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CASE I – S00-596 (AFIP 2743660)
Signalment: Abortion (at day 40-45), male, weisses Alpenschaf sheep, ovine
History: This flock in central Switzerland (canton Schwyz) had problems with several abortions.
Gross Pathology: The red-brown, opaque placenta had light-brown, soft cotyledons. Gross lesions of the fetus consisted of generalized subcutaneous edema and reddish fluid accumulation (approximately 2-3 ml) in the thoracic cavity.
Laboratory Results: Large numbers (3+) of Coxiella burnetii were found by microscopic examination of Köster-stained smears of the placenta. The organisms appeared as fine, acid-fast (red), partly intracellular, short rods. In contrast to Brucella species, they stained well (red) by the method of Giménez.
Contributor’s Diagnosis and Comment: Placentitis, necrotizing, multifocal, severe with masses of intraepithelial Coxiella burnetii organisms.
There is multifocal necrosis and neutrophilic infiltration in both the cotyledonary and intercotyledonary areas of the placenta, and foci of mineralization. The placental stroma is edematous and hyperemic. Stamp’s stain of the placental histologic sections revealed masses of intraepithelial, acid-fast, rod-shaped bacteria (morphology consistent with Coxiella burnetii).
Differential diagnosis of bacterial abortion includes infections with Chlamydia and Brucella spp. However, Chlamydia spp. stain negative (blue) by the method of Köster and typical inclusion bodies are lacking in histological sections. On the other hand, Brucella spp. stain negative (blue) by the method of Giménez.
Coxiella burnetii, a member of the family Rickettsiaceae, causes Q (Query) fever in man, and infects sheep, goats, cattle and nearly all domestic animals. Q fever is distributed worldwide, with the exception of New Zealand. The disease is on the B list of the Office International des Epizooites (OIE). In 1999, 39 cases were reported in Switzerland in sheep and goats; in 1998 there were 41 cases. In 1998, ten human cases occurred, and from 1990 to 1998 an average of 18 human cases per year were recorded.
The term “Q fever” is mainly used for the human infection, characterized by atypical pneumonia, fever, and hepatitis. Recent studies describe cases of pericarditis associated with Q fever, and that Coxiella burnetii infection may cause long-term complications such as vascular disease. Farmers with seropositive animals have the highest risk of contracting the disease, but seropositivity is also found among veterinarians, and abattoir and laboratory workers. The disease is transmitted by aerosol.
In sheep and goats, Coxiella burnetii is responsible for abortion or birth of dead or weak lambs, preferentially in newly exposed animals. Animals get infected through Coxiella-containing feces of ticks. Infection in the flock spreads by aerosol or through licking and eating highly contaminated placentas or discharges after parturition. Sheep, goats, and cattle are important reservoirs of Coxiella burnetii.
Rickettsiae are very small, coccoid to rod-shaped organisms, that were originally parasites in the intestines of insects. Coxiella differs from other rickettsiae in their high tenacity. In a dried status, they survive 2 to 6 months in the environment and 1.5 years in dried feces of ticks.
A recent study detected Coxiella infections from ovine genital swabs, milk, and fecal samples using polymerase chain reaction (PCR).
AFIP Diagnosis: Chorioallantois: Placentitis, cotyledonary and intercotyledonary, necrotizing, subacute, diffuse, moderate, with vasculitis and myriad intracellular bacteria, weisses Alpenschaf sheep, ovine.
Conference Comment: The contributor has provided an excellent review of Q Fever and Coxiella burnetii. Additional points made or reinforced during the conference included: 1. Unlike abortions in sheep due to Brucella ovis or Chlamydophila abortus (formerly Chlamydia psittaci), Coxiella burnetii affects intercotyledonary areas and the placentome. 2. Cats that associate with sheep from endemically infected flocks have been incriminated in spreading infection to humans.
