犊牛磺胺中毒的病理形态学观察

为了解犊牛磺胺中毒的病理形态学变化特点,对2头因磺胺中毒而死亡的犊牛进行了详细的病理学研究.结果表明,犊牛磺胺中毒的病理性损伤主要发生于肾脏和肝脏.宏观检查可见,肾脏肿胀,色泽变淡,皮质增宽,肾盂有多量豆腐渣样物质.肝脏肿胀,淡橘红色,质地脆易碎.微观检查可见,近曲小管上皮细胞肿胀,核浓缩,染色不良,大量上皮细胞脱落....     

Experimental infection of guinea pigs with Chlamydia. 1. Pathomorphological studies]

The changes that occurred following nasal instillation of a bovine strain of Chlamydia psittaci were characterized by hypertrophy and proliferation of epithelial cells and exudates containing polymorphonuclear leukocytes, with acute bronchopneumonia and less intense inflammatory reactions in nasal and tracheal mucosa, spleen and pulmonary lymph nodes. The intestines, liver, kidney and brain were scarcely affected. There was little prospect of complete recovery from the clinically mild, or even subclinical, pneumonia within the period of observation since the causal agent was present continuously from the 12th hour to the 91st day after infection.     

Pathology of sporotrichosis in 10 cats in Rio de Janeiro

Ten cats with sporotrichosis were examined clinically and pathologically. They were in very poor general condition, and had widespread ulcerated cutaneous lesions and respiratory signs. Gross internal abnormalities were found only in the lungs and lymph nodes. Histologically, an inflammatory infiltrate and yeast-like structures were observed in the skin, lungs, liver and lymph nodes. The spleen was congested and contained fungal elements. No microscopical changes were observed in the pancreas, kidneys and heart. Sporothix schenckii was isolated from all the skin samples and nasal swabs obtained in vivo, and from all the samples of lung, liver, spleen, lymph nodes, heart and kidney taken postmortem.     

Pathological Changes in Virus Enteritis of Mink

The lesions which characterize viral enteritis of mink (VEM) were studied in twenty-six, ten-week-old mink which had been infected by force feeding a tissue suspension containing a Wisconsin strain of mink enteritis virus. The pathogenesis of the lesions was reconstructed from gross and histopathological changes observed in animals which were selected randomly from the group each day for necropsy during the course of the disease.

Alterations were observed in the tissues of all mink examined from post-inoculation day (PID) 4 through 13. The principal macroscopic lesions which consisted of fibrinous enteritis, enlargement and hemorrhage of the spleen and edema of mesenteric and hepatic lymph nodes were most conspicuous on PID 7 and 8. Histopathological changes including necrosis and desquamation of intestinal epithelium, depletion of mature lymphocytes in lymph nodes, thymus and spleen and loss of partly differentiated myeloid and erythroid cells from spleen and bone marrow also reached full development on PID 7 and 8. However, nuclear inclusion bodies which were presumed to be a product of the causative agent and, therefore, of diagnostic significance were most prevalent on PID 3, 4 and 5. The inclusions were observed in mucosal epithelial cells of the intestine, parenchymal cells of the liver and in lymphocyte precursor cells of the spleen, intestinal lymph nodules and masenteric and hepatic lymph nodes.

     

Violet mink develop an acute disease after experimental infection with Aleutian disease virus (ADV) isolate ADV SL3

Six-Aleutian (aa)-genotype violet mink were infected intraperitoneally with the Aleutian Disease Virus (ADV) bone marrow derived isolate ADV SL3. All animals developed virus-specific antibodies and hypergammaglobulinaemia. Mortality during the fourteen week duration of the infection was 50%. The virus induced (histo)pathological lesions typical for Aleutian Disease. By immunohistochemical examination using a virus capsid-specific monoclonal antibody viral antigen was detected in lymph nodes, spleen, kidneys and once in hepatic Kupffer cells. By Southern blot and in situ hybridization studies with strand-specific RNA probes able to distinguish viral replicative forms from merely sequestered genomic DNA, ADV replication was detected in mesenteric lymph nodes and spleen. In one mink DNA replicative forms were also found in bone marrow cells or mononuclear cells of the peripheral blood, respectively. Only single-stranded viral DNA was detected in liver, kidney, gut and lung of infected animals. From Southern blot hybridization results a different, possibly organ-specific permissiveness of ADV in vivo is suggested.     

