Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Botulism”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 253 records · Page 14Linked to original sources
PubMed2003

Sequence of the gene for Clostridium botulinum type B neurotoxin associated with infant botulism, expression of the C-terminal half of heavy chain and its binding activity.

Previously, we demonstrated that the neurotoxin of strain 111 (111/NT) associated with type B infant botulism showed antigenic and biological properties different from that (Okra/NT) produced by a foodborne botulism-related strain, Okra. In this study, the neurotoxin genes of 111/NT and Okra/NT were amplified and the sequences determined. The nucleotide sequences of the genes for both neurotoxins possessed an open reading frame of 3873 bp that encoded 1291 amino acids. The identities of nucleotide sequences and amino acid sequences were 97.6% and 95.7%, respectively. The ratio of nonsynonymous to synonymous substitutions was 0.47. The amino acid substitutions between 111/NT and Okra/NT occurred mainly in the domain of the C-terminal half of heavy chain (H(C)) responsible for binding to its receptor complex of protein and ganglioside. To characterize the binding capability of the H(C), recombinant genes for the H(C) and two hybrid H(C) in which one half of Okra/NT was replaced by the homologous half of 111/NT were constructed and expressed in Escherichia coli. The binding activity of the recombinant H(C) of 111/NT to the protein receptor synaptotagmin II, in the presence of ganglioside GT1b, was 4.2-fold less than Okra/NT, consistent with the corresponding two NTs. The use of hybrid H(C) revealed that mutation of 23 residues in carboxy terminal half of H(C) (1029-1291) of Okra/NT could be attributed to the lower binding activity of 111/NT and thus the differences in binding affinity between the two BoNT/B.

Amino Acid Sequence↗
PubMed1998

Type E botulism associated with vacuum-packaged hot-smoked whitefish.

On January 16, 1997 two Germans got botulism after eating hot-smoked Canadian whitefish produced in Finland. The serum sample of one of the patients contained 6 MLD/ml of botulinum toxin. The type of toxin was identified as E by the toxin neutralization test and the botulinum neurotoxin type E (BoNT/E) gene was also amplified from the serum by polymerase chain reaction (PCR), but C. botulinum could not be isolated from the positive serum sample. The remains of the hot-smoked whitefish eaten by the patients contained botulinum toxin detected by the mouse bioassay and the BoNT/E gene as determined by PCR. C. botulinum was isolated from the fish sample and it was confirmed to be type E by the mouse bioassay and by PCR. Eleven other fish samples from the same lot did not contain botulinum toxin nor any BoNT gene. The incriminated food was processed on the 9th and 10th of January, 1997 from frozen whitefish imported to Finland from Canada. The pulsed-field gel electrophoretic pattern of the isolated C. botulinum strain resembled a reference strain of North American origin. It did not match any C. botulinum strains isolated from the Baltic sea-bottom or from the fish caught in the area indicating that the fish was contaminated by C. botulinum in Canada. The conditions resulting in toxin production could not be identified. The safety problems associated with vacuum-packaged hot-smoked fish seem to be of utmost concern and the product is one of the most important botulism food vehicles processed on an industrial scale. Temperature monitoring and the use of time-temperature indicators are to be recommended in order to ensure adequate storage temperature from processing through to consumption. Allowing the use of nitrate and nitrite together with sufficiently high NaC1 concentration in this particular product should also be considered.

Adult↗
PubMedDate not supplied

Development of vaccines for prevention of botulism.

Botulism is a potentially lethal disease caused by one of seven homologous neurotoxic proteins usually produced by the bacterium, Clostridium botulinum. This neuromuscular disorder occurs through an exquisite series of molecular events, ultimately ending with the arrest of acetylcholine release and hence, flaccid paralysis. The development of vaccines that protect against botulism dates back to the 1940s. Currently, a pentavalent vaccine that protects against BoNT serotypes A-E and a separate monovalent vaccine that protects against BoNT serotype F are available as Investigational New Drugs. However, due to the numerous shortcomings associated with the toxoid vaccines, several groups have efforts towards developing next-generation vaccines. Identifying a synthetic peptide that harbors a neutralizing epitope is one approach to a BoNT vaccine, while another employs the use of a Venezuelan equine encephalitis virus replicon vector to produce protective antigens in vivo against BoNT. The strategy used in our laboratory is to design synthetic genes encoding non-toxic, carboxy-terminal fragments of the C. botulinum neurotoxins (rBoNT(H(C))). The gene products are expressed in the yeast, Pichia pastoris, and purified to greater than 98% with yields typically ranging from 200-500 mg per kg of wet cells. Protective immunity to the purified products against high-level challenges of neurotoxin is elicited in mice and in non-human primates. A pre-Investigational New Drug meeting was held with the Food and Drug Administration, and the next milestone for the vaccine candidates will be clinical trials.

