Periventricular changes associated with spontaneous canine hydrocephalus

Causes of canine juvenile hydrocephalus have been well documented. However, the effects of hydrocephalus on periventricular white matter have been only partially described. The present report shows that hydrocephalus-associated lesions of the periventricular white matter, i.e., formation of diverticula, clefts, and tears, are prevalent. Marked hydrocephalus was identified at necropsy in 20 juvenile dogs between 1990 and 1999. The severity grade was based upon a ratio of lateral ventricular dimensions to cortical thickness. All animals exhibited ependymal lesions consisting of attenuation, with or without abortive attempts of ependymal regeneration, and ulceration. In 10 dogs (50%), unilateral or bilateral periventricular diverticula and cleft formation in the region of the caudate nucleus were observed. The diverticula were formed at the caudal pole of the caudate nucleus, communicated with the ventricular lumen, and were associated with ependymal denudation. Loss of the ependymal lining probably contributes to a bulk shift of cerebrospinal fluid from the ventricular lumen to the periventricular white matter, leading to diverticulum formation. Clefts were observed within the parenchyma at the border of the internal capsule and putamen, consistent with an ischemic insult. Occasionally tearing with separation of the caudate nucleus from the subcortical white matter was found, representing unification of expanding clefts and diverticula. In one of the few clinically well-documented cases, tearing was correlated with a sudden decline in neurologic function, culminating in euthanasia. However, tears and clefts may exhibit a chronicity of several days, as indicated by the presence of astroglial scars along the lesion margins.     

Canine respiratory viruses

Acute contagious respiratory disease (kennel cough) is commonly described in dogs worldwide. The disease appears to be multifactorial and a number of viral and bacterial pathogens have been reported as potential aetiological agents, including canine parainfluenza virus, canine adenovirus and Bordetella bronchiseptica, as well as mycoplasmas, Streptococcus equi subsp. zooepidemicus, canine herpesvirus and reovirus-1,-2 and -3. Enhancement of pathogenicity by multiple infections can result in more severe clinical forms. In addition, acute respiratory diseases associated with infection by influenza A virus, and group I and II coronaviruses, have been described recently in dogs. Host species shifts and tropism changes are likely responsible for the onset of these new pathogens. The importance of the viral agents in the kennel cough complex is discussed.     

Serologic survey of selected viral agents in recently captured wild North American river otters (Lontra canadensis).

Blood samples were collected from 64 wild North American river otters (Lontra [Lutra] canadensis) from northern and eastern New York State and analyzed for serologic evidence of exposure to selected viral agents during a 1995 1996 translocation program. No clinical signs of disease nor lesions suggestive of prior viral exposure were seen. Titers were detected for antibodies against canine distemper virus, canine herpesvirus-1, and canine parvovirus-2 but not for antibodies against canine adenovirus-1, canine coronavirus, canine parainfluenza virus, rabies virus, feline herpesvirus-1, feline calicivirus, or feline coronavirus. This is the first report of titers for antibodies against canine herpesvirus-1 in North American river otters, and it suggests a low prevalence of antibody titers against most canine viruses in otter populations in northern and eastern New York. Confounding variables in this study could include exposure to domestic dogs associated with the project, prolonged time spent in captivity, and concurrent bacterial or parasitic infection. Stress-associated humoral immune suppression could have altered serologic profiles, especially in otters exposed to dogs after trapping but before venipuncture.     

EPENDYMAL AND PERIVENTRICULAR MAGNETIC RESONANCE IMAGING CHANGES IN FOUR DOGS WITH CENTRAL NERVOUS SYSTEM BLASTOMYCOSIS

Rapid detection of central nervous system (CNS) involvement is important for dogs with blastomycosis, as this can affect antifungal drug selection and has been associated with an increased risk of death. Previous reports describing magnetic resonance imaging (MRI) characteristics of canine CNS blastomycosis primarily identified mass lesions. The purpose of this retrospective study was to determine whether other MRI characteristics of CNS blastomycosis may also occur. Medical records of the Purdue University Veterinary Teaching Hospital were searched and four dogs met inclusion criteria. Magnetic resonance imaging characteristics included periventricular edema, periventricular and meningeal contrast enhancement, and ventriculomegaly. Periventricular lesions most commonly involved the rostral horn of the lateral ventricles and the third ventricle. Increased meningeal contrast enhancement involved the cerebrum, thalamus, sella turcica, and brainstem. Findings indicated that, in addition to mass lesions, MRI characteristics of periventricular hyperintensity, contrast enhancement, and ventriculomegaly may also occur in dogs with CNS blastomycosis.     

