Form Of Paralysis Research Articles

On the interference of clinical outcome on rabies transmission an perpetuation

Rabies is a viral zoonotic infectious disease that affects mammals and is caused by genotypes/species of the Lyssavirus genus (Rhabdoviridae, Mononegavirales), with the genotype 1 (classic rabies virus - RABV) being the most prevalent. Despite continuous efforts, rabies is still an incurable disease that causes thousands of deaths amongst humans worldwide. Due to a wide range of hosts and the different evolutionary paths of RABV in each host, several host-specific variants have arisen in an ongoing process. The result of RABV replication in nervous tissues may lead to two opposite clinical outcomes, i.e., paralytic/dumb form and encephalitic/furious one. The paralytic form creates dead-end hosts mainly amongst herbivores, while the furious form of the disease allows for augmented transmission when manifested in gregarious carnivores, as their natural aggressive behavior is accentuated by the disease itself. The aim of this article is to propose a theoretical model intended to explore how the rabies virus intrinsically modulates the immune system of different host classes, the pathological changes that the virus causes in these animals and how these elements favor its own perpetuation in nature, thus providing a basis for better prediction of the patterns this disease may present.

Brain–computer interface in paralysis

Communication with patients suffering from locked-in syndrome and other forms of paralysis is an unsolved challenge. Movement restoration for patients with chronic stroke or other brain damage also remains a therapeutic problem and available treatments do not offer significant improvements. This review considers recent research in brain-computer interfaces (BCIs) as promising solutions to these challenges. Experimentation with nonhuman primates suggests that intentional goal directed movements of the upper limbs can be reconstructed and transmitted to external manipulandum or robotic devices controlled from a relatively small number of microelectrodes implanted into movement-relevant brain areas after some training, opening the door for the development of BCI or brain-machine interfaces in humans. Although noninvasive BCIs using electroencephalographic recordings or event-related-brain-potentials in healthy individuals and patients with amyotrophic lateral sclerosis or stroke can transmit up to 80 bits/min of information, the use of BCIs - invasive or noninvasive - in severely or totally paralyzed patients has met some unforeseen difficulties. Invasive and noninvasive BCIs using recordings from nerve cells, large neuronal pools such as electrocorticogram and electroencephalography, or blood flow based measures such as functional magnetic resonance imaging and near-infrared spectroscopy show potential for communication in locked-in syndrome and movement restoration in chronic stroke, but controlled phase III clinical trials with larger populations of severely disturbed patients are urgently needed.

A clinical lecture on shaking palsy. By Thomas Buzzard, MD, FRCP. (Physician to the National Hospital for the Paralyzed and Epileptic). Brain 1882; 4: 473-492 and On-off fluctuations in Parkinson's disease. A clinical and neuropharmacological study. By RJ Hardie, AJ Lees and GM Stern. (From the Department of Neurology, University College Hospital, London WC1). Brain 1984; 107: 487-506.

Thomas Buzzard (1831–1919) never attended medical school but was one of the last doctors to enter medicine through apprenticeship to a general practitioner. Appointed to the staff of the National Hospital for the Paralyzed and Epileptic in 1867, at the suggestion of Hughlings Jackson, Buzzard was one of that small group of physicians who helped ‘Queen Square’ acquire its international reputation (Fig. 1). He doubled-up as a medical journalist; dealt with the Soho (London) outbreak of cholera in 1854; and served with the Turkish army in the Crimean War. He resigned his hospital appointment in 1906. Sir Gordon Holmes did not consider that Thomas Buzzard contributed much to the advance of neurology but acknowledged that he was a sound and practical physician who taught well. Buzzard wrote on The simulation of hysteria by organic disease (1891), delivered the Harveian Lectures for 1885 on Some forms of paralysis from peripheral neuritis (1886) and published on Clinical aspects of syphilitic nervous affections (1874). In 1882, Buzzard published a series of 25 lectures, mostly delivered at the National Hospital, as Clinical lectures on disease of the nervous system . The one on paralysis agitans is also the first article in Brain on Parkinson's disease (printed without mutual attribution having a few sentences omitted or inserted but otherwise unchanged). Fig. 1 The honorary medical staff of the national hospital, Queen Square, 1897. Thomas Buzzard is standing at the back right. From Holmes, G., The National Hospital Queen Square, 1860–1948 (1954). Edinburgh and London: E. & S. Livingstone. Plate III facing page 41. So graphic and admirable is James Parkinson's original description that little remains for subsequent observers to add: ‘involuntary tremulous motion, with lessened muscular power, in parts not in action and even when supported; with a propensity to bend the trunk forwards and to pass …

