Common Foodborne Pathogens - VII

Clostridium botulinum Risk Profile 

Clostridium botulinum is gram-positive, spore-forming rod-shaped, an anaerobic bacterium that produces a protein, which has characteristic neurotoxicity. The spores are heat-resistant and can survive in foods that are incorrectly or minimally processed. C. botulinum may grow in foods under certain conditions while producing toxin(s), where a severe form of food poisoning (botulism) results when the toxin-containing foods are ingested. Although it is rare, its mortality rate is high. 
 
There are seven serotypes of C. botulinum have been identified (A, B, C, D, E, F, and G), based on the antigenic specificity of the toxin produced by each strain. Further, types A, B, E, and F cause human botulism, and types C and D cause botulism in animals including birds and fish. Besides, type G outbreaks have never been reported yet. Although most strains produce only one type of toxin, dual toxin-producing strains also been reported. 
 
Spores produced by the C. botulinum are heat-resistant, and both bacterium and the spores are widely distributed in nature. The spores germinate in the absence of oxygen, grow, and excrete toxins. They are found in both cultivated and forest soils, bottom sediments of streams, lakes, and coastal waters as well as in the intestinal tracts of fish and mammals, and on the gills and viscera of crabs and other shellfish.
 
Growth Factors
Temperature:
            Minimum – 10°C      Maximum – 48°C     (Optimum 35 - 40°C)
pH:
            Minimum – 4.6         Maximum – 9.0         (Optimum -)
Water Activity (aW):
            Minimum – 0.93       Maximum – -            (Optimum -)
Water Phase Salt:
            Maximum – 10%     
 
Sources

The food types that are susceptible to botulism vary according to the specific food preservation and cooking practices. Almost any food that is not very acidic, where pH is above 4.6 can be susceptible to the proliferation, growth, and toxin production by C. botulinum. Hence, 4% to 5% salt concentration is required for inhibition of its spores (especially regarding type E), while a 5% salt concentration can completely inhibiting growth. Salt concentrations slightly lower than those providing inhibition tend to extend spore outgrowth time at low temperatures.
 
Thus, any food that is conducive to outgrowth and toxin production of C. botulinum can be associated with botulism, when inadequate food processing practices that will allow survival of spores and that are not subsequently heated before consumption, to eliminate any live cells. 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 can be caused due to 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. 
 
Disease

Botulism is a serious and sometimes fatal, rare non-transmittable foodborne infection caused by C. botulinum due to a potent neurotoxin formed during growth. The recommended treatment for foodborne botulism includes early administration of botulinum antitoxin, and intensive supportive care, including mechanical breathing assistance. An antitoxin for infant botulism (Botulism Immune Globulin Intravenous or BIG-IV) also is available, which should be administered as early in the illness as possible. However, antimicrobial therapy is not recommended, due to concerns about increased toxin release as a result of cell lysis. 
 

Mortality: 

The general fatality of botulinum is in-between 5% to 10% of the cases, but the mortality rate is high if treatment is not immediately administered. 

 

Infective dose: 

An extremely small amount such as “a few nanograms” of the toxin can cause infection.

 

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.

Complications: 

The infection results in flaccid paralysis of muscles due to neurotoxin, including those of the respiratory tract. The botulinum causes flaccid paralysis due to toxin by blocking motor nerve terminals at the neuromuscular junction, which progresses symmetrically downward, usually starting with the eyes and face, to the throat, chest, and extremities. Once the diaphragm and chest muscles become fully involved, respiration is inhibited and death can result from asphyxia without intervention. 

 

There are three major types of botulism are to be known and foodborne botulism and infant botulism, which also is foodborne. The third type, wound botulism, is not a foodborne infection. Nonetheless, there is a fourth undecided category, which might be the result of intestinal colonization in adults, with in vivo production of toxin. 

 

Foodborne botulism – A severe type of food poisoning caused by the ingestion of foods contaminated with the toxin produced by C. botulinum, which mostly develops symptoms often after consumption of improperly processed and inadequately cooked home-preserved foods. Home-canned or, occasionally, commercially produced foods have been involved in botulism outbreaks. Foodborne botulism is a rare occurrence in most commercially produced food products, but of considerable concern, because of its high mortality rate if not treated immediately and properly. 

 

Infant botulism – Colonization of C. botulinum in the intestinal tracts of infants due to the ingestion of spores that produce toxin is a serious infection such as intestinal toxemia botulism. 

 

Wound botulism - The rarest form of botulism and it does not involve food, which occurs when C. botulinum colonizes in a wound and produces toxins. The toxins are transported through 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. 

Symptoms:

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

 

Infant – Constipation is often the first sign of normal development of infant botulism, which 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, botulinum toxins are ingested through improperly processed food in which the bacteria or the spores survive, then grow and produce the toxins. Though mainly a foodborne intoxication, human botulism can also be caused by intestinal infection with C. botulinum in infants, wound infections, and inhalation.

 

Pathway: 

Clinical symptoms develop 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, which is 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. 

 

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. 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 neuron, resulting in flaccid muscle paralysis. 

 
Frequency
Although this food illness is rare, its mortality rate is high if the disease is not treated immediately and properly. There are 962 recorded botulism outbreaks in the United States from 1899 to 1990 involved 2320 cases and 1036 deaths. In outbreaks in which the toxin type was determined, 384 were caused by type A, 106 by type B, 105 by type E, and 3 by type F. In two outbreaks, the foods implicated contained both types A and B toxins. Some cases of botulism may go undiagnosed because symptoms are transient or mild or are misdiagnosed as Guillain-Barré syndrome.
 
Target Populations
All people are believed to be susceptible to botulism.
 
Diagnosis

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

Food Analysis
Determination of the source of an outbreak is usually based on the detection and identification of toxin in the food since botulism results from the ingestion of preformed C. botulinum toxin. Hence, the most widely accepted method is the mouse neutralization test, where extracts of the food injected into passively immunized mice, and results can be obtained in 48 hours. The mouse neutralization is followed by culturing of all suspected food in an enrichment medium, to detect and isolate the causative organism.

Reference:

FDA Bad Bug Book, Foodborne Pathogenic Microorganisms and Natural Toxins. Second Edition. 2013
Preventive Controls for Human Foods. 2016
www.cdc.gov