Acute encephalitis and hydrocephalus in dogs caused by canine parainfluenza virus

Gnotobiotic puppies were inoculated intracerebrally with a strain of canine parainfluenza virus (CPI-78-238). Four of eight dogs developed histological evidence of acute encephalitis. Clinical signs of encephalitis were seen in two of these four dogs; one had signs and lesions of interstitial pneumonia. Of six inoculated dogs observed for six months after infection, five developed internal hydrocephalus. Virus was reisolated from two dogs with acute encephalitis but not from dogs with hydrocephalus. Hemagglutination-inhibition antibodies persisted throughout the observation period of six months at high levels in the serum and cerebrospinal fluid of hydrocephalic dogs.     

Leukoencephalitis associated with selective viral replication in the brain of a pony with experimental chronic equine infectious anemia virus infection

Neurologic disease occurs sporadically in horses infected with the equine infectious anemia virus (EIAV). This report describes a case of clinically severe neurologic disease in a pony experimentally infected with EIAV. This pony did not have fever or anemia, which are the characteristic clinical signs of disease. The histopathologic changes were characterized as lymphohistiocytic periventricular leukoencephalitis. Polymerase chain reaction and in situ hybridization data showed that the brain lesions were directly associated with viral replication and that high-level viral replication occurred selectively within the lesion and not in other tissues. These findings suggest that EIAV-associated neurologic disease is the direct result of viral replication.     

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.     

Cryptococcal infection of the central nervous system of a dog in the United Kingdom

Cryptococcal infection of the C.N.S. is described in a two-year-old Borzoi dog. The animal showed limb weakness progressing over a period of five months to spastic paraplegia with head tremor, stiffness of the neck and nystagmus. On post-mortem examination there was severe hydrocephalus and granulomatous ependymitis. Cryptococci were found in the lesions and were identified on the basis of morphology and reaction to specific fluorescent antibody. This is believed to be the first case of canine cryptococcosis reported in the United Kingdom.     

The impact of bluetongue virus on reproduction

Bluetongue virus has been recognized as an important noncontagious, arthropodborne infectious viral disease of ruminants. 24 different serotypes of virus have been recognized world-wide. The most severe clinical disease has been associated with severe clinical disease in sheep and some free ranging wild ruminants. A number of reports have implicated the viruses as causing reproductive disorders in both males and females. The bluetongue related reproductive disorders include early embryonic deaths, abortions, malformed fetal calves or lambs, transient infertility in bulls and rams, and shedding of virus in semen. Recently, bluetongue virus contamination of modified live commercial canine vaccine was associated with abortion and acute death of pregnant bitches. The pathogenesis of these various aspects of reproductive failure are discussed herein.     

Pathogenesis of canine parvovirus enteritis: sequential virus distribution and passive immunization studies

After oral inoculation, the sequential distribution of canine parvovirus was studied in 14 nine-week-old seronegative beagle dogs. Two or three dogs were necropsied on days 1 through 6 after inoculation. Tissues were collected for virus isolation, immunofluorescence testing, and light microscopy. Virus was isolated from, and fluorescent cells were seen in the tonsil, retropharyngeal and mesenteric lymph nodes one and two days after inoculation. Virus infection of systemic and intestinal lymphoid tissues occurred as early as three days after inoculation and was associated with viremia. Intestinal epithelial infection was first seen four days after oral inoculation. All dogs were viremic before intestinal epithelial infection was found. Fecal virus excretion first occurred four days after oral virus inoculation. Intestinal virus infection and lesions became progressively more severe between four and six days after inoculation. The severity of intestinal lesions was variable and related to the severity of systemic lymphoid tissue lesions and the magnitude and duration of viremia. Four littermates of virus-infected dogs were passively immunized against canine parvovirus with convalescent canine serum 24 hours after oral virus inoculation. Neither clinical signs, lymphopenia, nor fecal virus excretion occurred in passively immunized dogs. Intestinal epithelial infection was not demonstrable by immunofluorescence testing when passively immunized dogs were necropsied four, five, and six days after virus inoculation.     

"Dog pox": some clinical aspects of an eruptive condition of certain mucous surfaces in dogs.

An eruptive condition seen on certain mucous membranes of dogs occurs frequently but often asymptomatically. Lesions have been found to be present in over 60 percent of male dogs. The infection is probably due to a canine herpes virus and has been termed conveniently but inaccurately "dog pox". In many cases lesions are present without observable clinical signs but severe irritation, especially related to lesions in the lower bowel, can give rise to marked symptoms which may be confused with abnormality of the para-anal sacs, or to chronic diarrhoea of a type suggestive of colitis. The incidence, sites of infection and possible syndromes which may be ascribed to the condition are briefly discussed on a clinical basis only.     

