Canine distemper infection associated with acute nervous signs in dogs.

Eight vaccinated dogs suddenly developed progressive ataxia, paresis or paralysis of short duration. A histopathological examination revealed a non-suppurative meningoencephalitis suggestive of a viral infection, and immunohistochemical examination confirmed the presence of canine distemper virus antigen in five of the dogs. Distemper had not been suspected from the clinical examination of the dogs.     

Anosmia associated with canine distemper

The sense of smell in dogs infected with canine distemper virus (CDV) was examined by use of EEG olfactometry, behavioral olfactometry, and electro-olfactography. Infection with CDV was confirmed by a direct immunofluorescence technique in 8 active cases and was suggested by clinical history compatible with canine distemper 10 to 26 weeks earlier in 6 cases. Pathologic alterations of the olfactory mucosa in 3 clinically affected dogs was examined by light microscopy. Infection with CDV was found to be associated with anosmia and lack of recorded responses on electro-olfactogram in 8 of 8 dogs with clinical signs of acute distemper from naturally acquired infections. Anosmia was found in 5 of 6 dogs that had recovered from acute distemper 10 to 26 weeks earlier. The sixth dog had hyposmia, with abnormalities on the electro-olfactogram. Histologic examination was not performed on the 6 dogs that had recovered. Histologic lesions observed at necropsy in 3 dogs that had had clinical signs of acute distemper were those of subacute purulent rhinitis and atrophy of the olfactory epithelium. Altered olfactory function could be explained by mucopurulent exudate blocking odors from olfactory receptors in the acutely affected dogs, but alteration of olfactory function in the dogs that had recovered without clinical evidence of rhinitis could not be explained.     

犬瘟热的临床诊断技术与疫苗研究进展

犬瘟热是由犬瘟热病毒引起的犬科、鼬科和浣熊科等动物的一种高度接触性烈性传染病。该病在临床上可根据临床症状和流行特点作出初步诊断,结合病原学检查和血清学诊断即可确诊。目前一直缺少治疗犬瘟热的有效药物,所以犬瘟热的预防主要依靠接种疫苗。结合已有研究报道,总结了犬瘟热的临床诊断技术和犬瘟热疫苗方面的研究进展,以期为兽医同仁提供参考。     

Canine distemper virus infection: proliferation of canine footpad keratinocytes

The proliferation of footpad keratinocytes of canine distemper virus (CDV)-infected dogs was investigated. Footpads of 19 dogs inoculated experimentally with a virulent distemper strain (A75/17) and of two noninoculated control dogs were collected at necropsy. Dogs were divided into four groups according to results of the postmortem examination: dogs with severe distemper (group 1), dogs with mild distemper (group 2), inoculated dogs without distemper (group 3) and noninoculated dogs (group 4). There was no distinct difference of epidermal thickness among the four groups. Infection of the footpad epidermis with CDV was demonstrated using immunohistochemistry for viral nucleoprotein and in situ hybridization for nucleoprotein messenger ribonucleic acid (mRNA). Only group 1 dogs had viral antigen and mRNA in the footpad epidermis with the same distribution. Footpad epidermis of group 1 dogs had more mitotic figures in the basal layer, and significantly more basal keratinocytes were positive for the proliferation markers Ki-67 and proliferating cell nuclear antigen. Double-staining for Ki-67 and viral nucleoprotein identified rare double-labeled basal keratinocytes. These findings suggest that the presence of CDV particles in the footpad epidermis is associated with keratinocyte proliferation.     

Immunoperoxidase study of canine distemper virus pneumonia

Forty-two cases of canine pneumonia were examined for the presence of canine distemper virus. For that purpose canine distemper virus inclusion bodies were located. The histopathological lesions were related to the presence of canine distemper antigen, as demonstrated with an immunoperoxidase technique. This technique was more sensitive for detecting canine distemper infection in lung tissue than was the study of inclusion bodies. Attention was also paid to combined infection with canine adenovirus and Bordetella bronchiseptica.     

