Botulism historical perspective
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Michael Maddaleni, B.S., Keanu Ngo[2]
Overview
Clostridium botulinum botulism was named In 1870 by Muller (German physician). In 1895 Clostridium botulinum was first isolated by Emile Van Ermengem and It was in 1949 when Burgen's group discovered that botulinum toxin blocks neuromuscular transmission.
Historical Perspective
Recognition of botulism as a foodborne disease (1793–1822)
The first well-documented outbreaks of foodborne botulism were recorded in late 18th- and early 19th-century southwestern Germany (Kingdom of Württemberg), where consumption of spoiled meat and blood sausages caused numerous deaths.[1]
The district medical officer and poet Justinus Kerner (1786–1862) published the first accurate and complete descriptions of the clinical syndrome between 1817 and 1822, correctly attributing it to a biological poison formed under anaerobic conditions that was lethal in minute quantities. He termed it "sausage poison," and the illness became known as "Kerner's disease." [2][3]
Notably, Kerner recognized that the toxin disrupted somatic and autonomic cholinergic transmission while sparing sensory function and cognition, and he proposed—more than a century before it was realized—that it might be used therapeutically to reduce hypersecretion and abnormal movements. He is regarded as the intellectual founder of botulinum toxin therapy.[3]
Discovery of the organism and toxin (1895–1949)
In 1895, Emile Pierre van Ermengem, professor of bacteriology at the University of Ghent, isolated the causative anaerobic bacillus following an outbreak of botulism after a funeral dinner featuring smoked ham in Ellezelles, Belgium. He named it after the Latin botulus (sausage), reflecting the disease's historical association with sausage rather than the organism's morphology.[4][2]
Subsequent work established that botulism could arise from foods other than cured meats; a 1913 Stanford outbreak from a string-bean salad implicated home-canned vegetables, marking an important expansion in recognition of foodborne sources.[3]
Edward Schantz began culturing Clostridium botulinum and developing bulk purification of the toxin in 1944, work that led to the 1946 crystallization of type A botulinum toxin.[4]
In 1949, Arnold Burgen demonstrated that botulinum toxin acts by blocking acetylcholine release at the neuromuscular junction—the mechanistic basis for both the disease and its later therapeutic use.[5][4]
From poison to therapy (1968–1989)
Modern therapeutic use originated with ophthalmologist Alan B. Scott, who—building on Daniel Drachman's observation that botulinum neurotoxin weakened chick hind-limb muscles—contacted Edward J. Schantz at Fort Detrick in 1968 seeking an injectable agent to weaken extraocular muscles as an alternative to strabismus surgery. Schantz, and later Eric A. Johnson, supplied purified botulinum neurotoxin type A.[6]
Crystalline toxin was first injected into rhesus monkeys for strabismus in 1972, Scott published his primate results in 1973, and he first injected a human patient with strabismus in 1977.[6][7]
Scott's product, initially marketed as Oculinum, received its first FDA approvals in December 1989 for strabismus and blepharospasm associated with dystonia in patients 12 years and older. Allergan acquired Oculinum in 1991 and renamed it Botox.[6][8]
Expansion of therapeutic indications (1989–present)
Following the 1989 approval, indications broadened across neurology, ophthalmology, urology, dermatology, and other fields. Major historical milestones include:
- 2000 — onabotulinumtoxinA (Botox) and rimabotulinumtoxinB (Myobloc/NeuroBloc) were approved for cervical dystonia.
- 2002 — onabotulinumtoxinA (Botox Cosmetic) was approved for glabellar lines; the cosmetic effect had been reported by Jean and Alastair Carruthers in 1991.
- 2004 — onabotulinumtoxinA was approved for severe primary axillary hyperhidrosis.
- 2009 — abobotulinumtoxinA (Dysport) was approved; the FDA introduced distinct nonproprietary "-botulinumtoxin" names to distinguish non-interchangeable products.
- 2010 — onabotulinumtoxinA was approved for chronic migraine and upper-limb spasticity; incobotulinumtoxinA (Xeomin) was approved for cervical dystonia and blepharospasm.
