Stroke units.
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Cerebrovascular Disorders↗
Biomedical subjects
L Ritchie
Publications and source records attributed to L Ritchie.
Is Bell's palsy a reactivation of varicella zoster virus?
Despite various pointers to an infectious aetiology, the cause of Bell's palsy remains obscure. We examined paired sera from 62 patients with facial palsy and 50 age and sex matched contemporaneous controls. Significantly more patients than controls had IgM antibodies by ELISA to varicella zoster virus (56.5% vs. 20%, P = 0.0001) and herpes simplex virus (41.9% vs. 18%, P = 0.006). Additionally, significantly more patients than controls were positive for CF antibody to varicella zoster virus (14.5% vs. 0%, P = 0.004) but not to herpes simplex or cytomegalovirus. Significantly more controls than patients (54% vs. 25.8%, P = 0.002) had no evidence of antigenic stimulation by any of the herpesvirus group. No significant difference between patients and controls in seropositivity by IgM ELISA to cytomegalovirus. Epstein-Barr virus and IFA for human herpes virus 6 was found. Furthermore, there was no significant difference between the two groups as to evidence of recent infection by the following agents: rubella virus and Borrelia burgdorferi by IgM ELISA, influenza A. influenza B, adenovirus, respiratory syncytial virus, mumps and measles. Mycoplasma pneumoniae, Coxiella burnetii and chlamydia spp. by complement fixation test. The first reported case of clinically and serologically proven Mycoplasma pneumoniae pneumonia associated with Bell's palsy is described. The rate of complete recovery at 6-8 weeks after onset was not significantly different in patients who were given steroids compared to those who were not. Ear related symptoms were the most common, occurring in 12 of 65 cases, but only three (4.6%) had clinical shingles (vesicles in ear).(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Bovine spongiform encephalopathy: a scrapie-like disease of British cattle.
Scrapie is a CNS degenerative infection of sheep and goats, which is invariably fatal after incubation periods of several months to years. Related disorders are found naturally in man and other species. There is a impairment of protein catabolism in scrapie and related diseases which leads to the accumulation of sparingly-soluble protein deposits in brain. These protein aggregates may share with the amyloid of Alzheimer's disease (AD) some common stage in the biochemical pathways of their formation, although different proteins are affected in scrapie (the PrP protein) and AD (the A4-precursor protein). Recently, cattle with the clinical signs and brain pathology of a neurodegenerative disease have been reported, and this cattle disorder has been called bovine spongiform encephalopathy (BSE). BSE-affected brains contain abnormal forms of the bovine homologue of PrP. This provides biochemical evidence that BSE is cattle scrapie rather than cattle AD.
Animals↗
A mutation in the DNA adenine methylase gene (dam) of Salmonella typhimurium decreases susceptibility to 9-aminoacridine-induced frameshift mutagenesis.
A mutant of Salmonella typhimurium with a reduced response to mutation induction by 9-aminoacridine (9AA) has been isolated. The mutation (dam-2) is located in the DNA adenine methylase gene. The dam-2 mutant strain exhibits a level of sensitivity to 2-aminopurine (2AP) intermediate between that of the dam+ and the DNA adenine methylation-deficit dam-1 strain, and 2AP sensitivity was reversed by introduction of a mutH mutation or of the plasmid pMQ148 (which carries a functional Escherichia coli dam+ gene). However, the dam-2 strain is not grossly defective in DNA adenine methylase activity. Whole cell DNA appears full methylated at -GATC- sites. The levels of 9AA required to induce equivalent levels of frameshift mutagenesis in the dam-2 strain were approximately 2-fold higher than for the dam+ strain. Introduction of pMQ148 dam+ reduced the level of 9AA required for induction of frameshift mutations 4-fold in the dam-2 strain and 2-fold in the dam+ strain. The dam-2 mutation had no effect on the levels of ICR191 required for induction of frameshift mutations, but introduction of pMQ148 reduced the ICR191-induced mutagenesis 2-fold. The dam+/pMQ148, dam-2/pMQ148 and dam-1/pMQ148 strains showed identical dose-response curves for both 9AA and ICR191. These results are consistent with a slightly reduced (dam-2) or increased (pMQ148) rate of methylation at the replication fork. The 2AP sensitivity of the dam-2 strain cannot be simply explained. Furthermore, addition of methionine to the assay medium reverses the 2AP sensitivity of the dam-2 strain, but has no effect on 9AA mutagenesis.
