Multifocal Coagulative Necrosis Research Articles

Hepatic encephalopathy in swine experimentally poisoned with Senna occidentalis seeds: Effects on astrocytes

Senna occidentalis may be accidently ingested by humans and animals. In this study, the percentages of S. occidentalis seeds necessary for experimental reproduction of hepatic encephalopathy were determined in a pig model and the biochemical and microscopic pathology is described in detail, with emphasis on the astrocytes. The experimental groups (G1, G2 and G3) were fed rations containing 5%, 7.5% and 10% of S. occidentalis seeds for 7–11 days. Pigs from the three experimental groups showed incoordination, ataxia, disorientation, head pressing, anorexia, recumbency and depression. In addition, the enzymes aspartate aminotransferase, alkaline phosphatase and creatine phosphokinase increased in all treated animals, which also showed higher serum total bilirubin and ammonia levels than in the control group (C). Microscopically, all experimental animals revealed acute hepatocellular swelling, multifocal coagulative necrosis in the pancreas, necrosis in the cardiac muscle, severe spongiosis in brain white and grey matter, and Alzheimer type II astrocytes in grey matter of the cerebral cortex. These cells were glial fibrillary acidic protein (GFAP) negative in G3. In white matter, a decrease in the positive area occupied by GFAP-immunolabelling and in the number of astrocytes per immunoreactive area was observed in G3 animals (5.35 ± 1.14% and 410 ± 45 cells/mm2, respectively) compared to the C animals (13.93 ± 1.59% and 581 ± 36 cells/mm2, respectively). This loss of GFAP was accompanied by alterations in astrocyte morphology, such as shrinkage of the cell body and retraction of the extending processes. This pig model of ammonia-mediated astrocyte damage could be used to study not only poisoning by S. occidentalis, but also other medical conditions resulting in hepatoencephalopathy.

Abortion in Captive Gray Brocket Deer (Mazama gouazoubira) Associated with Colloid Goiter, Hemonchosis and Necrotizing Rumenitis

Background: The gray brocket deer (Mazama gouazoubira) is a specie that shows great adaptability in different habitats and it is the most abundant deer specie in South America. The present work describes for the first time a case of abortion followed by death associated with colloid goiter, massive hemonchosis and necrotizing rumenitis in a captive female gray brocket deer. Case: A 4-year-old female gray brocket deer (M. gouazoubira) raised in captivity had a history of abortion during the last third of gestation. The animal was kept in an enclosure together with 3 other gray brockets deers, being 1 male of the same age and 2 juvenile brocket deer of approximately 1 and 2 years old. The animals were fed with concentrated used as cattle feed and dewormed annually with 1% Ivermectin. The animals' enclosure had vegetation cover formed by grasses and soil. The animals appeared healthy with no behavioral changes. The day after the stillbirth, the mother was found dead in the enclosure and sent to the animal pathology sector of the University of Vila Velha (UVV), Brazil. Necropsy revealed that thyroid lobules were highly increased in volume and histopathological findings were compatible with colloid goiter. A large number of nematodes were found in the abomasal content,totalizing 11,626 helminths, which were morphologically characterized as Haemonchus contortus. Grossly, the serous and ruminal mucosa exhibited an extensively reddish focal area with irregular contour, surface ulceration and a firm consistency. Microscopically, a severe necrotizing rumenitis was diagnosed. The liver showed pale multifocal areas on the subcapsular surface,friable to the touch which deepened when cut. Histopathological analysis revealed an accentuated multifocal panlobular coagulative necrosis, characterizing an acute liver necrosis.Discussion: Iodine is a mineral of great importance for thyroid hormones synthesis and your requirements are higher during pregnancy and lactation. Diets deficient in iodine causes a reduction in the basal activity of the hormones triiodothyronine (T3) and thyroxine (T4) and over-stimulation of the thyroid by thyroid stimulating hormone (TSH), resulting in goiter. In the present case, it is possible that the shortage of iodine in diet caused a goiter and, as a consequence, triggered the abortion. Haemonchus contortus is a pathogenic nematode of small ruminants, leading to decreased productivity and death in some cases as a result of anemia and hypoxia. The contact between domestic and wild animals, resulting in the emergence of infectious diseases and the spread of pathogens among species. In the present case, manual counting accounted for 11,626 H. contortus larvae, characterizing a massive infection and justifying the condition of severe anemia. The high parasitic load shown in this case points out this parasite's importance related to this species in captivity. In general, inflammatory lesions in the rumen are results of excessive intake of fermentable carbohydrates, which leads to a considerable decrease in ruminal pH and leads to a high proliferation of lactic acid bacteria. This lesion has been previously reported in cervids. This case of comorbidities demonstrates that failures in nutritional and health handling, may cause simultaneous multiple diseases leading to death. Preventive measures for helminth parasite control and a proper feeding management with an adequate diet must be provided in order to preserve the species in captivity. Keywords: colloid goiter, abortion, cervids, Haemonchus contortus.