Greyhound meningoencephalitis: PCR-based detection methods highlight an absence of the most likely primary inducing agents

Greyhound meningoencephalitis is currently classified as a breed-associated idiopathic central nervous system inflammatory disorder. The non-suppurative inflammatory response can be distinguished from the other breed-associated disorders based on histopathology and lesion topography, however the nature of the response primarily suggests a viral infection. In the present study PCR and RT-PCR technologies were employed on frozen cerebral tissue from confirmed cases of meningoencephalitis to target specific viruses and protozoa likely to be implicated and to exclude the presence of bacterial 16SrRNA. Secondly, degenerate primers were used to detect viruses of the herpesvirus and flavivirus families. In addition cerebral tissues were probed for West Nile Virus. Viral nucleic acid sequences to Borna disease virus, to louping ill, tick borne encephalitis, West Nile and other flaviviruses were not detected. Canine distemper virus was detected in one animal with 97% homology to strain A75/15. Degenerate PCR for herpesviruses detected viral amplification products in one animal with 90% homology to canine herpesvirus DNA polymerase gene. Protozoal amplification products were only detected in a single dog with pathological confirmation of a combination of lesions of greyhound meningoencephalitis and a protozoal encephalomyelitis. Neospora was confirmed with sequence homology to Austrian strain 1. Bacterial 16SrRNA was not detected. The present study supports previous observations that many of the known microbial causes of canine meningoencephalitis are not involved. Findings could reflect that the causal agent was not specifically targeted for detection, or that the agent is at undetectable levels or has been eliminated from brain tissue. The potential roles of genetics and of molecular mimicry also cannot be discounted.     

The ACVD task force on canine atopic dermatitis (XVIII): histopathology of skin lesions.

For years, the histopathology of skin lesions of canine atopic dermatitis was deemed non-specific for this diagnosis. However, more recent studies have established that canine atopic skin lesions exhibit an inflammatory pattern characterized as a chronic, hyperplastic and spongiotic, mixed perivascular dermatitis. The nature of epidermal and dermal inflammatory cell infiltrates has now been characterized using modern immunological techniques. Epitheliotropic cells include Langerhans' cells, T-lymphocytes and rare eosinophils. Dermal cells are composed of mast cells, dermal antigen-presenting cells, T-lymphocytes and occasional intact and degranulated eosinophils. This paper provides an historical review of the landmark papers that have elucidated the pathology of canine atopic dermatitis.     

自发性急性犬瘟热的原发性脱髓性脑病

为了进一步观察犬瘟热病毒引起的原发性脑损伤和包涵体形成的特点，调查脑组织的损伤与神经症状的关系，对10只急性犬瘟热病犬的脑组织进行了详细的病理学研究。为了仔细地观察病变，本试验按照解剖学关系将脑组织分成3个大部分和11个切面，即大脑(4个切面)，脑干(5个切面)和小脑(2个切面)。组织切片经HE、LFB和免疫组织化学染色后进行检查，结果表明：在大脑，脱髓呈弥漫性发生，程度较轻；脑干的周围或靠近第三脑室的白质脱髓较重；小脑在轻度或中度脱髓的基础上常出现严重的多发性脱髓灶。脱髓部呈空泡或海绵状，有少量胶质细胞存在，但无炎性反应。脱髓性病损是非时称性发生，对神经束没有特殊的亲和力。在脑室的室管膜细胞内发现有较多的嗜酸性胞浆或核内包涵体。用抗犬瘟热病毒抗体染色，带有包涵体的室管膜细胞呈现强阳性反应。部分锥体细胞，神经核细胞和漓氏细胞变性、溶解或胞浆深染。胞核浓缩。这种变化以小锥体神经细胞表现得最为明显。根据此研究结果，作者认为由犬瘟热病毒引起的原发性脑组织损伤是一种脱髓性脑病，而不是脑炎变化；位于室管膜细胞内的包涵体对于脑组织犬瘟热的确诊具有重要的作用；由于犬瘟热病毒引起神经细胞的损伤是非特异性的，对脑组织的侵害是非对称性的。对神经束的作用无特殊的亲和力，所以患犬瘟热的犬在临床上可出现不同的神经症状。     

Necrotizing encephalitis in Yorkshire terriers

During the past six years these authors have observed a distinctive multifocal non-suppurative necrotizing encephalitis in Yorkshire terriers. Histopathological findings were different from those in canine encephalitides of known and unknown causes. Clinically, the Yorkshire terriers presented primarily brain stem signs or evidence of cerebral involvement, including seizures. The course of the disease was mostly chronic and progressive. Protozoal, bacterial and mycotic organisms were not found on histopathological examinations. The morphology of the lesions was strongly suggestive of a viral aetiology. Immunocytochemistry as well as in situ hybridisation failed to provide evidence for canine distemper virus infection. Likewise, canine herpesvirus was not detected by immunocytochemistry. Other known canine encephalitides could be excluded on clinical and morphological grounds; however, certain similarities may exist to pug dog encephalitis.     

