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Background
This bacteria has gained noteriety because of the cosmetic benefits of the botulinum toxin as well as the potential destructive use as a weapon of bio-terrorism.
OUTLINE
EPIDEMIOLOGY CHARACTERIZATION SYNONYMS INCIDENCE/
PREVALENCEAGE SEX GEOGRAPHY Botulism in the United States: a clinical and epidemiologic review.
Shapiro RL, Hatheway C, Swerdlow DL.
Centers for Disease Control and Prevention, Atlanta, Georgia 30333, USA.
Ann Intern Med. 1998 Aug 1;129(3):221-8. Abstract quote
Botulism is caused by a neurotoxin produced from the anaerobic, spore-forming bacterium Clostridium botulinum. Botulism in humans is usually caused by toxin types A, B, and E. Since 1973, a median of 24 cases of foodborne botulism, 3 cases of wound botulism, and 71 cases of infant botulism have been reported annually to the Centers for Disease Control and Prevention (CDC).
New vehicles for transmission have emerged in recent decades, and wound botulism associated with black tar heroin has increased dramatically since 1994. Recently, the potential terrorist use of botulinum toxin has become an important concern. Botulism is characterized by symmetric, descending, flaccid paralysis of motor and autonomic nerves, usually beginning with the cranial nerves. Blurred vision, dysphagia, and dysarthria are common initial complaints. The diagnosis of botulism is based on compatible clinical findings; history of exposure to suspect foods; and supportive ancillary testing to rule out other causes of neurologic dysfunction that mimic botulism, such as stroke, the Guillain-Barre syndrome, and myasthenia gravis. Laboratory confirmation of suspected cases is performed at the CDC and some state laboratories. Treatment includes supportive care and trivalent equine antitoxin, which reduces mortality if administered early.
The CDC releases botulism antitoxin through an emergency distribution system. Although rare, botulism outbreaks are a public health emergency that require rapid recognition to prevent additional cases and to effectively treat patients. Because clinicians are the first to treat patients in any type of botulism outbreak, they must know how to recognize, diagnose, and treat this rare but potentially lethal disease.Clinical and laboratory comparison of botulism from toxin types A, B, and E in the United States, 1975-1988.
Woodruff BA, Griffin PM, McCroskey LM, Smart JF, Wainwright RB, Bryant RG, Hutwagner LC, Hatheway CL.
Enteric Diseases Branch, Centers for Disease Control, Atlanta, Georgia 30333.
J Infect Dis. 1992 Dec;166(6):1281-6. Abstract quote
Cases of adult botulism (n = 309) were studied to identify clinical differences between toxin types and to evaluate the sensitivity of diagnostic laboratory testing. Patients with illness from type E toxin had the shortest incubation periods. Sporadic case-patients were more severely ill: 85% required intubation compared with only 42% in multiperson outbreaks.
Of patients with type A botulism, 67% required intubation compared with 52% with type B and 39% with type E. Toxin testing was positive for 40%-44% of serum and stool specimens obtained within 3 days of toxin ingestion and for 15%-23% of specimens obtained thereafter, while 37% of stool specimens obtained > 3 days after toxin ingestion were positive by culture. Patients with type A botulism have more severe illness.
In general, specimens obtained early are more likely to be positive by toxin assay, and stool cultures are more sensitive than toxin detection for specimens obtained later in the illness.EPIDEMIOLOGIC ASSOCIATIONS HONEY Honey and other environmental risk factors for infant botulism.
Arnon SS, Midura TF, Damus K, Thompson B, Wood RM, Chin J.
J Pediatr. 1979 Feb;94(2):331-6. Abstract quote
Infant botulism results from the in vivo production of toxin by Clostridium botulinum after it has colonized the infant's gut. Epidemiologic and laboratory investigations of this recently recognized disease were undertaken to identify risk factors and routes by which C. botulinum spores might reach susceptible infants.
Clostridium botulinum organisms, but no preformed toxin, were identified in six different honey specimens fed to three California patients with infant botulism, as well as from 10% (9/90) of honey specimens studied. By food exposure history, honey was significantly associated with type B infant botulism (P = 0.005). In California, 29.2% (12/41) of hospitalized patients had been fed honey prior to onset of constipation; worldwide, honey exposure occurred in 34.7% (28/75) of hospitalized cases. Of all food items tested, only honey contained C. botulinum organisms. On household vacuum cleaner dust specimens and five soil specimens (three from case homes, two from control homes) contained Clostridium botulinum.
The known ubiquitous distribution of C. botulinum implies that exposure to its spores is universal and that host factors contribute importantly to the pathogenesis of infant botulism. However, honey is now an identified and avoidable source of C. botulinum spores, and it therefore should not be fed to infants.
DISEASE ASSOCIATIONS CHARACTERIZATION SIDS Is there a link between infant botulism and sudden infant death? Bacteriological results obtained in central Germany.
Bohnel H, Behrens S, Loch P, Lube K, Gessler F.
Institute for Tropical Animal Health, Georg-August-University Gottingen, Germany.
