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PubMed2004

The hydropericardium syndrome in poultry--a current scenario.

Inclusion-body hepatitis hydropericardium syndrome (IBH-HPS) is an important, recently emerged, disease of poultry, particularly of 3- to 6-week-old broiler chicks, characterized by its sudden onset, with high mortality ranging from 20% to 70%, typical hydropericardium and enlarged mottled and friable livers, with intranuclear inclusion bodies in the hepatocytes. The causative agent is a non-enveloped icosahedral fowl adenovirus (FAV) serotype 4, belonging to the Adenovirus genus of the family Adenoviridae, which can be propagated or cultivated in chicken embryo liver and kidney primary cell cultures. The transmission of disease occurs vertically and laterally by the oral-faecal route. The liver of infected birds shows necrotic foci and basophilic intranuclear inclusion bodies in the hepatocytes. The disease can be diagnosed from its gross and histopathological changes in the liver and by various serological tests, such as agar gel immunodiffusion, counterimmunoelectrophoresis, indirect haemagglutination, the fluorescent antibody technique, enzyme-linked immunosorbent assay and the polymerase chain reaction. The disease has been brought under control by the use of formalin-inactivated vaccines, prepared from infected liver homogenate, and of inactivated cell culture vaccines. The vaccines are effective in the face of natural outbreaks or experimental challenge and significantly reduce the mortality.

Adenoviridae Infections↗

PubMed1980

Changes of the central nervous system in herpes zoster.

Postmortem examination was conducted in eight cases of neurocutaneous herpes zoster. One generalized case with diffuse and focal meningoencephalomyelitis showed numerous infiltrates in the subarachnoid space and along the cerebral ventricles. Intranuclear inclusion bodies could be demonstrated for the first time in ependymal and in arachnoidal cells, and viral capsids were found in the latter. The parenchymal lesions, lying predominantly in the white matter, were characterized by inflammation, hemorrhage, axonal swellings, demyelination, and intranuclear inclusions in oligodendrocytes. In the second generalized case there was a granulomatous giant cell angiitis with intranuclear inclusions bodies in the vessel walls. Out of four cases with localized damage of the central nervous system (CNS), three showed demyelination as the main alteration. In another case there was a hitherto undescribed calcifying coagulation necrosis of a spinal ganglion.

Adult↗

PubMed1999

[Elephant herpes virus--a problem for breeding and housing of elephants].

Herpesvirus infections which take a fatal turn on African elephants as well as on Asian elephants seem to occur increasingly not only in the USA but also in European stocks. The endotheliotropic herpesvirus causes a rapidly progressing and severe disease which makes any therapeutical effort unsuccessful and finally results in death of the animal, especially in young Asian elephants. As all attempts to culture the virus failed up to now, molecular biological procedures have to be used more often for diagnostical purpose together with the common methods of pathology, virology, and electronmicroscopical evaluation. This is a report on the case of 'KIBA', an eleven year old male elephant at the Zoological Garden Berlin, infected with the endotheliotropic elephants herpesvirus. 'KIBA' was born at the Zoo in Houston, Texas, and raised within his herd. Upon arriving in Berlin in November 1997 he adapted to the new premises and climate and new social circumstances without any problems. In June 1998 he already serviced three females of his new herd several times. In August 1998 he died after passing a peracute progression of the disease after residenting in Berlin for only 9 months. The dissection of the animal revealed some evidence on an agent damaging the endothelium. Major signs indicating this agent were bleedings in several serous membranes, mucosa and on the the right atrium, as well as other parts of the myocardium. Furthermore there have been ulcerations at various localisations of the whole digestive tract. Slightly basophilic intranuclear inclusion bodies have been found histologically in endothelial cells of different organ samples. An examination of altered organ-material by electronmicroscopy made some herpesvirus-like particles visible. A virological investigation first revealed evidence of giant cell formations with solitary basophilic intranuclear inclusion bodies in different cell cultures, however, without any distinct cytopathogenic effect. Supported by molecular biological procedures the infection of 'KIBA' could be verified as the elephants herpesvirus. By means of PCR and subsequent sequence analysis a DNA-sequence typical for the elephants herpesvirus could be obtained which showed an identity of 97% with the terminase sequence of the elephant herpesvirus described by American authors. The deduced amino acid-sequences were 100% identical. To the terminase of the human cytomegalovirus, the elephant sequence had an identity of 53% (similarity: 74%). Based on the cooperation of ILAT, Institute of Veterinary-Pathology/Free University Berlin, Robert-Koch-Institut Berlin, and Zoological Garden Berlin, the cause of 'KIBA's' death could be discovered immediately. Possible implications of this case especially on breeding and keeping elephants are discussed briefly.