Perubahan Patologi Sistem Hepatobiliari Sapi Bali Terinfeksi Fasciola gigantica

Liver fluke infections is an important parasitic disease that common attack cattle, buffalo and others ruminant. The disease in the tropics is caused by Fasciola gigantica trematodes. Fasciolosis found in Bali cattle besides causing high economic loss also has the opportunity infect humans. This study aims to determine the pathology changes of Bali cattle hepatobiliary system infected by F. gigantica. In January 2019 were examined a hundred of liver tissue Bali cattle. Based on the sex as many as 75 bali cattle are cows and 25 are bulls. On macroscopic examination was found fifteen bali cattles in gallbladder containing of F. gigantica. In positive Fasciolosis the surface of liver look uneven with enlargement of lymph nodes. The tissue of Bali cattle liver infected with F. gigantica is cut into 1x1x1 cm and put in a pot that has been filled with 10% neutral buffered formaline. The fixed tissue then processed in a tissue processor and stained with hematoxylin-eosin (HE). Microscopic examination was found bile ducts proliferation and blocked of the lumen accompanied by cholangio cirrhosis. Found longitudinal pieces of Fasciola gigantica liver fluke surrounded by fibrous connective tissue and multifocal coagulative necrosis with fibroblast proliferation. In some location the infiltration of neutrophil cells around the bile ducts can also be seen. Congestion, bleeding, and neutrophil infiltration are also seen in areas of necrosis. In the bile duct wall bleeding, adenomatus hyperplasia, infiltration of mononuclear cells with mild intensity and foci of calcification are found. It can be concluded that there was a change with severe intensity accompanied by chronic inflammation in the hepatobiliary system of Bali cattle with Fasciolosis.

Outbreak of Oleander (Nerium oleander) Poisoning in Dairy Cattle: Clinical and Food Safety Implications.

Oleander is a spontaneous shrub widely occurring in Mediterranean regions. Poisoning is sporadically reported in livestock, mainly due to the ingestion of leaves containing toxic cardiac glycosides (primarily oleandrin). In this study, 50 lactating Fleckvieh cows were affected after being offered a diet containing dry oleander pruning wastes accidentally mixed with fodder. Clinical examination, electrocardiogram, and blood sampling were conducted. Dead animals were necropsied, and heart, liver, kidney, spleen, and intestine were submitted to histological investigation. Oleandrin detection was performed through ultra-high performance liquid chromatography-tandem mass spectrometry in blood, serum, liver, heart, milk, and cheese samples. Severe depression, anorexia, ruminal atony, diarrhea, serous nasal discharge, tachycardia, and irregular heartbeat were the most common clinical signs. The first animal died within 48 h, and a total of 13 cows died in 4 days. Disseminated hyperemia and hemorrhages, multifocal coagulative necrosis of the cardiac muscle fibers, and severe and diffuse enteritis were suggestive of oleander poisoning. The diagnosis was confirmed by the presence of oleandrin in serum, liver, heart, milk, and cheese. Our results confirm the high toxicity of oleander in cattle and report for the first time the transfer into milk and dairy products, suggesting a potential risk for the consumers.

