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 217 records · Page 12Linked to original sources
PubMed1981

Infant botulism type B in central Europe.

A case of moderately severe botulism was diagnosed in a 4 weeks old white female. Clostridium botulinum toxin was identified repeatedly in the infant's faeces by means of the mouse protection assay. Clostridium botulinum was isolated in pure culture from faecal material. Both the organism and the toxin were type B. The onset of illness was characterized by mild constipation, apathy, weak sucking and difficulty with swallowing. Incipient, probably aspiration, pneumonia was diagnosed at the same time. Further signs of botulism developed during hospitalization, viz. loss of head control, pooled oral secretion, weak cry, mild ptosis, reduced facial expression, generalized muscular weakness and reduced spontaneous activity. A nasogastric feeding tube was needed because the ability to suck and swallow was impaired. Immediately on admission of the infant to hospital emergency treatment was started with ampicillin, which was followed by penicillin injections. The infant recovered in 60 days. Subsequent medical examinations demonstrated that the recovery was complete and the development normal. The case represents the first instance of infant botulism detected on the European Continent.

Botulinum Toxins↗
PubMedDate not supplied

Cases of type C botulism in broiler chickens.

Twenty-seven cases of type C botulism were studied in integrated broiler operations on the Delmarva Peninsula. Single and repeated outbreaks in broiler flocks were observed. No botulinum toxin was found in litter and feed samples despite repeated testing. Clostridium botulinum type C was cultured from litter, feed, and tissues of morbid and clinically normal chickens sampled from farms in which flocks experienced botulism. Clostridium botulinum type C could not be cultured from tissues of clinically normal chickens taken from a farm without a flock history of botulism or from caged broilers reared in semi-isolation.

Animal Feed↗
PubMed1982

[Type E botulism. Two recent cases (author's transl)].

Two brothers, aged 29 and 31, developed severe type E botulism 12 hours after eating salted herrings. The younger died rapidly, the other survived after treatment with type E botulinus antitoxin under intensive care. Limited electromyographic exploration of the surviving patient showed characteristic signs of presynaptic block. This method may be helpful in the diagnosis of atypical forms of the disease. Type E botulism is uncommon in France. It is almost exclusively transmitted by raw, smoked or salted fish and, for some obscure reason, rarely affects all those who shared the same meal. Contrary to types A and B botulism, it usually responds to its specific antitoxin, which must be administered as early as possible. The other therapeutic measures (tracheostomy, controlled ventilation, tube feeding) are the same for all types.

Adult↗
PubMed1995

[Botulism in infancy].

According to international references the publication ascertains the etiologic role of neurotoxin producing Clostridial spp., other than C. botulinum in Infant botulism. Authors report on the first Hungarian case of Infant botulism. The organism isolated -- C. barati -- is responsible only for a small proportion of published cases. Authors point out the conjunction of Infantile botulism and crib death.

Age Factors↗
PubMed1995

Two outbreaks of type C and type D botulism in sheep and goats in south Africa.

Two outbreaks of botulism in sheep and goats are described; in one, 329 out of 900 sheep in a feedlot died within 9 d of the onset of the disease and in the other, 100 sheep and goats out of 330 succumbed over a period of about 3 weeks. Animals were found dead or died suddenly, without exhibiting clinical signs. Others stood with lowered heads and showed drooling of saliva or a stiff gait. Paresis and/or paralysis were frequent signs in the terminal stages of the disease. Gross lesions such as the accumulation of fluids in body cavities, pulmonary oedema, foam in the trachea, epicardial haemorrhages and congestion of the mucosa of the small intestine, suggestive of heart failure, were present in animals from both outbreaks. Botulism was confirmed via the mouse toxicity test, by the demonstration of Type C and Type D toxins in the feed and intestinal contents of sheep from the first outbreak and Type D toxin in intestinal contents of sheep from the second. The clinical signs and macropathology in the outbreaks of botulism in sheep and goats in South Africa may resemble "krimpsiekte" and cardiac glycoside and ionophore poisoning, as well as other conditions causing heart failure.

Animals↗
PubMed1999

Surveillance of foodborne botulism in Poland: 1960-1998.

Human foodborne botulism, in contrast to the other two forms of botulism (wound and infant botulism), is an intoxication that results when preformed botulinum toxin is ingested. Sporadic cases and family and general outbreaks occur when food products are

Journal Article↗
PubMed1975

Guanidine in type B botulism.

On two occasions, guanidine produced clinical and electrophysiological improvement in a 54-year-old man with botulism, type B. However, guanidine was ineffective for autonomic dysfunction. There were no intolerable side effects. Our experience showed that guanidine is also effective in botulism, type B, as adjunctive therapy.