Neurological manifestations of canine distemper virus infection

Canine distemper virus causes a multi systemic disease in dogs often with severe neurological signs. These signs are the result of viral replication in neurons and glial cells leading to grey matter lesions and demyelination. Inflammation leads to further destruction of the tissue. As extraneural signs are often lacking and only one localisation may be found on neurological examination, distemper may be difficult to diagnose. Myoclonus is almost pathognomonic for this disease but occurs in less than half of the cases. The inflammation of the central nervous system that occurs during the chronic stage of the disease can be detected on examination of the cerebrospinal fluid, in particular by determination of the IgG index. Viral antigen can be demonstrated in cerebrospinal fluid cells by fluorescent antibody techniques. The prognosis of nervous distemper is generally poor although dogs can recover from this disease. Treatment is largely supportive and symptomatic. The importance of regular vaccination is stressed.     

Canine distemper virus infection of canine footpad epidermis

Infection of the footpad epidermis can occur in natural canine distemper virus (CDV) infection of dogs. Footpads from 19 dogs experimentally inoculated with virulent distemper strain A75/17 and from two nonexposed dogs were examined histopathologically and assessed for the presence of viral antigen and nucleoprotein mRNA, as well as number of inflammatory and apoptotic cells. Dogs were divided into four groups based on inoculation status and postmortem examination: inoculated dogs with severe distemper (group 1, n = 7); inoculated dogs with mild distemper (group 2, n = 4); inoculated dogs without distemper (group 3, n = 8); and noninoculated dogs (group 4, n = 2). Footpads from dogs of all groups had a comparably thick epidermis. Eosinophilic viral inclusions and syncytial cells were present in footpad epidermis of one dog of group 1. Footpads of group 1 dogs contained viral antigen and mRNA in the epidermis with strongest staining in a subcorneal location. Additionally, in these dogs footpad dermal structures including eccrine glands and vascular walls were positive for virus particles. No CDV antigen or mRNA was present in the footpad epidermis and dermis of any other dog. Group 1 dogs had more CD3-positive cells and apoptotic cells within the basal layer of the epidermis when compared to the other groups. These findings demonstrate that in experimental infection CDV antigen and mRNA were colocalized in all layers of the infected canine footpad epidermis. The scarcity of overt pathological reactions with absence of keratinocyte degeneration indicates a noncytocidal persisting infection of footpad keratinocytes by CDV.     

Mass mortality in seals caused by a newly discovered morbillivirus

During a recent disease outbreak among harbour seals (Phoca vitulina) in the North and Baltic seas, more than 17,000 animals have died. The clinical symptoms and pathological findings were similar to those of distemper in dogs. Based on a seroepizootiological study, using a canine distemper virus (CDV) neutralization assay, it was shown that CDV or a closely related morbillivirus (phocid distemper virus-PDV) was the primary cause of the disease. The virus was isolated in cell culture from the organs of dead seals and characterized as a morbillivirus by serology (immunofluorescence neutralization and enzyme-linked immunosorbent assays) and by negative contrast electron microscopy. Experimental infection of SPF dogs resulted in the development of mild clinical signs of distemper and CDV-neutralizing antibodies. The disease was reproduced in seals by experimental inoculation of organ material from animals that had died during the outbreak. However, seals that had been vaccinated with experimental inactivated CDV vaccines were protected against this challenge. This fulfilled the last of Koch's postulates, confirming that the morbillivirus isolated from the seal organs, was the primary cause of the disease outbreak. The recent demonstration of the presence of a similar virus in Lake Baikal seals (Phoca sibirica), which infected these Siberian seals 1 year before the northwestern European seals were infected, raises new questions about the origin of this infectious disease in pinnipeds.     

Canine distemper viral inclusions in blood cells of four vaccinated dogs

Four cases of canine distemper were detected by the presence of numerous cytoplasmic inclusions in various circulating blood cells. Fluorescent antibody techniques and electron microscopy confirmed the identity of the viral inclusions. The cases occurred in the same geographic area and within a short time span. All four dogs had been vaccinated against canine distemper, but stress or other factors may have compromised their immune status. The possibility of an unusually virulent virus strain was also considered.     

Follow-up studies by large intestinal biopsies and necropsy in dogs with clinical signs of large bowel disease.