Pathological changes associated with an outbreak of colibacillosis in a commercial broiler flock

Escherichia coli infection was diagnosed in 5-week old broiler chickens raised intensively on a medium-sized commercial farm in Gaube-Kuje, Abuja, Nigeria. Signs of weakness, depression and inappetance with ruffled feathers and pasted vents were reportedly observed in affected birds within the flock. Detailed post mortem examinations revealed diffuse splenomegaly and hepatomegaly with multifocal greyish areas on their surfaces while the diffusely enlarged kidneys were congested with mottled pale appearance. Histopathologically, the liver of affected broilers showed diffuse congestion, multifocal coagulative necrosis and cellular infiltration. Generalized perivascular and inter-septal oedema and haemorrhage were observed in the lungs of affected broilers with generalized lymphocytic depletion within the spleen as well as locally extensive congestion and haemorrhage within the kidney, and cellular infiltration and necrosis within heart musculatures. Microbiological evaluation of liver samples yielded pure E. coli growth only. A diagnosis of colibacillosis, especially colisepticaemia, was made with appropriate treatment based on culture and sensitivity test result involving Levofloxacin(R). The client was consequently advised to guard against possible predisposing factors as control and preventive measures for the disease outbreak on the farm. Keywords : Broiler chickens, Colibacillosis, Gross pathology, Histopathology, Natural infection

Pathology and Tissue Distribution of an LPAI H5N8 of North American Lineage Isolated from an Outbreak in Commercial Japanese Quail (Coturnix c. japonica) in the Central Valley of California

This report describes the pathology and tissue distribution of avian influenza (AI) antigens by immunohistochemistry (IHC) in the tissues of commercial layer quail from a natural outbreak of low pathogenic avian influenza (LPAI) H5N8. LPAI virus H5N8 of North American lineage was diagnosed in commercial Japanese quail hens ( Coturnix coturnix japonica) in California based on serology, reverse-transcriptase real-time polymerase chain reaction, virus isolation, and sequencing. The sudden increase in mortality in a flock of laying quail hens had prompted the submission of 15 live and 5 dead, 10- to 15-wk-old quail to the California Animal Health and Food Safety Laboratory System, Turlock branch in the beginning of April 2014. There was mild bilateral swelling of the eyelids and greenish diarrhea in 4/15 live quail submitted. On postmortem examination, there were severe, extensive hemorrhages and multifocal, confluent pale foci in the pancreas in 10/20 birds. Liver gross lesions in five birds ranged from a few pale areas to numerous disseminated foci. Histology revealed moderate to severe necrosis of acinar cells in the pancreas with little or no inflammation in most of the birds. Livers had acute multifocal coagulative necrosis of hepatocytes with fibrin exudation and infiltration of few to large numbers of heterophils and lymphocytes randomly scattered throughout. The AI virus was detected in the nucleus and cytoplasm of pancreatic acinar cells and hepatocytes by IHC targeting the nucleoprotein of the AI virus. A few birds had AI antigen in the reticuloendothelial cells of the spleen, endothelial cells of the lungs, epithelium of the respiratory mucosa, and lamina propria of the intestine. The severity of the lesions observed in this natural outbreak of LPAI in quail was higher than that expected for the pathotypic presentation in this species.

VITAMIN B6 (PYRIDOXINE HYDROCHLORIDE) TOXICOSIS IN FALCONS.