Isolation of C. burnetii from animal tissues is not routinely performed as a diagnostic measure because it is time consuming and requires a bio-safety level 3 laboratory. The development of a simple method of DNA preparation which inactives Coxiella, combined with a PCR assay, has reduced the risk to laboratory personnel, while providing sensitive and specific detection. Similarly, immunohistochemistry staining can demonstrate Coxiella in formalin-fixed, paraffin-processed placental tissue, providing a low risk, rapid diagnosis.
Contributor: ity of Zürich, Institute of Veterinary Pathology, Winterthurerstrasse 268, CH-8057 Zurich, Switzerland
References: 1. Berri M, Laroucau K, Rodolakis A: The detection of Coxiella burnetii from ovine genital swabs, milk and fecal samples by the use of single touchdown polymerase chain reaction. Vet Microbiol 72(3-4):285-293, 2000
2. Cetinkaya B, Kalender H, Ertas HB, Muz A, Arslan N, Ongor H, Gurcay M: Seroprevalence of coxiellosis in cattle, sheep and people in the east of Turkey. Vet Rec 146(5):131-136, 2000
3. Damoser J, Hofer E, Müller M: Aborte in einem niederösterreichischen Schafbetrieb hervorgerufen durch Coxiella burnetii. Berl Münch Tierärztl Wschr 106:361-364, 1993
4. Levy PY, Carrieri P, Raoult D: Coxiella burnetii pericarditis: report of 15 cases and review. Clin Infect Dis 29(2):393-397, 1999
5. Lovey PY, Morabia A, Bleed D, Péter O, Dupuis G, Petite J: Long term vascular complications of Coxiella burnetii infection in Switzerland: cohort study. BMJ 319(7205):284-286, 1999
6. Maurin M, Raoult D: Q fever. Clin Microbiol Rev 12(4):518-553, 1999
CASE II – 270626 (AFIP 2741444)
Signalment: Four-month-old, male kid goat
History: The kid had a history of mild fever (40.8_ C), with mild dyspnea, cough, and marked mucopurulent nasal discharge. Several other kids in the herd were showing similar clinical signs.
Gross Pathology: On post mortem examination, crusting of the lips, with multifocal erosions of the oral mucosa, hard and soft palate were present. Multifocal hemorrhage and ulceration of the laryngeal mucosa and trachea, with flakes of mucopurulent discharge were seen. The lungs were partially consolidated, especially in the anteroventral lobes. A small amount of bloodstained content was present in the gastrointestinal tract, especially in the large intestine.
Laboratory Results: Peste des petit ruminants virus was diagnosed by immunofluorescent antibody (IF), agar gel immunodiffusion test (AGID), and polymerase chain reaction (PCR).
Contributor’s Diagnoses and Comment: 1. Lung: Bronchopneumonia, subacute, diffuse, severe, with necrotizing bronchiolitis.
2. Interstitial pneumonia, subacute, diffuse, severe, with type II pneumocyte hyperplasia, syncytial cell formation, and intraepithelial intranuclear and intracytoplasmic eosinophilic inclusion bodies.
AFIP Diagnosis: Lung: Pneumonia, bronchointerstitial, subacute, diffuse, moderate, with type II pneumocyte hyperplasia, syncytial cells, and epithelial intranuclear and intracytoplasmic eosinophilic inclusion bodies, goat, breed not specified, caprine.
Conference Comment: Antigenically and morphologically closely related, the morbilliviral diseases of peste des petits ruminants (PPR) in sheep and goats, and rinderpest in cattle, have similar clinical signs of depression, oral erosions, conjunctivitis, diarrhea, dehydration, and death. Animals with rinderpest usually die of dehydration from profuse diarrhea, and rarely develop significant pneumonia. In contrast, PPR is more acute in onset, mainly affecting animals 6 to 12 months-of-age, with marked involvement of the respiratory tract. If animals survive the consolidating, interstitial pneumonia with necrotizing bronchiolitis, they usually succumb to diarrhea and dehydration that develops later. Close contact is necessary for spread of the fragile, enveloped virus, as the virus cannot survive in the environment for more than a few hours.