Experimental bedsonia infections in calf. 2. Pathomorphologic studies]

Tracheal inoculation of bovine strains of Bedsonia was often followed by inflammatory processes in lung, trachea, nasal mucosa and also spleen, lymph nodes and brain. Lesions in the duct system and alveoli of the lung consisted of exudates containing neutrophilic granulocytes and proliferation of epithelial and mesenchymal cells. The initial changes were evidently located in the bronchioli. Elementary bodies were present in variable numbers. The formation of lesions seemed to be influenced by route of infection and concentration of the causal organisms in the inoculum.     

Mycobacterium avium abortion in a sow.

A 2-year-old sow aborted her entire near-term litter of 11. Gross and histologic examination of a fetus suggested a tuberculous infection, and a yellow-pigmented Mycobacterium avium serotype 1 was subsequently isolated from the fetal tissue. Efforts to rebreed the sow were unsuccessful. She was anergic to skin tests with purified protein derivative of M. avium on two occasions but had M. avium specific in vitro lymphocyte immunostimulation. Gross granulomatous lesions were found in the liver, kidneys, and endometrium when the sow was necropsied 5 months after the abortion. Histologic examination showed diffuse and focal non-encapsulated granulomas in lymph nodes, tonsils, kidney, liver, spleen, lung, and uterine and vaginal walls. There were a few encapsulated calcified foci in the endometrium. The centers of some granulomas in the tonsils, liver, kidneys, and some lymph nodes were caseated. The yellow-pigmented M. avium was isolated from the reproductive organs and from 11 of 12 other tissues cultured.     

The dynamics of the microbial count in experimentally-induced salmonellosis of calves

Numerical developments of pathogens were followed up in intestinal matter, mucosa, and lymph nodes as well as in spleen and liver of calves which had been orally infected with Salmonella (S.) dublin or S. typhimurium. Massive flooding of the organism with Salmonellae and eventually fatal proliferation were found to be possible immediately after infection or after some days of pathogen-host equilibrium. Complete elimination of Salmonellae was found to be achievable even after infestation of spleen and liver. Intestinal lymph nodes, in addition to intestinal mucosa and intestinal matter, proved to be of decisive relevance to pathogenesis of the infection and to persistence of germs.     

Visceral leishmaniasis in the German shepherd dog. II. Pathology

Three German shepherd dogs were inoculated with Leishmania chagasi and three with Leishmania donovani and the infection was followed for 82 days. All infected dogs developed splenomegaly and lymphadenomegaly. In lymph nodes there was a reduction in lymphocyte population in paracortical areas, extensive proliferation of macrophages in paracortical areas and medullary cords, follicular hyperplasia, and increased numbers of plasma cells. The spleen had decreased numbers of lymphocytes in periarteriolar lymphoid sheaths, proliferation of macrophages in these regions, follicular hyperplasia, and enlargement of the red pulp with clusters of macrophages and plasma cells. The morphology of the tonsil was similar to the lymph nodes. Clusters of macrophages, often containing Leishmania spp, were present in liver, bone marrow, lung, and the intestines. The morphologic changes in lymph nodes and spleen were suggestive of a suppressed cell-mediated immunity and an active humoral immunity. The German shepherd dog may be a useful laboratory model for the study of immunopathologic changes in visceral leishmaniasis.     