This manuscript reports three independent accidental cases of vitamin (Vit) B6 toxicosis in gyrfalcons (Falco rusticolus) and peregrine falcons (Falco peregrinus) and a toxicology study that was conducted to characterize the clinical responses of gyrfalcons and gyrfalcon × peregrine falcons to a range of single intramuscular (IM) and oral (PO) doses of Vit B6. Both lethal and nonlethal doses were determined. Twelve female gyrfalcons died following IM injection of 1 ml of a vitamin B preparation. Within 30 min of injection, the birds passed pistachio green-colored urates and progressed to vomiting, anorexia, cessation of normal activity, ptosis, collapse, and death, occurring 24-36 hr post injections. Three individuals vomited frothy, partially digested blood and had clonic spasms and convulsions. Postmortem and histopathology revealed multifocal severe hepatic necrosis, splenic lymphoid tissue depletion and hemorrhages with arterial necrosis, and acute renal tubular necrosis. Following administration of a different, oral, mineral-vitamin supplement, a total of 21 peregrine falcons in two separate European facilities died suddenly. Histology of the liver showed diffuse congestion and multifocal coagulative necrosis with mild infiltration of heterophils. The particular nutritional supplement, used by both breeders, was analyzed and found to contain 5-9.7% Vit B6. Other randomly selected lots of the product contained 0.007-0.27% Vit B6. According to the product label, Vit B6 should have been present at 0.004%. To confirm the hypothesis that Vit B6 was responsible for the deaths of the falcons in Abu Dhabi, Vit B6 (British Pharmacopoeia [BP] grade) in powder form was diluted in water for injection and administered IM to four groups of falcons. Groups of four gyrfalcon × peregrine hybrid falcons or gyrfalcons (or both) were given a single IM dose of 5, 10, 15, or 20 mg/kg of Vit B6 or received an oral dose of 25, 50, or 75 mg of Vit B6. Only birds in the lowest-dose groups survived. The maximum nonlethal single doses of Vit B6 in falcons were 5 mg/kg i.m. and 25 mg/kg p.o.

Lawsonia intracellularis and Porcine Circovirus type-2 infection in Estonia.

The present study describes the reasons of post-weaning distress in Estonian pig herds. Here we examined the natural cases of Lawsonia intracellularis and porcine circovirus 2 (PCV2) infection and co-infections. The presence of L. intracellularis in swine herds were tested by PCR and by histopathological methods, whereas PCV2 was detected by real-time-PCR and immunohistochemical stainings. Seven of the 11 investigated herds with signs of post-weaning wasting were infected with L. intracellularis and all 11 herds with PCV2. From the analysed samples 22.2% were infected with L. intracellularis and 25% with PCV2. The results of microbiological studies suggested that the piglets suffered from enteritis and pneumonia. Escherichia coli and Pasteurella multocida often aggravated the process of illness. The frequency of L. intracellularis was high in pigs 7-12 weeks old (18.5-42.7%) and PCV2 infection was too high in pigs 7-12 weeks old (24.8-32.7%). E. coli was often a co-factor with L. intracellularis and PCV2. The primary reasons of post weaning wasting were PCV2 and E. coli, later aggravated by L. intracellularis and other pathogens. Our results indicated that different pathogens have an important role in developing post-weaning wasting. Proliferative intestinal inflammation caused by L. intracellularis is mainly characterised by its localization and morphological findings. The main gross lesions were the enlargement of mesenteric lymph nodes and thickening of the wall of ileum. In post-weaning multi-systemic wasting syndrome there are characteristic histological lesions in lymphoid tissues. They consist of a variable degree of lymphocyte depletion, together with histiocytic and/or multinucleate giant cell infiltration. This basic lymphoid lesions is observable in almost all tissues of a single severely affected animal, including lymph nodes, Peyer's patches and spleen. Sporadically, multifocal coagulative necrosis may be observed.