Animals↗
PubMed1977

Infantile botulism.

Botulism has not traditionally been considered as occurring in infants under one year of age because they generally do not ingest foods potentially containing preformed Clostridium botulinum toxin. We report a case of infantile botulism in a 3 1/2 month old infant who presented as a "floppy baby," and discuss the probable pathobiology involved.

Botulism↗
PubMed2006

[Botulism and pregnancy].

Botulism during pregnancy is uncommon and raises concern due uncertainty about fetal impairment. This type of situation has not been reported to date. Treatment is basically symptomatic and based on nursing care. The prognosis is tightly correlated with the maternal status. Dietary hygiene is the basis of prevention. We describe a case of botulism occurring during the second quarter of pregnancy.

Adult↗
PubMed1998

Infant botulism during a one year period in San Luis, Argentina.

Five cases of infant botulism which occurred during the period from May 1995 to May 1996 in San Luis, Argentina, are reported. Infant botulism was confirmed in all patients by isolation of Clostridium botulinum type A from stool culture and by the toxin assay. Toxin was found in the serum of one of them. All patients required hospitalization with treatment consisting of supportive especially respiratory and nutritional care. At the time of discharge from the hospital, three patients had a good recovery, although two of them had mild difficulties in sucking or constipation. C. botulinum was not detected in samples of honey which had been given to two of the patients.

Argentina↗
PubMed1994

Landfill sites, botulism and gulls.

Botulism due to Clostridium botulinum type C causes considerable mortality in gulls in the UK, and refuse disposal sites are suspected as a major source of toxin. C. botulinum types B, C and D were each found in 12 (63.2%) of 19 landfill sites examined. Type E was detected in only one (5.2%) and types A, F and G were not found. The prevalence of type C spores was much higher than that demonstrated in the UK environment by earlier surveys. The presence of these spores, together with the rotting organic matter and generated heat associated with landfill sites, undoubtedly leads to bacterial proliferation and toxigenesis. This is likely to result in botulism in scavenging gulls unless skilled landfill management prevents the ingestion of toxic material. Type D spores were previously shown to be rare in the UK environment and their high prevalence on landfill sites was therefore surprising. Four composite samples of refuse collected before distribution on a landfill gave negative results for C. botulinum and it seems likely that the gulls themselves play a major role in introducing contamination.

Animals↗
PubMed2006

[Botulism in cattle].

Botulism is an intoxication caused by ingestion of feed or water contaminated with the toxin of Clostridium botulinum. In cattle, intoxication usually results from the ingestion of feed containing preformed type C or D toxin, either in feed which has been contaminated with toxin-containing carcasses or in feed in which there has been primary multiplication of C. botulinum and toxin production. The initial signs of botulism are progressive difficulty in chewing and swallowing, caused by paralysis of the tongue and muscles of mastication. This results in slow prehension and chewing of feed, water and feed falling out of the mouth, excessive salivation and weakness of the tongue. After 1 to 3 days, generalised paralysis occurs followed by death due to respiratory paralysis. Intravenous fluid therapy is the recommended treatment. The administration of antiserum is of limited value in advanced stages and is used mainly as a prophylactic measure in cattle herds in which an outbreak has just started. Active immunization of cattle in high-risk herds is also an option. It is critical that cattle not be fed feed contaminated with soil or carcasses.

Animal Feed↗
PubMed1994

Neuro-ophthalmic findings in botulism type B.