Botulism↗
PubMed1976

Pathophysiologic aspects of human botulism.

Physiologic studies were carried out in six patients with botulism. Abnormalities were those of a defect of acetylcholine release. Although the most consistent findings were small, evoked muscle action potentials (MAP) and posttetanic facilitation similar to the Eaton-Lambert syndrome, there were differences. In botulism as opposed to the Eaton-Lambert syndrome, the following were true: (1) posttetanic facilitation of the amplitude of the evoked MAP was considerably less and did not approach the normal value when the block was severe; (2) posttetanic facilitation persisted at least several minutes during the postactivation cycle; (3) posttetanic depression did not occur; (4) significant tetanic facilitation of the amplitude of the MAP occurred in less than half the patients and, even then, did not approach normal (on the other hand, a decremental response, as in myasthenia gravis, is not seen); and (5) no decremental response of the MAP occurred during slow rates (two per second) of nerve stimulation. Evidence of transient physiologic denervation occurred as in experimental animals affected by botulinum toxin. All physiologic abnormalities revert to normal in association with clinical recovery.

Adult↗
PubMed1980

Botulism and memory.

Although botulinum toxin is thought not to affect the human CNS, previous studies have not examined those behaviors, such as memory, that have been shown to be dependent on central acetylcholine transmission. In eight patients with type A botulism, subjective analysis, bedside memory testing, and formal memory testing with Hebb's verbal sequencing test, Corsi's nonverbal sequencing test, and Buschke's verbal serial list learning test failed to demonstrate impairment in immediate and recent memory. Botulism severe enough to block peripheral nicotinic and muscarinic cholinergic transmission does not block those central cholinergic synapses involved in memory.

Acetylcholine↗
PubMed1982

Botulism: a case with associated sensory abnormalities.

A 25-year-old man with type A botulism had prominent sensory symptoms and signs, which are findings that have not been previously reported to date. A sensory mononeuropathy multiplex was suspected. Sensory abnormalities do not exclude the diagnosis of botulism.

Adult↗
PubMed1987

Cardiovascular-reflex testing and single-fiber electromyography in botulism. A longitudinal study.

Four patients with botulism were studied on admission and at different times after intoxication, using a battery of cardiovascular autonomic tests. The results were compared with clinical status and single-fiber electromyographic findings. In the early stage of intoxication, the control of heart-rate and blood-pressure responsivity was markedly impaired, as was the neuromuscular transmission. At follow-up, results of sympathetic tests normalized earlier than those of parasympathetic tests. The recovery of autonomic function was slower than that of neuromuscular transmission in three patients. Monitoring autonomic derangement in botulism adds further information on the course of the disease and may identify patients at risk for cardiac or respiratory arrest. Further clinical investigation can help in determining more precisely the autonomic sites where the toxin acts.

Adolescent↗
PubMed1987

Antidiuretic hormone excess in infant botulism.

Two infants developed evidence of antidiuretic hormone excess as a complication of infant botulism. Neither child received mechanical ventilatory support before the development of hyponatremia, serum hyposmolality, and urinary hyperosmolality. Both infants responded to fluid-intake restriction. The appearance of hyponatremia in an infant with botulism should suggest antidiuretic hormone excess. The recognition of this entity will lead to its appropriate management with fluid-intake restriction.

Botulism↗
PubMed1989

Risk factors for infant botulism in the United States.

To define risk factors for infant botulism, we performed a 2-year prospective case-control study of 68 laboratory-confirmed cases in infants living in the United States, outside of California. For each case patient, two control subjects were matched by date and hospital of birth or county birth records. By univariate analysis, breast-feeding (odds ratio = 2.9) and consumption of honey (odds ratio = 9.8) were associated with disease, but only 11 case patients (16%) had eaten honey. Decreased frequency of bowel movement (less than one per day for at least 2 months) was also associated with disease in infants 2 months of age and older (odds ratio = 5.2). Risk factors changed with the age of the patient at disease onset when analyzed by multivariate logistic regression methods. For infants less than 2 months old, living in a rural area or on a farm was the only significant risk factor (odds ratio = 6.4). For infants 2 months of age and older, breast-feeding (odds ratio = 3.8), less than one bowel movement per day for at least 2 months (odds ratio = 2.9), and ingestion of corn syrup (odds ratio = 5.2) were associated with disease. The severity of the disease was similar for breast- and bottle-fed infants. Clearly defined food exposures account for a minority of infant botulism cases. Preexisting host factors, such as intestinal flora and frequency of bowel movements, may be the most important risk factors for development of disease.

