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PubMedDate not supplied

Recurrent transient paresis in a turkey flock.

Recurring episodes of extreme leg weakness and associated mortality were documented in a turkey flock at 8 to 15 weeks of age. Flock mortality attributed to posterior paresis was approximately 12%, or 4800 of 40,000 turkeys. Four of six open-confinement units were affected. Gross and histological examinations revealed no significant lesions. Immunology and virology were uninformative. There were no significant differences in serum chemistry between clinically affected and normal turkeys. Testing of feed, water, soil, and tissues revealed no common toxicants. Isolation and supportive care for affected turkeys, both in the laboratory and in the field, frequently resulted in full recovery. Injection of a test group of affected turkeys with Type C botulism antitoxin appeared to enhance recovery. However, repeated attempts to detect botulism toxin in serum, liver, or cecal contents using mouse bioassay procedures were unsuccessful.

Animals↗
PubMed2004

[Some epidemiologic characteristics of foodborne intoxications in Croatia during the 1992-2001 period].

Epidemiologic characteristics of foodborne intoxications registered in Croatia during the 1992-2001 period are described. Salmonellosis, as well as staphylococcal food intoxication, foodborne botulism, Clostridium perfringens food intoxication, histamine poisoning and food intoxication caused by other pathogens, especially conditionally pathogenic bacteria, were analyzed. During the study period, 87,782 cases were reported, 45,721 (52.1%) of them related to salmonellosis and the rest of 42,061 (47.9%) cases to foodborne intoxications of various etiology. The diseases occurred throughout the year, with a higher proportion in summer than at any other time of year. During the study period, 480 outbreaks of foodborne intoxications with 10,567 cases were reported, 405 (84.4%) of them with 8476 cases related to salmonellosis. The most frequently isolated pathogen in salmonellosis outbreaks was Salmonella enteritidis with 345 (85.2%) outbreaks. The outbreaks of salmonellosis were primarily associated with the intake of pastries (40.1%). Ice-cream was associated with a high risk of staphylococcal food intoxication, and bean salad of Clostridium perfringens food intoxication. The food vehicle of transmission most often associated with foodborne botulism outbreaks was smoked ham. Histamine poisoning, recorded in four outbreaks, occurred after consumption of fish and fish products. Salmonellosis outbreaks most frequently occurred at home (n=149; 36.8%), followed by pastry shops with 47 (11.6%) outbreaks, the latter also ranking first in the outbreaks of staphylococcal food intoxication (40%).

Croatia↗
PubMed1979

[Studies on the persistence of Clostridium botulinum on a cattle farm (author's transl)].

In the winter of 1978-1979, the presence of Clostridium botulinum was studied on a cattle farm, on which botulism caused by feeding the animals contaminated brewers' grains occurred in 1977. Cl. botulinum type B, the cause of mortality among cattle at the time, was detected in grass silage prepared in 1978. This organism was not detectable in a grass silage pit dating from 1977 and made prior to the outbreak of botulism. Investigations showed that proteolytic types of C. botulinum having grass as the substrate may produce large amounts of toxin. The production of toxin in grass silage pits may, however, be prevented by a low pH in conjunction with low water activity. The present study showed that the faeces of cattle were also contaminated with Cl. botulinum type B. The degree of infection ran parallel with the degree of contamination of silage feeding in these cases.

Animal Feed↗
PubMed1981

Potentiation of Clostridium botulinum toxin aminoglycoside antibiotics: clinical and laboratory observations.

A child with infant botulism became apneic and died while receiving ampicillin and gentamicin therapy. As aminoglycosides have been implicated in the induction and/or exacerbation of neuromuscular blockade, we used an animal model to test the hypothesis that aminoglycosides potentiate neuromuscular blockade of botulinum toxin. In the range of aminoglycoside doses utilized in these experiments, both gentamicin and tobramycin enhance neuromuscular impairment and death of botulinum toxin-exposed mice. These results support recently published clinical observations that aminoglycosides may potentiate neuromuscular weakness caused by botulinum toxin, and suggest that these antibiotics should be used with caution in suspected cases of infant botulism.