H3N2 canine influenza virus causes severe morbidity in dogs with induction of genes related to inflammation and apoptosis

Dogs are companion animals that live in close proximity with humans. Canine H3N2 influenza virus has been isolated from pet dogs that showed severe respiratory signs and other clinical symptoms such as fever, reduced body weight, and interstitial pneumonia. The canine H3N2 influenza virus can be highly transmissible among dogs via aerosols. When we analyzed global gene expression in the lungs of infected dogs, the genes associated with the immune response and cell death were greatly elevated. Taken together, our results suggest that canine H3N2 influenza virus can be easily transmitted among dogs, and that severe pneumonia in the infected dogs may be partially due to the elevated expression of genes related to inflammation and apoptosis.     

Immunohistochemical detection of canine adenovirus in paraffin sections of liver

An avidin-biotin immunoperoxidase procedure was optimized for detection of canine adenoviral antigens in formalin-fixed, paraffin-embedded liver. Long-term stability of viral antigen was shown by successful demonstration of virus in liver tissue preserved up to six years from dogs with infectious canine hepatitis. This immunohistochemical stain was applied to sections from livers with a wide range of inflammatory lesions. Examination of sections from 53 dogs yielded five livers with small amounts of adenovirus. An additional virus-positive liver was identified from a dog with no hepatic inflammation. Although a cause and effect relationship remains to be determined, these findings suggest a possible connection between canine adenovirus and spontaneous chronic hepatitis.     

Pathology in dogs with experimental canine H3N2 influenza virus infection

Avian-lineage H3N2 canine influenza virus (CIV)-associated respiratory disease, which can be fatal, emerged in South Korean dogs in 2007. We show here that dogs experimentally infected with CIV only developed respiratory tract diseases, as no extrapulmonary lesions and virus antigens were detected. This differs from the multiorgan diseases that avian influenza H5N1 induces in small experimental animals. However, the CIV-infected dogs developed a distinctively severe, long-persistent bronchointerstitial pneumonia, which differs from the acute but short-term bronchopneumonia that human (H1N1 and H3N2) influenza cause in rodents and ferrets. Histopathology and in situ TUNEL assays revealed that the neutrophils infiltrating the lesions were undergoing apoptosis, which probably reflects the attempts by the body to maintain appropriate numbers of neutrophils for defense against secondary bacterial infections. Our observations suggest that neutrophils along with the related chemoattractant cytokines (TNF-α, IL-1 and IL-8, etc.) may play a key role in the pathogenesis of H3N2 CIV in dogs.     

Atypical necrotizing encephalitis associated with systemic canine distemper virus infection in pups

This report describes the naturally occurring atypical neuropathological manifestation of systemic canine distemper virus (CDV) infection in two 16-day-old Pit Bull pups. CDV-induced changes affected the gray and white matter of the forebrain while sparing the hindbrain. Histologically, there was necrosis with destruction of the nervous parenchyma due to an influx of inflammatory and reactive cells associated with eosinophilic intranuclear inclusion bodies within glial cells. Positive immunoreactivity against CDV antigens was predominantly observed within astrocytes and neurons. RT-PCR was used to amplify CDV-specific amplicons from brain fragments. These findings suggest the participation of CDV in the etiopathogenesis of these lesions.     

Therapeutic potential of canine bone marrow stromal cells (BMSCs) in the carbon tetrachloride (CCl4) induced chronic liver dysfunction mouse model

Regenerative medicine using bone marrow cells is an attractive therapy for the cure of patients with severe liver disease. Here, we show the therapeutic potential of canine bone marrow stromal cells (BMSCs) in mouse models of CCl(4)-induced chronic liver dysfunction. We used two different models for xenotransplantation, nude mice and cyclosporine A (CSA) immunosuppressed mice. Serum parameters from a standard liver panel were not improved following transplantation. However, fibrotic liver lesions with severe inflammation were decreased in CCl(4)-treated CSA mice following BMSC transplantation. Effective migration of transplanted canine BMSCs was limited to persistently injured liver in CCl(4)-treated CSA mice, where they may be effective in resolving inflammatory fibrotic lesions. These results suggest that canine BMSCs are an effective cell source for liver regeneration.