Botulism: a laboratory investigation on biological and food samples from cases and outbreaks in Brazil (1982-2001). (65/694)

Laboratory investigation of botulism from 1982 to 2001 confirmed the occurrence of eight positive outbreaks/cases of botulism in Brazil. From those, type A botulism was observed in seven of them. Biological material of one case (serum and feces) was positive in the first step of the bioassay, but the amount of sample was not sufficient for typification. One of the outbreaks that occurred in 2001 was negative for botulinum toxin in samples of serum, gastric washing and feces, collected eight days before the onset of the symptoms in the affected person who was clinically diagnosed as presenting the disease. Other two cases presenting compatible clinical diagnoses presented negative results. However, in those cases, the collection of samples was (1) after antiserum administration or (2) later than eight days of the onset of symptoms. Investigation was performed by mouse bioassay, as described in the Compendium of Methods for the Microbiological Examination of Foods (compiled by American Public Health Association--APHA)11, using specific antiserum from Centers for Disease Control (CDC), USA.  (+info)

Inhalational poisoning by botulinum toxin and inhalation vaccination with its heavy-chain component. (66/694)

Botulinum toxin is the etiologic agent responsible for the disease botulism, which is characterized by peripheral neuromuscular blockade. Botulism is ordinarily encountered as a form of oral poisoning. The toxin is absorbed from the lumen of the gut to reach the general circulation and is then distributed to peripheral cholinergic nerve endings. However, there is a widespread presumption that botulinum toxin can also act as an inhalation poison, which would require that it be absorbed from the airway. Experiments have been done to show that both pure toxin and progenitor toxin (a complex with auxiliary proteins) are inhalation poisons. Interestingly, the data indicate that auxiliary proteins are not necessary to protect the toxin or to facilitate its absorption. When studied on rat primary alveolar epithelial cells or on immortalized human pulmonary adenocarcinoma (Calu-3) cells, botulinum toxin displayed both specific binding and transcytosis. The rate of transport was greater in the apical-to-basolateral direction than in the basolateral-to-apical direction. Transcytosis was energy dependent, and it was blocked by serotype-specific antibody. The results demonstrated that the holotoxin was not essential for the process of binding and transcytosis. Both in vivo and in vitro experiments showed that the heavy-chain component of the toxin was transported across epithelial monolayers, which indicates that the structural determinants governing binding and transcytosis are found in this fragment. The heavy chain was not toxic, and therefore it was tested for utility as an inhalation vaccine against the parent molecule. This fragment was shown to evoke complete protection against toxin doses of at least 10(4) times the 50% lethal dose.  (+info)

Inhibitory effects of botulinum toxin on pyloric and antral smooth muscle. (67/694)

Botulinum toxin injection into the pylorus is reported to improve gastric emptying in gastroparesis. Classically, botulinum toxin inhibits ACh release from cholinergic nerves in skeletal muscle. The aim of this study was to determine the effects of botulinum toxin on pyloric smooth muscle. Guinea pig pyloric muscle strips were studied in vitro. Botulinum toxin type A was added; electric field stimulation (EFS) was performed every 30 min for 6 h. ACh (100 microM)-induced contractile responses were determined before and after 6 h. Botulinum toxin caused a concentration-dependent decrease of pyloric contractions to EFS. At a low concentration (2 U/ml), botulinum toxin decreased pyloric contractions to EFS by 43 +/- 9% without affecting ACh-induced contractions. At higher concentrations (10 U/ml), botulinum toxin decreased pyloric contraction to EFS by 75 +/- 7% and decreased ACh-induced contraction by 79 +/- 9%. In conclusion, botulinum toxin inhibits pyloric smooth muscle contractility. At a low concentration, botulinum toxin decreases EFS-induced contractile responses without affecting ACh-induced contractions suggesting inhibition of ACh release from cholinergic nerves. At higher concentrations, botulinum toxin directly inhibits smooth muscle contractility as evidenced by the decreased contractile response to ACh.  (+info)

A case of primary spinal myoclonus: clinical presentation and possible mechanisms involved. (68/694)