Contributor: Kimron Veterinary Institute, Department of Pathology, P.O. Box 12, Beit-Dagan, Israel 50250
References: 1. 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. 159-163. Academic Press, Inc, New York, NY, 1993
2. Brown CC, Mariner JC, Olander HJ: An immunohistochemical study of the pneumonia caused by peste des petits ruminants virus. Vet Pathol 28(2):166-170, 1991
3. Kulkarni DD, Bhikane AU, Shaila MS, Varalakshmi P, Apte MP, Narladkar BW: Peste des petits ruminants in goats in India. Vet Rec 138:187-188, 1996
4. Kulkarni DD, Bhikane AU, Kulkarni GB, Narladkar BW: Clinico-pathological investigations in goats experimentally infected with peste des petits ruminants. Indian Vet J 75:591-594, 1998
5. Perl S, Alexander A, Yakobson B, Nyska A, Harmelin A, Sheikhat N, Shimshony A, Davidson M, Abramson M, Rapaport E: Peste des petits ruminants (PPR) of sheep in Israel: case report. Israel J Vet Med 49(2):59-61, 1994
CASE III – S 31/00 (AFIP 2742238)
Signalment: 8-week-old, female mixed breed, domestic pig
History: This animal was part of a vaccination study and was challenged by intramuscular administration of 105.75 TCID50 of the virulent Koslov strain of classical swine fever virus (CSFV). After developing fever on day 3 post-infection (p.i.), the animal became depressed, tachypneic, and developed a cough on day 6 p.i. The pig became recumbent on day 11 p.i., and died 2 days later with multiple, variably sized cutaneous hemorrhages.
Gross Pathology: Numerous coalescing cutaneous hemorrhages were present on the ears, limbs, and ventral parts of the trunk. Tonsillar necrosis and peripheral hemorrhages in the edematous and swollen (3 x 4 x 3 cm) mandibular, mediastinal, renal, and gastric lymph nodes were present. Lymph nodes had a marbled grey-red cut surface. Kidneys and urinary bladder showed multiple petechiae. More than 50% of the cranioventral lung was consolidated and grey-purple.
Laboratory Results: CSFV was re-isolated by tissue culture; CSFV-RNA was detectable by RT-PCR in multiple organs.
Contributor’s Diagnoses and Comment: 1. Mandibular lymph node: Hyperemia and hemorrhage, peripheral, diffuse, moderate, subacute, with hemosiderosis (arterial fibrin thrombi were present in some sections).
2. Mandibular lymph node: Depletion, lymphoid follicular, diffuse, moderate.
3. Mandibular lymph node: Hyperplasia, reticuloendothelial, multifocal, mild.
Classical swine fever (CSF, hog cholera) is a highly contagious systemic disease of domestic pigs and wild boar. It is caused by a 40-50 nm, enveloped, RNA virus (CSFV). It is a member of the family Flaviviridae, genus pestivirus, along with bovine viral diarrhea virus (BVDV) and border disease virus (BDV). CSFV has worldwide distribution, except in the countries of: Australia, Belgium, Canada, France, Great Britain, Iceland, Ireland, New Zealand, Portugal, Spain, Scandinavia, Switzerland, and the United States. CSFV infections can display a peracute, acute, subacute, chronic, atypical, or inapparent course. Pathogenicity is highly dependent on virulence and infective dose of the virus, age, breed, and species of the host domestic pig or wild boar.
CSFV of high virulence causes acute disease, resulting in high morbidity and mortality. After initial replication in the tonsillar crypt epithelium, viremia develops, infecting the surrounding lymphoreticular tissue, draining lymph nodes, spleen, bone marrow, and intestinal lymphoid tissue. Later, epithelial cells of lung, kidney, and liver are also targeted. Infection of arteriolar capillary endothelium, with subsequent degeneration and necrosis, is responsible for the characteristic hemorrhage, or thrombosis and infarction.
