家兔亚硒酸中毒的病理形态学研究

给家兔分别肌肉注射不同剂量的亚硒酸钠，历时入周，复制出亚急性硒中毒的动物模型。病理形态学变化为：家兔的生长受到明显抑制，肝，肾，心，脾等组织器官损害严重如肝实质细胞变性，坏死；肾实质退行病变；心肌纤维变性，充血，肺淤血，水肿：脾萎缩，淋巴细胞坏死，肝，肾，心细胞内线粒高度肿胀，嵴减少，断裂或消失成空泡。     

An outbreak of influenza (H1N1) in turkey breeder hens

Outbreaks of influenza were diagnosed in two turkey breeder flocks on the same premises in eastern North Carolina during the "dark-out" period of recycling for a second lay. Clinical history included increased mortality from acute death with no apparent predisposing illness. Mortality attributed to the disease was 4.5% in one flock and 3.3% in the other. Necropsy findings included severe diffuse congestion and edema of both lungs, with little or no pleural exudate. Spleens were moderately to markedly enlarged and mottled, and kidneys were swollen and congested. Microscopic lesions included moderate to severe serofibrinous pneumonia with severe pulmonary congestion. Splenic changes included fibrin deposition and severe congestion, and severe congestion was noted in kidneys. Influenza virus (H1N1) was isolated from pools of tissues including lung, spleen, liver, and kidney, and both flocks seroconverted to influenza (H1N1) virus.     

Septicemic proteus infection in Japanese quail chicks (Coturnix coturnix japonica)

Proteus infection was incriminated as the cause of severe depression, coma, and high mortality in successive broods of quail chicks. The pathological lesions comprised congestion of lungs, liver, and kidneys and mucus exudation in the trachea. The organism, isolated from the heart blood and lungs of affected chicks, was identified on biochemical tests as Proteus mirabilis. Pathogenicity of the isolate was tested in young albino mice and week-old quail chicks, which succumbed to infection within 48 hours of inoculation. Association of P. mirabilis with septicemic disease in Japanese quails has apparently been demonstrated for the first time.     

Pathologic and immunohistochemical studies of Newcastle disease (ND) in broiler chickens vaccinated with ND: severe nonpurulent encephalitis and necrotizing pancreatitis

Twenty-five 22- to 46-day-old broilers with Newcastle disease (ND) were investigated pathologically and immunohistochemically in order to evaluate the mechanism of ND outbreak in vaccinated broilers. The broilers were vaccinated with ND live vaccine via drinking water. Clinical signs were neurologic and respiratory in nature. Macroscopically, bursal atrophy, white spots on the pancreas, and discoloration and enlargement of kidneys and spleen were observed in the broilers. Histologically, perivascular cuffing, neuronal degeneration and necrosis, and glial proliferation were present in the cerebrum, cerebellum, and medulla oblongata. There was extensive rarefaction and malacia in the parenchyma of severely affected brains. There were extensive degeneration, necrosis, and depletion of acinar cells in the pancreas. There was proliferation of macrophages in the lungs with congestion, tubulointerstitial nephritis, hepatocytic necrosis with thrombi in the sinusoids, and lymphocytic depletion in the cloacal bursa. Immunohistochemically, ND virus antigens were detected in the lesions. ND virus isolated from the present cases did not cause encephalitis or pancreatitis in specific-pathogen-free chickens, but it induced mortality with hepatocytic sinusoidal thrombi, splenic necrosis, lymphoid necrosis and depletion, and conjunctival hemorrhage. Severe nonpurulent encephalitis with extensive rarefaction and malacia, and necrotizing pancreatitis in the present case may suggest a close possibly causal relation with vaccination.     