Spontaneous poisoning by Ricinus communis (Euphorbiaceae) in cattle

The aim of this study is to report cases of spontaneous poisoning of cattle by Ricinus communis (castor beans) in Paraíba, a semiarid region of northeastern Brazil. The cases were observed in 2 herds on neighboring properties in 2013. Clinical signs developed within 6-24 h and consisted of weakness, tachycardia, dyspnea, profuse watery diarrhea, dehydration, depression, instability, cramps, permanent lateral recumbency and death within 48-72 h. Of the 60 cattle at risk, 19 were affected and 14 died. Five fully recovered after the course of 12 days. Three animals were necropsied. The main gross lesions were hemopericardium, hemothorax, pulmonary edema, petechial hemorrhages in the epicardium and endocardium, ecchymoses at the papillary muscles and suffusions on the intercostal muscles. Hemorrhages were also observed in the abdominal cavity, spleen and mucosa of the abomasum and small intestine. The rumen content was liquid with a large amount of castor bean seeds. There were circular, whitish and focally diffuse areas in the liver parenchyma. The main microscopic lesions consisted of multifocal coagulative myocardial necrosis with the presence of mononuclear cell infiltration and varying degrees of bleeding between cardiac muscle fibers. The abomasum and small intestine mucosae and submucosa had mild edema and mononuclear and polymorphonuclear inflammatory cell infiltration. The diagnosis of R. communis was based on the history of plant consumption, clinical signs, pathology of the disease and the presence of large amounts of castor bean seeds in the forestomachs.

Angiotensin‐converting enzyme (ACE and ACE2) imbalance correlates with the severity of cerulein‐induced acute pancreatitis in mice

Angiotensin-converting enzyme (ACE) and its effector peptide angiotensin II (Ang II) have been implicated in the pathogenesis of pancreatitis. Angiotensin-converting enzyme 2 (ACE2) degrades Ang II to angiotensin-(1-7) [Ang-(1-7)] and has recently been described to have an antagonistic effect on ACE signalling. However, the specific underlying role of ACE2 in the pathogenesis of severe acute pancreatitis (SAP) is unclear. In the present study, the local imbalance of ACE and ACE2, as well as Ang II and Ang-(1-7) expression, was compared in wild-type (WT) and ACE2 knock-out (KO) or ACE2 transgenic (TG) mice subjected to cerulein-induced SAP. Serum amylase, tumour necrosis factor-α, interleukin (IL)-1β, IL-6 and IL-10 levels and histological morphometry were used to determine the severity of pancreatitis. In WT mice, pancreatic ACE and Ang II and serum Ang II expression increased (P < 0.05), while pancreatic ACE2 and Ang-(1-7) and serum Ang-(1-7) levels were also significantly elevated (P < 0.05) from 2 to 72 h after the onset of SAP. However, the ratio of pancreatic ACE2 to ACE expression was significantly reduced (from 1.46 ± 0.09 to 0.27 ± 0.05, P < 0.001) and paralleled the severity of pancreatitis. The Ace2 KO mice exhibited increased levels of tumour necrosis factor-α, IL-1β, IL-6, multifocal coagulative necrosis and inflammatory infiltrate, and lower levels of serum IL-10 and pancreatic Ang-(1-7) (4.70 ± 2.13 versus 10.87 ± 2.51, P < 0.001) compared with cerulein-treated WT mice at the same time point. Conversely, Ace2 TG mice with normal ACE expression were more resistant to SAP challenge as evidenced by a decreased inflammatory response, attenuated pathological changes and increased survival rates. These data suggest that the ACE2-ACE imbalance plays an important role in the pathogenesis of SAP and that pancreatic ACE2 is an important factor in determining the severity of SAP.

Lethal Herpesvirosis in 16 Captive Horned Vipers (Vipera ammodytes ammodytes): Pathological and Ultrastructural Findings

Sixteen captive adult horned vipers (Vipera ammodytes ammodytes) were submitted for necropsy examination following a 2-week history of lethargy, anorexia and dyspnoea. Gross lesions included widespread haemorrhage, serosanguineous effusions in the body cavities and multiple pinpoint white to yellow foci in the liver. Microscopically, there was multifocal hepatic coagulative necrosis associated with intranuclear acidophilic inclusion bodies in sinusoidal endothelial cells. Similar endothelial lesions were observed in the myocardium, fat bodies, kidneys and spleen. Transmission electron microscopy revealed numerous virions (100-110 nm) in the nuclei of endothelial cells and intracytoplasmic enveloped virions (140-150 nm) were also found. The gross and histological findings and the ultrastructural features of the intranuclear inclusions and viral particles were consistent with herpesviral infection. To the best of our knowledge, these are the first reported cases of a lethal herpesvirosis in horned vipers and the second report in snakes.

