Clostridium botulinum

Clostridium botulinum has a close connection to the craft, including in its name. Clostridium comes from the Greek kloster, a spindle, for the shape of the spore-swollen cell; botulinum comes from the Latin botulus, a sausage. It is named after sausage because the disease was, for most of its recorded history, associated with sausages. A series of well-documented outbreaks in Wurttemberg, in southern Germany, led the district medical officer Justinus Kerner to write the first full description of food-borne botulism between 1817 and 1822. He named the unknown agent Wurstgift, sausage poison, and suggested it might one day have a medical use, which it later did, as Botox. The word botulism was coined in 1870, and in 1895 Emile van Ermengem isolated the bacterium from smoked and pickled ham eaten at a funeral in the Belgian village of Ellezelles. He named it Bacillus botulinus; it was moved to the genus Clostridium in 1917.

It is a gram-positive, obligately anaerobic, spore-forming rod, and both properties matter. Obligately anaerobic means it grows only where oxygen is excluded. Spore-forming means it survives: the spores are heat-resistant and pass through ordinary cooking, so cooking kills the growing cell but leaves spores that can germinate later. The hazard is not the cell but the toxin it produces, botulinum neurotoxin, the most poisonous substance known. It is an enzyme that cuts the proteins a nerve ending needs to release acetylcholine, so the signal from nerve to muscle stops and a descending paralysis follows, which is fatal if it reaches the muscles of breathing.

For the curesmith the species divides into two groups. Group I, the proteolytic strains, produce toxin types A and B, have highly heat-resistant spores, and tolerate salt, acid and nitrite relatively well; they grow best near blood heat and are the strains behind botulism in ambient dry-cured and canned products. Group II, the non-proteolytic strains, produce types B and E, have less heat-resistant spores, and grow down to about 3 degrees C; they are the risk in chilled, vacuum-packed and cold-smoked foods, and type E is the marine type associated with cold-smoked fish. Because Group II grows in the cold, refrigeration alone is not a sufficient control.

**How it endangers cured meat.** The spores are widespread, in soil, dust, sediment, on hides and in the gut, and they reach the surface of the meat. Where they become dangerous depends on the form of the product. In an intact whole muscle the interior is essentially sterile, so surface spores are the only route and a whole-muscle cure carries low risk on that count, with one exception: in a large brine- or dry-cured ham the deep centre can become anaerobic and spoil before salt and cure reach it, which is part of why long cures use nitrate as a reservoir and why the cure must reach the core. The main risk is in comminuted and stuffed products. Grinding distributes surface spores through the whole mass, and stuffing into a casing provides the anaerobic core they need, so dry-cured and fermented sausages are the principal concern, controlled by nitrite together with a prompt fall in pH and water activity. Smoked products are the other setting to watch: warm- and cold-smoking hold meat or fish in the danger zone with little oxygen, and cold-smoked fish carrying type E is a recognised botulism vehicle, as are vacuum-packed smoked products.

The Safety Triangle and the curing salts exist largely to control this organism. The figures are specific: Group I is stopped by a water activity below about 0.94 or a pH below 4.6, and Group II by a water activity of about 0.97 and a pH of about 5.0. Because cold does not stop Group II, and salt and acid alone are not sufficient, nitrite is the specific hurdle, and Cure #1 is used first of all to control it. The toxin, unlike the spore, is destroyed by proper boiling, but the correct approach is to prevent its formation, not to rely on destroying it.