Amino Acid Sequence↗

PubMed2002

Spontaneous human herpes virus type 1 infection in a chinchilla (Chinchilla lanigera f. dom.).

A 1-year-old male chinchilla with a 2-week history of conjunctivitis suffered subsequently from neurological signs comprising seizures, disorientation, recumbency and apathy. After 3 weeks of progressive central nervous disease the animal was killed in view of the poor prognosis. A non-suppurative meningitis and polioencephalitis with neuronal necrosis and intranuclear inclusion bodies were observed at necropsy and by light microscopy. The brain stem and cerebral cortices were most severely affected. Both eyes displayed ulcerative keratitis, uveitis, retinitis and retinal degeneration, and optical neuritis. Additionally, a purulent rhinitis with focal erosions, epithelial degeneration and intranuclear inclusion bodies was present. Ultrastructurally, herpes virus particles were detected in neurons of the brain. Immunohistochemistry with antisera specific for human herpes virus types 1 and 2 resulted in viral antigen labeling in neurons, glial cells and in neuronal processes. Viral antigen was found in the rhinencephalon, cerebral cortices, hippocampus, numerous nuclei of the brain stem, single foci in the cerebellum, and in a solitary erosive lesion of the right nasal vestibulum. Viral antigen was not detected in the eyes. The virus was isolated from the CNS, and nucleic acid sequence analysis of the glycoprotein B and the DNA polymerase revealed a sequence homology with human herpes virus type 1 of 99% and 100%, respectively. The clinical signs, the distribution of the lesions and the viral antigen suggest a primary ocular infection with subsequent spread to the CNS. Chinchillas are susceptible to human herpes virus 1 and may play a role as a temporary reservoir for human infections.

Animals↗

PubMed1991

[Fluorescence serologic and histologic studies of antigen distribution in parvovirus infections in dogs and cats].

In organs known as replication sites of parvovirus and additionally in stratified squamous epithelia from different regions of 35 dogs with lethal parvovirus enteritis and 19 cats with lethal panleukopenia the distribution of antigen and the prevalence of histologic lesions were studied by immunofluorescence and histologic techniques. The findings showed no striking differences between dogs and cats. Antigen was found in the epithelia of the dorsal side of the tongue (96.3%), pharynx (81.0%), esophagus (50.0%), ventral side of the tongue (20.4%) and planum nasale (5.6%). The epithelia of the skin and the mucous membranes of the male and female genital organs never contained antigen. Moreover antigen was detected in the mucosa of the small intestine (85.2%), bone marrow (81.6%), spleen (79.6%), thymus (66.7%), mesenteric lymph nodes (60.4%), tonsilla palatina (58.5%), smooth muscle cells of the tunica muscularis of the small intestine (9.3%) and myocardium (1.9%). The histologic lesions found in intestinal mucosa, lymphatic tissues, bone marrow and myocardium are in accordance with literature. The tunica muscularis of the small intestine and the epithelium of tongue, pharynx and esophagus contained intranuclear inclusion bodies, the epithelium of tongue and pharynx showed necroses additionally. Tongue- and esophagus-erosions as well as -ulcers reported mainly in panleukopenia according to our results may be explained as a sequel of parvovirus infection of the epithelia of these organs. The prevalence of antigen and intranuclear inclusion bodies in the myocardium and smooth muscle cells of the small intestine--tissues with low or no mitotic activity,--allows to question the postulate of the parvoviruses' exclusive affinity to rapidly dividing cells.

Animals↗

PubMed1956

Electron microscopy of HeLa cells infected with adenoviruses.