Severe economic losses due to past CSF epidemics in Europe forced the European Community to eliminate CSFV from its member countries. Slaughter of infected herds, with restrictions in trade of live pigs and the sale of fresh meat of domestic pigs and wild boar only recently allowed the eradication of CSF in endemic areas. The high density of pig and wild boar populations in central European countries like the Netherlands and Germany, and the predominance of low virulence CSFV strains in endemic areas due to co-evolution, were complicating factors in the eradication effort. These factors can result in mild disease or subclinical infections, and are significant in the risk of CSF spread in the field. Virulence is often enhanced after repeated passages in pigs. Viewed together, these factors indicate a need for development of global certification and use of a marker vaccine against CSFV.
AFIP Diagnoses: 1. Lymph node: Hemorrhage, medullary, diffuse, moderate, with erythrophagocytosis and hemosiderosis, mixed breed pig, porcine.
2. Lymph node: Lymphoid depletion, diffuse, moderate, with dendritic cell and lymphoblastic hyperplasia (regeneration).
Conference Comment: Acute classical swine fever may appear similar, clinically and histopathologically, to African swine fever, erysipelas, or septicemic salmonellosis. Hemorrhage in lymph nodes, kidney, and other organs due to widespread vasculopathy is the most diagnostic feature. Infarction of the spleen, often listed as being almost pathognomonic for CSF, is not reported in necropsy findings from recent outbreaks, and is considered a feature of older field strains of the virus.
In this case, the lack of dense cortical cellularity, and follicular structures with distinct mantle zones indicate lymphoid depletion. Expansion of the cortex by hyperplastic dendritic cells and many large lymphoblasts with numerous mitotic figures is interpreted as a regenerative response to previous acute lymphoid necrosis.
Contributor: Federal Research Centre for Virus Diseases of Animals, Friedrich-Loeffler-Institutes, Boddenblick 5A, 17498 Insel Riems, Germany
References: 1. Kaden V: Classical swine fever (hog cholera). In: Applied Veterinary Epidemiology, ed. Blaha T, pp. 61-66. Elsevier Publishing, New York, NY, 1989
2. Kaden V: Bekämpfung der Klassischen Schweinepest beim Schwarzwild. Z Jagdwiss 45:45-59, 1999
3. Röhrer H: Histologische Untersuchungen bei Schweinepest: Lymphknotenveränderungen in akuten Fällen. Arch wiss prakt Tierheilkde 62:345-372, 1930
4. Van Oirschot JT: Classical swine fever (hog cholera). In: Diseases of Swine, ed. Straw BE, D’Allaire S, Mengeling WL, Taylor DJ, pp. 159-172. Iowa State ity Press, Ames, IA, 1999
CASE IV – 98/311 (AFIP 2643754)
Signalment: 15-month-old, female Norwegian Landrace pig, Sus scrofa domestica
History: This sow was from a commercial herd on a farm that also raised sheep. The sow was about 3 weeks from farrowing when she developed hyperemic conjunctiva, vomiting, restlessness and anorexia. The rectal temperature was 41° C, the respiratory rate was 33 per minute, and the heart rate was 110 per minute. Despite parenteral antibiotic treatment, the symptoms worsened and the pig died 5 days after onset of disease. Over a short period, three other adult swine in the same herd died after showing similar clinical signs.
Gross Pathology: The pig was in normal body condition. The sclera, conjunctiva, and meninges were hyperemic. The sow also had an atrial septal defect and the right ventricle was dilated. The uterus contained 14 normally developed piglets, ranging in size from 20 to 30 cm.
Laboratory Results: The sow had moderate neutrophilia and slightly raised creatinine and blood urea nitrogen levels.
Contributor’s Diagnoses and Comment: 1. Brain: Vasculitis, lymphocytic, acute, multifocal, moderate to severe.