The results of follow-up studies in 77 dogs with clinical signs of large bowel disease are presented. In 32 dogs colonic and/or rectal biopsy follow-up studies were done, combined with necropsy in seven dogs. In 45 dogs a follow-up necropsy only was done. The time between the first and the last series of biopsies varied from three to 729 days and between the first series of biopsies and necropsy from one to 980 days. Colitis found in 45 dogs in the initial biopsies was still present in 29 cases in the follow-up biopsy studies and/or at necropsy. Eleven cases showed hystiocytic ulcerative colitis. In general, adenoma, carcinoma and lymphosarcoma were confirmed in the follow-up examination, except for one adenoma, which appeared to be a carcinoma at necropsy. In cases in which the differential diagnosis was adenoma or carcinoma, the necropsy diagnosis was always carcinoma and in cases of a differential diagnosis of lymphosarcoma and/or colitis, lymphosarcoma was always diagnosed at necropsy. Several dogs without colonic changes in the initial biopsies had other gastric or small intestinal lesions at necropsy such as gastritis and enteritis of the small intestine, or tumors, in these areas.     

Retrospective serological analysis of spontaneous CDV infection in 192 dogs

Spontaneous cases of canine distemper virus (CDV) infection were serologically evaluated. The 192 dogs in which CDV antigen was confirmed from tonsil by immunohistological examination were 2- to 4-months old, of various breeds, and unvaccinated. The prognoses were good in 74 dogs with significantly high levels of anti-CDV passive hemolytic aggregation (PHA) titer. In the other 118 dogs with poor prognoses, anti-CDV PHA titer was not detected. Anti-CDV PHA titer had the most significant association with the prognoses of CDV infection, and could be the most reliable and useful indicator for evaluating such prognoses.     

Transmissible Gastroenteritis in Feeder Swine: Clinical, Immunofluorescence and Histopathological Observations

Eight feeder swine (four to six months of age) were inoculated orally with 200,000 to 500,000 pig infectious doses (PID) of the Purdue strain of transmissible gastroenteritis (TGE) virus. Biopsies obtained from their small intestines were examined histopathologically and by fluorescent antibody tissue section technique at intervals that included 24, 48, 72 and 96 hours postexposure, and similar examinations were carried out at necropsy 168 hours postexposure. Evidence of virus infection was demonstrated in all segments of the small intestine except the upper duodenum and the viral antigen was found only in the cytoplasm of the absorptive cells covering the villi. Although six of the eight pigs failed to show clinical signs of TGE, typical microscopic lesions of villous atrophy with replacement of columnar absorptive cells by cuboidal cells were observed in seven pigs, and TGE virus antigen was demonstrated in the intestinal cells of four of eight pigs during the first week postexposure. The infection was usually mild to moderate and focal in the pigs without clinical signs of the disease and more severe and extensive in the pigs with clinical signs of the disease variable in severity. It was concluded that TGE virus probably replicated in all feeder swine exposed, and that the presence or absence of clinical signs of TGE in these pigs was related to the severity and extent of the villous atrophy and columnar cell replacement induced in their small intestines.     

Natural distemper in vaccinated and unvaccinated dogs in Warsaw

Two hundred and twenty-four dogs with clinical signs of distemper were examined for the presence of canine distemper virus (CDV) in mucous membranes by direct immunofluorescence assay. The study showed that 22% of the animals were CDV-positive. Most (33/50; 66%) of the infected dogs had never been vaccinated against distemper, whereas only 11 of 50 (22%) CDV-positive animals were immunized at least once. The difference in the infection rate between vaccinated and unvaccinated animals was statistically significant (P < 0.001), as assessed by the chi2 test. It is concluded that distemper is an important disease among dogs in Warsaw and the vaccination significantly reduces the risk of this disease.     

An unusual presentation of canine distemper virus infection in a domestic ferret (Mustela putorius furo)

A 4.5-year-old, male castrated ferret was examined with a 27-day history of severe pruritus, generalized erythema and scaling. Skin scrapings and a trichogram were negative for mites and dermatophyte organisms. A fungal culture of hair samples was negative. The ferret was treated presumptively for scabies and secondary bacterial and yeast infection with selamectin, enrofloxacin, fluconazole, diphenhydramine and a miconazole–chlorhexidine shampoo. The ferret showed mild improvement in clinical signs over the subsequent 3 weeks, but was inappetent and required supportive feeding and subcutaneous fluids by the owner. The ferret was then examined on an emergency basis at the end of 3 weeks (53 days following initial signs of illness) for severe blood loss from a haematoma over the interscapular region, hypotension and shock. The owners elected euthanasia due to a poor prognosis and deteriorating condition. On post-mortem examination intraepithelial canine distemper viral inclusions were identified systemically, and abundant canine distemper virus antigen was identified with immunohistochemical staining. It is important to note the prolonged course of disease along with the absence of respiratory and neurological signs because this differs from the classic presentation of canine distemper virus infection in ferrets. Canine distemper virus should remain a clinical suspicion for ferrets with skin lesions that do not respond to appropriate therapy, even in animals that were previously vaccinated.     

