Wintering of neurotropic velogenic Newcastle disease virus and West Nile virus in double-crested cormorants (Phalacrocorax auritus) from the Florida Keys

During November 2002, six double-crested cormorants (DCCs; Phalacrocorax auritus) were found moribund in Big Pine Key, FL, exhibiting clinical signs indicative of neurologic disease. Postmortem diagnostic evaluations were performed on two adult birds. Virulent Newcastle disease virus (NDV) was isolated from a cloacal swab from cormorant 1. West Nile virus (WNV) was isolated from the brain and lung of cormorant 2. Nucleotide sequence analysis of a portion of the fusion (F) protein gene of the NDV cormorant isolate revealed it shared a 100% deduced amino acid identity with only two viruses: the 1992 epizootic cormorant isolate from Minnesota and the 1992 turkey isolate from North Dakota. The epidemiologic significance of the recognition of virulent NDV on cormorant wintering grounds during a nonepizootic period, in addition to the potential implications of the concurrent isolation of NDV and WNV from cormorants, is discussed.     

Domoic acid toxicity in Californian sea lions (Zalophus californianus): clinical signs, treatment and survival

Eighty-one Californian sea lions (Zalophus californianus) with signs of domoic acid toxicity stranded along the coast of California in 1998 when there were blooms of the domoic acid-producing alga Pseudonitzschia australis off-shore. In 2000, a further 184 sea lions stranded with similar clinical signs, but the strandings occurred both during detectable algal blooms and after the blooms had subsided. The clinical signs in these 265 Californian sea lions included seizures, ataxia, head weaving, decreased responsiveness to stimuli and scratching behaviour. Affected animals had high haematocrits, and eosinophil counts, and high activities of serum creatine kinase. They were treated supportively by using fluid therapy, diazepam, lorazepam and phenobarbitone. Fifty-five of the 81 sea lions (68 per cent) affected in 1998 and 81 of the 184 (44 per cent) affected in 2000 died despite the treatment. Three of the 23 sea lions which survived in 1998 were tracked with satellite and radiotransmitters; they travelled as far south as San Miguel Island, California, and survived for at least three months. Eleven of the 129 animals which were released stranded within four months of being released.     

Newcastle disease in wild water birds in western Canada, 1990

This report describes the investigation of mortality of double-crested cormorants (Phalacrocorax auritus), white pelicans (Pelecanus erythrorhynchos), and gulls (Larus spp.) in Alberta, Saskatchewan, and Manitoba during late summer 1990. Techniques used varied among areas, but virological and histopathological examination of birds was done in each area. The major clinical sign in cormorants was inability to fly, often with unilateral wing or leg paralysis. Focal nonsuppurative inflammation was present in the brain and spinal cord of cormorants and pelicans. Newcastle disease virus (NDV) was isolated from cormorants, a pelican, and a ring-billed gull (Larus delawarensls) from Saskatchewan. Cormorants from Alberta were positive for NDV in an immunofluorescent test. Most of the viruses were classed as velogenic and all had a similar monoclonal antibody profile to viruses from the 1970 to 1974 panzootic. Approximately half of cormorant, pelican, and gull eggs collected from affected colonies in the spring of 1991 had antibody to NDV. Antibody was also present in cormorant eggs from the Great Lakes. No unusual mortality was detected at any colony in 1991. Fledgling cormorants and gulls from colonies where mortality occurred in 1990 did not have antibody to NDV in June-July 1991. The overall extent of mortality among water birds and the source of the virus were not determined.     

Quantitative assessment of clinical signs for the detection of classical swine fever outbreaks during an epidemic

The performance of clinical signs as a diagnostic test for the detection of classical swine fever (CSF) outbreaks during the 1997-1998 CSF epidemic in The Netherlands was evaluated by constructing and analysing a receiver operating characteristic (ROC) curve. This curve assesses the discriminating ability of a diagnostic test over a range of test signals. The cut-off values for a defined diagnostic test to detect CSF outbreaks were set by different combinations of clinical signs observed. The area under the ROC curve, which is a quantitative measure of test performance, was significantly (P<0.001) larger than the area under the random ROC curve. This indicates that clinical signs have a significantly higher performance as a diagnostic test for the detection of CSF than for flipping a coin. However, the gain in diagnostic performance compared to a random process is not as much as we would wish it to be. The optimal efficient diagnostic test combined a sensitivity of 72.7% with a specificity of 52.7%, with a combination of the following clinical signs: unsteady gait/ataxia, not eating, not reacting to antibiotic treatment, conjunctivitis, hard faecal pellets.     