The Pilgrimage Topos and the Problem of Modernity: A Transatlantic View of Selected Hispanic Texts

Góngora's Soledades can be used as a base from which to examine failed pilgrimage as a recurring topos in Latin American texts which confront the Baroque legacy of frustrated modernity. Carpentier's 'El camino de Santiago', Rulfo's Pedro Páramo and Vallejo's 'Trilce LXV' constitute a sort of progeny of this Gongorine topos, contrasting in their different relation to the messianic. While Góngora, Rulfo, and Carpentier present historical repetition as a form of paralysis, Vallejo presents the frustration of historical progress in equally graphic terms, but also offers hope in his engagement with possibility from a socialist perspective. His poem suggests the 'weak Messianic power' of which Benjamin writes, one which engages the future without a pre-established teleology, locating pilgrimage instead in the collective and open space of human potential.

Rabies: Epidemiology, pathogenesis, and prophylaxis

Rabies is a viral zoonosis that causes approximately 50,000 to 100,000 deaths per year worldwide. Most deaths occur in developing countries. Dogs are the major vector, especially in developing countries. The virus is usually transmitted to humans by infected saliva through the bite of a rabid animal; the incubation period averages 30 to 90 d. Hyperexcitability, autonomic dysfunction, hydrophobia, and aerophobia are characteristic of encephalitic rabies, which accounts for 80% of cases. The paralytic form is characterized by flaccid paralysis in the bitten limb, which ascends symmetrically or asymmetrically. Once symptoms develop, the disease is invariably fatal. Animal rabies can be controlled by proper induction of herd immunity, humane removal of stray animals, promotion of responsible pet ownership through education, and enactment of leash laws. Preexposure vaccination with modern cell culture vaccine is recommended for people at high risk of exposure to rabies and for travelers who spend longer than 1 mo in countries where rabies is a constant threat, or who travel in a country where immediate access to appropriate care is limited. Postexposure prophylaxis consists of prompt and thorough wound cleansing and immunization with modern cell culture vaccine, together with administration of rabies immune globulin to those individuals who have not previously received preexposure prophylaxis.

Letters to the Editor

1 March 2007 Dear Editor, POLIOMYELITIS – ACUTE FLACCID PARALYSIS AND STOOL VIROLOGY I write on behalf of the Poliomyelitis Expert Committee of the Commonwealth Department of Health and Ageing, to stress the importance of submitting stool specimens for virological analysis, in cases of acute flaccid paralysis (AFP), and particularly in those cases where poliomyelitis, however, unlikely, must be included in the differential diagnosis. The last case of wild-type poliomyelitis occurred in Australia in the early 1970s, and the last case of vaccine-associated poliomyelitis occurred in 1996. Since that time, Australia has been poliomyelitis-free. Nevertheless, every year there have been cluster outbreaks of poliomyelitis in countries that Australians visit and from which Australians return. The 2005/6 outbreak of clinical poliomyelitis in Indonesia was of significant concern to all monitoring bodies. Currently, almost three million Australians travel overseas each year and almost six million overseas visitors come here. The current immunisation-completion rate for poliomyelitis, for Australians, is 86% after the age of 6 years. There is obviously great need for meticulous surveillance, early diagnosis in the event of any clinical case occurring in Australia, and continued promotion of immunisation. The poliomyelitis virus remains viable and potentially infectious outside the body for some 8 weeks in faecal-contaminated soil or water. If poliomyelitis were reintroduced into Australia, the personal, logistic and administrative costs of eradication would be great, and have huge repercussions. Such would be further exacerbated by delayed diagnosis. The national Poliomyelitis Expert Committee, a committee of the Commonwealth Department of Health and Ageing, functions executively from the Victorian Infectious Diseases Reference Laboratory based in Melbourne. The Poliomyelitis Expert Committee monitors every case of AFP reported to it from multiple sources of case finding, principally through reports from the Australian Paediatric Surveillance Unit. Approximately 70 cases of AFP are reviewed in detail each year with final diagnoses ranging from Guillaine–Barré syndrome to tick paralysis. The ‘gold standard’, by which children with various forms of paralysis can be certified not to have poliomyelitis, is by negative culture of two stool-specimens submitted for virological culture, collected 24 h apart and within 14 days of onset of paralysis. Currently, the rate of submission of such stool specimens is only 16%. It is essential, in any newly presenting child with AFP, in which acute poliomyelitis or other neurotropic viruses must be considered in the differential diagnosis, to have such stool specimens submitted for culturing. This is done through one’s own local hospital pathology laboratory, to be forwarded to the National Polio Reference Laboratory located at the Victorian Infectious Diseases Reference Laboratory, 10 Wreckyn Street, North Melbourne, Victoria 3051, Australia (Tel: 03 9342 2600; Fax: 03 9342 2665; email: polio@mh.org.au). In the context of the ongoing ever-present risk of a poliomyelitis case occurring in Australia, may I join with many colleagues in promoting the strongest advocacy for the submission of stool specimens for virological analysis in all non-traumatic patients with AFP.

