BOTULISM—A Rare, But Deadly Disease

Botulism is a rare, life-threatening paralytic illness caused by neurotoxins produced by an anaerobic, gram-positive, spore-forming bacterium, Clostridium botulinum.[1]  Unlike Clostridium perfringens, which requires the ingestion of large numbers of viable cells to cause symptoms, the symptoms of botulism are caused by the ingestion of highly toxic, soluble exotoxins produced by C. botulinum while growing in foods.[2]  These rod-shaped bacteria grow best under anaerobic (or, low oxygen), low-salt, and low-acid conditions.[3]  Bacterial growth is inhibited by refrigeration below 4° C., heating above 121° C, and high water-activity or acidity.[4]  And although the toxin is destroyed by heating to 85° C. for at least five minutes, the spores formed by the bacteria are not inactivated unless the food is heated under high pressure to 121° C. for at least twenty minutes.[5] C. botulinum bacteria and spores are widely distributed in nature, because they are indigenous to soils and waters.[6] They occur in both cultivated and forest soils, bottom sediment of streams, lakes, and coastal waters, in the intestinal tracts of fish and mammals, and in the gills and viscera of crabs and other shellfish.[7]

The incidence of foodborne botulism is extremely low.[8]  Nonetheless, the extreme danger posed by the bacteria has required that “intensive surveillance is maintained for botulism cases in the United States, and every case is treated as a public health emergency.”[9] This danger includes a mortality rate of up to 65% when victims are not treated immediately and properly.[10] Most of the botulism events[11] that are reported annually in the United States are associated with home-canned foods that have not been safely processed.[12]  Occasionally, though, commercially-processed foods are implicated as the source of a botulism events, including sausages, beef stew, canned vegetables, and seafood products.[13]

Symptoms of Botulism

After their ingestion, botulinum neurotoxins are absorbed primarily in the duodenum and jejunum, pass into the bloodstream, and travel to synapses in the nervous system.[14] There, the neurotoxins cause flaccid paralysis by preventing the release of acetylcholine, a neurotransmitter, at neuromuscular junctions, thereby preventing motor-fiber stimulation.[15] The flaccid paralysis progresses symmetrically downward, usually beginning with the eyes and face before moving to the throat, chest, and extremities.[16] When the diaphragm and chest muscles become fully involved, respiration is inhibited and, unless the patient is ventilated, death from asphyxia results.[17]

Classic symptoms of botulism include nausea, vomiting, fatigue, dizziness, double vision, drooping eyelids, slurred speech, difficulty swallowing, dryness of skin, mouth, and throat, lack of fever, muscle weakness, and paralysis.[18]  Infants with botulism appear lethargic, feed poorly, are constipated, and have a weak cry and poor muscle tone.[19] Throughout all such symptoms, the victims are fully alert and the results of sensory examination are normal.[20]

In foodborne botulism cases, symptoms usually begin anywhere between 12 and 72 hours after the ingestion of toxin-containing food.[21]  Longer incubation periods—up to 10 days—are not unknown, however.  The duration of the illness is from 1 to 10 (or more) days, depending on host-resistance, the amount of toxin ingested, and other factors.[22]  Full recovery often takes from weeks to months.[23] And, as earlier indicated, mortality rate can be from 30% to 65%, with rates generally lower in European countries than in the United States.[24]

Detection and Treatment  of Botulism

Although botulism can be diagnosed based on clinical symptoms, its differentiation from other diseases is often difficult—especially in the absence of other known persons affected by the condition.[25] Once suspected, the most direct and effective way to confirm the diagnosis of botulism in the laboratory is testing for the presence of the botulinum toxin in the serum, stool, or gastric secretions of the patient.[26]  The food consumed by the patient can also be tested for the presence of toxins.[27]  Currently, the most sensitive and widely used method for the detection of the toxins is the mouse neutralization test, which involves injecting serum into mice and looking for signs of botulism.[28]  This test typically takes 48 hours, while the direct culturing of specimens takes 5-7 days.[29] Some cases of botulism may go undiagnosed because symptoms are transient or mild, or are misdiagnosed as Guillain-Barre Syndrome.[30]

