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Toxicoinfectious botulism in commercial caponized chickens.

During the summer of 2003, two flocks of commercial broiler chickens experienced unusually high death losses following caponizing at 3 wk of age and again between 8 and 14 wk of age. In September, fifteen 11-wk-old live capons were submitted to the Iowa State University Veterinary Diagnostic Laboratory for assistance. In both flocks, the second episode of elevated mortality was associated with incoordination, flaccid paralysis of leg, wing, and neck muscles, a recumbent body posture characterized by neck extension, and diarrhea. No macroscopic or microscopic lesions were detected in affected chickens. Hearts containing dotted blood and ceca were submitted to the National Wildlife Health Center in Madison, WI. Type C. botulinum toxin was identified in heart blood and ceca by mouse bioassay tests. Enzyme-linked immunosorbent assay tests on heart blood samples were also positive for type C. botulinum toxin. Clostridium botulinum was isolated from the ceca and genes encoding type C. botulinum toxin were detected in cecal contents by a polymerase chain reaction test. Chickens are less susceptible to botulism as they age, and this disease has not previously been documented in broilers as old as 14 wk of age. Wound contamination by spores of C. botulinum may have contributed to the unusually high death losses following caponizing.

Animals↗

Effect of guanidine, germine, and steroids in a case of botulism.

A patient with severe type A botulism demonstrated several interesting features. Characteristic electrophysiologic findings are not necessary for the diagnosis. Guanidine hydrochloride provided mild improvement. High doses of steroids and low dose of germine-monoacetate had no effect.

Action Potentials↗

A novel neurotoxoid vaccine prevents mucosal botulism.

The threat posed by botulism, classically a food- and waterborne disease with a high morbidity and mortality, has increased exponentially in an age of bioterrorism. Because botulinum neurotoxin (BoNT) could be easily disseminated by terrorists using an aerosol or could be used to contaminate the food or water supply, the Centers for Disease Control and Prevention and the National Institute of Allergy and Infectious Diseases has classified it as a category A agent. Although clearly the development of a safe and effective mucosal vaccine against this toxin should be a high priority, essentially no studies to date have assessed mucosal immune responses to this disease. To bridge this gap in our knowledge, we immunized mice weekly for 4 wk with nasal doses of BoNT type A toxoid and a mutant of cholera toxin termed E112K. We found elevated levels of BoNT-specific IgG Abs in plasma and of secretory IgA Abs in external secretions (nasal washes, saliva, and fecal extracts). When mice given nasal BoNT vaccine were challenged with 4 x 10(3) LD50 of BoNT type A (BoNT/A) via the i.p. route, complete protection was seen, while naive mice given the same dosage died within 2 h. To further confirm the efficacy of this nasal BoNT vaccine, an oral LD50 was determined. When mice were given an oral challenge of 5 microg (2 x oral LD50) of progenitor BoNT/A, all immunized mice survived beyond 5 days, while nonimmunized mice did not. The fecal extract samples from nasally vaccinated mice were found to contain neutralizing secretory IgA Abs. Taken together, these results show that nasal BoNT/A vaccine effectively prevents mucosal BoNT intoxication.

Adjuvants, Immunologic↗

Infant botulism--the first reported case from Queensland.

Infant botulism is a rare disease with previous reports in Australia originating from its southern states. The first case to be recognized from Queensland is described in a four-month-old white girl. Complications included respiratory failure, the syndrome of inappropriate antidiuretic hormone secretion, urinary tract infection and autonomic dysfunction.

Australia↗

Evaluation of coproexamination as a diagnostic test for avian botulism.

Fecal extracts and blood sera from 113 ducks showing clinical signs of botulism were examined for Clostridium botulinum type C toxin by means of the mouse toxicity test to evaluate coproexamination as a diagnostic procedure, as compared with demonstration of toxin in serum. When death of test mice unprotected with type specific antitoxin (while protected controls survived) was the criterion, 78.8% of the sera and 5.3% of the fecal extracts were positive. When characteristic signs of intoxication in the unprotected mice was included as evidence of toxin in the specimens, these percentages increased to 86.7 and 6.2, respectively. Fecal specimens were collected hourly for the first 6 h after peroral dosing of eight mallards (Anas platyrhynchos) with 1.0 LD50 of type C toxin and at 24, 48, and 72 h from birds surviving that long. From 2 to 4 toxin-positive specimens were passed by all eight ducks during the first 6 h, five specimens were positive at 24 h, and three were positive at 48 h. Only three specimens were collected at 72 h, all of which were negative. These findings suggest that attempts to detect toxin in the feces of wild ducks might have been more successful had the birds been captured earlier in the course of the disease.