Eur J Pediatr. 2001 Oct;160(10):623-8. Abstract quote
Despite the fact that botulism was described in Germany for the first time by Kerner in 1820, the disease is almost forgotten in this country. Only about 10-20 cases of classical botulism (intoxication) are recorded every year, including 1-2 cases of clinical infant botulism. As we assumed a high incidence of botulism to be connected with cases of sudden infant death (SID), we undertook the research work presented here.
From every case of unexpected infant death up to 12 months of age, standardised specimens (blood, liver and intestine) were taken at autopsy. They were tested for the presence of botulinum neurotoxin (BoNT) and/or bacterial forms of Clostridium botulinum with subsequent BoNT neutralisation tests by the international standard mouse bioassay. Age, sex, pathological findings and season were recorded. Over a 5-year period, 75 samples including 57 SID cases were tested. Free toxin was found in nine and bacterial forms were detected in six samples. Toxin neutralisation revealed the definite presence of BoNT/BoNT producing bacteria (mainly type E), whereas another 11 toxin tests were inconclusive. According to international literature, these 15 cases are to be interpreted as infant botulism.
Conclusion: the results show a remarkable incidence of infant botulism without any known previous medical history, partly hidden as sudden infant death. We propose to systematically search for botulism in connection with sudden infant death.
PATHOGENESIS CHARACTERIZATION
LABORATORY/
RADIOLOGIC/
OTHER TESTSCHARACTERIZATION RADIOLOGIC LABORATORY MARKERS PCR Polymerase chain reaction for detection of Clostridium botulinum types A, B and E in food, soil and infant faeces.
Szabo EA, Pemberton JM, Gibson AM, Eyles MJ, Desmarchelier PM.
Department of Microbiology, University of Queensland, Australia.
J Appl Bacteriol. 1994 Jun;76(6):539-45. Abstract quote
The application of the polymerase chain reaction (PCR) for detection of Clostridium botulinum types A, B and E in foods, environmental and clinical samples was evaluated and compared to the mouse bioassay.
Samples inoculated with 10, 100 and 1000 spores of Cl. botulinum types A and B included pasteurized milk, UHT milk, infant formula, infant faeces, meat juice, canned tuna, mushrooms, blood sausage and soil. Clostridium botulinum type E spores were inoculated into fish eggs, canned tuna, picked herring, raw fish and soil at similar levels. Spores were added to 2.5 g of each sample with the exception of soil which was inoculated in 10 g samples. The presence of Cl. botulinum in sample enrichments was determined by both PCR and the bioassay. An overall correlation of 95.6% was observed between PCR results and the mouse bioassay.
Of the total of 114 samples tested there was disparity between the mouse bioassay and the PCR in three samples of soil inoculated with 100 type A or E spores and 10 type B spores per 10 g, respectively, and two samples of infant faeces inoculated with 10 type A or B spores per 2.5 g. All of these samples gave negative animal results and positive PCR results.
GROSS APPEARANCE/
CLINICAL VARIANTSCHARACTERIZATION GENERAL VARIANTS ANTIBIOTIC ASSOCIATED COLITIS (C. DIFFICILE) BOTULISM Clostridium botulinum and the clinical laboratorian: a detailed review of botulism, including biological warfare ramifications of botulinum toxin.
Caya JG, Agni R, Miller JE.
Department of Pathology and Laboratory Medicine, University of Wisconsin Hospital and Clinics, Madison, USA.
Arch Pathol Lab Med. 2004 Jun;128(6):653-62. Abstract quote
OBJECTIVE: This review article is designed to thoroughly familiarize all health care professionals with the history, classification, epidemiology, clinical characteristics, differential diagnosis, diagnostic evaluation (including laboratory-based testing), treatment, and prognosis of botulism. It is especially targeted toward clinical laboratorians and includes a detailed enumeration of the important clinical laboratory contributions to the diagnosis, treatment, and monitoring of patients with botulism. Finally, the bioterrorism potential for botulism is discussed, with an emphasis on the clinical laboratory ramifications of this possibility.
DATA SOURCES: Included medical periodicals and textbooks accessioned from computerized and manual medical literature searches. More than 1000 medical works published from the 1800s through 2003 were retrieved and reviewed in this process.
DATA SYNTHESIS: Pertinent data are presented in textual and tabular formats, the latter including 6 tables presenting detailed information regarding the clinical parameters, differential diagnosis, diagnostic studies, laboratory testing, and therapeutic approaches to botulism.
CONCLUSIONS: Because botulism is such a rare disease, a keen awareness of its manifestations and prompt diagnosis are absolutely crucial for its successful treatment. The bioterrorism potential of botulism adds further urgency to the need for all health care professionals to be familiar with this disease, its proper evaluation, and timely treatment; the need for such urgency clearly includes the clinical laboratory.Wound botulism.
Burningham MD, Walter FG, Mechem C, Haber J, Ekins BR.
Department of Emergency Medicine, Valley Medical Center, University of California, San Francisco School of Medicine.