HeLa cells were infected with adenoviruses (types 1-4) and sectioned for electron microscopy after intervals of 20 to 48 hours. Clusters of virus-like particles were found within the nuclei of infected cultures but not in those of uninfected controls. The particles were often arranged in rows as if in crystalline formation. Maximal diameter of particles was approximately 65 mmicro, and internal bodies were demonstrated. Lesions of infected cells included target-like structures of the nuclear membrane, large nuclear vacuoles (type 2), and increased numbers of large irregular electron-dense granules in the cytoplasm 48 hours after infection. Examination of infected cultures by light microscopy, using the Feulgen reaction, showed intranuclear inclusion bodies and a cytopathogenic effect consisting of clumping of cells without pyknosis of nuclei. A lipide stain showed numerous cytoplasmic granules that were not identical with the large, irregular, electron-dense granules of the cytoplasm. Practically all the cells showed the viral cytopathogenic effect, but only a minority of cells were found to contain virus-like particles or intranuclear inclusion bodies.

Adenoviridae↗

PubMed1987

A necrotizing pneumonia in lambs caused by pseudorabies virus (Aujesky's disease virus).

An outbreak of pseudorabies occurred in sheep housed with swine in the same building. Although the sheep and swine were not in physical contact, the lambs and ewes were exposed to air from the sows' section. Three dead lambs were submitted to the Iowa State University Veterinary Diagnostic Laboratory for necropsy. Grossly there were pulmonary congestion and multifocal pulmonary hemorrhages. Microscopic lesions were severe acute multifocal necrotizing bronchopneumonia with necrotizing vasculitis and intranuclear inclusion bodies within the neurons of the parabronchial ganglia. Bacterial cultures were negative for pathogenic agents; pseudorabies virus was isolated from ovine brain tissue. Viral antigen was demonstrated in the neurons of the parabronchial ganglia by immunoperoxidase staining. Electron microscopy revealed nucleocapsids in the parabronchial ganglionic neurons which contained basophilic intranuclear inclusion bodies. Viral DNA prepared from the ovine pseudorabies virus isolate was found by restriction endonuclease analysis to be related to the Indiana Funkhauser strain of pseudorabies virus.

Animals↗

PubMed1984

Karyokinetic reactions in rat kidney proximal convoluted segment epithelium on long-term lead supply with drinking water.

In the rat kidney proximal convoluted segment epithelium the development of intranuclear inclusion bodies was observed after long-term lead administration with the drinking water. The inclusion bodies were PAS-positive. By electron microscopy they were identified as composed of filaments and granules lacking any kind of surrounding membrane. During the experiment, the nuclear volumes increased commensurately with the duration of lead exposure. The nuclear volume increase was considered a physiological reaction since it began long before the first appearance of intranuclear inclusion bodies.

Animals↗

PubMed1976

Disseminated cytomegalic inclusion disease in an adult with cirrhosis of liver and review of literatures.

We reported a 44 year old man with micronodular cirrhosis who eventually died from massive hematemesis and melena. At postmortem studies, there were disseminated cytomegalic inclusion bodies detected in various organs. In liver, intranuclear inclusion bodies were observed in cirrhotic liver. We discussed here possible pathogenesis of CMV (cytomegalovirus) infection in adults, in reviewing literatures.

Adult↗

PubMed1984

An immunofluorescent study of generalized infection of human cytomegalovirus in a patient with systemic lupus erythematosus.

An autopsy case of generalized infection of cytomegalovirus (CMV) in an adult with systemic lupus erythematosus is reported. CMV infection was histologically diagnosed postmortem by the presence of the characteristic cytomegalic cells with inclusion body. In the lungs, viral antigen was seen not only in the cytomegalic cells with inclusion body but also in the cells without intranuclear inclusion body in both of the frozen and the formalin-fixed paraffin sections. Viral antigen was also detected in frozen sections of the liver. CMV was isolated from the lung and liver.

Adult↗

PubMed2002

Immunohistopathology of calf pneumonia induced by endobronchial inoculation with bovine adenovirus 3.