Aminoglycosides↗
PubMed1998

Hemagglutinin binding mediated protection of botulinum neurotoxin from proteolysis.

Type A Clostridium botulinum, the causative agent of the food poisoning botulism disease, secretes botulinum neurotoxins along with seven neurotoxin associated proteins (NAPs). The function of NAPs has been shown to protect the neurotoxin from acidity, heat, and proteolytic attack in the environmental and gastrointestinal tract during the toxicogenesis of the botulism disease. One of the NAPs, purified from type A botulinum neurotoxin complex, showed hemagglutination activity. A direct interaction has been demonstrated between purified NAP, a 33-kDa hemagglutinin or Hn-33, and the neurotoxin by using Sephadex G-200 column chromatography. Furthermore, Hn-33 has complete resistance against proteolytic attack at pH 2.0 as well as at normal physiological pH. We have investigated digestion of the neurotoxin in the presence and absence of Hn-33. The neurotoxin alone has been found to be more susceptible to the enzymatic digestion than neurotoxin with Hn-33. The presence of Hn-33 changes the proteolytic fragmentation pattern of the neurotoxin. It seems that Hn-33 protects the neurotoxin from proteolysis either by structural modification of the neurotoxin or by blocking the protease accessible sites of the neurotoxin.

Botulinum Toxins, Type A↗
PubMed1963

Botulinus toxin: effect on the central nervous system of man.

Electrical stimulation of multiple peripheral nerves, elicited "H" reflexes in a patient, 61 years old, with botulism. These reflexes are extremely suggestive of some central release or failure of inhibitory control of a monosynaptic or polysynaptic spinal reflex arc. This "central" action of botulinus toxin is similar to that suggested for tetanus toxin.

Antitoxins↗
PubMed1965

MYASTHENIA GRAVIS: MEDICAL ASPECTS.

The diagnosis of myasthenia gravis is often difficult and calls for a broader use of pharmacological and electrodiagnostic tests. The decamethonium-edrophonium test, which has proved superior to other procedures for this purpose, is based on neurophysiological principles and depicts the behaviour of the neuromuscular junction. A state of resistance to depolarizing agents in the limited form of myasthenia and a state of a non-depolarizing (competitive) block in advanced cases has been shown. This test has demonstrated that the neuromuscular defect exists throughout the skeletal musculature, including muscles clinically unaffected. It produced no false-positive results either in normal or neurasthenic persons or in patients with neurological diseases with myasthenic symptoms. In a patient with botulism and in a patient with ocular palsies from brain-stem encephalitis the edrophonium test gave a false-positive result, while the decamethonium-edrophonium test was negative.Diagnosis, treatment and management of myasthenic emergencies are described.

Acetylcholine↗
PubMed1982

Head and neck manifestations of uncommon infectious diseases.

Certain uncommon systemic infections may be present with head and neck manifestations either initially or during the course of the disease. A high index of suspicion is required on the part of the otolaryngologist with the subsequent procedures leading to the appropriate diagnosis. The manifestations of infectious diseases such as erysipelas, histoplasmosis, rabies, tetanus, botulism, and cysticercosis must be understood by the head and neck specialist. For successful management, many of the infections require prompt identification and initiation of therapy. Airway maintenance, ventilatory support, and medical chemotherapy may be required.

Botulism↗
PubMed1985

[Value of bacteriologic studies within the scope of forensic autopsies].

The various questions regarding bacteriological investigations within the scope of forensic autopsies are discussed in the light of our own cases and with regard to the relevant literature: estimate of the age of the corpse on the basis of decomposition changes caused by bacteria; determination of so-called bacteriograms from the point of view of criminalistics; supplementary investigations of the cause of death. Iatrogenic infections (e.g., gangrene) are gone into in more detail, as is so-called infantile botulism within the scope of the "sudden infant death syndrome". Finally, it is pointed out that when doing forensic autopsies, thought should also be given to illnesses that have only been known for a few years, examples being legionnaires' disease and the toxic shock syndrome ("tampon sickness").