The chronic toxicity of inorganic mercury in goats: clinical signs,toxicopathological changes and residual concentrations

Chronic mercury toxicity was induced in goats by administering mercuric chloride at 100 µg/ml in deionized drinking water offered ad libitum for 90 days. Toxic signs of gastrointestinal disturbances and renal dysfunction developed from 43 days onwards without any mortality. The toxicity also induced nephrosis and tubular nephritis; centrilobular necrosis of liver; mild to moderate necrosis in spleen, intestine and lymph node; Zenker's degeneration of cardiac muscles; exudative pneumonia; and pial congestion, oedema and vacuolation in the brain. In addition, hyperaemia, oedema and tissue haemorrhages were evident in most of the organs. The kidneys contained the largest residues of mercury, followed by liver, spleen, intestine, lymph node, skeletal muscles, lungs, heart, brain and the omental fat. The intensity of the cytotoxic changes in the various organs was proportional to the amount of mercury accumulated.     

Gossypol toxicosis in a dog consequent to ingestion of cottonseed bedding.

Six dogs died after accidental ingestion of cottonseed bedding. No clinical signs of illness were observed prior to death. A full diagnostic workup was performed on one of these dogs. At necropsy, the lungs were congested and edematous, and the liver was firm, congested, and had a marked reticular pattern. There was also moderate ascites. Histopathologic examination revealed multifocal myocardial degeneration and necrosis, severe pulmonary edema, and chronic passive congestion of the lungs, heart, liver, and kidneys. Transmission electron microscopy of the myocardium revealed disruption of myofibrils, chromatin condensation, and disrupted and swollen mitochondria. The cottonseed bedding contained 1,600 mg/kg of free gossypol, a concentration considered toxic for monogastric animals. The stomach content revealed the presence of gossypol, thus confirming ingestion of cottonseed. Gossypol poisoning in dogs is extremely rare and has not yet been associated with cottonseed bedding. This first documented case of gossypol poisoning in a dog, caused by the ingestion of cottonseed bedding, demonstrates how specific toxicological analysis is crucial in reaching an accurate diagnosis.     

Pathology of Aujeszky's disease in mink

Lesions in 21 mink which died of Aujeszky's disease included hemorrhages in lungs, heart, mediastinum, thymus, diaphragm, gastric wall, pancreas, and enteric wall. Microscopically, hyalin and fibrinoid degeneration and necrosis of vessel walls were present in cardiac muscle, brain, gastrointestinal wall and occasionally elsewhere in the body. Hemorrhages, exudation of plasma proteins and necrosis were associated with the angiopathy. Inflammation was minimal or absent. Other findings were congestion and extravasation of blood (lungs, liver), necrosis of lymphoid cells, and hemoglobinuric nephrosis. Aujeszky's disease virus was isolated from all but three animals. After experimental infection of three mink, similar though less pronounced lesions were found to those observed in the field cases.     

Dirofilariasis in wild canids from the Gulf coastal prairies of Texas and Louisiana,U.S.A.

Heartworms, Dirofilaria immitis, were recovered from 17 out of 24 (71%) coyotes, Canis latrans, 38 out of 46 (83%) coyote × red wolf hybrids and all of 8 (100%) red wolves, Canis rufus gregoryi, collected from the Gulf coastal prairies of southeast Texas and southwest Louisiana. Intensities of infection ranged from 1 to 176 ($\text{x}\text{=25}$) worms per host. There was a significantly (P<0.05) higher intensity of infection in red wolves. Prevalence of heartworms increased significantly with increasing age. There were no significant differences between coyotes, hybrids and red wolves or between different host sexes in terms of prevalence. The female to male ratio of heartworms was close to unity (1.2:1) and was not correlated with worm burdens. Nematodes were primarily localized in the right heart, frequently extending into the pulmonary artery and the pulmonary arterial tree in the lungs. In 13 instances, 1–4 adult heartworms were recovered from the venae cavae. Pathological responses in the right heart were variable, depending on the intensity of infection. In severe infections, there were small areas of infarctive necrosis with mild to severe interstitial edema in the myocardium. Lesions in the pulmonary artery and pulmonary arterial trunk varied from mild focal hyperplastic intimal changes to extensive exudative villous endarteritis. The latter was characterized by a hyperplastic collagenous stroma with numerous histiocytes, plasma cells and eosinophils. Lung pathology varied from patchy to extensive areas of congestion, edema, hemorrhage, interstitial pneumonitis and infarction. In cases with heartworms in the venae cavae, hepatic changes were minimal and associated with liver changes such as passive congestion and centrolobular necrosis seen in cases without adult worms in the venae cavae. In heavily infected animals, hemosiderosis of the liver, spleen and kidneys was pronounced. A microfilaremia was noted in 46% of the infected wild canids. Microfilariae were observed in tissue sections of the myocardium, lungs, liver, kidney, spleen, lymph nodes, pancreas and appendix. Wild canids from this area are regarded as natural definitive hosts and primary reservoirs for heartworms and it appears that this infection is an important factor in the morbidity and mortality of these hosts.     