If diagnosed early, foodborne botulism can be treated with an antitoxin that blocks the action of toxin circulating in the blood.[31] This can prevent patients from worsening, but recovery still takes many weeks.[32] The mainstay of therapy is supportive treatment in intensive care, and mechanical ventilation in case of respiratory failure, which is common.[33]

Long-Term and Permanent Injury

Although a minority of botulism patients eventually recover their pre-infection health, the majority do not. For those who fully recover, the greatest improvement in muscle strength occurs in the first three months after the acute phase of illness.[34]  The outside limit for such improvement appears, however, to be one year.[35]  Consequently, physical limitations that still exist beyond the one-year mark are more probably than not permanent.  Recovery from acute botulism symptoms may also be followed by persistent psychological dysfunction that may require intervention.[36]

According to a recently-published study that tracked the long-term outcomes of 217 cases of botulism, a large majority of patients reported “significant health, functional, and psychosocial limitations that are likely the consequences of the illness.”[37]  These limitations included: fatigue, weakness, dizziness, dry mouth, and difficulty lifting things.  The victims also reported difficulty breathing caused by moderate exertions, such as walking or lifting heavy items.  They were also more likely to have limitations in vigorous activities, like running or playing sports, climbing up three flights of stairs, or carrying groceries. Summarizing its finding, the study concluded that:

Even several years after acute illness, patients who had botulism were more likely than control subjects to experience fatigue, generalized weakness, dizziness, dry mouth, difficulty lifting things, and difficulty breathing caused by moderate exertion….In addition, patients…reported worse overall psycho-social status than did control subjects, with patients being significantly less likely to report feeling happy, calm and peaceful, or full of pep.[38]

There is, as a result, no question that the damaging effects of botulism are life-long.

[1]           See J. Sobel, et al., Foodborne Botulism in the United States, 1990-2000, Emerging Infectious Diseases, Vol. 10, No. 9, at 1606 (Sept. 2004).

[2]           James M. Jay, MODERN FOOD MICROBIOLOGY, 466 (6th Ed. 2000)

[3]           Id. at 469-71; see also Sobel, supra note 2, at 1606.

[4]           Sobel, supra note 2, at 1606.

[5]           Id.

[6]           Jay, supra note 3, at 467-69.  See also, generally H. Houschild, Clostridium Botulinum, in FOODBORNE BACTERIAL PATHOGENS, at 112-89  (M. Doyle Ed. 1989)

[7]           Jay, supra note 3, at 467-69.

[8]           Sobel, supra note 2, at 1607-09; Jay, supra note 3, at 472-76.

[9]           Sobel, supra note 2, at 1606-07 (also noting that the CDC maintains a 24-hour clinical consultation and emergency antitoxin release service).

[10]          Jay, supra note 3, at 474.

[11]          With botulism, the broader term “event” is used to encompass both outbreaks—i.e., two or more cases of botulism caused by a common-source, as well as individual (or sporadic) cases.

[12]          Sobel, supra note 2, at 1610; Jay, supra note 3, at 474.

[13]          Id.

[14]          Thomas P. Bleck, Clostridium botulinum (Botulism), in MANDELL, DOUGLAS AND BENNETT’S PRINCIPLES AND PRACTICE OF INFECTIOUS DISEASE 2543, 2544 (5th ed. 2000).

[15]          Id.; Sobel, supra note 2, at 1606.

[16]          Bleck, supra note 15, at 2545; see also BOTULISM FACT SHEET, National Agricultural Bio-Security Center, Kansas State University, online at http://nabc.ksu.edu/content/factsheets/category/Botulism#f26

[17]          Bleck, supra note 15, at 2545; Sobel, supra note 2, at 1606.

[18]          Sobel, supra note 2, at 1606; Jay, supra note 3, at 474.

[19]          Jay, supra note 3, at 476-77.

[20]          Sobel, supra note 2, at 1606.