21-Year-Old Male Trauma Patient With Skin and Liver Lesions, Hepatitis, and Coagulopathy

A 21-year-old African-American male suffered multiple injuries from an improvised explosive device while deployed in Afghanistan. His trauma resulted in severe soft tissue injuries involving the posterior upper arms and left shoulder, as well as the left flank, which communicates with the abdominal cavity. A splenectomy was required due to the splenic lacerations that he received. During his hospital course, the complication of polymicrobial wound infection occurred, which required repeated debridements with wound vacuum (WV) placement and broad spectrum antibiotic coverage. Ten days after his injury, he developed coagulopathy with persistently bloody WV output that required multiple transfusions of packed red blood cells, platelets, and cryoprecipitate. The patient had no known prior medical problems, and there was no report of unusual exposures to pathogens during his 8 months of deployment. On examination, the patient was febrile, hypotensive, tachycardic, intubated, and sedated. Two weeks after his injury and during surgical intervention for wound debridement and wound hemostasis, his surgeon noted several yellow, soft, slightly raised, pustular lesions on the surface of his liver, 1 of which was biopsied. The patient also developed pustular skin lesions on his forehead, right axilla, and right thorax, 1 of which was also biopsied (Figure 1). His laboratory test results during this episode were as follows: white blood cell count 20.6 × 10(3)/μL with 23% bands; hemoglobin 11.5 g/dL; hematocrit 22.2%; platelet count 47 × 10 (3)/μL; prothrombin time 17 seconds; partial thromboplastin time 33 seconds; international normalized ratio 1.3; aspartate aminotransferase 873 U/L; alanine aminotransferase 470 U/L; total bilirubin 7.1 mg/dL, and direct bilirubin 6.9 mg/dL. His liver biopsy showed multifocal coagulative necrosis without zonation. His skin biopsy was diagnostic (Figure 2). What is your diagnosis?

Haemolytic anaemia and acute pancreatitis associated with zinc toxicosis in a dog

We describe a case of zinc toxicity in a 14-month-old, female, neutered, Cavalier King Charles spaniel with a 48-hour history of haematochezia, icterus and collapse. Regenerative anaemia with a packed-cell...

Detection of Infectious Bovine Rhinotracheitis in Natural Cases of Bovine Abortion by PCR and Histopathology Assays

Bovine herpesvirus 1 (BHV-1), the causative agent of infectious bovine rhinotracheitis (IBR), is considered to be the most common viral pathogen found in bovine. Bovine Herpesvirus 1(BHV-1) belongs to the genus of Varicellovirus and the family of Herpesviridae which contains three main gB, gC and gD genes. The objective of this study was to determine the relation between type of macroscopic lesions and bovine herpesvirus-1(BHV-1) infection; hence the aborted fetus specimens were initially prepared for PCR test. In this study, 23 of fetus samples, which were transferred to Veterinary Laboratories during 2009-2012, were assessed for BHV-1 with PCR in lung and spleen tissues and all of positive samples undergone histopathological study. The results indicated myocarditis and necrosis of cardiac tissue in 8 cases (42.1%), and 6 cases encompassed interstitial lymphocytic pneumonia (28.57%), whereas 5 cases revealed bronchopneumonia (23.8%) and in 8 cases (38.09%) severe interstitial edema was observed. In addition, the lesions may be associated with BHV-1, so that in brain tissue 9 cases (36 %) possessed encephalitis and necrosis, 8 cases (38.09%) indicated interstitial nephritis, 2 cases (9.52%) developed acute tubular necrosis, 2 cases (9.52%) revealed vacuolar degeneration inrenal tubular epithelium, 1 case had (4.76%) renal hemorrhage and in 3 cases (14.28%) renal autolysis was observable. In liver, 10 cases (47.61%) were affected to lymphocytic hepatitis, 5 cases (23.8%) possessed necrotic hepatitis, 6 cases (28.57%) of multifocal coagulative necrosis without inflammatory reaction and 3 cases (14.28%) with lymphocytic portal hepatitis were observed. In this assessment, 10 specimens (52.17%) of spleen tissues revealed necrosis and lymphatic tissues emptying and in 10 cases (100%) severe enteritis, which may be associated with IBR, were recorded. This study suggests based on lesions in several organs induced by IBR virus and real time PCR confirmation there is direct correlation between virus and lesions, and in order to obtain more reliable results of IBR infection the histopathological examination may be efficient.