Necrotizing encephalitis of unknown cause in Fennoscandian Arctic foxes (Alopex lagopus).

A neurologic disease affected a colony of endangered Fennoscandian arctic foxes (Alopex lagopus) kept in captivity for breeding purposes. Several outbreaks of disease occurred between 1994 and 2004. The clinical signs included ataxia, indications of anosmia, blindness, and abnormal behavior. The disease was characterized by severe necrotizing encephalitis affecting mostly the cranial cerebrum, basal ganglia, and olfactory bulbs. Investigations to identify the etiology of the disease included testing for several infectious agents known to cause encephalitis in carnivores. Tests for Toxoplasma gondii, Encephalitozoon cuniculi, Neospora caninum, canine distemper virus, rabies, adenovirus type 1, Borna disease virus, and Listeria monocytogenes were negative. The colony was closed, and the cause of the disease remains undetermined.     

Molecular sexing of Japanese cormorants used for traditional fishing on the Nagara River in Gifu City

The Japanese cormorants used in traditional fishing in Japan are wild derived and their sex cannot be determined from their appearance. Applicability of molecular sex determination based on the size difference between CHD1Z and CHD1W introns was confirmed in male and female Japanese cormorants whose sexes had been ascertained by pathological autopsy. All of 21 birds of unknown sex reared by a cormorant fishing master were identified as males. The molecular sexing method will provide valuable information on sex differences of wild Japanese cormorants, including tameness, trainability, behavior and fishing capability, as well as for future trials involving artificial reproduction.     

Aural Cholesteatoma in Twenty Dogs

Objective— To determine the clinical course in dogs with aural cholesteatoma. Study Design— Case series. Animals— Dogs (n=20) with aural cholesteatoma. Methods— Case review (1998–2007). Results— Twenty dogs were identified. Clinical signs other than those of chronic otitis externa included head tilt (6 dogs), unilateral facial palsy (4), pain on opening or inability to open the mouth (4), and ataxia (3). Computed tomography (CT) was performed in 19 dogs, abnormalities included osteoproliferation (13 dogs), lysis of the bulla (12), expansion of the bulla (11), bone lysis in the squamous or petrosal portion of the temporal bone (4) and enlargement of associated lymph nodes (7). Nineteen dogs had total ear canal ablation–lateral bulla osteotomy or ventral bulla osteotomy with the intent to cure; 9 dogs had no further signs of middle ear disease whereas 10 had persistent or recurrent clinical signs. Risk factors for recurrence after surgery were inability to open the mouth or neurologic signs on admission and lysis of any portion of the temporal bone on CT imaging. Dogs admitted with neurologic signs or inability to open the mouth had a median survival of 16 months. Conclusions— Early surgical treatment of aural cholesteatoma may be curative. Recurrence after surgery is associated with advanced disease, typically indicated by inability to open the jaw, neurologic disease, or bone lysis on CT imaging. Clinical Relevance— Presence of aural cholesteatoma may affect the prognosis for successful surgical treatment of middle ear disease.     

The classical swine fever epidemic 1997-1998 in The Netherlands: descriptive epidemiology

The objective of this paper is to describe the severe epidemic of classical swine fever (CSF) in The Netherlands in 1997–1998 under a policy of non-vaccination, intensive surveillance, pre-emptive slaughter and stamping out in an area which has one of the highest pig and herd densities in Europe.

The primary outbreak was detected on 4 February 1997 on a mixed sow and finishing pig herd. A total of 429 outbreaks was observed during the epidemic, and approximately 700 000 pigs from these herds were slaughtered. Among these outbreaks were two artificial insemination centres, which resulted in a CSF-suspect declaration of 1680 pig herds (mainly located in the southern part of The Netherlands). The time between introduction of CSF virus (CSFV) into the country and diagnosis of CSF in the primary outbreak was estimated to be approximately 6 weeks. It is presumed that CSFV was spread from The Netherlands to Italy and Spain via shipment of infected piglets in the beginning of February 1997, before the establishment of a total stand-still of transportation. In June 1997, CSFV is presumed to be introduced into Belgium from The Netherlands.