[21]          Jay, supra note 3, at 474.

[22]          Id.

[23]          R. Shapiro, et al., Botulism in the United States: A Clinical and Epidemiologic Review, Ann. Intern. Med. 1998; 129:221-28.

[24]          Jay, supra note 3, at 474.

[25]          Bleck, supra note 15, at 2546 (noting that “botulism has a limited differential diagnosis”).

[26]          Sobel, supra note 2, at 1607; see also FDA/CFSAN Bad Bug Book, Clostridium Botulinum, available at http://vm.cfsan.fda.gov/~mow/chap2.html

[27]          Id.

[28]          Bleck, supra note 15, at 2546.  See also, e.g. MMWWR, supra note 1, at 2 (“CDC detected botulinum toxin Type A by mouse bioassay in the man’s serum sample”).

[29]          Bad Bug Book, supra note at 25.

[30]          Sobel, supra note 2, at 1606; Shapiro, supra note 23, at 223.

[31]          Jay, supra note 3, at 474; Sobel, supra note 2, at 1606.

[32]          Id.; Bleck, supra note 15, at 2546-67.

[33]          Sobel, supra note 2, at 1606.

[34]          Bleck, supra note 15, at 2547. See also P. Wilcox, et al., Recovery of Ventilatory and Upper Airway Muscles and Exercise Performance After Type-A Botulism, Chest, 98:620-26 (1990); J. Mann, et al., Patient Recovery From Type-A Botulism: Morbidity Assessment Following a Large Outbreak, Am. J. Public Health, 71 (3):266-69 (Mar. 1981).

[35]          Id.

[36]          Bleck, supra note 15, at 2547. See also F. Cohen, et al., Physical and Psychosocial Health Status 3 Years After Catastrophic Illness—Botulism, Issues Mental Health Nurs., 9:387098 (1988)

[37]          S. Gottlieb, et al., Long-Term Outcomes of 217 Botulism Cases in the Republic of Georgia, Clin. Infectious Disease, 45: 174-80, at 180 (220&).

[38]          Id. at 179.

34380zdyq33t7dg-300x225The Tokyo Metropolitan Government has announced that a 6-month-old Adachi Ward boy died of infant botulism after his family gave him honey.

According to the metro government, it is the first death caused by infant botulism reported in Japan since 1986, when statistics started being kept.

The government warned that babies younger than 1 should not be given honey, after announcing on Friday that the boy died on March 30. Government officials said the boy had been having coughs since Feb. 16, and was taken to a hospital by ambulance on Feb. 20 after developing convulsions and suffering respiratory failure. He was diagnosed as having infant botulism on Feb. 28.

They said that the boy’s family had been giving him honey by mixing it into juice twice a day for about a month, and that the family told them they were not aware babies should not be given honey.

The bacteria Clostridium botulinum was found from an unsealed honey container kept at the boy’s house and in the boy’s stool, and a public health center confirmed that the boy’s death was caused by botulism poisoning.

Phil-am Trading, Inc. of Jersey City, NJ is recalling Phil-am Smoked Mackerel (Hasa-Hasa), because it has the potential to be contaminated with Clostridium botulinum, a bacterium which can cause life-threatening illness or death. Consumers are warned not to use the product even if it does not look or smell spoiled.

Botulism, a potentially fatal form of food poisoning, can cause the following symptoms: general weakness, dizziness, double-vision and trouble with speaking or swallowing. Difficulty in breathing, weakness of other muscles, abdominal distension and constipation may also be common symptoms. People experiencing these problems should seek immediate medical attention.

Phil-am Smoked Mackerel (Hasa-Hasa) was distributed in New Jersey, New York, Georgia and Pennsylvania.

Phil-am Smoked Mackerel (Hasa-Hasa) comes in 200 g. (7.05 oz) packs and is packaged in a clear flexible plastic pouch and is topped by a predominantly red tag affixed to the top seal which has the product’s information. Its UPC code is 814487015147, and the product was distributed to stores between February and November 2016. Stores will be notified of their receipt of product and will be provided with recall instructions.