Rabies—Update on a Global Disease

Rabies, a fatal viral zoonosis, persists in both developed and developing countries worldwide in spite of successful preventive public health measures and postexposure therapies. Considering the years of life lost, rabies ranks seventh among all infectious diseases in the world. Public health campaigns, emphasizing rabies immunization of pets and development of effective preand postexposure immunization regimens, have reduced acquired human rabiesrelated fatalities in the U.S. to less than 3 per year. These few cases almost always involve a bat variant of the rabies virus causing fatal encephalitis. Etiology. The RNA, neurotropic virus causing rabies has a bullet-shaped nucleocapsid surrounded by a lipoprotein envelope. The unique genetic patterns in the nucleocapsid and glycoprotein components of rabies virus isolates provide an opportunity through molecular techniques to identify reservoir hosts (eg, bat, dog, fox, raccoon, skunk) providing useful epidemiological data. Epidemiology. Each year, an estimated 55,000 people die of rabies in Africa and Asia where infection is endemic in dogs. In contrast, only 19 indigenously acquired rabies-related human fatalities were reported in the U.S. from 2000 to 2006, 17 of which were associated with rabies virus variants maintained by bats. Mass immunization of pet dogs and cats at an estimated annual cost of 300 million dollars in great part accounts for the low incidence of human rabies in the U.S. Wildlife, primarily raccoons, skunks, bats and foxes, accounted for more than 92% of all animal rabies cases reported to the CDC in 2005. Oral rabies vaccine projects are being evaluated to control rabies in wildlife in Texas, Florida, Alabama and Ohio with over 4.1 million baits distributed in July of 2006. Transmission. Transmission requires introduction of rabies virus from saliva or infected neural tissue into bite wounds or open cuts in skin or mucous membranes. Minor, possibly unrecognized bites from bats (contributing to inaccurate recall), appear to have played a role in recent human fatalities in the U.S. Human to human transmission of rabies has been described in 8 patients receiving corneal transplants and, recently, 4 U.S. patients receiving organ transplants (lung, liver, and kidney) from one donor, raising new questions about tissue tropism and rabies screening of organ and tissue donors. Clinical Signs. The incubation period ranges from 2 weeks to 6 years, averaging 2 to 3 months, depending upon inoculum and proximity to the brain. Viral replication at dorsal root ganglion causes the first clinical sign of neuropathic pain near the inoculation site. The virus migrates to the central nervous system at 15–100 mm per day and then outward within peripheral nerves infecting adjacent organs such as salivary glands with viral shedding in saliva. Two clinical presentations, furious form (anterior horn cell dysfunction) and paralytic form (peripheral nerve dysfunction), lead to death within 5 days without intensive care. Diagnosis. Diagnosis based on clinical signs of phobic spasms (hydroor aerophobia), paralytic or Guillaine–Barrelike syndrome, or excitation is difficult and unreliable especially considering that typical or nonclassic rabies is being increasingly recognized. Magnetic resonance imaging, specifically hypersignal T2 images in brainstem, hippocampus, hypothalamus, deep subcortical and cortical white and gray matter, respectively, as well as gadolinium enhancement contribute to a rabies diagnosis. Antigen detection using fluorescent antibody test in skin biopsies taken from From the Department of Comparative Medicine, University of Rochester, Rochester, NY. Copyright © 2007 by Lippincott Williams & Wilkins ISSN: 0891-3668/07/2604-0351 DOI: 10.1097/01.inf.0000258776.47697.97 CONTENTS Rabies Update Autoinflammatory Syndromes