Haemolytic anaemia and acute pancreatitis associated with zinc toxicosis in a dog

We describe a case of zinc toxicity in a 14-month-old, female, neutered, Cavalier King Charles spaniel with a 48-hour history of haematochezia, icterus and collapse. Regenerative anaemia with a packed-cell...

Intestinal Volvulus with Coagulative Hepatic Necrosis in a Chicken

A 7-week-old SPF chicken inoculated at 4 weeks of age with chicken anemia virus was puffed up depressed and had ruffled feathers and a good body condition. Intestinal volvulus involving the jejunum and part of the duodenum forming two loops with one knob was observed. Microscopically, venous infarction of the obstructed loops, periportal and sublobular multifocal coagulative hepatic necrosis and granulomatous inflammation of the cecal tonsils were observed. Gram staining revealed no bacteria in hepatic tissue; however, gram-positive bacilli were detected in the necrotic debris in the intestinal lumen. Immunosuppression might have predisposed the chicken to intestinal and cecal tonsil infection that then progressed to volvulus. Loss of the mucosal barrier in infarction might allow bacterial toxins and vasoactive factors to escape into the systemic circulation (toxemia) and be responsible for the hepatic necrosis.

Microscopical Lesions and Antigen Distribution in Bovine Fetal Tissues and Placentae Following Experimental Infection with Bovine Herpesvirus-1 during Pregnancy

As part of a larger investigation, gross and histopathological examinations were carried out on six aborted and one non-viable calf born to heifers inoculated with bovine herpesvirus-1 (BHV-1) early in the third trimester of pregnancy. Antibody titres in sera collected from the dams confirmed seroconversion following inoculation. Samples of liver, lung, kidney, brain, heart, spleen, hepatic lymph node and placenta were subjected to histopathological examination. Immunohistochemistry for the detection of BHV-1 antigen was performed on liver and placenta from each calf, and on the full range of tissue from three of the six calves. Six dams aborted between 15 and 50 days post-inoculation (dpi) whilst one produced a live but non-viable calf at 51dpi. Consistent microscopical findings in tissues from the six aborted calves were multifocal coagulative necrosis in the liver and necrotic placentitis. The latter was characterized by villous necrosis, necrosis of vascular endothelium and infiltration of necrotic villi by mixed inflammatory cells. Other findings included multifocal necrosis in kidney, spleen and hepatic lymph node as well as haemorrhage in the lung and kidney. Immunohistochemistry confirmed the presence of BHV-1 antigen in association with these lesions and also revealed focal labelling of the endothelium of small blood vessels and surrounding glial processes in the brains of three calves. Virus isolation confirmed the presence of BHV-1 in the placentae from the six aborted calves and in pooled tissues of three of the fetuses. It is concluded that the pathogenesis of BHV-1 abortion involves infection of vascular endothelial cells in multiple tissues including placenta and brain. Furthermore, histopathological examination in suspected cases of BHV-1 abortion should include placenta as well as fetal viscera, and immunohistochemistry is a valuable tool for confirming a diagnosis of infection with the virus.

Clostridium piliforme Infection in Two Farm-raised White-tailed Deer Fawns (Odocoileus virginianus) and Association with Copper Toxicosis

Necropsy of 2 white-tailed deer fawns who died acutely revealed diarrhea and melena in case No. 1 and no gross changes in case No. 2. Histologically, the livers of both deer displayed multifocal coagulative necrosis, with infiltrations of neutrophils, macrophages, and lymphocytes. By Warthin-Starry staining, bundles of filamentous bacteria were identified within hepatocytes at the periphery of the necrotic foci in case No. 1. There was multifocal myocardiocyte necrosis in case No. 1 and multifocal lymphoid necrosis of the Peyer's patches in case No. 2. Clostridium piliforme 16S ribosomal ribonucleic acid gene was detected in both livers by polymerase chain reaction (PCR) with C. piliforme-specific primers. The liver copper levels in both cases were normal to slightly elevated. The kidney copper level in case No. 2 was elevated. This represents the first published cases of Tyzzer's disease in deer, a novel use of PCR for the diagnosis of C. piliforme infection, and a possible association between copper toxicosis and Tyzzer's disease.