NYSDAM laboratory and sampling analysis revealed that the product is uneviscerated.

No illnesses have been reported to date.

Homemade of Leavenworth, Washington is recalling pickle and sauce products because they may have been improperly produced. Washington State Department of Agriculture routine sampling discovered that a bottle of Homemade Bread and Butter Pickles had a pH level high enough to allow the growth of Clostridium botulinum. Required records were not available to support that safe processing guidelines were followed on all sauce and pickle products produced at Homemade.

Foodborne botulism is a severe type of food poisoning caused by the ingestion of foods containing the potent neurotoxin formed during growth of the organism. Foodborne botulism can cause the following symptoms: general weakness, dizziness, double-vision and trouble with speaking or swallowing. Difficulty in breathing, weakness of other muscles, abdominal distension and constipation may also be common symptoms. People experiencing these problems should seek immediate medical attention. Consumers are warned not to use the product even if it does not look or smell spoiled.

Recalled products are packaged in clear glass bottles with metal caps. There are no lot codes or expiration dates on recalled products. The following products have been recalled:

Bread and Butter Pickles (16 oz./454 g)
Icicle Pickles (16 oz./454 g)
Pickled Beets (16 oz./454 g)
Chili Sauce (12 oz./340 g)
Lite BBQ Sauce (12 oz./ 340 g)
Medium BBQ Sauce (12 oz./340 g)
Hot BBQ Sauce (12 oz./340 g)
Horseradish BBQ Sauce (12 oz./340 g)

The recalled products were sold from small retailers and fruit stands in Chelan and Douglas counties in Washington State.

Scientific American reports that Scientists have discovered a new strain—the first in 40 years—of Clostridium botulinum, the bacterium that is ultimately responsible for causing botulism. And although they have reported their findings in a scientific journal, the investigators have taken the extraordinary step of withholding key details of the discovery. That’s because the toxins made by C. botulinum are the most dangerous known to humankind and currently there is no antidote for a toxin generated by the new strain. The fear is that malevolent organizations or rogue governments might use the information to reverse engineer their own version of the new bug, making it a potent and real bioterrorism threat.

The public is being warned not to eat Central-Epicure Gefilte Fish, Ready to Serve, Sweet and Savoury.

The Canadian Food Inspection Agency says the product may be contaminated with the bacteria that can cause botulism, a sometimes life-threatening illness.

The fish was sold in Ontario and Quebec in 600 gram packages with a best before date of April 13, 2013 (UPC code 061279 00440 3 & 061279 00440 7).

So far no reported illnesses have been linked the fish.

The manufacturer, Central-Epicure Food Products Ltd., of Toronto, has recalled the affected products from the marketplace and the CFIA is monitoring the recall.

The California Department of Public Health (CDPH) is warning consumers not to eat Harry’s Berries Salsa (mild or hot flavors) or Harry’s Berries Dilled Beans, packed by Gean Farms, Inc., because they may have been improperly produced, making them susceptible to contamination with Clostridium botulinum. No illnesses have been linked to any of the affected products at this time.

Gean Farms, Inc., of Oxnard, California, is voluntarily recalling the products after CDPH discovered they were produced without the required controls to prevent botulism toxin. Ingestion of botulism toxin from improperly processed foods can lead to serious illness and death.

These products were sold under the Gean Farms, Inc. label and packaged in one-pint glass canning jars with screw-on metal lids, labeled as “Harry’s Berries Salsa” and “Harry’s Berries Dilled Beans.” These products do not contain production or date codes. Additional product information, including photos of affected products, can be found on the CDPH website.

The products were sold between May 2011 and November 2012 at certified farmers markets in Los Angeles, Ventura and Santa Barbara counties.

Botulism toxin is odorless and colorless. Symptoms generally begin 18- to-36 hours after eating contaminated food, but can occur as early as six hours, or as late as ten days. Symptoms typically begin with blurred or double vision, followed by trouble speaking and swallowing, progressing to muscle weakness that starts in the upper body. Botulism can lead to life-threatening paralysis of the muscles used in breathing.