Presence of rabies specific immune complexes in cerebro-spinal fluid can help in ante-mortem diagnosis of human paralytic rabies

Background Human rabies presents in two clinical forms, viz. furious or encephalitic and paralytic. Clinical diagnosis of paralytic form is difficult and requires laboratory confirmation. Presently available diagnostic techniques are not very sensitive for ante-mortem confirmation of rabies. Objective In the present study, we investigated whether presence of rabies specific immune complexes in cerebro-spinal fluid (CSF) of paralytic rabies patients could help in ante-mortem diagnosis of rabies. Study design A capture ELISA based on monoclonal antibodies to rabies nucleoprotein (N) and glycoprotein (G) was developed to detect immune complexes to rabies N and G proteins. We studied CSF samples collected ante-mortem from 30 suspected paralytic rabies patients in whom diagnosis was later confirmed by autopsy. We included 30 CSF samples from people undergoing spinal anesthesia as negative controls and 30 CSF samples from other viral encephalitis as disease controls. Results Twenty-three out of 30 CSF samples (76.6%) showed presence of immune complexes to both rabies N and G proteins. None of the negative controls and CSFs from other confirmed viral infections were positive. Thus, the results were 100% specific and the sensitivity of this test was 76.6%. Conclusions Detection of immune complexes to rabies antigens may be used as one of the techniques for rapid ante-mortem diagnosis of human rabies.

Postmortem Confirmation of Human Rabies Source

Postmortem Confirmation of Human Rabies Source

Specific clinical and epidemiological features of tick-borne encephalitis in Western Siberia

In Western Siberia, tick-borne encephalitis (TBE) morbidity among residents of all ages and social groups has remained high over many years. The frequency of tick bites is high, and 2.6–5.7% of bitten persons are hospitalized each year because of suspected TBE infection. According to official statistical data, children <14 years account for 20–30% of TBE cases. Adult, working-age people (20–49 years) are at highest risk of infection. TBE may progress in a febrile, meningeal, or focal (paralytic) form, becoming chronic in 1–1.7% of cases. Severe progression and fatal outcomes of the disease have been recorded in all age groups. Over the past 20 years, mortality varied from 1.8% to 3%, increasing in periods of high TBE morbidity. This data stresses the necessity for more effective measures aimed at preventing TBE infection in the region. The results of our analyses of TBE peculiarities in Western Siberia lead to the conclusion that people in that region have been at high risk of infection and developing the most complicated forms of TBE.

Healing of back pain and some other neurological problems using preparations from the skin of the Arabian Gulf catfish (Arius Bilineatus Val.)

The Arabian Gulf catfish elaborates gel-like proteinacious secretions when threatened or injured. It was established that preparations from the skin of the catfish can lead to accelerated wound healing and healing of diabetic foot ulcers. The preparations contain highly active proteins and lipids, including a group of enzymes, growth factors, high levels of arachidonic acid and it,s metabolites, cholesterol and chlesterol esters, components that act on blood vessels, components that act on blood cells and factors that cause vascular permeabilty. The preparations which were found to cure 80% of treated back pain patients, sciatica, some forms of paralysis, facial palsy and demyelination, were found to have noticeable effecs on a spastic case resulting from spinal chord injury. Both lipids and proteins seem to play important roles in the healing proceses. Such results provide new venues in understanding and curing a number of neurological problems. (Partly funded by His Highness Shaikh Jaber Al-Ahmad Al-Sabah, The Amir of Kuwait; Shaikh Nasser. Mohd. Al-Ahmad Al-Sabah, Minister of the Amiri Diwan; Kuwait foundation for the Advancement of Sciences grant No.; Kuwait University grant No. SBO-19; and Jassim M. Al-Hassan).

