The effects of chemical or surgical deafferentation on [3H]-acetylcholine release from rat spinal cord.

Cholinergic modulation of nociceptive transmission through both nicotinic and muscarinic receptors in the spinal cord represents an important mechanism in pain signaling. However, what neuronal elements release acetylcholine and how release might change in response to deafferentation are unclear. The present studies demonstrated Ca++- and K+-dependent release of [3H]-acetylcholine from slices of regional areas of rat spinal cord. That [3H]-acetylcholine was synthesized from [3H]-choline was demonstrated by the lack of [3H]-acetylcholine release following incubation with either the choline uptake inhibitor hemicholinium or the choline acetyltransferase inhibitor bromoacetylcholine. Rats treated neonatally with capsaicin or with spinal nerve ligation as adults showed a significantly decreased K+-stimulated release of [3H]-acetylcholine from dorsal horn but not ventral horn lumbar spinal cord slices. In rats subjected to dorsal rhizotomy, while basal release from lumbar dorsal spinal cord slices was reduced, K+-stimulated [3H]-acetylcholine release, while decreased, was not significantly different compared with controls. The data presented here show that there are regional differences in the release of acetylcholine from spinal cord and that this release can be modulated by chemical or surgical deafferentation. These results also indicate that the source of acetylcholine in the dorsal cord originates mainly from resident somata and their collaterals, interneurons and/or descending terminals, with only very minor contributions coming from primary afferents. The present data help to further elucidate the role of acetylcholine in spinal signaling, particularly with respect to the effects of nerve injury and nociceptive neurotransmission.

Antitoxin levels in botulism patients treated with trivalent equine botulism antitoxin to toxin types A, B, and E.

Serum levels of equine-botulism antitoxin to toxin types A, B, and E were measured in four type-A botulism patients who had received equine-botulism antitoxin. High circulating levels capable of neutralizing in excess of 1 X 10(8), 9 X 10(7), and 6 X 10(6) 50% mouse lethal doses of toxin of types A, B, and E, respectively, were detected. There was little depletion of type-A antitoxin even though two of the patients had circulating type-A toxin before treatment. The half-life for antitoxin persistence for one patient was calculated as being 6.5, 7.6, and 5.3 days for antitoxin types A, B, and E, respectively. Antitoxin levels were not proportionate to the amount (range, 2-4 vials) injected and did not appear to be affected by whether the route of administration was iv or im. Peak serum levels of antitoxin were 10-1,000 times higher than amounts needed to neutralize the toxin measured in the serum of these and other patients with botulism.

Restaurant-associated type A botulism: transmission by potato salad.

In the period November 13-18, 1978, seven cases of type A botulism occurred in persons who had eaten in a restaurant in Colorado. The outbreak was recognized when two persons who had independently eaten at the restaurant were hospitalized with an illness compatible with botulism. Surveillance efforts identified five additional cases. Potato salad made at the restaurant and available for service during an 11-day period was epidemiologically incriminated as the vehicle of botulinal toxin transmission (p less than 0.00001). Laboratory studies showed that Clostridium botulinum spores on the surface of potatoes could survive baking in the manner used by the restaurant and that botulinal toxin could be produced in potatoes contaminated with C. botulinum spores.

Tick-borne relapsing fever in Colorado. Historical review and report of cases.

Since 1915 the front range of the Colorado Rocky Mountains has been postulated as a focus of endemic tick-borne relapsing fever. However, the disease has rarely been identified: only two cases have been reported in Colorado since 1944. Three sporadic cases in 1977--tightly grouped geographically and temporally--prompted an epidemiologic review. Tick-borne relapsing fever should be considered in the differential diagnosis of recurrent paroxysmal fever--with or without known presence of ticks--whenever exposure in an endemic area is part of a patient's history.