Bad Bug Book – Foodborne Pathogenic Microorganisms and Natural Toxins – Second Edition

botulism.jpg1. Organism

Clostridium botulinum is an anaerobic, Gram-positive, spore-forming rod that produces a potent neurotoxin. The spores are heat-resistant and can survive in foods that are incorrectly or minimally processed.

Seven types of botulinum are recognized (A, B, C, D, E, F and G), based on the antigenic specificity of the toxin produced by each strain. Types A, B, E and F cause human botulism. (Types C and D cause botulism in animals. Types C and E also cause botulism in birds. No outbreaks of type G have been reported.) Most strains produce only one type of toxin, but strains producing dual toxin types have been reported.

The organism and its spores are widely distributed in nature. They are found in both cultivated and forest soils; bottom sediments of streams, lakes, and coastal waters; in the intestinal tracts of fish and mammals; and in the gills and viscera of crabs and other shellfish.

(Another species of Clostridium, i.e., perfringens, causes foodborne illness, but does not cause botulism. It is addressed in another chapter.)

2. Disease

Overview: Botulism is a serious,
sometimes fatal, disease caused by a potent
neurotoxin formed during growth of C. botulinum. The infection results in flaccid paralysis of muscles, including those of the respiratory tract. Three major types of botulism are known, two of which will be discussed in this chapter: foodborne botulism and infant botulism, which also is foodborne. The third type, wound botulism, is not foodborne and will not be covered extensively in this chapter.

Botulinum toxin causes flaccid paralysis by blocking motor nerve terminals at the neuromuscular junction. The flaccid paralysis progresses symmetrically downward, usually starting with the eyes and face, to the throat, chest, and extremities. When the diaphragm and chest muscles become fully involved, respiration is inhibited and, without intervention, death from asphyxia results.

Foodborne botulism is a severe type of food poisoning caused by ingestion of foods containing the toxin produced by C. botulinum. This type of botulism most often develops after consumption of improperly processed and inadequately cooked home-preserved foods. Home- canned or, occasionally, commercially produced foods have been involved in botulism outbreaks in the United States. Although the incidence of the disease is low, the disease is of considerable concern because of its high mortality rate if not treated immediately and properly.

Infant botulism is a serious illness caused by ingestion of C. botulinum spores that colonize and produce toxin in the intestinal tracts of infants (i.e., intestinal toxemia botulism).

Wound botulism is the rarest form of botulism and is discussed only briefly here, because it does not involve food. It results when C. botulinum colonizes in a wound and produces toxins, which reach other parts of the body via the bloodstream. Whereas foodborne botulism is limited to the amount of toxin ingested, C. botulinum in wounds produce toxin in situ (gas gangrene) until the pathogen is gone.

A fourth, “undetermined” category consists of adult cases in which a food or wound source cannot be identified. It has been suggested that some cases of botulism assigned to this category might result from intestinal colonization in adults, with in vivo production of toxin.

The medical literature suggests the existence of an adult form of botulism similar to infant botulism. In these cases, patients have had surgical alterations of the gastrointestinal tract and/or antibiotic therapy. It is proposed that these procedures may have altered the normal bacterial population of the gut and allowed C. botulinum to colonize the intestinal tract.

Recommended treatment for foodborne botulism includes early administration of botulinum antitoxin, available from the Centers for Disease Control and Prevention (CDC), and intensive supportive care, including mechanical breathing assistance. An antitoxin for infant botulism (Botulism Immune Globulin Intravenous, abbreviated BIG-IV) also is available and should be administered as early in the illness as possible. Antimicrobial therapy is not recommended, due to concerns about increased toxin release as a result of cell lysis.

• Mortality: The mortality rate is high if treatment is not immediately administered. The disease is generally fatal in 5% to 10% of cases.

• Infective dose: An extremely small amount – a few nanograms – of the toxin can cause illness.

• Onset:
Adult: Usually 18 to 36 hours after ingesting food containing the toxin, although times 
have varied from 4 hours to 8 days. 
Infant: Generally follows a period of normal development.