Three 1-week-old and three 3-month-old Holstein calves that had received colostrum were inoculated endobronchially with bovine adenovirus 3 (BAV-3). The gross and histologic lesions in these six infected calves were localized mainly in the right caudal lobe of the lung and were closely associated with the site of the deposition of the inoculum. The pneumonic lesions were severe necrotizing bronchitis, bronchiolitis, and alveolitis, accompanied by infiltration of inflammatory cells and proliferation of type 2 pneumocytes. Intranuclear inclusion bodies, BAV-3 antigen, and virus particles were detected in the degenerated epithelial cells in the 1-week-old but not the 3-month-old calves. After infection, the total cell count in the bronchoalveolar lavage (BAL) fluid cells was increased. The results of BAV-3 isolation from BAL fluid were correlated with the detection of intranuclear inclusion bodies in the desquamated epithelial cells in the BAL fluid cells from the right caudal lobe but not in cells from the left caudal lobe. CD8+ T lymphocytes in the pneumonic lesion were found only in the 3-month-old infected calves. The difference in the immunopathologic reactions between the 1-week-old and the 3-month-old infected calves may be attributed to differences in immune system development.

Adenoviridae Infections↗

PubMedDate not supplied

Epizootic outbreaks of gizzard erosion associated with adenovirus infection in chickens.

Two outbreaks of gizzard erosion in slaughtered broiler chickens in Japan were examined pathologically and microbiologically. The prevalences of such lesions were 9%-11% and 4%-50% in the affected flocks. Affected chickens had no clinical signs. Group I fowl adenovirus (FAV) serotype 1 was isolated from gizzard lesions. Histologically, gizzard mucosa were necrotic. Intranuclear inclusion bodies were seen in the enlarged nuclei of degenerating epithelial cells of the gizzard. The keratinoid layer in the erosion was edematous and desquamated and contained degenerative cells. Moderate to marked inflammatory cell infiltration was observed in the lamina propria and perivascular connective tissue in the submucosa and muscle layer. Immunohistochemical staining showed evidence of FAV antigens in the intranuclear inclusion bodies within degenerating epithelial cells. Ultrastructurally, numerous viral particles were demonstrated in the inclusions.

Adenoviridae Infections↗

PubMed1986

Chronic lead intoxication causes a brain-specific nuclear protein to accumulate in the nuclei of cells lining kidney tubules.

A characteristic feature of chronic lead intoxication is the induction of intranuclear inclusion bodies in cells lining kidney proximal tubules. These are relatively insoluble lead- and protein-rich structures which may serve a protective function by sequestering lead. The most abundant protein of isolated inclusion bodies, p32/6.3, has been partially characterized by use of a monoclonal antibody. As predicted by biochemical analysis, p32/6.3 occurs in kidney only in conjunction with lead intoxication and inclusion body formation. It does not accumulate in other tissues as a result of lead exposure. Unexpectedly, p32/6.3 was found to be a constitutive protein of adult brain, occurring primarily in the cerebral cortex. Within this tissue, both neurons and astrocytes contained p32/6.3. The brain p32/6.3 was concentrated in the insoluble nuclear protein or matrix fraction, a localization reminiscent of the intranuclear inclusion bodies from lead-exposed kidney. Brain p32/6.3 was detected in rat, mouse, dog, man, and chicken. In rat brain, the appearance of p32/6.3 was developmentally regulated. Only traces were detected 3 days after birth but within 1-2 weeks adult levels were achieved. The presence in brain of a protein which is involved in a potentially protective response to lead suggests that the brain may also have such a protective mechanism.

Age Factors↗

PubMed1992

Acute simian varicella infection. Clinical, laboratory, pathologic, and virologic features.

Five African green monkeys inoculated intratracheally with 7.5 x 10(3) to 1.4 x 10(5) plaque-forming units of simian varicella virus (SVV) were subjected to clinical, laboratory, pathologic, and virologic analyses to study the pathogenesis of acute varicella. All animals developed viremia and rash and were sacrificed 8 to 11 days post-infection. No serum was available for postmortem serologic studies. Examination of multiple organs for pathologic changes and for SVV-specific antigen and nucleic acid revealed inflammation, hemorrhagic necrosis, and intranuclear Cowdry A inclusions in liver, lung, lymph node, and spleen; mild inflammation without necrosis in adrenal gland, kidney, and bone marrow, and SVV-specific antigen and nucleic acids in all viscera examined. No pathologic changes, SVV antigen or nucleic acids were detected in the spinal cord or in the brain from any of the monkeys. Ganglia revealed mild inflammation but no necrosis, and intranuclear inclusion bodies in non-neuronal cells of one trigeminal ganglion; SVV antigen and nucleic acids were detected in both non-neuronal and neuronal cells in ganglia. The pathologic and virologic findings in viscera are consistent with those described in viscera of humans with disseminated zoster, but the mild inflammatory changes in ganglia during acute simian varicella infection contrast with the extensive hemorrhagic necrosis and intranuclear inclusion bodies seen in human ganglia after disseminated varicella or zoster. Nevertheless, these studies show that ganglia become infected with varicella virus during primary infection, although the route of primary ganglionic infection remains to be determined, and indicate the possible usefulness of the SVV model to study varicella pathogenesis in humans.