In June 1989, the largest recorded outbreak of food-borne botulism occurred in the United Kingdom. Twenty-seven patients were affected during the outbreak with type B botulism. A case note review of 14 patients admitted with this condition was performed and the neuro-ophthalmic findings are presented. Patients with severe disease presented with a combination of ocular and bulbar symptoms; in mild cases dysphagia was noted first and visual disturbance followed within 24 hours. Clustering of cases and bilaterality of cranial nerve signs aided in the diagnosis. Accommodative paresis and sixth cranial nerve palsy were frequent early signs. When there was respiratory paralysis and ventilatory failure, it occurred within 12 hours of the onset of a third cranial nerve palsy.

Abducens Nerve↗
PubMed1999

Botulism: a case associated with pyramidal signs.

Botulism is a widespread neuroparalytic disease that may be confused with other neurological disorders. As it is potentially lethal, clinicians are required to be aware of its diagnosis and management. We report a case of botulism complicated by pyramidal signs in a 35-year-old woman. Clinical aspects, differential diagnoses and therapeutic problems are discussed.

Adult↗
PubMed2002

[Wound botulism after drug injection].

CLINICAL PRESENTATION: A 32-year old male drug user presented with diplopia, ataxia and general weakness. The patient had abscesses on arms and legs at injection sites, bilateral ptosis, a bifacial weakness, nasal speech, severely reduced ability to raise his arms and a positive Trendelelenburg sign with normal motor neuron reflexes and normal sensation. CLINICAL AND LABORATORY TESTS: The haematological values indicated a hypochromic, microcytic anaemia (12,1 mg/dl), a slight leuko (10,8 G/L) - and thrombocytosis (582G/l) with elevated erythrocyte sedimentation rate (74 mm/h), and a reduced prothrombin time (67%). The HIV test was negative. The MRI scan of the brain and the bacterial, serological and cytological results of a lumbar puncture were normal. In the bloodculture no bacterial growth and no botulinum toxin was found. In a culture of the wound material grew coagulase-negative staphylococcus and Clostridium perfringens, diagnosed with PCR. The serum anti-acethylcholine antibodies were negative. The motor-nerve conduction test with repetitive stimulation of the ulnari nerve with a 3 Hz trigger showed no change in the amplitude, while a 20 Hz trigger showed an increment up to 160 %. DIAGNOSIS, TREATMENT AND RESPONSE TO THERAPY: Another possible diagnosis was excluded through MRI, CSF and serum examination. The typical presentation of a rapidly progressive descending paralysis without loss of sensation and the typical motor-nerve conduction disorder of a presynaptic block established the diagnosis of wound botulism. This was treated immediately by surgical removal of wound debris, antitoxin- and penicillin therapy. After 28 days the patient left the hospital with slight residual problems. He had been admitted to the intensive care unit for a short period only and intubation was not necessary at any time. CONCLUSION: After exclusion of any other possible diagnosis, it is possible to establish an early diagnosis of injection related wound botulism by its typical symptoms and signs. These are presented as wound abcesses at intramuscular drug injection sites together with rapidly progressive descending paralysis with preserved sensation. Treatment consists of surgical excision of wound debris combined with antitoxin and penicillin administration in order to prevent a possible build-up of residues. Early diagnosis and associated therapy overcome the necessity of intubation and prolonged intensive care.

Adult↗
PubMed2006

[Wound botulism in heroin addicts in Germany].

HISTORY AND ADMISSION FINDINGS: 5 heroin addicts (aged 31-44 years; 1 female, 4 men) presented with a history of blurred vision and diplopia followed by dysarthria. 3 of the patients also developed respiratory failure requiring long-term ventilatory support. Physical examination revealed cranial nerve deficits and abscesses at injection sites in 3 of them. DIAGNOSIS: In 4 patients wound botulism was diagnosed on the basis of symptoms, course of the illness and response to specific treatment. Clostridium botulinum was grown from wound swab in one patient. TREATMENT AND COURSE: Two of the patients, having been injected with antitoxin immediately after admission, were discharged almost symptom-free after only a few days. Adjuvant antibiotics and, in 3 patients, surgical débridement of the abscesses were needed. CONCLUSIONS: Progressive cranial nerve pareses in addicts who inject drugs intravenously or intramuscularly should raise the suspicion of wound botulism and require hospitalization. While indirect demonstration of toxin supports the diagnosis, false-negative results are common.