Abortion in goats by Caprine alphaherpesvirus 1 in Spain

An abortion outbreak occurred in a goat herd of Murciano‐Granadina breed in Almeria Region in Spain where 80 pregnant females aborted. All bacteriological and parasitological examinations resulted negative, whereas virological investigations and real‐time PCR assay showed the presence of Caprine alphaherpesvirus 1 DNA in the pathological specimens from aborted foetuses. Nucleotide sequence analysis revealed that the DNA was highly close related to the Swiss strain E‐CH (99.7%) and a little less extent to the Italian BA.1 strain (99.4%). Histopathological examination revealed multifocal, well‐circumscribed, 50‐ to 200‐μm‐diameter foci of coagulative necrosis in the liver, lungs and kidneys of three foetuses. In the periphery of the necrosis, there were frequently epithelial cells with the chromatin emarginated by large, round, amphophilic intranuclear viral inclusion bodies. The source of the infection in the herd could not clearly find out even some hypothesis were formulated. This seems to be the first report of an abortion outbreak due to Caprine alphaherpesvirus 1 in a goat herd in Spain.     

Pathogenesis of Aspergillus fumigatus infection in pigeons in the Sudan.

The pathogenesis of a pigeon isolate of Aspergillus fumigatus in a local breed of pigeons in the Sudan was tested. The spores inoculated intravenously resulted in an acute disease with 100% of mortality within six days. At necropsy, pinpoint and miliary lesions were prominent in the liver, spleen, lungs and kidneys. Histopathological examination detected lesions in the liver, heart, lungs, kidneys, spleen and brain. Hyphae and/or spores were encountered in all these organs. The presence of A. fumigatus was confirmed by reisolation from the liver, lungs and kidneys.     

Fatal intraoperative pulmonary fat embolism during cemented total hip arthroplasty in a dog

A 3-year-old, German shepherd dog died suddenly during cemented total hip arthroplasty. Gross necropsy findings included severe pulmonary edema and congestion as well as congestion of the liver and kidneys. Acute pulmonary embolism was suspected as the cause of death. Microscopic examination of hematoxylin and eosin-stained, formalin-fixed, and oil red O-stained frozen tissue sections confirmed the presence of large numbers of fat globules in blood vessels in the lungs, liver, and kidneys. Fat embolism during total hip arthroplasty is a common surgical complication in humans, but it is uncommon in veterinary cases and is rarely a cause of death.     

Pathological Studies of “Sudden Death Syndrome” in Broiler Chickens

Sudden death syndrome usually occurs in heavy, fast-growing and healthy-looking broilers. Most of the affected birds are males. The characteristic necropsy changes are seen in well-fleshed broilers with edema and generalized pulmonary congestion, recently ingested feed in the crop and gizzard, distended intestine with creamy content and empty gall bladder. The liver and kidneys are slightly enlarged and the latter have patchy areas of subcapsular hemorrhage. The heart contains clotted blood in the atria but the ventricles are often empty and the left ventricle in particular assumes a hypertrophied appearance.Microscopic examination of heart muscle reveals degeneration of fibers, separation of cardiac muscle fibers by edema and infiltration of heterophils. The lungs have severe vascular congestion, inflammatory cell infiltration in the mucosa of the secondary bronchi and edema fluid in the tertiary bronchi and interlobular connective tissue. The liver has moderate bile duct hyperplasia, periportal hepatitis and mononuclear cell infiltration adjacent to bile ducts which possibly leads to bile duct constriction. The kidneys have subcapsular and parenchymatous hemorrhage.     