Sinais clínicos, distribuição das lesões no sistema nervoso e epidemiologia da raiva em herbívoros na região Nordeste do Brasil

Descrevem-se 24 surtos de raiva em bovinos (25 casos), 4 em eqüinos (5 casos), 2 em caprinos (2 casos) e 2 em ovinos (4 casos). Todos os surtos ocorreram na Paraíba, exceto um em eqüinos que ocorreu no Rio Grande do Norte. Todos os surtos, com a exceção de um em ovinos, foram transmitidos provavelmente por morcegos hematófagos; no entanto, não se descarta a possibilidade de transmissão por raposas (Dusicyon vetulus). Os sinais clínicos foram representativos da localização das lesões no sistema nervoso central (SNC). Em bovinos os sinais eram, principalmente, da forma paralítica, causados por lesões da medula, tronco encefálico e cerebelo; mas alguns animais apresentaram depressão, excitação e outros sinais associados a lesões cerebrais. Três dos 5 eqüinos apresentaram sinais de lesões cerebrais e 2 apresentaram a forma paralítica. De 4 ovinos e 2 caprinos, 4 apresentaram a forma paralítica, mas em um caprino e um ovino os sinais foram predominantemente de lesões cerebrais. Todos os animais afetados, exceto um caprino, tiveram um curso clínico de 2-8 dias. As únicas lesões macros-cópicas observadas foram a dilatação da bexiga em 4 bovinos e a dilatação da ampola retal em 2. Dois cavalos apresentaram lesões da pele causadas por traumatismos. As lesões histológicas foram de encefalomielite e meningite difusa não supurativa. Nos eqüinos e em um caprino com evolução clínica de 35 dias as lesões foram mais severas, observando-se necrose neuronal, neuronofagia e presença de esferóides axonais. Corpúsculos de Negri foram observados em 87% (20/23) dos bovinos examinados e em 83% (5/6) dos ovinos e caprinos. Nessas 3 espécies os corpúsculos foram mais freqüentes no cerebelo, mas ocorreram também no tronco encefálico, medula e cérebro. Em cavalos, corpúsculos de Negri foram menos numerosos, sendo observados somente no córtex de um animal e no córtex e hipocampo em outro. No gânglio trigeminal, as lesões histológicas e os corpúsculos de Negri foram menos freqüentes que no SNC. Esses resultados mostram que na raiva dos herbívoros os sinais clínicos e a distribuição das lesões histológicas do SNC são variáveis, e que para o correto diagnóstico da enfermidade são necessários um bom exame clínico e o estudo histológico das diferentes regiões do SNC. Sugere-se, também, que perante resultados negativos nos testes de imunofluo-rescência e inoculação em camundongos, estes devam ser repetidos com amostras de diferentes regiões do SNC. Utilizando-se dados sobre a freqüência de doenças, de 4 laboratórios de diagnóstico, foi realizada uma estimativa das mortes de bovinos causadas pela raiva, anualmente, em 3 Estados. Na Paraíba, com uma população de 918.262 bovinos, o número de mortes é estimado em 8.609 cabeças por ano. No Mato Grosso do Sul, com uma população de 23 milhões de bovinos, as perdas por raiva são estimadas em 149.500 cabeças e, no Rio Grande do Sul, com uma população de 13 milhões de bovinos, as mortes são estimadas em 13.000 a 16.250 animais por ano. Se estas estimativas forem extrapoladas para todo o Brasil, com 195 milhões de bovinos, as mortes podem ser estimadas em 842.688 cabeças por ano.