Adult↗
PubMed1997

Infant botulism. The first culture-confirmed Danish case.

Infant botulism is caused by intestinal colonization by Clostridium botulinum, C. barati or C. butyricum. Infant botulism has only rarely been reported outside the USA. A 3-month-old boy developed constipation, lethargy, feeding difficulties and descending, severe, symmetric weakness. He was breastfed but had also been fed honey. Supportive care led to complete recovery. The serum was positive for C. botulinum toxin type A-F (mouse toxin neutralization assay). A strain of C. botulinum producing toxin type A and E was identified in the stool. C. botulinum was identified in a jar of honey of the same brand as the honey fed to the patient.

Botulinum Toxins↗
PubMed1979

Outbreak of botulism in Kenyan nomads.

During disease surveillance in Kenya, a series of deaths were investigated among a group of nomadic Gabra in Marsabit. The cause was identified as botulism (Clostridium botulinum Type A), contracted from sour milk prepared traditionally in a gourd. Reported outbreaks of botulism in Africa would appear to be extremely rare.

Adult↗
PubMed1998

An outbreak of food-borne botulism associated with contaminated locally made cheese in Iran.

Cases of botulism in the northern province of Iran were studied in March and April 1997. A total of 27 patients were affected; 1 patient died. The samples were sent to the Department of Bacteriology, Pasteur Institute of Iran, for investigation. To identify the food source, several patients were interviewed and a case control investigation was conducted among families of hospitalized patients. Clinical and food specimens were tested. Toxin testing was positive for 37% of serum and stool specimens. Type A botulinal toxin was detected in cheese and Clostridium botulinum type A was isolated from cultures of clinical specimens and the cheese. This is the first documented outbreak of botulism due to Clostridium botulinum type A following consumption of cheese in Iran.

Botulism↗
PubMed1978

Infant botulism: new guise for an old disease.

While classic botulism is usually due to preformed toxin in improperly prepared food, the newly recognized infant syndrome occurs when spores or vegetative cells germinate in the gut of the very young and elaborate toxin there. The resulting illness may range from inapparent to fulminant, sometimes causing respiratory arrest and death. Infant botulism may also account for at least some cases of sudden infant death syndrome.

Adolescent↗
PubMed1998

A large outbreak of botulism: the hazardous baked potato.

In April 1994, the largest outbreak of botulism in the United States since 1978 occurred in El Paso, Texas. Thirty persons were affected; 4 required mechanical ventilation. All ate food from a Greek restaurant. The attack rate among persons who ate a potato-based dip was 86% (19/22) compared with 6% (11/176) among persons who did not eat the dip (relative risk [RR] = 13.8; 95% confidence interval [CI], 7.6-25.1). The attack rate among persons who ate an eggplant-based dip was 67% (6/9) compared with 13% (241189) among persons who did not (RR = 5.2; 95% CI, 2.9-9.5). Botulism toxin type A was detected from patients and in both dips. Toxin formation resulted from holding aluminum foil-wrapped baked potatoes at room temperature, apparently for several days, before they were used in the dips. Consumers should be informed of the potential hazards caused by holding foil-wrapped potatoes at ambient temperatures after cooking.

Animals↗
PubMed2004

Proteolytic Clostridium botulinum type B in the gastric content of a patient with type E botulism due to whitefish eggs.

Whitefish eggs were confirmed by pulsed-field gel electrophoresis to cause type E foodborne botulism in a 54-year-old patient in Finland. Botulinum neurotoxin and/or nonproteolytic Clostridium botulinum type E organisms were detected in fecal and gastric samples from the patient and in suspected whitefish eggs. Apart from C. botulinum type E, proteolytic type B organisms were detected in the patient's gastric content. This was considered to be insignificant with respect to the clinical disease, suggesting botulinal spores to be occasionally present in the human gastrointestinal tract without any apparent clinical significance. This is the first domestic case of foodborne botulism in Finland.

Animals↗