Adult↗
PubMed1992

Clostridium botulinum toxins: a general review of involvement in disease, structure, mode of action and preparation for clinical use.

The neurotoxins produced by Clostridium botulinum are the most potent acute toxins known and are the causative agents of the neuroparalytic disease botulism. The toxins act primarily at peripheral cholinergic synapses by blocking the evoked release of the neurotransmitter acetylcholine. There are seven distinct serotypes of toxin. All are polypeptides of Mr about 150 kDa that have similar structure and pharmacological action. In their most active forms the toxins exist as dichain molecules in which a heavy (H) chain is linked by disulphide bonding to a light (L) chain. The H chain is believed to be associated with the highly specific and avid binding of toxin to the motor nerve end plates and also with the process of internalisation of the toxin. The toxic activity appears to be associated with the L chain which blockades the calcium-mediated release of acetylcholine, probably by interfering at the molecular level with the mechanisms whereby neurotransmitter-containing vesicles merge with the plasmalemma. The type A toxin is now used therapeutically to treat a variety of conditions involving involuntary muscle spasm. The therapeutic toxin is a neurotoxin-haemagglutinin complex isolated from cultures of C. botulinum. A controlled manufacturing process has been developed for the therapeutic toxin which is specially formulated to give a freeze-dried product having good stability.

Acetylcholine↗
PubMed1975

Preparation, measurement and possible use of human antitoxin against Cl. botulinum A, B, and E toxins.

Human antibodies against botulinum toxins A, B, and E have been raised by repeated injections of pentavalent toxoid in a healthy volunteer. The final titer was 3.2 U anti-A, 0.4 U anti-B, and 2.5 U anti-E/ml. In mice, the efficacy of the antitoxin decreases with the time between poisoning and application of the antiserum. The dose recommended for prophylactic purposes in man is 1 ml/kg. In overt poisoning, therapy should be started with higher titer animal serum since in animal experiments high titer sera can stop (although not reverse) the symptoms of overt botulism within an-admittedly not too broad-rnage of time and dosage. Later on, therapy can be continued with human antiserum. An inverse radioimmunassay for botulinum A antitoxin using labeled botulinum toxin and antibody-coated tubes is described. The serum is available upon request from the author.

Animals↗
PubMed1999

Botulinum toxin as a carrier for oral vaccines.

Botulinum toxin is an unusually potent substance that acts on the nervous system to produce the clinical outcome of flaccid paralysis. To produce this effect, the toxin ordinarily proceeds through two separate but essential sequences of events. During the first, the toxin is ingested, it traverses a portion of the gastrointestinal system and then it is transcytosed from the lumen of the gut to the general circulation. During the second, circulating toxin binds to peripheral cholinergic nerve endings, it is endocytosed and then it acts as a metalloendoprotease to cleave polypeptides that are essential for exocytosis. Although botulinum toxin is antigenic, it ordinarily does not evoke an immune response during or after cases of oral poisoning. This is due to the fact that the dose of toxin that produces flaccid paralysis-and potentially death-is less than the dose needed to evoke an antibody response. In the recent past, the techniques of molecular biology have been used to generate an expression product of botulinum toxin that retains the ability to escape the gut and reach the general circulation, retains the ability to evoke an immune response, but has lost the ability to produce neurotoxicity. This modified toxin may have two clinical applications. The expression product itself may have utility as an oral vaccine against botulism. Beyond this, the modified toxin, or a truncation mutant of the toxin, may have utility as a carrier in the construction of other oral vaccines. Both potential applications could lead to the expression of oral vaccines in common foods.

Animals↗
PubMed2005

Botulinal neurotoxins: revival of an old killer.