- 2011 — onabotulinumtoxinA received FDA approval for urinary incontinence due to neurogenic detrusor overactivity (idiopathic overactive bladder with urge incontinence followed in 2013).[9]
Four botulinum neurotoxin products are described in the source evidence as approved in the United States: onabotulinumtoxinA (Botox), abobotulinumtoxinA (Dysport), incobotulinumtoxinA (Xeomin), and rimabotulinumtoxinB (Myobloc). Their units of potency are not interchangeable.[10][11]
Historical clinical implications
- Kerner (1817–1822) — first detailed clinical description of botulism and early proposal for therapeutic use of the toxin.
- van Ermengem (1895) — isolation of the causative organism.
- Schantz (1944–1946) — purification work leading to crystallization of type A toxin.
- Burgen (1949) — demonstration of blockade of acetylcholine release at the neuromuscular junction.
- Scott and Schantz (1968–1977) — development of therapeutic botulinum toxin for strabismus, progressing from the initial collaboration to animal studies and the first human treatment.
- FDA approval (1989) — beginning of the modern approved therapeutic era with Oculinum.
The historical development of independently manufactured botulinum neurotoxin products also explains why their potency units are not interchangeable; units should not be converted between products using a simple equivalence factor.[8][10]
References
- ↑ Erbguth FJ (2007). "From Poison to Remedy: The Chequered History of Botulinum Toxin". Journal of Neural Transmission. doi:10.1007/s00702-007-0728-2. PMID 17458494.
- ↑ 2.0 2.1 Erbguth FJ (2004). "Historical notes on botulism, Clostridium botulinum, botulinum toxin, and the idea of the therapeutic use of the toxin". Movement Disorders. 19 (Suppl 8): S2–S6. doi:10.1002/mds.20003. PMID 15027048.
- ↑ 3.0 3.1 3.2 Patil S; Willett O; Thompkins T; et al. (2016). "Botulinum Toxin: Pharmacology and Therapeutic Roles in Pain States". Current Pain and Headache Reports. 20 (3): 15. doi:10.1007/s11916-016-0545-0.
- ↑ 4.0 4.1 4.2 Jankovic J (2017). "Botulinum toxin: State of the art". Movement Disorders. 32 (8): 1131–1138. doi:10.1002/mds.27072.
- ↑ Comella CL; Pullman SL (2004). "Botulinum toxins in neurological disease". Muscle & Nerve. 29 (5): 628–644. doi:10.1002/mus.20033.
- ↑ 6.0 6.1 6.2 Johnson EA (2026). "Manufacture of the first FDA-approved batches of 900 kilodalton crystalline type a botulinum toxin for clinical use: a personal remembrance". Journal of Neural Transmission. 133 (6): 939–944. doi:10.1007/s00702-026-03124-0.
- ↑ Scott AB; Fahn S; Brin MF (2023). "Treatment of Strabismus and Blepharospasm With Botox (onabotulinumtoxinA): Development, Insights, and Impact". Medicine. 102 (Suppl 1): e32374. doi:10.1097/MD.0000000000032374. PMID 37499080 Check
|pmid=value (help). - ↑ 8.0 8.1 Dressler D (2016). "Botulinum toxin drugs: brief history and outlook". Journal of Neural Transmission. 123 (3): 277–279. doi:10.1007/s00702-015-1478-1.
- ↑ U.S. Food and Drug Administration. FDA Orange Book: Approved Drug Products with Therapeutic Equivalence Evaluations. OnabotulinumtoxinA (Botox). 2024.
- ↑ 10.0 10.1 Jankovic J (2013). "Medical treatment of dystonia". Movement Disorders. 28 (7): 1001–1012. doi:10.1002/mds.25552.
- ↑ Mills R; Bahroo L; Pagan F (2015). "An Update on the Use of Botulinum Toxin Therapy in Parkinson's Disease". Current Neurology and Neuroscience Reports. 15 (1): 511. doi:10.1007/s11910-014-0511-3.