Letter: Rapid diagnostic techniques for detection of porcine parvovirus infection in mummified foetuses.
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Biomedical subjects
Publications and source records attributed to R H Johnson.
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Basic variables of the haemagglutination inhibition (HI) test for porcine parvovirus antibody were investigated. Nonspecific serum inhibitors were satisfactorily removed without loss of specific antibody when undiluted serum was adsorbed with 25 percent kaolin in borate saline at pH 9.0. Natural haemagglutinins in test serums could be completely removed using 0.1 ml of packed erythrocytes to 0.6 ml of kaolin treated serums. Adsorption of prediluted serum resulted in a depression of specific antibody titres. Highest HI titres were obtained using guinea pig erythrocytes, following incubation of virus-serum mixtures for 18 hours at 4 degrees C, 3 hours at 25 degrees C or 2 hours at 37 degrees C. Micro- and macro-tests gave comparable HI titres.
Evidence presented suggests that porcine parvovirus is highly stable and infective. Introduction of virus to susceptible herds results in 100% infection rate within the following 3 months. Active immunity is associated with high persistent levels of haemagglutination-inhibitating (HI) antibody (greater than 256), piglets suckling immune sows acquiring HI titres between 10,000 and 40,000. Loss of passive immunity, measured by HI, occurs in a majority of pigs between 14 and 26 weeks of age (mean 21 weeks), whilst an average of 25% (2-47%) of pigs lose HI titres between 26 and 36 weeks of age. Susceptibility to challenge with virus does not occur until 3-5 weeks following loss of HI titres. In endemically infected herds 98-100% of adult pigs show serological evidence of active immunity. A significant proportion of gilts may not be actively immune to porcine parvovirus at the time of first service, and subsequent infection may occur while these gilts are pregnant.
1. Six well-trained cyclists and six untrained subjects were studied during and immediately after four successive 7 min periods of exercise at 30, 45, 60 and 75% of their maximal work capacity. 2. Venous blood samples were taken at rest, at the end of each exercise period and 5 min following the end of exercise, for estimation of metabolites in blood and plasma insulin, growth hormone, cortisol and catecholamines. 3. The results showed significant differences in the mobilization and utilization of muscle fuels between the athletically fit cyclists and the untrained group. In the cyclists, glucose, glycerol and free fatty acid concentrations were higher, but lactate, pyruvate and alanine were lower than in the untrained subjects during exercise. 4. Plasma catecholamines rose in both groups during exercise but the rise was significantly less in the racing cyclists. Plasma insulin was depressed to a greater extent in the untrained subjects during exercise and plasma glucagon rose to a greater extent during strenuous exercise and remained elevated after the end of exercise in the untrained group. Plasma human growth hormone rose to a greater extent during exercise and remained elevated after the end of exercise in the untrained group. Plasma cortisol fell at low and moderate exercise rates in both groups, but to a smaller extent in the cyclists. Cortisol values rose at higher workloads and were significantly higher in the cyclists at the end of exercise. 5. It is concluded that there are significant differences in the metabolic and hormonal responses to exercise between athletically trained and untrained individuals, even when the physically fit subjects work at the same percentage of their maximal capacity as the unfit subjects.
Three patients who suffer from spastic paraplegia are described who belong to two generations in one family. One of the patients, who has had symptoms and signs for at least 10 years, has a monozygous twin who is unaffected. Using blood groups and chromosomal polymorphisms, the probability of monozygosity is estimated to be 0.99986. The observation of nonpenetrance in familial spastic paraplegia suggests that environmental factors may be involved in provocation and emphasises the need for careful genetic counselling in this and related diseases.
Glucose tolerance tests have been performed on five patients with Huntington's chorea and no difference in response has been observed compared with seven controls. Insulin tolerance tests have been performed on 12 patients with Huntington's chorea and 10 controls. Blood samples were taken at regular intervals for 75 minutes and analysed for blood glucose, insulin, and growth hormone (HGH). There was no difference between the groups in the hypoglycaemia which developed. The patients, however, had an earlier elevation of HGH than the controls. The difference was highly significant (P less than 0.001, P less than 0.02) 30 and 35 minutes after the intravenous injection of insulin. The patients, although awake, ceased to have choreiform movements for at least the last 60 minutes of the insulin tolerance tests. Our observations of HGH release imply that hypothalamic activity is altered in Huntington's chorea. Further observations of HGH release may therefore be of value in its diagnosis.