Animals↗

Avian botulism during late autumn and early spring in Saskatchewan.

Two outbreaks of botulism in central Saskatchewan in which mortality of waterfowl continued into late autumn and then recurred in the same marshes the following spring are described. Small numbers of birds were involved in each instance. Dabbling ducks (predominantly mallards, Anas platyrhynchos and pintails, Anas acuta) and American coots, Fulica americana were affected most commonly in autumn, whereas only diving ducks (predominantly lesser scaup, Aythya affinis) were found to be involved in spring. Live maggots present in carcasses despite sub-freezing temperatures were the probable source of intoxication in the autumn; the source of toxin in the spring was not determined.

Animals↗

Prevalence of Clostridium botulinum type C in substrates of phosphate-mine settling ponds and implications for epizootics of avian botulism.

Prevalence and conditions for occurrence of Clostridium botulinum type C were examined on phosphate-mine settling ponds and a natural wetland in northern Florida between April 1981 and March 1982. Substrate samples were collected monthly (winter) and semi-monthly (summer) from 16 locations on seven ponds. Selected environmental parameters were measured at each location at the time of sampling. Mouse inoculation tests and toxin neutralization tests using enrichment culture filtrates were conducted to identify C. botulinum type C in the samples. The bacteria were identified in 26 (5.6%) of 467 sediment samples. Occurrences were distributed over four of the seven ponds and included nine of the 16 sample locations, but were restricted to the months April through October. The organism occurred over a wide range of ecological conditions found on the ponds during these months. If the presence of C. botulinum type C in the substrate is a prerequisite for botulism to occur, the prevalence and fairly wide distribution of this organism on settling ponds makes it difficult to predict where future outbreaks may occur.

Animals↗

Internal temperature of decomposing duck carcasses in relation to botulism.

Under spring conditions (mean daily maximum 22 C, mean daily minimum 9 C), the temperature within duck carcasses paralleled air temperature for 3 days; on days 4 and 5 the internal temperature rose above 30 C for approximately 30 hr and maximum temperatures of 40-47 C occurred. This coincided with the period of maximum blowfly maggot activity in the carcasses. Carcasses screened from blowflies did not experience this period of high internal temperature. Under autumn conditions (mean daily maximum 13 C, mean daily minimum 1 C), the internal temperature of carcasses paralleled air temperature for approximately 2 wk. Following a warm day (23.5 C), maggots appeared in the carcasses and the internal temperature rose markedly higher than air temperature. Maggots moved into the soil on cold nights and reinhabited the carcasses during the day. The microclimate within maggot-infested carcasses appeared very suitable for growth and toxin production by Clostridium botulinum and this phenomenon may help explain the occurrence of botulism outbreaks during cool weather.

Animals↗

An outbreak of botulism in wild waterbirds in southern Australia.

An outbreak of Type C botulism in waterbirds was investigated at Lake Lalbert in northwestern Victoria, Australia. Total losses were estimated at 1,500 birds, with 80% of affected birds being grey teal (Anas gibberifrons). The outbreak was associated with a falling water level, and extensive decomposition of plant material.

Animals↗

Observations on waterfowl carcasses during a botulism epizootic.

Several features related to waterfowl carcasses were studied at Eyebrow Lake, Saskatchewan, Canada, during a botulism epizootic in the summer of 1989. Dummy carcasses, constructed by stretching duck skins over wooden forms, were used to assess the reaction of waterbirds to carcasses. There was no significant difference in the number of American coots, ducks, grebes, or total birds present when dummy carcasses were or were not present. Only one of 42 freshly-dead bird carcasses marked and observed twice each day was removed by a scavenger prior to the development of large maggots. Maggots developed in all carcasses and were visible externally a mean of 3.9 days after placement of the carcasses. The effectiveness of carcass collection and disposal operations was tested by marking carcasses on the day prior to two scheduled clean-ups. Only 32% of marked carcasses were recovered. Large carcasses and carcasses on or near islands were recovered at a higher frequency than were small carcasses and carcasses not near islands, respectively.

Animals↗

Experimental botulism in chickens: the cecum as the site of production and absorption of botulinum toxin.