Botulinal neurotoxins (BoNTs) produced by anaerobic bacteria of the genus Clostridium are the most toxic proteins known, with mouse LD(50) values in the range of 1-5 ng/kg. They are responsible for the pathophysiology of botulism. BoNTs are metalloproteinases that enter peripheral cholinergic nerve terminals, where they cleave one or two of the three core proteins of the neuroexocytosis apparatus and elicit persistent but reversible inhibition of neurotransmitter release. Their specificity of action has made them useful therapeutic agents for many human syndromes caused by hyperactivity of cholinergic nerve terminals. Their range of clinical applications is continuously growing, and BoNT/A is being used extensively as a pharmaco-cosmetic.

Animals↗
PubMed2004

Prevalence of Clostridium species and behaviour of Clostridium botulinum in gnocchi, a REPFED of italian origin.

Sales and consumption of refrigerated processed foods of extended durability (REPFEDs) have increased many-fold in Europe over the last 10 years. The safety and quality of these convenient ready-to-eat foods relies on a combination of mild heat treatment and refrigerated storage, sometimes in combination with other hurdles such as mild preservative factors. The major hazard to the microbiological safety of these foods is Clostridium botulinum. This paper reports on the prevalence and behaviour of proteolytic C. botulinum and non-proteolytic C. botulinum in gnocchi, a potato-based REPFED of Italian origin. Attempts to isolate proteolytic C. botulinum and non-proteolytic C. botulinum from gnocchi and its ingredients were unsuccessful. Based on assessment of the adequacy of the methods used, it was estimated that for proteolytic C. botulinum there was < 25 spores/kg of gnocchi and < 70 spores/kg of ingredients. The total anaerobic microbial load of gnocchi and its ingredients was low, with an estimated 1 MPN/g in processed gnocchi. Most of the anaerobic flora was facultatively anaerobic. A few obligately anaerobic bacteria were isolated from gnocchi and its ingredients and belonged to different Clostridium species. The protection factor, number of decimal reductions in the probability of toxigenesis from a single spore, was determined for eight different gnocchi formulations by challenge test studies. For all gnocchi stored at 8 degrees C (as recommended by the manufacturer) or 12 degrees C (mild temperature abuse), growth and toxin production were not detected in 75 days. The protection factor was >4.2 for proteolytic C. botulinum, and >6.2 for non-proteolytic C. botulinum. When inoculated packs were stored at 20 degrees C (severe temperature abuse), toxin production in 75 days was prevented by the inclusion of 0.09% (w/w) sorbic acid (protection factors as above), however in the absence of sorbic acid the packs became toxic before the end of the intended shelf-life and the protection factors were lower. Providing sorbic acid (0.09% w/w) is included in the gnocchi, the safety margin would seem to be very large with respect to the foodborne botulism hazard.

Ascorbic Acid↗
PubMed2006

Hazard and control of group II (non-proteolytic) Clostridium botulinum in modern food processing.

Group II (non-proteolytic) Clostridium botulinum poses a safety hazard in modern food processing, which consists of mild pasteurization treatments, anaerobic packaging, extended shelf lives and chilled storage. The high risk is reflected in the relatively large number of botulism cases due to group II C. botulinum in commercially produced foods during the past decades. Because of the high prevalence of group II C. botulinum in the environment, food raw materials may carry spores. Although group II spores are less heat-resistant than group I (proteolytic) spores, they can tolerate the heat treatments employed in the chilled food industry. Some food components may actually provide spores with protection from heat. Spore heat resistance should therefore be investigated for each food in order to determine the efficiency of industrial heat treatments. Group II strains are psychrotrophic and thus they are able to grow at refrigeration temperatures. Anaerobic packages and extended shelf lives provide C. botulinum with favourable conditions for growth and toxin formation. As the use of salt and other preservatives in these foods is limited, microbiological safety relies mainly on refrigerated storage. This sets great challenges on the production of chilled packaged foods. To ensure the safety of these foods, more than one factor should safeguard against botulinal growth and toxin production.

Botulinum Toxins↗
PubMed2006

Recovery from botulinum neurotoxin poisoning in vivo.