• Illness / complications: See above.

• Symptoms:

Adult: Initial symptoms may include double vision, blurred vision, drooping eyelids, slurred speech, difficulty swallowing, dry mouth, and muscle weakness. If the disease is not treated, symptoms may progress to paralysis of the arms, legs, trunk, and respiratory muscles.

Early signs of intoxication consist of marked lassitude, weakness and vertigo, usually followed by double vision and progressive difficulty in speaking and swallowing. Difficulty in breathing, weakness of other muscles, abdominal distention, and constipation may also be common symptoms

Infant: Constipation after a period of normal development is often the first sign of infant botulism. This is followed by flat facial expression; poor feeding (weak sucking); weak cry; decreased movement; trouble swallowing, with excessive drooling; muscle weakness; and breathing problems.

• Duration: Patients with severe cases that involve paralysis of the respiratory muscles may need mechanical ventilation and intensive care for weeks or months.

• Route of entry: Oral, for foodborne infection. (Infection of wounds also occurs).

• Pathway: Clinical presentation develops after a person ingests the pre-formed toxin, or if the organisms grow in the intestines or in wounds, followed by toxin release. The ingested botulinum toxin (an endopeptidase enzyme) blocks peripheral cholinergic neurotransmission at the neuromuscular junction and cholinergic autonomic nervous system. The toxin acts by binding presynaptically to high-affinity recognition sites on the cholinergic nerve terminals and decreasing the release of acetylcholine, causing a neuromuscular blocking effect. (This mechanism laid the foundation for development of the toxin as a therapeutic tool; e.g., when temporary inactivation of specific muscles is needed for therapeutic or cosmetic purposes.) 
C. botulinum produces the toxin as a complex of proteins, among which is the neurotoxic moiety. The toxin is synthesized as a relatively inactive single-chain polypeptide with a molecular weight of ~150 kDa. It becomes an active toxin by selective proteolytic cleavage to yield the heavy and light chains that are linked by a single disulphide bond and non-covalent interactions. The toxin’s light chain is a Zn++-containing endopeptidase that blocks acetylcholine-containing vesicles from fusing with the terminal membrane of the motor neuron, resulting in flaccid muscle paralysis.

3. Frequency

As noted, the incidence of the disease is low, but the mortality rate is high, if the disease is not treated immediately and properly. Some cases of botulism may go undiagnosed because symptoms are transient or mild or are misdiagnosed as Guillain-Barré syndrome.

4. Sources

General info: The types of foods involved in botulism vary according to food preservation and cooking practices. Any food conducive to outgrowth and toxin production can be associated with botulism. This can occur when food processing allows spore survival and the food is not subsequently heated before consumption, to eliminate any live cells.

Almost any type of food that is not very acidic (pH above 4.6) can support growth and toxin production by C. botulinum. Salt concentration from 4% to 5% is needed for inhibition of its spores (especially regarding type E), with a 5% concentration completely inhibiting their growth. Salt concentrations slightly lower than those providing inhibition tend to extend spore outgrowth time at low temperatures.

A variety of foods, such as canned corn, peppers, green beans, soups, beets, asparagus, mushrooms, ripe olives, spinach, tuna fish, chicken and chicken livers, liver pate, luncheon meats, ham, sausage, stuffed eggplant, lobster, and smoked and salted fish have been associated with botulinum toxin.

Infant botulism: Of the various potential environmental sources, such as soil, cistern water, dust, and foods, honey is the one dietary reservoir of C. botulinum spores linked to infant botulism by both laboratory and epidemiologic studies. Honey should not be fed to infants under 12 months of age.

5. Target Populations

All people are believed to be susceptible to botulism.

6. Diagnosis

Although botulism can be diagnosed by clinical symptoms alone, differentiation from other diseases may be difficult. The most direct and effective way to confirm the clinical diagnosis of botulism in the laboratory is to demonstrate the presence of toxin in the serum or feces of the patient or in the food the patient consumed. Currently, the most sensitive and widely used method for detecting toxin is the mouse neutralization test. This test takes 48 hours. Culturing of specimens takes 5 to 7 days.

