicles were often attached to the ovarian cluster by long, pedunculated fibrous stalks. Small numbers of follicles were tightly adhered to the surrounding abdominal wall, liver, and loops of intestine. Scant amounts of faintly yellow exudate were present in the oviduct.
Laboratory Results: Salmonella pullorum was recovered from the reproductive pool (ovary and oviduct) and organ pool (apex of heart, lung, liver, kidney, and spleen). Salmonella was not recovered from the cecum. The National Veterinary Services Laboratory (NVSL) confirmed the identity of this isolate.
Contributor’s Diagnosis and Comment: Severe, chronic, multifocal to coalescing pyogranulomatous oophoritis with intralesional bacteria (Salmonella pullorum), minimal fibrosis, and egg-yolk peritonitis.
Pullorum disease (PD) is caused by Salmonella pullorum. PD was originally described in 1899 and termed “fatal septicemia of young chicks”. Prior to 1929, PD was also known as bacillary white diarrhea, a rather descriptive term used to denote clinical signs often observed in infected chicks. Although chickens and turkeys are the most significant species affected, many other bird species may be infected, to include quail, ducks, peafowl, pheasants, and guinea fowl.
In poultry flocks, PD is primarily a disease of chicks and poults resulting from transovarian (vertical) transmission. In young birds, clinical signs may vary from incubator deaths to weakness, inappetence, and pasting of the vent with white fecal matter. Often PD does not manifest until chicks and poults are 5-10 days of age with peak mortality around 14-21 days of age. The clinical signs are generally nonspecific and may include lethargy, weakness, underdevelopment, poor feathering, and droopy wings. Gross lesions in young birds reflect a peracute to acute bacterial sepsis and consist of visceral congestion, creamy to caseous yolk material, white nodules in the lungs, fibrinous pericardial exudate, caseous cores in the ceca, and swollen joints. Exudate may also be present in the anterior chamber of the eye.
In adult birds, lesions are frequently minimal and include a few misshapen, discolored and pedunculated ova interspersed with unremarkable ova or the presence of exudate within the oviduct. Pericarditis is often observed in more advanced and protracted cases.
Considerable measures have been taken in an attempt to control and eradicate S. pullorum from commercial poultry flocks in the United States. Nevertheless, the impact of PD was felt in 1990 and 1991 with an outbreak in a broiler operation that involved five states. The primary means of control for PD has been through intense serologic screening of flocks. Presently, serologic tests are routinely performed on birds for exhibition and sale in many states. It should be noted that positive reactions may occur from infections with agents other than S. pullorum, therefore serologic evidence of infection should be confirmed with repeated tests and bacteriologic examination.
AFIP Diagnosis: Ovary and mesentery: Oophoritis and egg yolk peritonitis, granulomatous and heterophilic, diffuse, severe, with bacilli, White Rock chicken, avian.
Conference Comment: The clinical signs and disease manifestations of pullorum disease are highly variable among chickens. Age, breed, flock management and means of exposure can influence morbidity and mortality. Infections that localize in joints and tendon sheaths may resemble infections by Mycoplasma synoviae, Staphylococcus aureus, Pasteurella multocida, or Erysipelothrix rhusiopathiae. Ovarian infections may appear similar to infections caused by bacteria such as Escherichia coli, staphylococci, streptococci, P. multocida, and other salmonellae. Birds of any age may be infected and definitive diagnosis can only be made following isolation and identification.
Contributor: Veterinary Diagnostic Laboratory, College of Veterinary Medicine, P.O. Box U, 2001 S. Lincoln Avenue, Urbana, IL 61801
Reference: Shivaprasad HL: Pullorum disease and fowl
typhoid. In: Diseases of Poultry, ed. Calneck BW, Barnes
HJ, Beard CW, McDougald LR, Saif YM, 10th ed., pp.
82-96. Iowa State University Press, Ames, IA, 1997
*Sponsored by the American Veterinary Medical Association, the American College of Veterinary Pathologists and the C. L. Davis Foundation.
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