C. botulinum produces heat-resistant endospores that are commonly found in soil and are able to survive under adverse conditions.

Seven serotypes of toxins have been identified that are allocated a letter (A–G), several of which can cause disease in humans.

C. botulinum producing B and F toxin types have been isolated from human botulism cases in New Mexico and California.

However, these integrations sites are degraded (except for the C and D types), indicating that the C. botulinum acquired the toxin genes quite far in the evolutionary past.

[28] Physiological differences and genome sequencing at 16S rRNA level support the subdivision of the C. botulinum species into groups I-IV.

[32] In the laboratory, C. botulinum is usually isolated in tryptose sulfite cycloserine (TSC) growth medium in an anaerobic environment with less than 2% oxygen.

C. botulinum (groups I through III) is a lipase-positive microorganism that grows between pH of 4.8 and 7.0 and cannot use lactose as a primary carbon source, characteristics important for biochemical identification.

In spore form, it is a heat resistant pathogen that can survive in low acid foods and grow to produce toxins.

[41] Botulinum toxin can be destroyed by holding food at 100 °C for 10 minutes; however, because of its potency, this is not recommended by the USA's FDA as a means of control.

However, pickles are sufficiently acidic to prevent growth;[44] even if the spores are present, they pose no danger to the consumer.

As soon as infants begin eating solid food, the digestive juices become too acidic for the bacterium to grow.

[47] C. botulinum was first recognized and isolated in 1895 by Emile van Ermengem from home-cured ham implicated in a botulism outbreak.

This argument is not accepted by the LPSN and would cause an unjustified change of the type strain under the Prokaryotic Code.

)[29] Dobritsa et al. (2018) argues, without formal descriptions, that group II can potentially be made into two new species.

[56] Physicians may consider the diagnosis of botulism based on a patient's clinical presentation, which classically includes an acute onset of bilateral cranial neuropathies and symmetric descending weakness.

[59][60] A careful history and physical examination is paramount to diagnose the type of botulism, as well as to rule out other conditions with similar findings, such as Guillain–Barré syndrome, stroke, and myasthenia gravis.

Other tests that may be helpful in ruling out other conditions are: Signs and symptoms of foodborne botulism typically begin between 18 and 36 hours after the toxin gets into your body, but can range from a few hours to several days, depending on the amount of toxin ingested.

Additionally if botulism is suspected, patients should be treated immediately with antitoxin therapy in order to reduce mortality.

Immediate intubation is also highly recommended, as respiratory failure is the primary cause of death from botulism.

[77][78][79] In North America, an equine-derived heptavalent botulinum antitoxin is used to treat all serotypes of non-infant naturally occurring botulism.

It has other "off-label" medical purposes, such as treating severe facial pain, such as that caused by trigeminal neuralgia.

[84] Botulinum toxin produced by C. botulinum is often believed to be a potential bioweapon as it is so potent that it takes about 75 nanograms to kill a person (LD50 of 1 ng/kg,[41] assuming an average person weighs ~75 kg); 1 kilogram of it would be enough to kill the entire human population.

[20] A number of quantitative surveys for C. botulinum spores in the environment have suggested a prevalence of specific toxin types in given geographic areas, which remain unexplained.

In Italy, a survey conducted in the vicinity of Rome found a low level of contamination; all strains were proteolytic C. botulinum types A or B.