It is now recognized that orthostatic hypotension occurs as a complication of many neurological diseases. An account is given of some of those in which it may develop. The pathological lesions frequently allow studies to be made of physiological mechanisms remaining in the isolated parts of the nervous system. For example transection of the cervical spinal cord causes complete separation of peripheral sympathetic pathways from the control of the brain. It was possible, therefore, to examine the control of renin release and also cerebral blood flow regulation during change of blood pressure in patients with some of these disorders. Evidence has been obtained that the renin-angiotensin system is active in paraplegia and in many other patients with orthostatic hypotension. In addition symptoms of cerebrovascular insufficiency are minimized by the retention of autoregulation of cerebral blood flow (CBF) in patients with failure of sympathetic function. Autoregulation maintains CBF within wide limits of blood pressure and symptoms of orthostatic hypotension only develop if the blood pressure falls below the lower limit, usually about 70 mm Hg.
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Although disease caused by Arizona hinshawii is known to resemble the spectrum of clinical syndromes seen with Salmonella infections, little is known of their sensitivity to antimicrobials. We present three cases that are illustrative of Arizona sepsis, localized infection, or both; review the literature; and report sensitivities to 12 antimicrobials for 32 human and animal isolates of Arizona hinshawii from various geographic areas. With the exception of erythromycin and streptomycin, most strains were sensitive to many of the commonly used antibiotics. As with Salmonella infections, ampicillin or chloramphenicol appear to be the initial antimicrobial agents of choice for severe infections with A. hinshawii. Definitive antimicrobial therapy must be individualized on the basis of sensitivity testing and with regard to host factors.
The clinical response of treatment with a chemical preparation of tyramine and tranylcypromine, a monoamine oxidase inhibitor, is described in six patients wit neurogenic orthostatic hypotension. Previous therapy with fluorocortisone, ephedrine, elastic garments, postural training and, in one patient, an anti-G suit was unsuccessful. Oral and intravenous tyramine produced no pressor response. However, after treatment with tranylcypromine five of the patients when supine showed a marked rise of blood pressure to intravenous tyramine which was sustained for over two hours when they stood up. Tyramine given orally with tranylcypromine produced a moderate rise of blood pressure in the supine position which was sustained for over 3-4 hours in the erect position enabling patients to walk about without symptoms of orthostatic hypotension. Measurement of circulating adrenaline and noradrenaline during therapy suggested that the pressor response was due to release of noradrenaline. Three patients have had marked improvement for four, fifteen and twenty-four months respectively. In a further patient, therapy has been successful in treating his orthostatic hypotension although his mobility has been restricted due to cerebellar ataxia. One patient developed a confusional state during treatment and the therapy was stopped. The only patient in whom the drugs produced no pressor response had orthostatic hypotension with evidence of adrenergic innervation of blood vessels, but failure of noradrenaline release. It is suggested that the pressor response to a monoamine oxidase inhibitor and tyramine should be examined in patients to a monoamine oxidase inhibitor and tyramine should be examined in patients with neurogenic orthostatic hypotension in whom conventional therapy is unsatisfactory and those who respond should receive a trial of this treatment.
Although hospital-associated spread of vaccinia has been reported in the past, there have been no recent reports. This paper describes hospital-associated spread of vaccinia virus infection, supplies data on the environmental survival of vaccinia virus and offers recommendations for the management of patients with vaccinia that may minimize the hazard of infection in other high-risk patients.
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Genital samples collected at autopsy from 193 beef cows representing 22 different herds in Northern Australia yielded only one isolate of infectious bovine rhinotracheitis (IBR) virus. Serological evidence showed 59 per cent of similar cows had prior infection with this virus and of 19 sero-positive cows tested, 11 (58-2 per cent) shed detectable IBR virus from the vagina after treatment with corticosteroids. Transitory lesions of the vagina and vulva developed in five of the treated cows. Twenty-six (65 per cent) of 40 sero-positive bulls shed detectable IBR virus into the prepuce after corticosteroid treatment. Except for one bull, virus was not isolated after corticosteroid treatment of sero-negative animals. IBR virus and mucosal disease (MD) virus were not isolated from nasal swabs before or after corticosteroid administration. No correlation was observed between initial circulating antiboyd titre and virus excretion after treatment. There were no significant changes in levels of serum antibody during the virus excretion period.
Porcine, feline and rat parvoviruses were shown to be antigenically distinct. Specific antibody to feline and rat parvoviruses was shown in a high proportion of porcine sera, and to the porcine parvovirus in sera from cattle, sheep, cats, guinea-pigs, mice and rats, but not from horse, dog, rabbit, chicken or human.
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