Highly purified preparations of Clostridium botulinum toxins were administered to chickens by various routes. Chickens were highly susceptible to type A toxin, but relatively resistant to toxins of other types. Type C toxin (12S) at a dose of 1 X 10(7) mouse ip LD50 failed to kill the chicken by the oral route. Oral administration of 10 or more of type A, C, or D spores killed normal chickens, whereas cecoligated chickens were insusceptible to oral administration of 10(6) spores. These results show that the site of production and absorption of botulinum toxin in chickens is the cecum. Peroral administration of spores of a type C strain cured of its prophages and producing the C2 factor only also killed normal chickens. Chickens appeared to the more susceptible to the C2 factor than to the C1 toxin. The C2 factor, therefore, may play more important role in chicken deaths from toxico-infection with type C organisms. The optimum temperature for growth of C. botulinum types C and D was found to be 40-42 C. Type C and D toxins were significantly more stable than type A toxin in the cecum contents with pH above 7. These characteristics and the high density of distribution of type C spores in the environment may explain prevailing cases of type C botulism among broiler chickens.

Animals↗

A case report on human type B botulism.

A case of type B human botulism was found in Tochigi Prefecture in November, 1984. Botulinum type B toxin was detected in the serum and feces of the patient. The serum toxin was activated by trypsinization. Type B toxin was demonstrated in cooked meat medium cultures of the fecal specimens. The patient recovered after administration of type A, B, E and F quadrivalent antitoxin.

Botulinum Toxins↗

Quantification of Clostridium botulinum type A toxin and organisms in the feces of a case of infant botulism and examination of other related specimens.

Bacteriological examinations were performed on the first case of infant botulism in Japan (an infant boy aged 79 days at onset of illness). Clostridium botulinum type A toxin and organisms were detected continually in the stools of the infant for at least 31 days and 39 days, respectively. The highest levels of the toxin and of the population of the organisms, 7.8 X 10(4) LD50/g and 1.3 X 10(6) colony forming units (cfu)/g, were detected in the stool specimen taken on the 20th day of illness. Type A organisms were detected also in the honey fed to the infant before onset of illness, teats of his feeding bottle, soil specimens taken at the house entry and the vacuum-cleaner dust. Fecal excretion of the toxin and organisms was no longer detected from the 68th day of illness and he recovered.

Botulinum Toxins↗

Comparative studies on Clostridium botulinum type A strains associated with infant botulism in Japan and in California, USA.

Twenty strains of Clostridium botulinum type A associated with infant botulism cases, six in Japan and 14 in California, USA, were compared in their characters. All six Japanese strains produced medium-sized progenitor toxin (M toxin; Mr 300 k) but no hemagglutinin and showed lower 50% infective doses (ID50) in the infant mouse test; whereas most American strains produced large-sized progenitor toxin (L + LL toxins; Mr 500 k and 900 k) and hemagglutinin in addition to M toxin and showed higher ID50 in infant mice. No marked difference in the biochemical properties was found between the two groups except for two American strains.

Animals↗

[Botulism in 1997].

In 1997 81 cases of botulism in Poland were registered. The morbidity amounted 0.21/100,000. In the rural regions were registered 55, and in urban regions 26 cases. The morbidity in the rural regions amounted 0.37, and in urban regions 0.13. The morbidity of men (0.23) outnumbered the morbidity of women (0.19). In 1997 there were 8 outbreaks of two people noted, 2 outbreaks of three people and 2 of four people. Among the vehicles of the botulinum toxin dishes from meat remained on the first position (65.4% of cases), and in these numbers prevailed wecks of home production (19.8%). No deaths caused by botulinum toxin were noted in 1997.

Adolescent↗

[The men of the Andrée expedition probably died of botulism. A new hypothesis explains these mysterious deaths].

The last camp of the three members of the 1897 Swedish Andrée balloon expedition to the North Pole was found in Svalbard in 1930. The human remains and the paraphernalia of the expedition including diaries were brought to Sweden and are presently housed in a museum. The cause of the deaths has never been determined, but several hypotheses have been put forward over the years. Trichinosis, scurvy, and poisoning by carbon-monoxide, vitamin-A or lead are some of them. In this article it is argued that botulism is a plausible explanation which is in better accord with known facts.

Botulism↗

Botulism-like syndrome after injections of botulinum toxin.

Botulinum type A toxin (BTA) is an orphan drug used to treat several disorders of muscle spasticity. We report the first known case of systemic botulism-like syndrome induced by BTA therapy which resulted in respiratory arrest. Clinicians should be aware that systemic effects may occur with localized BTA therapy and may be life-threatening.

Adult↗

An outbreak of type-C botulism in three-weeek-old broilers.

Botulism was diagnosed in 3-week-old broilers from clinical signs, absence of postmortem and histopathological lesions, and demonstration of toxin in the serum of comatose birds. Passive immunization of mice with Clostridium botulinum type-C antitoxin protected against a challenge with serum from comatose birds containing the Cl. botulinum toxin. Total mortality for the grow-out period exceeded 27% and was not altered by water medication with penicillin. Bacitracin at 100 g per ton reduced mortality to 5-7 birds per day.

Animals↗