7. Food Analysis

Since botulism is foodborne and results from ingestion of preformed C. botulinum toxin, determination of the source of an outbreak is based on detection and identification of toxin in the food involved. The most widely accepted method is the injection of extracts of the food into passively immunized mice (mouse neutralization test). The test takes 48 hours. This analysis is followed by culturing all suspect food in an enrichment medium, for detection and isolation of the causative organism.

8. Examples of Outbreaks

See CDC information on surveillance and investigation.

9. Other Resources

• Loci index for genome Clostridium botulinum is available from GenBank.

• CDC’s Emergency Preparedness and Response for Botulism.

Continue Reading Bad Bug Book – Foodborne Pathogenic Microorganisms and Natural Toxins – Second Edition – Clostridium botulinum – Botulism

A story of a young man temporarily paralyzed by the neurotixin produced by Clostridium botulinum: 

In 36 hours he went from being a young healthy college student to complete paralysis and being kept alive by tubes and machines.

A rare illness almost stole Brent Ocker’s life. The U of L graduate says his toughest test was far from the classroom.

Brent Ocker has earned a master’s degree in Sports Administration and at just 26 years old learned lessons most will never know. “A year ago I was on my death bed,” he says. That was September 10, 2010. He says he, “woke up that day felt very dizzy, blurred vision, and I couldn’t walk straight…My lungs were collapsing and I was unable to breathe.”

Ocker says doctors went into a guess-and-check method of diagnosis Like a medical mystery from a television drama. First they thought he had vertigo, then maybe meningitis.

“Botulism was down here, no one was even beginning to contemplate that,” he says. But that was the diagnosis.

Botulism is a neuro-cognitive disorder where bacteria that Ocker ingested started in the brain and attacked the nerve ending that sent messages to his muscles.

“I have paralysis,” he says, “I am essentially trapped in my own body. I can hear but I can’t see or move. It was really frightening.”

Botulism is so rare the federal government guards the antidote. As doctors waited for it to be flown in from Georgia, they told his family the drug is so strong 25 percent of patients die during treatment.

Even though the drug was working, Ocker had to withdraw from U of L because he had two more months in 24-hour rehab facilities learning to live again.

But friends rallied around him, hosting fundraisers to help with his seven-digit medical bills. U of L professor Mary Hums says, “The one thing I remember really well was the first day he came back to school to set up his semester, and that was an emotional meeting. I’ll admit it I cried.”

Ocker says, “I could literally only come to class because I could only be on my feet about 15 to 20 minutes from strength.” But he pushed through: “Absolutely, this is the toughest test.”

He will graduate Friday with University’s Alice Eaves Barns Award, which is given to just one master student each semester who has triumphed in the face of adversity.

And what has he learned? “The power that people have to love.”

The Food Safety Authority of Ireland announced the withdrawal of all products produced by Bio Gaudiano, the Italian company that manufactured and distributed botulism-tainted olives that have sickened several people, claiming the life of a woman from Helsinki, Finland.  Some of the recalled olives were distributed to companies in the United States, including to distributors in Massachussetts and United Natural Foods, who sent the FoodMatch Inc., Divina Stuffed Olives to many different states.

The withdrawal of Bio Gaudiano’s entire product line is an expansion of an earlier recall of Bio Gaudiano’s almond stuffed olives.  Foodborne botulism often occurs due to improper canning practices–i.e. failure to bring the product to a temperature sufficient to kill, or inactivate, the botulism bacteria–with low acid content foods, such as asparagus, green beans, beets and corn.  When the bacteria are not killed, under the right conditions the still-viable bacteria can germinate and produce the dangerous toxins that cause cases of botulism. 

It is likely that the investigation into Bio Gaudiano’s botulism outbreak and recall revealed that the companies practices, generally, were insufficient to prove that botulism bacteria had been killed during canning or bottling, resulting in the withdrawal of the company’s entire line of products.