The first outbreak of fowl cholera in Muscovy ducks (Cairina moschata) in Japan.

The first outbreak of fowl cholera occurred in a flock of Muscovy ducks (Cairina moschata) in Okinawa Prefecture of Japan in November 1990. Fifty (25%) of 200 birds in a farm died of an acute disease. Remaining birds recovered after treatment with oxytetracycline. Pasteurella multocida subsp. multocida was isolated in pure culture from all tissues tested from two dead birds. Serovars of the isolates were identified as Carter's capsular type A. Heddleston's type 3.4.12, and Namioka's type 5:A which have not been demonstrated in Japan. Pathologically, multiple necrosis and bacterial aggregates were prominent in several organs, particularly in the liver. The isolate killed chickens when inoculated intravenously at a concentration of 10(8) colony forming units.     

Caprine mycoplasmosis: an outbreak of mastitis and arthritis requiring the destruction of 700 goats

An acute outbreak of mastitis and arthritis in a herd of 700 goats required the destruction of all but the few animals that were held for observation. The milk of nearly all of about 400 lactating does contained almost pure cultures of Mycoplasma putrefaciens with counts in 150 samples up to 1 X 10(9) colony forming units/ml. At post mortem examination the joints of both the adults and kids contained a fibrinopurulent discharge. M putrefaciens was isolated in pure cultures and large numbers from joints, tissues and fluid not previously known to harbour this mycoplasma: brain, kidneys, lungs, lymph nodes, uterus and urine. The outbreak was milkborne and initiated by infusion of the pathogen into the teat canal by poor hygiene in the milking parlour and by feeding raw colostrum to kids. All but 12 of the herd of 700 goats were killed or sold for slaughter.     

The toxicity of Senecio inaequidens DC

This study was designed to confirm the toxicity of a plant implicated in an outbreak of poisoning of stock in Frankfort, Free State Province, South Africa. Cows died acutely after being introduced into a camp, where an abundant, green shrublet was noted to be heavily grazed. This plant was subsequently identified as Senecio inaequidens DC. (Asteraceae) by the South African National Biodiversity Institute (SANBI). Extraction and chemical analyses for pyrrolizidine alkaloids (PAs) in Senecio inaequidens revealed the presence of 4 different compounds, namely retrorsine and senecionine (known to be hepatotoxic) and 2 unidentified compounds. The average total PA (free base plus N-oxide) concentration in plant parts of S. inaequidens collected at Frankfort during the outbreak was 0.81%, compared with the total alkaloid content in the dried, milled S. inaequidens plant material, collected 7 weeks after the outbreak, of only 0.18%. Male Sprague-Dawley rats (n = 4), aged 8-9 weeks, were dosed per os. Each rat received a different dose of the crude Senecio inaequidens extract, ranging from 0.049 mg/g body weight (b.w.) to 0.25 mg/g b.w. No clinical signs were observed in the rat receiving the lowest dose. Rats receiving higher doses showed depression, an unsteady gait, pilo-erection and jaundice, which was particularly noticeable in the ears. Clinical chemistry evaluation revealed an increase in the activities of ALP (except Rat 4), AST and GGT in all animals. Total serum bilirubin, creatinine and urea concentrations were also elevated. All rats had low serum globulin concentrations with an A/G ratio above 1.2. Post mortem examination of the rats revealed marked hepatic lesions. Histopathologically, these changes were characterised by necrosis (variable in extent) of the centrilobular and midzonal hepatocytes (but sparing the portal hepatocytes), with extensive haemorrhage and congestion. Proliferation of the bile ducts, fibrosis and oedema were also present. Ultrastructural changes in affected rats were characterised by margination of chromatin, the presence of numerous autolysosomes in necrotic hepatocytes, intramitochondrial woolly inclusions and changes in the endoplasmic reticulum. A sheep, also dosed with the crude extract, failed to exhibit clinical signs, clinical chemistry aberrations or macroscopic lesions; however, examination of the liver of this sheep revealed histopathological and ultrastructural changes similar, though milder, to those displayed by the rats. Pyrrolizidine alkaloids were extracted from the liver and kidneys of the rats and the sheep. In the case of the sheep, retrorsine was also detected in the lungs, urine and bile.     