Pre-emptive slaughter of herds that had been in contact with infected herds or were located in close vicinity of infected herds, was carried out around the first two outbreaks. However, this policy was not further exercised till mid-April 1997, when pre-emptive slaughter became a standard operational procedure for the rest of the epidemic. In total, 1286 pig herds were pre-emptively slaughtered. (approximately 1.1 million pigs). A total of 44 outbreaks (10%) was detected via pre-emptive slaughter.

When there were clinical signs, the observed symptoms in infected herds were mainly atypical: fever, apathy, ataxia or a combination of these signs. In 322 out of 429 outbreaks (75%), detection was bases on clinical signs observed: 32% was detected by the farmer, 25% by the veterinary practitioner, 10% of the outbreaks by tracing teams and 8% by screening teams of the veterinary authorities. In 76% of the outbreaks detected by clinical signs, the farmer reported to have seen clinical symptoms for less than 1 week before diagnosis, in 22% for 1–4 weeks before diagnosis, and in 4 herds (1%) the farmer reported to have seen clinical symptoms for more than 4 weeks before diagnosis.

Transportation lorries played a major role in the transmission of CSFV before the primary outbreak was diagnosed. It is estimated that approximately 39 herds were already infected before the first measures of the eradication campaign came into force.

After the first measures to stop the spread of CSFV had been implemented, the distribution of the most likely routes of transmission markedly changed. In most outbreaks, a neighbourhood infection was indicated.

Basically, there were two reasons for this catastrophe. Firstly, there was the extent of the period between introduction of the virus in the region and detection of the first outbreak. As a result, CSFV had opportunities to spread from one herd to another during this period. Secondly, the measures initially taken did not prove sufficient in the swine- and herd-dense region involved.     

Comparison of Newcastle disease viruses isolated from cormorants in Canada and the USA in 1975, 1990 and 1992.

Seventeen Newcastle disease virus (NDV) isolates obtained from cormorants, turkeys, a pelican, and a gull in Canada and the USA collected in 1975, 1990 and 1992 were analyzed for relatedness by monoclonal antibody profiling. In addition, nucleotide sequence analysis was performed in two areas of the fusion (F) gene for 5 of the isolates. No difference in the antigenicity of these 17 viruses, as determined by monoclonal antibody binding patterns, was seen. The amino acid sequences obtained via nucleotide sequencing at the cleavage site of the F protein showed that all the isolates tested had two pairs of basic amino acids immediately upstream of the cleavage site, and a phenylalanine residue at the N-terminus of the F1 protein, which is consistent with velogenic NDV. The deduced amino acid sequence obtained at the cleavage site of the F protein from 6 of the isolates was virtually identical regardless of the species, year of isolation, or location. However, the 1975 cormorant isolate showed marked differences from the 1990-1992 isolates in the nucleotide and deduced amino acid sequence of the F gene signal region. These data indicate that the 1990 and 1992 outbreaks were caused by the same epizootic virus and further suggest that the population of NDV in these wild birds may be very stable. The belief that the velogenic NDV circulating in cormorants in 1992 was transmitted into the free-ranging turkey flocks located near the cormorants in North Dakota is supported by the present study in which no distinction could be made between the viruses isolated from turkeys or wild birds.     

Hexachlorophene toxicosis in a litter of Doberman pinschers

A litter of 5-week-old Doberman Pinschers with pustular dermatitis was treated dermally with a hexachlorophene-containing emulsion. Shortly after a second treatment, all of the puppies developed neurologic signs consisting of muscle tremors, ataxia, and apparent muscle weakness. The clinical history and signs, histologic lesions within the central nervous system, and measurement of hexachlorophene in liver and kidney tissue confirmed a diagnosis of hexachlorophene toxicosis.     

Toxoplasma gondii in an African crested porcupine (Hystrix cristata).