Pathophysiology of human paralytic rabies

Furious rabies is a well-recognized clinical disorder in humans but the paralytic form is not as easily identified. The mechanisms responsible for the weakness and longer survival periods are not clear. Several hypotheses have been proposed, including rabies virus variants associated with a particular vector, location of wounds, incubation period, influence of prior rabies vaccination, and virus localization in the central nervous system (CNS). However, none of these have been substantiated. Regarding molecular analyses of rabies viruses isolated from both furious and paralytic rabies patients, only minor genetic variations with no specific patterns in glyco- (G), phospho- (P), and nucleoprotein (N) sequences have been identified and arginine 333 in G protein was present in all samples. Regional distribution of rabies virus antigenin rabies patients whose survival periods were 7 days or less and magnetic resonance imaging (MRI) of the CNS indicated brainstem and spinal cord as predilection sites regardless of clinical presentations. There are clinical, electrophysiological, and pathological indications that peripheral nerve dysfunction is responsible for weakness in paralytic rabies whereas in furious rabies, even in the absence of clinical weakness, abundant denervation potentials with normal sensory nerve conduction studies and proximal motor latencies suggest anterior horn cell dysfunction. The lack of cellular immunity to rabies virus antigen accompanied by an absence of cerebrospinal fluid (CSF) rabies neutralizing antibody in most paralytic rabies patients may argue against role of an immune response against rabies virus-positive axons. Aberrant immune responses to peripheral nerve antigen, in particular those mediated by one or more cellular-dependent mechanisms, may be involved as is supported by the absence of putative anti-ganglioside antibodies commonly found in immune-mediated peripheral nerve diseases. Longer survival period in paralytic rabies may possibly be related to currently unidentified mechanism(s) on neuronal gene expression, required for virus transcription/replication and for maintaining neuronal survival.

Neuropathogenic properties of Argas ( Persicargas) walkerae larval homogenates

Several tick species have been demonstrated, described, or suspected to cause paralysis in their host during the repletion process, presumably by impairing neurotransmission. The resulting polyneuropathy gradually spreads to the upper limbs causing incoordination and ends in respiratory failure. This form of paralysis is commonly confused with Guillain-Barrè syndrome, botulism and myasthenia gravis and although the clinical symptoms of these diseases are similar, it is not clear whether the pathogenesis is also the same. During this study we investigated the mechanism of paralysis by the tick Argas ( Persicargas) walkerae by determining the effect of larval homogenates on both potassium-stimulated (calcium-dependent) and veratridine-stimulated (external calcium-independent) release of [ 3H]glycine from crude rat brain synaptosomes. The results indicated that larval homogenates inhibited both processes. These findings are reconcilable with the results obtained for two other paralysis-causing tick species, Ixodes holocyclus and Dermacentor andersoni, which were indicated to cause paralysis by decreasing the synthesis or release of acetylcholine at the neuromuscular junction.

Special article: Polio: Its history and its eradication

Poliomyelitis has a long history, dating back at least to the Egyptian eighteenth dynasty (1580-1350 BC). In 1835, the first account of an outbreak of the disease was described by John Badham, and in 1840, Jacob von Heine, a German orthopedist, provided the first description indicating the spinal cord as the primary site of the paralytic form of the disease. During the late 19th and early 20th centuries, numerous epidemics began to occur with increasing frequency and severity. Many of these epidemics were accompanied by hysterical reactions. Because the paralyzed patients experienced respiratory compromise, artificial breathing support was needed. One of the devices most effectively used to manage the breathing for paralytic polio patients was the iron lung. In 1949, John Enders, Thomas Weller, and Frederick Robbins showed that poliovirus caused visible damage to primate cells derived from tissues other than those of the nervous system. This technology ultimately provided the means for producing large quantities of standardized poliovirus for the production of the killed vaccine (Salk vaccine, inactivated polio vaccine) and, eventually, the live poliovirus vaccines (Sabin vaccine, oral polio vaccine). The last case of wild strain poliomyelitis in the United States occurred in 1979. In 1998, the national vaccine advisory bodies responsible for recommending immunization began advocating the use of the enhanced inactivated polio vaccine as an alternative to the oral vaccine. Copyright © 2000 by W.B. Saunders Company

The Relationship Between the Sense of Coherence and Adjustment to Disability Studied in the Context of Marital Interrelations

ABSTRACT The aim of this article was to examine the Sense of Coherence (SOC) as a personal disposition, accounting for differences in the ability of the individual to cope effectively with the stressful experience of disability in the marital context. The relationship between the SOC of both spouses and their adjustment to a postmarital disability of one partner was examined within the interpersonal context of the marital relationship, incorporating an environmental perspective. Two groups of subjects were assessed: the individuals with disability and their spouses. The dominant disabilities were Spinal Cord Injury and CVA, all resulting in some form of paralysis. The SOC was found to be significantly associated with adjustment, and positive correlations existed between the SOC of both partners as well as between the adjustment of both, indicating that the reciprocal relations are explained beyond the personal variables. The practical and theoretical implications of these findings are discussed.