Lysozyme in calves

Relatively high lysozyme concentrations, depending on age, were recorded from intestinal content, spleen, liver, kidney, lung, lymph nodes, and mucosa of calves. Yet, only minor quantities of lysozyme were found in blood serum or plasma and in granulocytes. Physicochemical characterisation, precipitation, using polyclonal antisera, and crosswise neutralisation of lysis reaction were likely to suggest occurrence of immunological relationship reactions as well as differences between organ lysozymes, on the one hand, and intestinal lysozymes, on the other.     

小尾寒羊绵羊痘病例的诊断

旨在对甘肃某羊场小尾寒羊疑似绵羊痘进行确诊,并深入探讨其病理变化特点。对临诊疑似患绵羊痘的小尾寒羊进行了羊痘间接ELISA抗体检测和PCR检测确诊,并对6只病羊进行病理剖检、病理组织学和超微结构研究。结果如下：羊痘间接ELISA抗体检测显示6例病羊样品均为阳性;同时,对2例病羊样品进行PCR检测,均扩增出绵羊痘病毒（SPV）585 bp的目的基因片段,表明本次小尾寒羊所患疫病为绵羊痘。病理剖检显示,病羊皮肤无毛或少毛处充血,局部有红斑和坏死,尾部常有感染化脓形成溃疡;消化道黏膜,尤其舌和瘤胃黏膜有大小不等痘疹与坏死病灶,局部甚至形成糜烂或溃疡。肺膈叶以及肝、脾等常有痘疹和坏死病灶。病理组织学观察显示,肺痘疹病灶主要呈现渗出-增生结节和坏死-增生结节变化,病灶内血管、细支气管等周围常有大量绵羊痘细胞,胞质内有嗜酸性包涵体;病变消化道黏膜局部,上皮细胞程度不等增生、水泡变性,固有层及黏膜下层充血、水肿,有大量绵羊痘细胞,其细胞质内包涵体明显。肝、脾、肾也有程度不等坏死-增生结节变化。肺超微结构观察显示,肺泡上皮细胞肿大,细胞核浓缩、染色质聚集,线粒体程度不等肿胀、嵴断裂、空泡化,可见细胞质内包涵体。研究证明,除局部皮肤病变外,消化道黏膜和肺等实质器官的痘疹病变是患绵羊痘小尾寒羊具代表性的病理变化,尤其痘疹病灶中大量绵羊痘细胞的出现具有证病性意义。     

Pathogenesis of Trypanosoma (brucei) evansi in small East African goats

Trypanosoma evansi is the cause of surra, a camel disease which is the most important single cause of economic losses in camel rearing areas. Sheep and goats herded with camels are the most likely hosts for T evansi. Upon intravenous infections goats developed erratic parasitaemia, lost weight and their packed cell volume dropped significantly (P<0–001). Trypanosomes were demonstrated by direct microscopy in extravascular locations such as synovial, peritoneal and cerebrospinal fluids and also in lymph by subinoculations into mice. The carcases were emaciated and pale. Histologically there was lymphatic tissue hyperplasia, muscular atrophy and nephrotic changes. Two animals had necrotic foci in the liver, kidneys, lymph nodes, spleen and lungs and also bronchopneumonia. Histologically there was depopulation of lymphocytes in lymphatic tissues, destruction of hepatocytes in the liver with infiltration by inflammatory cells in the liver, lymph nodes, spleen and the kidneys.     

Lesions in clinically healthy cattle persistently infected with the virus of bovine viral diarrhea--glomerulonephritis and encephalitis

Four clinically healthy cattle persistently infected with the virus of bovine viral diarrhea were examined for viral antigen and lesions. Antigen was seen by direct immunofluorescence in cytoplasm of the neurons of the brain and cervical part of the spinal cord, cells and basement membrane of renal glomeruli, reticular cells of lymph nodes and spleen, epithelial cells of small intestinal crypts and renal and testicular tubules, and endothelial cells of blood vessels. Infected neurons were pyknotic and surrounded by astrocytes and macrophages. A few blood vessels in the brains were cuffed with mononuclear cells. Basement membranes of renal glomeruli were irregularly thick with eosinophilic material, and mesangial cells in the glomeruli were plentiful. The virus had a direct effect on some tissues, but was restricted in its cytopathogenicity and was not eliminated by defense mechanisms of the host. Renal glomerular lesions were believed to have an immunologic basis.     