Botulism↗
PubMed1975

Wound botulism.

Botulism occurring in patients with wounds has been thought of as a rare disease. A patient with a lacerating wound of his hand and wrist and an avulsion of his fourth finger developed diplopia, dizziness, and slurred speech one week later, followed by generalized weakness and difficulty in swallowing. Repetitive nerve stimulation studies showed signs of neuromuscular block consistent with the diagnosis of botulism. Results of bacteriologic and immunologic tests were not revealing, but the subsequent course of progressing, and retrogressing, bulbar signs and symptoms with eventual nearcomplete recovery confirmed the diagnosis. Increasing awareness and employment of electrophysiologic studies are uncovering increasing numbers of cases.

Adult↗
PubMed1976

Botulism in Alaska, 1947 through 1974. Early detection of cases and investigation of outbreaks as a means of reducing mortality.

Since 1947, there have been 21 outbreaks of botulism in Alaska, involving 46 people with 13 deaths (28% fatality). In the last six months of 1974, there were four outbreaks. With one exception to date, type E toxin was involved in all outbreaks for which laboratory confirmation has been obtained, and in all instances, Eskimo and Indian foods were the source. Clinical signs and symptoms of nausea and vomiting, dysphagia, diplopia, dilated pupils, and dry throat occurred with great frequency, forming a diagnostic pentad. We recommend that treatment include close medical supervision, supportive care, and the use of antitoxin, cathartics, and possibly, penicillin. The source of an outbreak must be determined to prevent further cases. Only prompt recognition, therapy and epidemiologic investigation can reduce the death toll from botulism.

Adolescent↗
PubMed1983

Economic impact of a botulism outbreak. Importance of the legal component in food-borne disease.

Legal expenses arising from food-borne outbreaks have not been reported in the medical literature, to the best of our knowledge. Expenses of an outbreak of food-borne botulism involving 34 victims in 1978 exceeded +5.8 million. These included outbreak investigation and control (3.2% of total), medical care for patients with botulism from April 1978 through October 1981 (12.3%), and settlements and legal charges (84.4%). Legal actions following food-borne outbreaks must be recognized for several reasons. First, the delay between the outbreak and the conclusion of legal activity (three years in this instance) mandates prompt and meticulous written documentation of investigation and control work. Second, legal expenses may make a large contribution to the total societal impact of food-borne disease outbreaks. Finally, awareness of the legal expense strengthens the rationale for public and private expenditures on food-borne disease prevention in this country.

Botulism↗
PubMed1977

Botulism: electrophysiological studies.

In a patient with botulism type B, electrophysiological studies showed: (1) a pattern in the repetitive nerve stimulation test resembling that found in the Eaton-Lambert syndrome but without any significant increment at high rates of stimulation or posttetanic exhaustion phenomenon; (2) a prominent response to guanidine hydrochloride; (3) a short mean duration of motor unit potentials that reversed with recovery; (4) a mild, prolonged latency and low amplitude of the H-reflex; (5) mild peripheral nerve dysfunction; and (6) a long-lasting persistence of abnormalities beyond the time of clinical recovery. The literature reports two types of responses in the repetitive nerve stimulation test in botulism: in the severe form one obtains a low-amplitude muscle potential, a decremental response at low rates of stimulation, and an insignificant incremental response at high rates of stimulation; in the mild form a normal amplitude of muscle potential occurs together with a normal response to low rates of stimulation and a significant incremental response at high rates of stimulation.

Botulism↗
PubMed1985

Electrophysiologic study in benign human botulism type B.

Conventional electromyography (EMG) and single fiber EMG (SFEMG) were performed in a 64-year-old diabetic woman with mild type B botulism. The main clinical signs were autonomic dysfunction and cranial nerves paresis. Conventional EMG was normal, except for small changes that were consistent with mild mixed peripheral neuropathy in the lower limbs and were related to diabetes. Repetitive stimulation and results of single stimulus before and after full effort were normal. SFEMG showed increased jitter and impulse blocking in clinically normal muscles. The jitter was frequency dependent and improved at a higher innervation rate. Impulse blocking in potentials with only slightly increased jitter was found. The follow-up showed improvement of the jitter in agreement with clinical recovery. Jitter abnormalities were recorded after 16 weeks, when clinical signs of botulism had been reversed to normal. Motor unit fiber density increased progressively, and on examination at 8 weeks, some potentials showed very high jitter values. Both findings might suggest new endplate formation, perhaps due to ultraterminal sprouting development.

Botulism↗