2. Meninges: Meningitis, non-purulent, acute, focal, moderate.
3. Conjunctiva: Conjunctivitis, lymphocytic, acute, diffuse, moderate.
4. Uvea: Vasculitis, lymphocytic, acute, coalescing, moderate to severe.
5. Cornea: Edema.
6. Kidney: Interstitial tissue, non-purulent, multifocal, moderate to severe.
Etiologic diagnosis: Sheep-associated malignant catarrhal fever
This pig showed clinical signs and pathologic changes similar to three pigs described by LYken, et al. By polymerase chain reaction, tissues from the animals in that study were shown to contain DNA specific for ovine herpesvirus type 2. In 1950, Kurtze first described this disease in a single sow in Germany. Bratberg described 32 cases from Norway. It is also reported in Sweden and Switzerland. The pathological findings are, in many aspects, similar to the findings of malignant catarrhal fever in ruminants, but differ by a distinctive short course, predominant vascular changes, and relative lack of epithelial involvement. The lymphoid involvement in pigs seems to be inconsistent. The sheep-associated form of this disease is caused by ovine herpesvirus type 2. The majority of cases in swine and cattle have occurred in animals in close contact with sheep, and in the winter and spring, which is the lambing season in Norway.
Norway is regarded free of important swine diseases such as classical swine fever (hog cholera), African swine fever, swine influenza, Aujeszky’s disease, and swine vesicular disease. Polioencephalomyelitis (Talfan disease) of swine does occur, but is normally seen as pelvic limb ataxia and paresis, and not as an acute and fatal disease.
In this case, the diagnosis of malignant catarrhal fever was made based on the clinical history, especially the fact that the herd was in the near vicinity of sheep, and the relatively characteristic histopathological findings.
AFIP Diagnosis: Cerebrum and meninges: Vasculitis, lymphocytic, diffuse, mild to moderate, with perivascular edema, Norwegian Landrace pig, porcine.
Conference Comment: Recently, a newly recognized herpesvirus, representing the third known pathogenic virus in the malignant catarrhal fever group, has been documented in white-tailed deer (Odocoileus virginianus) from a zoo in the North Central United States. The causative virus has been shown by PCR to be a genetically distinct gammaherpesvirus that is closely related to ovine herpesvirus type 2 (OHV-2) and alcelaphine herpesvirus type 1 (AHV-1). The reservoir for this virus is not known, nor is its pathogenicity for other ruminants.
Conference participants preferred a differential diagnosis of graft versus host immune reaction, classical swine fever, and malignant catarrhal fever for the histopathological lesions present in the brain sections. Even with the provided clinical history, most participants preferred evidence of viral presence within the tissue, as with immunohistochemistry or in situ hybridization, to establish a definitive diagnosis.
Contributor: Norwegian College of Veterinary Medicine, Department of Morphology, Genetics and Aquatic Biology, Division of Pathology, P.O. Box 8146, Department N-0033, Oslo, Norway
References: 1. 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. 163-173. Academic Press, Inc, New York, NY, 1993
2. Bratberg B: Acute vasculitis in pigs: a porcine counterpart to malignant catarrhal fever. Proc Congress Internatl Pig Vet Soc, Copenhagen, Denmark, p. 353, 1980
3. Jarp J, Tharaldsen J: Dokumentasjon av infeksjonssykdommer hos svin i Norge. (In Norwegian). Proc HusdyrforsYksmYtet, 9s, Norway, pp. 171-181, 1998
4. Kurtze H: Überträgung des “Bösartigen Katarrhalfiebers des Rindes” auf ein Schwein. (In German). Deutsche Tierärtzliche Wochenschrift 57:261, 1950
5. Li H, Dyer N, Keller J, Crawford TB: Newly recognized herpesvirus causing malignant catarrhal fever in white-tailed deer (Odocoileus virginianus). J Clin Microbiol 38(4):1313-1318, 2000
6. Lium B, Baustad B: Viral encephalomyelitis of pigs (Teschen disease, Talfan disease). (In Norwegian) Norsk Veterinrtidsskrift. 108:719-720, 1996
7. LYken T, Aleksandersen M, Reid H, Pow I: Malignant catarrhal
fever in swine caused by Ovine herpesvirus-2 in Norway. Vet Rec
143:464-467, 1998
*Sponsored by the American Veterinary Medical Association, the American College of Veterinary Pathologists and the C. L. Davis Foundation.
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