Plasma cell myeloma producing IgG, IgM, and IgA immunoglobulins in a cow.

A diagnosis of plasma cell myeloma was made in a 6-year-old Holstein cow that showed continuous nosebleed, progressing emaciation, and hyperglobulinemia. Necropsy revealed enlargement of the caudal mesenteric lymph nodes. Lymph nodes and spleen were infiltrated by neoplastic plasma cells. Renal lymph nodes, bone marrow, and kidneys also were affected. Amyloid-like material that was negative for Congo red was present in most of the affected lymph nodes. Congo red-positive amyloid material was noted in spleen, kidneys, liver, and adrenal glands. Neoplastic plasma cells exhibited immunohistochemical reactions for lambda-light chain and 3 classes of heavy chain but not for kappa-light chain. Nonamyloid deposits were labeled with antisera against lambda-light chain and heavy chains. Plasmacytoid cells, which stained positively for IgG, IgM, or IgA, were intermingled in all lesions. Production of 3 types of immunoglobulins may be caused by heavy-chain class switching, constantly occurring in certain proportions.     

山西黄土高原地区羊鼻蝇蛆病流行病学调查和病理学观察

通过对山西黄土高原区域羊鼻蝇蛆感染情况调查和病理学研究,以明确该地区羊鼻蝇蛆的感染率和该病的病理变化。春秋两个季节对羊鼻蝇蛆感染情况进行调查,对307例绵羊进行羊头剖检,检查羊鼻蝇蛆病的各龄幼虫感染情况,同时观察病理变化,并采取感染羊的鼻黏膜、咽后淋巴结、脑和肺组织进行病理组织学检查。春季检查157例,鼻蝇蛆感染患羊34例,感染率达22%;秋季检查150例,感染患羊70例,感染率达47%;春秋两季平均感染率为34%。病理变化主要表现为:鼻黏膜出现不同损伤和增生性炎,咽后淋巴结炎性细胞浸润,有的病例出现肺气肿,脑组织水肿。免疫组织化学染色结果表明,检出虫体的羊与未检出虫体羊比较,咽后淋巴结IgA分泌细胞和IgG分泌细胞呈增高趋势,尤其是淋巴结髓质中IgA分泌细胞和IgG分泌细胞明显增多。     

Mycobacterium bovis infection in the brush-tailed possum (Trichosurus vulpecula): I. Preliminary observations on experimental infection

An Australian cattle strain of Mycobacterium bovis was injected intramuscularly into 10 brush-tailed possums (Trichosurus vulpecula) which were shown to be highly sensitive to experimental infection with this organism. The possums were killed and examined throughout the course of infection. At necropsy, gross and microscopic lesions were recorded and several tissues cultured for recovery of M. bovis. Infection spread rapidly via the lymphatic system from the injection site to the lumbar lymph nodes, then to the spleen. There was a bacteraemia after 2 week and by 6 weeks lesions were present in spleen, lymph nodes, lungs and kidneys; M. bovis proliferated rapidly and host response was minimal. Few organisms were detected in the liver where miliary lesions were found. M. bovis was excreted in large numbers in urine, faeces and discharging sinuses from subcutaneous abscesses. In two possums that died early in the infection, stress had rendered then more susceptible; infection spread more rapidly than in other possums and liver involvement was more severe. Although aerosol transmission was considered to be a possible means of spreading M. bovis, three in-contact possums did not acquire infection.     