Botulinum neurotoxins cause the disease botulism, which is characterized by prolonged muscle paralysis. In contrast, injections of low doses of purified botulinum neurotoxins do not cause systemic illness but produce localized muscle paralysis that is beneficial for treating several human medical disorders involving uncontrollable muscle contraction. Optimizing the therapeutic efficacy while diminishing adverse reactions requires precise knowledge of toxin potency as well as a clear understanding of how each toxin causes disease. A novel in vivo mouse assay has been used to correlate toxin dosage with the duration of muscle paralysis. Voluntary running activity performed by mice was proportional to the amount of toxin injected into the hind limbs and the subsequent rate of recovery over the ensuing days or weeks was a function of botulinum neurotoxin serotype A or B concentration. Botulinum neurotoxin A produced longer paralysis than botulinum neurotoxin B consistent with human observations. A third serotype, botulinum neurotoxin E, had the shortest duration of action, but unlike the other two toxins, dosage did not influence recovery time. Botulinum neurotoxin A recovery appeared biphasic with the initial phase about two-fold faster than the final phase. Over four weeks, muscle activity had gradually improved following the highest botulinum neurotoxin A dose, reaching about half of the normal running activity. Lower botulinum neurotoxin A doses led to incrementally faster and complete recovery. Persistence of maximum paralysis was exponentially related to botulinum neurotoxin A dosage, with a doubling of the paralysis time occurring with every 25% increase of the toxin concentration. In contrast, the rate of recovery from botulinum neurotoxin B was monophasic relative to toxin dosage and the duration of maximum paralysis was linear relative to dosage. Combinations of botulinum neurotoxin A and B and botulinum neurotoxin A and E were tested and shown to exacerbate paralysis compared with individually administered serotypes.

Animals↗
PubMed2006

Recombinant C fragment of botulinum neurotoxin B serotype (rBoNTB (HC)) immune response and protection in the rhesus monkey.

Botulinum neurotoxin B (BoNTB) is a distinct protein subtype of a family of neurotoxins with the potential for use in biological warfare or terrorist attacks. This study is one in a series evaluating the immunogenicity and protective effects of recombinant vaccines against the different subtypes of botulinum toxin. The recombinant subunit vaccines encoding the C fragment portion ( approximately 50 kDa) of the toxins are produced in the yeast, Pichia pastoris. In this study, groups of rhesus monkeys were vaccinated with three doses (1 and 5microg per dose) of rBoNTB(H(c)) vaccine. Total and neutralizing antibody titers were determined at various times during and postvaccination. Two groups of vaccinated monkeys plus non-vaccinated controls were actively challenged with B toxin by aerosol exposure. All monkeys receiving vaccine were protected from the toxin and no clinical signs of disease were observed, while controls displaying classic signs of botulism succumbed to the toxin challenge. Two additional groups of monkeys receiving the same vaccine regiment as the first two groups had significant levels of circulating neutralizing antibody titers up to 24 months postvaccination. This non-human primate study demonstrated the short- and long-term immunity afforded by the rBoNTB(H(c)) vaccine.

Animals↗
PubMed1987

Intestinal toxicoinfection by Clostridium botulinum type F in an adult. Case associated with Guillain-Barré syndrome.

A 27-year-old man with type F botulism (classification undetermined) had two episodes of botulinum toxaemia with identification of botulinum toxin and Clostridium botulinum organisms in faecal specimens during a three-month stay in hospital. Between these clinical episodes neither toxin nor Cl botulinum could be demonstrated. The illness was severe with quadriplegia, respiratory insufficiency, and bowel paralysis. In addition the patient had sensory abnormalities and a raised protein in the cerebrospinal fluid. The results demonstrate for the first time in detail an intestinal colonisation with and multiplication of C botulinum organisms and in-vivo production of toxin in an adult. The clinical findings at first pointed to Guillain-Barré syndrome, and it is suggested that patients with this syndrome should be examined for botulinum toxin in serum and for toxin and organisms in stool.

Adult↗