Ann Emerg Med. 1994 Dec;24(6):1184-7. Abstract quote
Wound botulism is a rare infectious and toxicologic complication of trauma and i.v. drug abuse.
Only 39 cases have been reported in detail in the English literature. This case report describes a patient with wound botulism who presented to four medical facilities before receiving definitive diagnosis and treatment. Although his history and physical examination were consistent with wound botulism, diagnosis and therapy were delayed because this rare disease was not considered initially in the differential diagnosis.
Wound botulism should be considered in trauma patients and i.v. drug abusers who present with cranial nerve palsies and descending paresis.Infant botulism. Epidemiological, clinical, and laboratory aspects.
Arnon SS, Midura TF, Clay SA, Wood RM, Chin J.
JAMA. 1977 May 2;237(18):1946-51. Abstract quote
Clostridium botulinum organisms and toxin were identified in the feces of six infants, aged 5 to 20 weeks, who had illnesses clinically consistent with botulism.
Five of the infants lived in California and became ill within a six-month period in 1976; one infant became ill in New Jersey in 1975. Three cases were type A botulism, and three were type B. No source of ingested botulinal toxin could be found in any case. However, one infant with type B botulism had ingested a food containing C botulinum type B organisms, and no toxin was found in it.
The clinical findings in these cases include constipation, weak sucking and crying ability, pooled oral secretions, cranial nerve deficits, generalized weakness, and, on occasion, sudden apnea. A characteristic electromyographic pattern termed "brief, small, abundant, motor-unit action potentials" (BSAP) was observed. The sources of C botulinum toxin for these six infants is thought to have been in vivo (gastrointestinal) production following ingestion of C botulinum organisms.
Studies are underway to determine the full clinical spectrum, incidence, and potential public health importance of this infectious disease newly recognized in infants.
HISTOLOGICAL TYPES CHARACTERIZATION GENERAL
SPECIAL STAINS/
IMMUNOPEROXIDASE/
OTHERCHARACTERIZATION SPECIAL STAINS IMMUNOPEROXIDASE ELECTRON MICROSCOPY
DIFFERENTIAL DIAGNOSIS KEY DIFFERENTIATING FEATURES
PROGNOSIS CHARACTERIZATION
TREATMENT CHARACTERIZATION GENERAL TOXIN USES Historical notes on botulism, Clostridium botulinum, botulinum toxin, and the idea of the therapeutic use of the toxin.
Erbguth FJ.
Department of Neurology, City Hospital Nurnberg, Nurnberg, Germany.
Mov Disord. 2004 Mar;19 Suppl 8:S2-6. Abstract quote
Food-borne botulism probably has accompanied mankind since its beginning. However, we have only few historical sources and documents on food poisoning before the 19th century. Some ancient dietary laws and taboos may reflect some knowledge about the life-threatening consumption of poisoned food.
One example of such a dietary taboo is the 10th century edict of Emperor Leo VI of Byzantium in which manufacturing of blood sausages was forbidden. Some ancient case reports on intoxications with Atropa belladonna probably described patients with food-borne botulism, because the combination of dilated pupils and fatal muscle paralysis cannot be attributed to an atropine intoxication. At the end of the 18th century, some well-documented outbreaks of "sausage poisoning" in Southern Germany, especially in Wurttemberg, prompted early systematic botulinum toxin research. The German poet and district medical officer Justinus Kerner (1786-1862) published the first accurate and complete descriptions of the symptoms of food-borne botulism between 1817 and 1822. Kerner did not succeed in defining the suspected "biological poison" which he called "sausage poison" or "fatty poison." However, he developed the idea of a possible therapeutic use of the toxin. Eighty years after Kerner's work, in 1895, a botulism outbreak after a funeral dinner with smoked ham in the small Belgian village of Ellezelles led to the discovery of the pathogen Clostridium botulinum by Emile Pierre van Ermengem, Professor of bacteriology at the University of Ghent.
The bacterium was so called because of its pathological association with the sausages (Latin word for sausage = "botulus") and not-as it was suggested-because of its shape. Modern botulinum toxin treatment was pioneered by Alan B. Scott and Edward J. Schantz.Henry JB. Clinical Diagnosis and Management by Laboratory Methods. Twentieth Edition. WB Saunders. 2001.
Rosai J. Ackerman's Surgical Pathology. Ninth Edition. Mosby 2004.
Sternberg S. Diagnostic Surgical Pathology. Fourth Edition. Lipincott Williams and Wilkins 2004.
Robbins Pathologic Basis of Disease. Sixth Edition. WB Saunders 1999.
DeMay RM. The Art and Science of Cytopathology. Volume 1 and 2. ASCP Press. 1996.
Weedon D. Weedon's Skin Pathology Second Edition. Churchill Livingstone. 2002
Fitzpatrick's Dermatology in General Medicine. 5th Edition. McGraw-Hill. 1999.
Weiss SW and Goldblum JR. Enzinger and Weiss's Soft Tissue Tumors. Fourth Edition. Mosby 2001.
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