Histological and ultrastructural studies of renal lesions in Babesia canis infected dogs treated with imidocarb

Histological and electron microscopic examinations of the kidneys of 8 dogs suffering from fatal, naturally acquired Babesia canis infection and nephropathy are presented. Seven animals were treated with imidocarb dipropionate on average 4.5 days prior to death. Severe anaemia was present only in 2 cases. Degenerative histological changes observed mostly in the proximal convoluted tubules included vacuolar-hydropic degeneration, necrosis and detachment of renal tubular epithelial (RTE) cells from the basement membrane. Necrotic debris occasionally formed acidophilic casts within the tubules. In some cases, necrosis of the whole tubule was observed. Haemoglobin casts in the tubules and haemoglobin droplets in RTE cells seldom appeared. No significant histological changes were seen in the glomeruli. Ultrastructural lesions in RTE cells included nuclear membrane hyperchromatosis, karyopyknosis, karyolysis, swelling or collapse of mitochondria with fragmentation of cristae and vacuolar-hydropic degeneration in the endoplasmic reticulum and microvilli. Nuclear oedema was also observed. Many RTE cells exhibiting necrosis collapsed. Vacuolar-hydropic degeneration and necrosis were also observed in the glomerular and interstitial capillary endothelium. The severe acute tubular necrosis described in this study is probably the result of hypoxic renal injury. Systemic hypotension leading to vasoconstriction in the kidneys might be the most important cause of renal hypoxia in B. canis infections, but anaemia may also contribute to inadequate oxygenation. Imidocarb should be applied with caution in patients with possible renal involvement until further data become available on its potential nephrotoxicity in dogs.     

Porcine postweaning multisystemic wasting syndrome in Korean pig: detection of porcine circovirus 2 infection by immunohistochemistry and polymerase chain reaction.

This report describes the first diagnosis of porcine circovirus (PCV) infection in weaned pigs with postweaning multisystemic wasting syndrome in Korea by immunohistochemistry and polymerase chain reaction. The most unique lesions were multifocal granulomatous inflammation affecting lymph nodes, liver, and spleen, characterized by infiltrates of epithelioid macrophages and multinucleated giant cells. Circoviral antigen was detected in formalin-fixed sections and was usually present in large, round, dendritic cells in the white pulp of spleen and remnants of follicles in lymph nodes. Lymphoid follicles in the tonsils also contained PCV antigen. A 530-bp DNA fragment of circovirus was successfully amplified from all tested lymph nodes, liver, and spleen.     

Adenovirus infection in lambs. II. Experimental infection of lambs.

Adenovirus strain GY/14 isolated during a natural outbreak was used in experimental infection. Three weeks old lambs responded with temperature rise, respiratory symptoms and diarrhoea to the infection. Infection spread to a contact animal, too. Reisolation of the virus was successful from the nasal discharge and feces from the 3rd to 10th, and the 3rd to 5th day following infection, respectively. In the killed experimental animals the pathological and histological changes observed were similar to those observed in natural cases. On comparing the natural outbreaks with the experimental infection the only difference appeared in the severity of the changes. Following the experimental infection characteristic nuclear inclusions appeared in the nasal and bronchiolar epithelium, in the alveolar septal cells and in the reticular cells of the lymph nodes. Epizootiologic observations and experimental results confirm the assumption that our adenovirus strains isolated from natural cases are pathogenic for lambs.     

Extracutaneous histologic changes accompanying zinc deficiency in pups

The extracutaneous tissues in pups fed a Zn-deficient diet were examined. Four pups were fed a Zn-deficient diet and 3 littermates were fed a Zn-adequate diet. After 5 weeks, the pups were euthanatized. Lesions found only in pups fed a Zn-deficient diet were located in the buccal mucosa, lymph nodes, spleen, and thymus. In the buccal mucosa, lesions consisted of irregular epithelial hyperplasia and disruption of epithelial cell layers. There was a marked absence of lymphocytes in the thymus and in T-cell areas of the lymph nodes and spleen.