An adult female crested porcupine (Hystrix cristata) was evaluated for acute onset of neurologic signs including head tilt, circling, and ataxia. She was found dead in her holding area 2 days after initially exhibiting clinical signs. Necropsy was unremarkable. Histopathology of brain tissue revealed the presence of protozoal cysts associated with inflammation as the underlying cause of clinical signs and death. Immunohistochemical staining of brain tissue for Toxoplasma gondii was strongly positive. PCR on fresh brain confirmed T. gondii as the causative organism. An adult male in the same enclosure has demonstrated similar neurologic signs over the past 3 years and has failed to respond to various medical treatments. Clinical disease associated with T. gondii has not been previously reported in this porcupine species or any other Old World porcupines, although there are several reports of clinical toxoplasmosis involving New World porcupine species.     

Neurologic abnormalities and cerebrospinal fluid changes in horses administered fumonisin B1 intravenously

The objective of this experiment was to characterize a dose-dependent toxic effect of fumonisin B1 (FB1) and to document initial neurologic signs, clinical progression, and terminal cerebrospinal fluid (CSF) changes in horses administered FB1 IV. Seventeen healthy horses were administered 0.00 (n = 4), 0.01 (n = 3), 0.05 (n = 3), 0.10 (n = 3), or 0.20 mg (n = 4) of purified FB1 IV q24h. When neurologic abnormalities observed by a masked observer became severe, atlanto-occipital CSF taps were performed and CSF pressure, cell count, cytology, protein, albumin and glucose concentrations, and creatine kinase activity were measured. Changes in CSF and number of days to 1st observation of neurologic abnormalities were compared between doses by ANOVA, with the level of significance set at P < .05. Control horses and low-dose horses (0.01 mg/kg) remained neurologically normal. In higher dose FB1-treated horses (n = 10), initial clinical signs (days 4-10) included hindlimb ataxia, delayed forelimb placing, and decreased tongue tone and movement. Hindlimb and trunkal ataxia, depression, hyperesthesia, and intermittent dementia gradually became apparent. When data from all horses with neurologic abnormalities were pooled (0.05-0.20 mg/kg FB1), mild clinical signs (mean day 6.3) occurred significantly earlier than did more severe (mean day 8.9) clinical signs (P = .009). Neurologic horses had high CSF protein, albumin, and IgG concentrations and increased albumin quotients (P < .05). It was concluded that FB1-induced neurologic and CSF changes in a dose-dependent manner, with a no-observable-limit of 0.01 mg FB1/kg IV q24h for 28 days. The neurologic and CSF changes were consistent with vasogenic cerebral edema.     

Clinical, clinicopathologic, and electroencephalographic features of lead poisoning in dogs.

Eleven dogs with signs of lead poisoning were examined. The principal clinical signs were neurologic and included ataxia, tremors, clonic-tonic seizures, amaurosis, and deafness. Basophilic stippling and circulating nucleated red cells were not common findings in blood films. Blood lead values varied from 0.22 ppm to 0.63 ppm before treatment. Electroencephalographic changes in nonsedated dogs were marked by intermittent high-amplitude slow wave activity.     

Intervertebral disk prolapse and diskospondylitis in a horse

Intervertebral disk prolapse was diagnosed in a mature horse with clinical signs of caudal ataxia. Radiography and myelography demonstrated a collapsed intervertebral space and loss of the dorsal and ventral dye columns. Results of CSF analysis were normal, as were a CBC and serum biochemical profile. High CSF WBC count and high CSF creatine kinase activity were noticed following acute neurologic deterioration. While common in certain breeds of dogs, intervertebral disk prolapse is rarely reported in horses. It should be considered in the differential diagnosis of horses with caudal ataxia.     