Hepatic Lobe Torsion as a Cause of Colic in a Horse

A 14-year-old Arabian gelding was examined for colic. An exploratory celiotomy was subsequently performed and the left lobe of the liver was found to be twisted. The lobe was resected using a TA-90 surgical stapling instrument. Histologic examination of the resected liver indicated portal vein and sinusoid dilation and congestion with blood. There were focal areas of necrosis and bacterial cocci and rods throughout the section. The histologic findings were consistent with hepatic lobe torsion. After surgery, the horse was treated with broad spectrum antibiotics, anti-inflammatory drugs, heparin, and intravenous fluids. The horse recovered without complications, although serum liver enzymes remained elevated for more than 1 week after surgery. Seven months after surgery the horse showed no adverse affects from the disease.     

MELIOIDOSIS IN A GALAH (CACATUA ROSEICAPILLA)

A second case of a natural infection of melioidosis in a native bird is described. Pseudomonas pseudomallei was isolated in pure culture from the liver, spleen and intestinal contents of a galah (Cacatua roseicapilla). The case was characterised by focal granuloma formation, often associated with necrosis, in the brain, lungs, liver, spleen and kidneys.     

Outbreak of salmonellosis in a zoologic collection of lorikeets and lories (Trichoglossus,Lorius, and Eos spp.)

During August 2001, a syndrome characterized by acute lethargy and dyspnea was observed in a population of 45 lorikeets and lories in an open-air zoologic exhibit. The first death occurred on August 10, and within the next 12 days, nine more birds died (22% mortality rate). Hepatomegaly, reddening and congestion of the lungs, and injection of the serosal surface of the intestines were the common gross findings. Histologic changes, including fibrinonecrotic hepatitis and splenitis, bacterial emboli (liver, spleen, lung, kidney, proventriculus), pulmonary congestion and hemorrhage, and enteritis, were indicative of an acute, overwhelming bacterial septicemia. Salmonella typhimurium, with the same antibiogram, was isolated from four birds. Several birds had attacked and killed a snake on July 24, and Salmonella serogroup B (untypeable) was isolated from intestine and kidney samples of a garter snake caught in the open-air exhibit on August 28. Salmonella was also isolated from environmental samples of the exhibit but not from food preparation areas. After antimicrobial therapy, Salmonella spp. was not isolated from the surviving birds. The source of Salmonella in this outbreak remains unknown, but infection either directly or indirectly from snakes in the exhibit is possible. Contact between captive psittacine populations and reptiles should be avoided to prevent the risk of salmonellosis.     

Note on the pathology of experimental infection of pigeons by the pigeon paramyxovirosis type I (PPMV-1)

Oral, intramuscular or intravenous experimentally induced infection of pigeons by paramyxovirosis serotype I (PPMV-1) resulted in nervous signs, and diarrhoea. Necropsic examination showed mild to moderate congestion of viscera and catarrhal enteritis. Histo-pathological changes were most frequent in the central nervous system, followed by kidneys, liver, pancreas, intestines and lungs, together with mild to severe non-purulent meningoencephalitis.     

Isolation and Identification of Respiratory Pathogens of Chicken

This study was aimed to provide the basis for prevention and control of development of a new product for bacterial respiratory disease of chicken.Diseased samples such as throat, trachea and lungs were inoculated on various selected media for isolating bacteria.17 isolated strains were identified by biochemistry assay and PCR, and then animal experiment were carried out.Black and glassy surface with metallic shine colony from EMB medium Gram-negative bacilli were observed under optical microscope.1 500 bp products were specifically amplified by PCR.DNA sequencing results were analyzed by BLAST and DNAStar with 16S rDNA sequence in GenBank.The results showed that the strains were identified as Escherichia coli.It could cause damage infection with the isolated bacteria through noses.Significant blood spots were observed on throat.Trachea was congestion, swelling and studded with blood points.Heart and liver were wrapped with yellow cheese substances.Air sac was yellow and opaque.The isolated bacteria could provide basis for developing a new product.