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PubMed1990

Outbreak of type A botulism caused by a commercial food product in Taiwan: clinical and epidemiological investigations.

In late September 1986, we found 7 patients from a printing factory in Chang-Hwa city who developed an endemic disease manifested by general malaise, ptosis, double vision, dysarthria, dysphagia, and proximal limb weakness. After clinical, epidemiological, microbiological, and toxicological investigations, an outbreak of botulism was confirmed 2 weeks later, Commercially canned peanuts made by an unlicensed cannery were identified as the vehicle of botulinum toxin transmission. Antitoxin was given to 2 patients who needed ventilator support. One of the 7 victims died from medical complications and the remaining 6 patients recovered. Several administrative problems exposed in this outbreak were the poor governmental supervision of canned food, the inadequate quantities of "orphan drugs" stored in this country, the inefficient system for recalling the problem products, and the delayed broadcasting of warnings to the public. Since commercially processed food is increasingly popular with modernization, the possibility of future botulism outbreaks should not be overlooked.

Adolescent↗
PubMed1989

Adverse reactions and serologic response to a booster dose of acellular pertussis vaccine in children immunized with acellular or whole-cell vaccine as infants.

Adverse reactions and antibody response to pertussis toxin, ie, antitoxin, after a booster injection of an acellular pertussis vaccine were studied in 2-year-old children. A majority (212/241) of the children had previously been immunized with either two or three doses of the acellular vaccine at the ages of 6, 7, and 8 months. The other 29/241 children had received three doses of a plain whole-cell pertussis vaccine at the same ages. In the children who received primary immunization with the acellular vaccine, two cases of more serious systemic reactions occurred in close temporal association with the booster injection. Less serious systemic reactions were few. Local reactions were more common in the children only immunized with the acellular vaccine. Large reactions (greater than 10 cm) were only seen in this group. A good antitoxin response was elicited in both groups. The geometric mean titer in the former whole-cell vaccine recipients was significantly higher than in the children who received only acellular vaccine. The study raised some questions concerning differences in reactogenicity and immune response after a booster injection of an acellular vaccine depending on the type of pertussis vaccine given to infants for the primary immunization.

Antibodies, Bacterial↗
PubMed1976

Oral immunization against tetanus.

Model experiments in mice were used for the investigation of oral immunization against tetanus. The efficacy of oral tetanus toxoid application was tested by subcutaneous challenge (10 LD50 tetanus toxin) and antitoxin determination by L+-method. Reasonable protection could only be achieved when toxoid was in intensive contact with the mucous membranes of the oral cavity, whereas immunization by way of the gastrointestinal tract failed completely. After a single oral vaccination with 200 Lf fluid tetanus toxoid onto mucous membranes of the oral cavity the efficiency index was 75. A 100% protection was obtained in challenge after 3 applications of 200 Lf toxoid. In comparison, a single subcutaneous dose of 2 Lf tetanus toxoid resulted in an efficiency index of 100 and a single intranasal immunization with 100 Lf in an efficiency index of 93. Development of immunity after oral immunization was much accelerated if compared with parenteral immunization. 20% of the orally treated animals were immune 5 days after vaccination. After the same period subcutaneously treated animals had failed to develop any protection at all. Antitoxin titers after one oral vaccination (200 Lf) were similar to the ones after one subcutaneous dose (2 Lf). A distinct increase in antitoxin titers could only be observed when revaccination was done subcutaneously. The results obtained with mice apply analogically to guinea pigs.

Administration, Intranasal↗
PubMed1989

Role of local IgA antitoxin-producing cells for intestinal protection against cholera toxin challenge.

We examined in mice, perorally immunized with cholera toxin (CT) or cholera B subunit (CTB), the association between protection against intestinal toxin challenge and frequency and function of gut mucosal IgA antitoxin-forming cells. The in vitro production of IgA antitoxin by isolated cells and the toxin-neutralizing ability of culture supernatants were determined. Repeated oral immunizations with CT gave rise to high numbers of IgA antitoxin 'spot-forming' cells (SFC) in the lamina propria as well as to protection against challenge with CT in ligated intestinal loops. In contrast, mice immunized with purified CTB, gave poor IgA antitoxin SFC responses in the lamina propria and little or no protection. When a small amount of CT was used to adjuvant the response to CTB, many IgA antitoxin SFC were found; however, protection in intestinal loops remained poor. This discrepancy was explained by the predominant localization of antitoxin SFC in the proximal small intestine following oral CTB/CT-adjuvant immunization, whereas relatively few SFC were found further down in the intestine where the loop-protection test was performed. Thus, when lamina propria plasma cells were isolated from challenged loops and cultured in vitro, they released only low titers of IgA antitoxin and CT-neutralizing antibodies in culture supernatants; this was in contrast to cells from optimally immunized mice which gave supernatants with high IgA antitoxin and toxin-neutralizing antibody titers. Increasing the dose of CT, added as adjuvant to the CTB, resulted in better protection and higher numbers of IgA antitoxin SFC in more distal parts of the intestine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1980

Production of Clostridium difficile antitoxin.

We have produced antitoxin to the toxin of Clostridium difficile in rabbits and in goats. Antitoxin dilutions of 1/8,000 and 1/5,120 were capable of neutralizing lethal doses of the toxin in mice and in tissue culture, respectively.

Animals↗