Isolation of Newcastle disease virus and Salmonella typhimurium from the brain of double-crested cormorants (Phalacrocorax auritus)

Avian paramyxovirus type 1 (Newcastle disease virus) and Salmonella typhimurium were isolated from the brain and lung tissues of double-crested cormorants (Phalacrocorax auritus) from Lac Canard, Alberta, Canada. More than 100 birds died during this outbreak in 1999. Affected birds presented signs of central nervous system disease characterized by unilateral wing and leg paralysis. Other geographic locations in the provinces of Alberta and Saskatchewan have reported cases of cormorants suffering from diseases with signs compatible with Newcastle disease. The virus isolated in the 1999 outbreak was characterized as mesogenic. These findings suggest that other pathogens, like S. typhimurium, may influence the clinical presentation of disease caused by mesogenic strains of Newcastle disease virus in cormorants.     

Multisystem Neuronal Degeneration in Cocker Spaniels

Four young Cocker Spaniels had slowly progressive neurologic signs with ataxia and mental deterioration. Pathologically, the lesions consisted of diffuse nerve cell loss, gliosis, axonal degeneration, and some demyelination in several areas of the brain. Pedigree analysis strongly suggests a hereditary cause for this disease, which is classified as a multisystem neuronal degeneration. This disorder has not been previously reported and has some resemblance to certain degenerative neurologic diseases found in humans. The clinical differential diagnosis includes cerebellar degeneration and lysosomal storage diseases. A definitive diagnosis requires postmortem examination.     

Smoke exposure in cats: 22 cases (1986-1997).

OBJECTIVE: To review clinical findings and clinical course for cats exposed to smoke in residential fires and to determine clinical variables that may have prognostic importance. DESIGN: Retrospective study. ANIMALS: 22 cats admitted to our veterinary teaching hospital between 1986 and 1997 with a history of smoke exposure during a residential fire. PROCEDURE: Medical records were reviewed for history, clinical signs, physical examination findings, changes in respiratory tract signs, initial hematologic analysis, treatment, results of thoracic radiography, and outcome. RESULTS: Fifteen of 22 (68%) cats were categorized in the uncomplicated group, 5 (23%) in the complicated group, and 2 (9%) were discharged after a short period because of financial considerations. Twenty (91%) cats survived, but 2 (9%) were euthanatized because of severe respiratory compromise or neurologic changes. Predominant thoracic radiographic changes were diffuse interstitial pattern (6 cats) and focal alveolar pattern (5). The majority (8/13) of cats that were stable or had improved by the day after admission had an uncomplicated clinical course while hospitalized, whereas cats that were worse on the day after admission tended to have a complicated clinical course. CONCLUSIONS AND CLINICAL RELEVANCE: Cats that survive a residential fire and are admitted to a hospital have a good chance to be discharged. Cats that do not have signs of respiratory tract dysfunction at admission probably will not develop severe respiratory complications. For cats with signs of respiratory dysfunction at admission, better prognostic information will be determined by monitoring progression of the respiratory condition on the day after admission.     

Equine encephalomyelitis outbreak caused by a genetic lineage 2 West Nile virus in Hungary

Background: The spread of lineage 2 West Nile virus (WNV) from sub‐Saharan regions to Europe and the unpredictable change in pathogenicity indicate a potential public and veterinary health threat and requires scientific awareness. Objectives: To describe the results of clinical and virological investigations of the 1st outbreak of a genetic lineage 2 WNV encephalomyelitis in horses. Animals: Seventeen horses with neurologic signs. Methods: Information regarding signalment, clinical signs, and outcome was obtained for each animal. Serology was performed in 15 cases, clinicopathological examination in 7 cases, and cerebrospinal fluid was collected from 2 horses. Histopathology was carried out in 4 horses, 2 of which were assessed for the presence of WNV in their nervous system. Results: WNV neutralizing antibody titers were between 10 and 270 (median, 90) and the results of other serological assays were in agreement with those of the plaque reduction neutralization test. Common signs included ataxia, weakness, asymmetric gait, muscle tremors, hypersensitivity, cranial nerve deficits, and recumbency. Twelve animals survived. Amplicons derived from the infection‐positive specimens allowed molecular characterization of the viral strain. Conclusions and Clinical Importance: From our results, we conclude that this outbreak was caused by a lineage 2 WNV strain, even though such strains often are considered nonpathogenic. Neurological signs and survival rates were similar to those reported for lineage 1 virus infections. The disease occurrence was not geographically limited as had been the typical case during European outbreaks; this report describes a substantial northwestern spread of the pathogen.