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The antitoxin titre against tetanus toxin has been evaluated in wounded subjects before and 24 after anti-tetanus serumprophylaxis by passive haemagglutination. Treatment with digested heterologous antiserum (3000-6000 I.U.) or with human hyperimmune immunoglobulins does not modify preexisting antitoxin titre. Serum negative subjects remain as such.
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In the present report the results indicate that the oral administration of one dose of CT in rats results in an antibody immune response in the spleen 48 h later, whereas no antitoxin antibody forming cells were found in the Peyer patches (PP), mesenteric lymph node (MLN) and lamina propria (LP) of the small intestine. At this time the main isotype of the antitoxin antibodies in the spleen were IgG and IgM, 5 days after the priming, few antitoxin AFC were observed in the MLN, IgG being the main isotype, whereas no IgM antitoxin AFC were found. At 1 week after priming the number of antitoxin AFC in the MLN reached similar values to those observed in the spleen. When cells from the spleen of rats primed orally with one dose of CT were cultured during 4 days in the presence of inhibitory doses of anti-Ia MAb (OX6), the number of antitoxin AFC was diminished when compared with that observed when cells were cultured in the absence of anti-Ia. The main isotype of antitoxin AFC observed when cells were analyzed after culture was IgM and it was the isotype most affected by the treatment with MAb anti-Ia. These results strongly suggest that an in situ presentation of the antigen did occur in the spleen. On the other hand, when the secondary immune response was studied 48 h after boosting, antitoxin AFC were found in the PP, MLN, SP and LP and 5 days after the booster a 20-30-fold increase was observed in all lymphoid tissues studied, indicating that the secondary immune response found in the spleen was mainly due to the recruitment of memory cells from Peyer's patches. However, when spleen cells were cultured 48 h after the immunization in the presence of inhibitory doses of anti-Ia a little decrease in the number of AFC was observed when compared with the controls (in absence of anti-Ia). The analysis of the antitoxin antibodies in sera and intestinal fluids were in line with the results presented above. The results shown in this report indicate that the systemic immune response observed after the oral administration of CT could be due in part to an in situ presentation of the antigen in the systemic compartments, especially in the spleen.
Two fragments with molecular weights of 111,000 (fragment I) and 59,000 (fragment II) were separated from each other by gel filtration of dithiothreitol and urea-treated, trypsinized derivative toxin (molecular weight, 170,000) of the proteolytic Okra strain of Clostridium botulinum type B on a column of Sephadex G-200 (superfine) with a buffer containing dithiothreitol and urea. Upon removal of dithiothreitol and urea by dialysis, the two fragments reassembled to reconstruct the derivative toxin molecule. Both fragments were immunogenic, and both anti-fragments neutralized type B toxin. The neutralizing activities of both anti-fragment I and anti-fragment II were, however, lower than that of the anti-derivative toxin, suggesting that the molecular integrity of derivative toxin is essential for sufficient production of the neutralizing antibody. The immunological difference found between type B toxin from a proteolytic strain and that from a nonproteolytic strain was ascribed to the antigenic difference of fragment I.
Botulinum neurotoxins (BoNTs) act within the synaptic terminal to block neurotransmitter release. The toxin enters the neuron by binding to neuronal membrane receptor(s), being taken up into an endosome-like compartment, and penetrating the endosome membrane via a pH-dependent translocation process. Once within the synaptic cytoplasm, BoNT serotypes A and E cleave separate sites on the C-terminus of the neuronal protein SNAP-25, one of the SNARE proteins required for synaptic vesicle fusion. In this study, we measured the effect of brief toxin exposure on SNAP-25 proteolysis in neuronal cell cultures as an indicator of toxin translocation. The results indicate that (1) uptake of both BoNT-A and -E is enhanced with synaptic activity induced by K+ depolarization in the presence of Ca2+ and (2) translocation of BoNT-A from the acidic endosomal compartment is slow relative to that of BoNT-E. Polyclonal antisera against each toxin protect cells when applied with the toxin during stimulation but has no effect when added immediately after toxin exposure, indicating that toxin endocytosis occurs with synaptic activity. Both serotypes cleave SNAP-25 at concentrations between 50 pM and 4 nM. IC50 values for SNAP-25 cleavage are approximately 0.5 nM for both serotypes. Inhibition of the pH-dependent translocation process by pretreating cultures with concanamycin A (Con A) prevents cleavage of SNAP-25 with IC50 values of approximately 25 nM. Addition of Con A at times up to 15 min after toxin exposure abrogated BoNT-A action; however, addition of Con A after 40 min was no longer protective. In contrast, Con A inhibited, but did not prevent, translocation of BoNT-E even when added immediately after toxin exposure, indicating that pH-dependent translocation of BoNT-E is rapid relative to that of BoNT-A. This study demonstrates that uptake of both BoNT-A and -E is enhanced with synaptic activity and that translocation of the toxin catalytic moiety into the cytosol occurs at different rates for these two serotypes.