Successful Treatment and Polymerase Chain Reaction (PCR) Confirmation of Tyzzer's Disease in a Foal and Clinical and Pathologic Characteristics of 6 Additional Foals (1986–2005)

Tyzzer's disease is a rapidly progressive and highly fatal hepatitis of foals caused by Clostridium piliforme. Survival of a confirmed case has not been reported previously. Successful therapy of C. piliforme infection in foals is possible. Polymerase chain reaction (PCR) can be used to diagnose Tyzzer's disease antemortem or postmortem. Seven foals were included in the study. Retrospective study was made to evaluate the clinical and pathologic characteristics of foals with Tyzzer's disease. Medical records of the Veterinary Medical Teaching Hospital at University of California Davis were reviewed. Foals <3 months old were included in the study if typical clinical signs were present and histologic examination identified multifocal coagulative necrosis and hepatitis with intracytoplasmic filamentous bacilli, consistent with C. piliforme. A real-time TaqMan assay was developed to detect C. piliforme gene sequences in liver tissue from affected foals. Median survival time from onset of disease in nonsurviving foals was 30 hours (mean 34.5 +/- 20.1; range, 16-62 hours). Common clinical findings included lethargy, recumbency, seizures, and fever. Laboratory findings included metabolic acidosis, hypoglycemia and increased activity of hepatobiliary enzymes. Treatment consisted of IV fluids, antimicrobial and antiinflammatory drugs, and parenteral nutrition. One filly survived, whereas 6 died. Postmortem examination of the 6 foals that died disclosed hepatomegaly with multifocal necrosis. Liver tissue from 4 foals was positive for C. piliforme gene sequences using PCR. Although the mortality rate of Tyzzer's disease is high, successful outcome is possible if intensive care is initiated promptly. PCR can be used for early and specific diagnosis.

Acute haemorrhagic and hypoxic-ischaemic brain damage in the neonate

Haemorrhage and hypoxic-ischaemic lesions are relatively frequent post-mortem findings in neonates, particularly in the context of low birth weight and prematurity. The most common of the acute abnormalities is germinal matrix haemorrhage, which is often accompanied by haemorrhage into the ventricles. Resolution of haematomas in the germinal matrix and brain parenchyma leaves gliotic cysts. The more severe grades of ventricular haemorrhage are often complicated by the development of hydrocephalus. Other occasional sites of non-traumatic haemorrhage in neonates include the choroid plexus (in which case the haemorrhage is usually an incidental finding), the cerebellum and the subpial region. The pattern of hypoxic-ischaemic damage in neonates varies with gestational age. In premature infants the cerebral white matter is particularly susceptible. The manifestations range from relatively selective apoptotic loss of oligodendrocytes in telencephalic leukomalacia to focal or multifocal coagulative necrosis in periventricular leukomalacia. Ischaemic degeneration of neurons may also occur, mainly in the basal ganglia, thalamus, cerebellar granule cell layer and brain stem, and apoptosis is usually prominent. In term infants, hypoxic-ischaemic damage is most prominent in the grey matter and manifests itself with various combinations of neuronal apoptosis, selective neuronal necrosis and frank infarction, that can involve the cerebral cortex, basal ganglia, thalamus, cerebellar cortex, cerebellar dentate nucleus and brain stem. Recent research has shed some light on the pathogenesis of neonatal haemorrhagic and hypoxic-ischaemic lesions and has helped ameliorate some of the complications. Accurate assessment and documentation of the pathology of perinatal brain damage is important for providing information for the studies on which these advances depend.