Acute Disease↗

PubMedDate not supplied

A case of acute pulmonary edema, splenomegaly, and ascites in guinea fowl.

Acute pulmonary edema, splenomegaly, and ascites were observed in a disease outbreak in adult white and pearl guinea fowl. The clinical history and gross and microscopic lesions resembled those described for marble spleen disease of pheasants and avian adenovirus group II splenomegaly of chickens. A small number of intranuclear inclusion bodies were found in liver, spleen, and lung sections of affected guinea fowl. Attempts to isolate virus and serological tests to detect the presence of viral antigens were unsuccessful. Adult female pearl guinea fowl experimentally exposed to pheasant and turkey isolates of type II avian adenoviruses developed gross and microscopic lesions similar to those seen in the field outbreak. The pheasant isolate was the more virulent. Intranuclear inclusion bodies were observed in liver, spleen, and lung sections of pearl guinea fowl inoculated with either of the virus isolates, and direct immunofluorescent examination revealed viral antigen in the spleen and lung.

Animals↗

PubMed1991

Retrospective study of myocardial canine parvovirus infection by in situ hybridization.

The diagnosis of myocardial canine parvovirus (CPV) infection used to depend on the presence of pathognomonic intranuclear inclusion bodies. The in situ hybridization technique, however, allowed to detect CPV specific nucleic acid in myocardial tissue where no inclusion bodies were found. Hence, we applied this technique to check formalin-fixed paraffin-embedded myocardial tissue from puppies with heart lesions for the presence of CPV. The tissues had been collected between 1977 and 1989. A biotinylated probe was used for in situ hybridization. This way CPV specific nucleic acid was detected in 3 dogs where CPV myocarditis had not been diagnosed on routinely stained slides because of the lack of intranuclear inclusion bodies. However, in spite of the application of the in situ hybridization technique no further myocardial CPV infection was detected in puppies with heart lesions from after 1979, confirming that the number of puppies with myocardial CPV infection declined after that year.

Animals↗

PubMed1982

Spontaneous paramyxoviral encephalitis in nonhuman primates (Macaca mulatta and M. nemestrina).

Two female rhesus macaques (Macaca mulatta) and one female pigtailed macaque (M. nemestrina) developed acute neurological signs including ataxia, muscular incoordination, and seizures. Light microscopy showed Cowdry Type A intranuclear inclusion bodies in astrocytes and neurons of the cerebral cortex and Purkinje's cells of the cerebellum. Many cells also had intracytoplasmic inclusion bodies. Electron microscopy identified paramyxoviral nucleocapsids in the intranuclear and intracytoplasmic inclusions in two monkeys. We believe these monkeys had measles encephalitis because measles virus is the only paramyxovirus known to cause inclusion bodies in macaques and because the lesions in these monkeys resembled measles encephalitis in man.

Animals↗

PubMed1999

Intranuclear inclusions in cells infected with Newcastle disease virus.

Cells infected by Newcastle Disease Virus were observed to contain both intracytoplasmic and intranuclear inclusion bodies. Ultrastructurally, they consisted of twisted strands of about 18-20 nm diameter resembling nucleocapsids. The presence of these inclusions was detected irrespective of host cell or pathogenicity of the virus. In immunofluorescence and immunogold labelling experiments, these structures were tagged by an anti-P protein monoclonal antibody. In summary, we show that intracytoplasmic and intranuclear inclusion bodies, hitherto used as a taxonomic characteristic for the genus Morbillivirus of the Paramyxoviridae, also occur in a member of the genus Rubulavirus.

Animals↗