Clinical presentation of experimentally induced rabies in horses.

Twelve naive and nine test-vaccinated horses which developed clinical signs of rabies as a result of the required protocol of a vaccine trial were prospectively observed. Nineteen of the 21 cases were confirmed positive for rabies infection of the brain by fluorescent antibody test. The two horses with negative results had ganglioneuritis of the trigeminal ganglion or lymphocytic perivascular cuffing in the brain stem in addition to clinical signs. Average incubation period was 12.3 days and average morbidity was 5.5 days. Naive animals had significantly shorter incubation and morbidity periods (P < 0.05). Muzzle tremors were the most frequently observed (81%) and most common initial sign. Other common signs were pharyngeal spasm or pharyngeal paresis (71%), ataxia or paresis (71%), lethargy or somnolence (71%). The furious form was manifested in 43% of rabid horses and some of these furious animals initially manifested the dumb form. The paralytic form was not observed. Histopathology was characteristics for rabies. The results of this trial do not reflect on the efficacy of commercially licensed equine rabies vaccines.

Dickens and disability.

The novels of Charles Dickens include many vivid portraits of individuals with physical disabilities or deformities, and these conditions are often used symbolically to highlight some of the author's recurring themes. Disabled children are depicted as innocent victims, while their older counterparts are most often viewed as corrupt victimizers whose physical deformities are outward manifestations of their inner depravity. Punishment for moral failings in non-disabled characters frequently takes the form of paralysis and/or aphasia resulting from a cerebrovascular accident. In this context the wheelchair becomes a potent metaphor of imprisonment as a form of retributive justice.

Sero- and Molecular-Epizootiological Studies on Equine Herpesvirus Type 1(EHV-1) Infection among Race Horses: an Occurrence of Respiratory Disease with Nervous Disorders.

Among race horses raised and trained at Ritto Training Center of the Japan Racing Association, an epizootic of respiratory disease was observed from January to February in 1989. During the epizootic, a total of 155 out of approximately 2, 000 race horses developed pyrexia. Following the respiratory symptoms, 7 Thoroughbred horses showed various degree of nervous disordersuch as incoordination of the hind limbs to recumbency with urinary incontinence. Previous study briefly reported a result of virus isolation, in which 10 EHV-1 strains were isolated from febrile horses involved in this epizootic. In this study, clinical, serological, and molecular-biological researches were conducted to elucidate an epizootiological aspect of this occurrence of EHV-1 infection. Serologically, 90 (67.7%), including 7 samples from the horses manifested nervous disorders, out of 133 paired serum samples collected from febrile horses showed significant antibody response (four-fold or greater increase in the antibody titer) against EHV-1 by complement fixation and/or serum neutralization tests. Majority (more than 85%) of the infected horses as judged by serological tests were 3 years old. By restriction enzyme and Southern blot analyses o f DNAs extracted from 10 EHV-1 isolates, including an isolate from one of the 7 horses manifested nervous disorders, the Bam HI cleavage pattern corresponded to that of the electropherotype 1 P of EHV-1 and closely resembled each other. However, minor variations were detected in the electrophoretic mobilities of certain Bam HI fragments. These results confirmed that the epizootic of respiratory disease occurred among race horses at Ritto Training Center in 1989 was caused by EHV-1 infection, and strongly suggest that the nervous disorders observed among febrile horses involved in the epizootic were caused by the paralytic form of EHV-1 infection, which had never been recognized among horses in Japan. However, no distinct difference was detected between DNAs o f the isolate from a horse with paralysis and of the isolates from horses without paralysis in the Bam HI restriction profile.

Diagnostic Approaches for the Detection of Bovine Viral Diarrhea (BVD) Virus and Related Pestiviruses

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