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We measured serum antibodies to botulinum toxin (ABT) in 96 patients with focal dystonia who had been treated with type A botulinum toxin. The frequency of detectable ABT was 3% (three patients). Patients with ABT had received more than 50 ng of botulinum toxin, and the shortest time between two injections was significantly less than in patients without ABT. The clinical evolution of the three patients was heterogeneous: one had decreased effectiveness with repeated injections, another had persistent improvement, and the third never responded to toxin injections.

Resistance to clindamycin, erythromycin, streptogramins, and tetracycline was shown to be transferable from a clinical isolate of Bacteroides fragilis subspecies distasonis to a sensitive strain of B. fragilis subspecies fragilis. Resistance to clindamycin, erythromycin, and streptogramins was transferable from a clinical isolate of B. fragilis subspecies fragilis to the sensitive strain of B. fragilis subspecies fragilis. Except for tetracycline, resistance to all of these antibiotics was spontaneously curable en bloc at a frequency of approximately 10(-2). These results suggest that resistance to these antibiotics is determined by a plasmid.

DNA sequence analysis of regions from plasmid pIP417 and chromosome BF8 which encode 5-nitroimidazole resistance in Bacteroides strains allowed the identification of two open reading frames corresponding to new genes, nimA (528 bp) and nimB (492 bp). Either gene may confer 5-nitroimidazole resistance to susceptible strains of Bacteroides. The encoded polypeptides have deduced molecular masses of 20.1 and 18.6 kDa, respectively, and share about 73% identity and 85% similarity. A new insertion sequence (IS) element named IS1168 lies 14 bases upstream of the nimA gene. The complete sequence of IS1168 was determined. A similar IS exists 12 bp upstream of the nimB gene. About 60% of the BF8 IS element was also sequenced and shown to be almost identical to IS1168.

The ability of Clostridium perfringens type A to produce an enterotoxin active in human food poisoning has been shown to be directly related to the ability of the organism to sporulate. Enterotoxin was produced only in a sporulation medium and not in a growth medium in which sporulation was repressed. Mutants with an altered ability to sporulate were isolated from an sp + ent + strain either as spontaneous mutants or after mutagenesis with acridine orange or nitrosoguanidine. All sp 0 − mutants were ent − . Except for one isolate, these mutants were not disturbed in other toxic functions characteristic of the wild type and unrelated to sporulation. A total of four of seven osp 0 mutants retained the ability to produce detectable levels of enterotoxin. None of the ent − mutants produced gene products serologically homologous to enterotoxin. A total of three sp − mutants, blocked at intermediate stages of sporulation, produced enterotoxin. Of these mutants, one was blocked at stage III, one probably at late stage IV, and one probably at stage V. A total of three sp + revertants isolated from an sp − ent − mutant regained not only the ability to sporulate but also the ability to produce enterotoxin. The enterotoxin appears to be a sporulation-specific gene product; however, the function of the enterotoxin in sporulation is unknown.

The genetic organization of two different 5-nitroimidazole (5-Ni) resistance genes was investigated: nimC and nimD from Bacteroides plasmids plP419 and plP421, respectively. The nimC gene (492 bp) and the nimD gene (495 bp) directed the synthesis of polypeptides with deduced molecular masses of 18.37 kDa and 1848 kDa, respectively. The predicted proteins showed 6 7 4 3 % identity and 78-91 O/ O similarity with the products of two other nimA and nimB genes previously described and could be derived from a common ancestral gene. An insertion sequence element (IS1170) was identified upstream of the nimC gene. IS1170 is 1604 bp in length and is flanked by'imperfect inverted repeats (15 bp). IS1770 is similar to the Bacteroides insertion sequence element IS942 with an identity of 70% a t the nucleotide level. The single copy of IS1170 present on plasmid plP419 is integrated 24 bp upstream of the initiation codon of nimC. Similar genetic organization was found on plasmid plP421. One copy of another insertion sequence (151169) was found 4 bp upstream of the first ATG codon of the nimD gene. This element (1325 bp) shows a strong homology a t the nucleotide level (70% identity) with IS1186 and IS1168 found to be associated with the Bacteroides carbapenem resistance gene cfiA, and the 5-Ni'genes nimA and nimB, respectively. There is strong evidence that, as in the case of the &A gene, the transcription of the four nim genes so far studied is directed by outward-oriented promoters, carried on the right ends of the different insertion sequence elements.

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