Spinal myoclonus is a rare movement disorder characterized by myoclonic involvement of a group of muscles supplied by a few contiguous segments of the spinal cord. Structural lesions are usually the cause, but in primary spinal myoclonus the etiology remains unknown. We present the case of a 26-year-old woman with cervical spinal myoclonus in which both clinical and electromyographic findings pointed to the segment C1-C3 as the origin of the myoclonus. Laboratorial examinations were normal and no structural lesion was found in magnetic resonance imaging (MRI). Botulinum toxin type A was injected in infrahyoid muscles and cervical paraspinal musculature. The patient remained free of symptoms for almost five months. The pathophysiology of spinal myoclonus remains speculative, but there is evidence that various possible mechanisms can be involved: loss of inhibitory function of local dorsal horn interneurons, abnormal hyperactivity of local anterior horn neurons, aberrant local axons re-excitations and loss of inhibition from suprasegmentar descending pathways.  (+info)

Use of botulinum toxin type A in a case of persistent parotid sialocele. (69/694)

Sialocele is an uncommon complication of parotidectomy. Most cases resolve after conservative therapy consisting of repeated aspiration and pressure dressing. The condition is, however, occasionally resistant to such therapy. We report on a 52-year-old Chinese man who had a 10-year history of right parotid swelling. Following fine-needle aspiration cytology, Warthin's tumour was diagnosed, but after elective parotidectomy, a swelling developed and parotid sialocele was diagnosed. Botulinum toxin type A was given after the sialocele had persisted for almost 3 weeks after surgery, and after conservative management had been tried; the sialocele disappeared after two doses of treatment. Botulinum toxin therapy was thus an effective method of treating persistent sialocele.  (+info)

Botulinum toxin in gastric submucosa reduces stimulated HCl production in rats. (70/694)

BACKGROUND: Botulinum toxin blocks acetylcholine release from nerve endings and acts as a long term, reversible inhibitor of muscle contraction as well as of salivary, sweat gland, adrenal and prostatic secretions. The aim of the present study is to investigate whether gastric submucosal injection of botulinum toxin type A reduces stimulated gastric production of HCl. METHODS: Sixty-four rats were randomized in two groups and laparotomized. One group was treated with botulinum toxin-A 10 U by multiple submucosal gastric injections, while the second group was injected with saline. Two weeks later, acid secretion was stimulated by pyloric ligation and acid output was measured. Body weight, food and water intake were also recorded daily. RESULTS: HCl production after pyloric ligation was found to be significantly lower in botulinum toxin-treated rats (657 +/- 90.25 micromol HCl vs. 1247 +/- 152. P = 0.0017). Botulinum toxin-treated rats also showed significantly lower food intake and weight gain. CONCLUSIONS: Botulinum toxin type A reduces stimulated gastric acidity. This is likely due either to inhibition of the cholinergic stimulation of gastric parietal cells, or to an action on the myenteric nervous plexuses. Reduction of growth and food intake may reflect both impaired digestion and decreased gastric motility.  (+info)

Activity-induced targeting of profilin and stabilization of dendritic spine morphology. (71/694)

Morphological changes in dendritic spines have been implicated in connective plasticity in brain circuitry, but the underlying pathway leading from synaptic transmission to structural change is unknown. Using primary neurons expressing GFP-tagged proteins, we found that profilin, a regulator of actin polymerization, is targeted to spine heads when postsynaptic NMDA receptors are activated and that actin-based changes in spine shape are concomitantly blocked. Profilin targeting was triggered by electrical stimulation patterns known to induce the long-term changes in synaptic responsiveness associated with memory formation. These results suggest that, in addition to electrophysiological changes, NMDA receptor activation initiates changes in the actin cytoskeleton of dendritic spines that stabilize synaptic structure.  (+info)

Treatment of hyperhidrosis with botulinum toxin A. (72/694)

Focal hyperhidrosis of axillae, palms or soles is a frequent, socially debilitating condition triggered by various emotional stimuli. There are several treatment options such as local application of metal sales (aluminum chloride) or tap water iontophoresis, which provide temporary relief for some patients. More recently, local intradermal injections of botulinum toxin A (BTX-A), a neurotoxin blocking the cholinergic stimulus of eccrine sweat glands, offers an effective treatment option with few side-effects. Patient satisfaction rates are high, although treatment effects only last a few months. For definite care, surgical procedures have to be considered.  (+info)