The heat-stable enterotoxin ST Ib produced by enterotoxigenic E. coli strains shares a sequence homology with the sea snail neurotoxin, conotoxin GI. Rabbit antisera were raised against synthetic analogs of these toxins and to a six-residue peptide representing the region common to both toxins. Results from enzyme-linked immunosorbent assays indicate that the homologous region of both toxins represents part of their antigenic site. The lack of cross-reactivity exhibited by the six-residue common domain with serum directed against either toxin suggests that this region probably retains a similar conformation in the intact toxins but not in the isolated fragment.
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The hamster model of clindamycin-induced enterocolitis was studied to determine the natural course of the disease and the response to five therapeutic regimens. Tissue culture assays of stools from untreated animals showed that colitis toxin is present at low titers within 24--36 hr after challenge with clindamycin; titers of toxin in subsequent specimens of stool increased progressively until the animals died on days 2--4 after challenge. Therapeutic regimens tested in this model were initiated 24 hr after clindamycin challenge when the majority of the animals had evidence of colitis toxin. Methylprednisilone, an anion exchange resin, and gas gangrene polyvalent antitoxin had a minimal effect on toxin titers in stool and failed to delay substantially death due to enterocolitis. Vancomycin and tetracycline eliminated toxin in stools and delayed death. However, the salutary effects of these antibiotics were noted only during the course of their administration since all animals died of enterocolitis and had high titers of toxin when treatment was discontinued.
The toxin produced by Clostridium botulinum type C 6813 (C-6813) was purified 1,009-fold from the culture supernatant in an overall yield of 30%. The specific toxicity was 1.1 X 10(7) mouse minimum lethal doses per mg of protein. The toxin had a molecular weight of 144,000, composed of the light and heavy chains with molecular weights of 52,000 and 92,000, respectively, linked by one or two disulfide bond(s). The purified C-6813 toxin heavy and light chains reacted strongly with anti-type D heavy chain immunoglobulin G and anti-type C1 light chain immunoglobulin G, respectively. The amino acid compositions of C-6813 toxin heavy and light chains were more similar to those of type D heavy chain and type C1 light chain than to those of type C1 heavy chain and type D light chain, respectively. These results suggest that in the toxin produced by the type C strain at least two subtypes exist.
The combination of the local disinfection therapy against Staphylococcus aureus with the conventional therapy for atopic dermatitis has been widely used, and the improvement in skin lesions has been reported to be associated with a remarkable decrease in IgE levels and reagin antibody titers. We have already reported that affected organs were not only the skin but also the gastrointestinal tract in a case with atopic dermatitis. In the present study, the duodenal tissues were examined by biopsy in 32 patients with atopic dermatitis, and mild or chronic duodenitis was observed in all samples. Toxins were examined by PCR from 180 Staphylococcus aureus strains obtained from our patients. The detection rate of toxins was 82.8%. In many patients, antitoxin IgE antibody titers corresponding to their types of toxin and IgE levels were decreased in a parallel manner as time passed. We found 1 patient who complained of paresthesia in all four limbs, and her neurological and radiological examinations showed moderate cervical spondylosis. Neurological examinations revealed some abnormalities in 43 out of 50 patients with atopic dermatitis, such as hyperreflexia of the legs. Cervical MRI was carried out randomly and showed abnormal findings in 21 of 25 patients, in whom 18 duodenal tissues were examined by biopsies.
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Intoxication with botulinum neurotoxin, which occurs frequently in Poland, may cause serious diagnostic difficulties. As no assays for laboratory detection of botulinum toxin are available and the biological test on mice requires time before results are obtained, diagnosis must be based on clinical findings and patient's epidemiological history. Quick diagnosis and early administration of therapy with equine antitoxin is essential for patient's recovery. The effectiveness of antitoxin therapy is considered to be significantly reduced if the treatment is not started shortly after the onset of the disease. We describe a case of a patient in whom, because of diagnostic difficulties, antitoxin therapy was introduced with much delay. However, it proved highly efficient and lead to gradual recovery.
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