Aminacrine↗
Changes in resistance in mixed infections of susceptible and benzimidazole resistant strains of Haemonchus contortus and Trichostrongylus colubriformis passaged in sheep.
Benzimidazole resistant strains of Haemonchus contortus and Trichostrongylus colubriformis were each diluted with equal numbers of their respective susceptible genotypes and passaged in separate worm-free sheep. The progeny of the mixed susceptible and resistant infections were diluted with equal numbers of susceptible genotypes before passaging on two further consecutive occasions in worm-free sheep. In H contortus the amount of thiabendazole required to prevent a 50 per cent egg hatching (LC50) was reduced at each generation, but the reduction was significant (P less than 0.05) only at the third passage. In T colubriformis the LC50 for thiabendazole was reduced only at the first passage and thereafter remained constant. The reduction was not significant. In another experiment, the dilution with susceptible genotypes was made only at the first passage. Thereafter for two further generations the progeny produced from the mixed infection were passaged in worm-free sheep. In H contortus a reduced amount of thiabendazole was required to prevent a 50 per cent egg hatching at each generation, but did not reach a level of significance. The result for T colubriformis was identical to the continuous dilution experiment.
Animals↗
Effect of removing anthelmintic selection pressure on the benzimidazole resistance status of Haemonchus contortus and Trichostrongylus colubriformis in sheep.
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Animals↗
Investigations for anthelmintic resistance in gastrointestinal nematodes from goats.
Field results from a commercial goat herd, based on egg counts and larval differentiation, suggested that anthelmintic resistance was present to albendazole, fenbendazole, levamisole, morantel, naphthalophos and phenothiazine. When the isolate was tested in sheep, using levamisole or oxfendazole, a possible resistance was shown for Trichostrongylus sp but no resistance was demonstrated in Haemonchus or Ostertagia spp. Ivermectin at a dose rate of 100 micrograms/kg was more than 98 per cent efficient in removing the adults of each of the three species of nematode. The phenomenon relating to the influence of the host on anthelmintic resistance is discussed.
Animals↗
Prolonged anthelmintic effect of closantel and disophenol against a thiabendazole selected resistant strain of Haemonchus contortus in sheep.
Two long-acting anthelmintics, closantel and disophenol, were tested by treatment 90, 60 and 30 days before challenge with a thiabendazole selected laboratory strain of Haemonchus contortus. The sheep were slaughtered 28 days after infection for total worm counts. A significant reduction in the number of adults remaining at autopsy was recorded after treatment with both anthelmintics 30 and 60 days before challenge but there was zero efficacy when the animals were treated 90 days before challenge. No significant difference was exhibited between the two compounds. Variability in response was recorded between animals on the 60 day period of treatment, which for disophenol may be dose related because animals receiving the lower volumes showed higher worm counts. For both anthelmintics a variability in the rate of metabolism may be responsible. The possibility offered by both anthelmintics for treating benzimidazole resistant strains of H contortus is discussed.
Animals↗
Effects of cerebellar lesions on saccadic eye movements.
1. Areas of cerebellar cortex related to saccadic eye movements were ablated in three Macaca mulatta monkeys trained to fixate visual targets. There followed a postoperative dysmetria of saccadic eye movements which appeared to be the result of an impairment specifically within the saccadic system. 2. Convergent evidence from two experimental paradigms indicated that the saccadic deficit was a function of the position of the eye in the orbit and did not involve retinal error processing. 3. The pattern of this position-dependent dysmetria suggests that the eye was no longer fully compensating for the elastic restoring forces imposed by the orbital medium and antagonist muscle(s). 4. The similarity of these data to saccadic eye movements of human cerebellar patients and arm movements of rhesus monkeys with cerebellar lesions indicates that the inability to compensate for the differential loads placed on motor systems by the mechanics of those systems may explain several cerebellar symptoms.
Animals↗