Granulomatous peritonitis and pleuritis in interferon-gamma gene knockout mice naturally infected with mouse hepatitis virus

OBJECTIVE: To investigate a disease outbreak in a colony of laboratory mice with targeted disruption of the gene for interferon-gamma. FORMAT: A case report based on necropsy, histopathology, serology and immunohistochemistry. RESULTS: Affected mice exhibited depression and variable ascites. Necropsy revealed a granulomatous peritonitis and pleuritis with extensive adhesions although parenchymal lesions were minimal. Serum samples had high concentrations of antibody to mouse hepatitis virus and immunohistochemical examination revealed the presence of mouse hepatitis virus antigen in granuloma macrophages. Sero-logical testing for other infectious agents and bacterial culture were negative and wild type mice kept in the same facility remained healthy. Despite the association between the disease and mouse hepatitis virus infection, the precise role played by mouse hepatitis virus was not determined. While the disease is superficially similar to feline infectious peritonitis (another coronavirus-induced serositis), differences exist between the histopathological findings in these two conditions. CONCLUSION: This unusual disease process illustrates how new diagnostic challenges can arise in novel mouse genotypes created through molecular genetics. Furthermore, the association between the disease and mouse hepatitis virus illustrates the importance of maintaining laboratory animals under specific-pathogen free conditions.     

狐犬瘟热继发细菌感染的诊断及防治

通过对一送检病狐临床症状的调查,剖检病变和细菌学检查,并进行RT-PCR检测犬瘟热病毒,确诊该狐为犬瘟热继发大肠杆菌感染,通过疫苗注射和治疗细菌感染,较好地控制了该病。     

Transcranial Doppler sonographic findings in granulomatous meningoencephalitis in small breed dogs

Granulomatous meningoencephalitis (GME) is an acute, progressive, and often fatal inflammatory disease of the central nervous system, affecting mainly small and toy dog breeds. A definitive diagnosis of GME can only be achieved through histopathologic examination of samples collected after death. This retrospective study describes transcranial Doppler ultrasonography (TDS) findings in dogs with confirmed clinical histopathology of GME. Eleven dogs were selected for this study. Sonographic findings in B-mode demonstrated diffuse decreased brain parenchyma echogenicity in 9 dogs, ventriculomegaly in 8 dogs, brain atrophy in 4 dogs, and hyperechoic focal lesions in 6 dogs. Color Doppler imaging revealed more obvious vessels of the arterial circle in 10 dogs. Spectral Doppler examination was performed in 10 dogs to detect the 6 major cerebral arteries of interest. The examination showed normal and high resistive index (RI) values in the outlined arteries. The TDS findings were consistent with pathology found on postmortem examination.     

Evaluation of the efficacy and duration of immunity of a canine combination vaccine against virulent parvovirus, infectious canine hepatitis virus, and distemper virus experimental challenges

The results of this study confirmed that dogs vaccinated subcutaneously with a commercially available multivalent vaccine containing modified-live canine distemper virus, canine adenovirus type 2, canine parvovirus type 2b, and canine parainfluenza virus antigens were protected against sequential experimental challenge 55 to 57 months after initial vaccination given at 7 to 8 weeks of age. All 10 vaccinates were protected against clinical diseases and mortality following parvovirus and infectious canine hepatitis experimental infections. All vaccinates were protected against mortality and 90% against clinical disease following distemper challenge. These data support at least a 4-year duration of immunity for these three "core" fractions in the combination vaccine.     

Uncommon acute neurologic presentation of canine distemper in 4 adult dogs

Four uncommon cases of canine distemper (CD) were diagnosed in vaccinated adult dogs. All dogs had acute onset of neurologic signs, including seizures, abnormal mentation, ataxia, and proprioceptive deficits. Polymerase chain reaction for CD virus was positive on cerebrospinal fluid in 2 cases. Due to rapid deterioration the dogs were euthanized and CD was confirmed by postmortem examination.