Common Foodborne Pathogens - IX

Clostridium perfringens Risk Profile 

Clostridium perfringens is an anaerobic and aero-tolerant, gram-positive, spore-forming rod that is relatively cold-tolerant and produces enterotoxins, where its spores are heat-resistant. Nonpathogenic C. perfringens is widely distributed in the environment and is frequently found in the intestines of humans and many domestic and feral animals. The spores persist in soil, sediments, and areas subject to human or animal fecal pollution. Isotype A almost always contains the “cpe” gene or the enterotoxin gene, which causes food poisoning, and types B, C, D, and E sometimes contain this gene among many C. perfringens isotypes found in nature. 
 
Sources 
The actual cause of poisoning happens due to temperature abuse of cooked foods in most instances. C. perfringens can be present in small numbers often after the food is cooked due to germination of its spores, which can survive high heat and can multiply rapidly as a result of a fast doubling time (<10 minutes for vegetative cells), depending on temperature and food matrix. Therefore, during cool-down (109-113°F) and storage of prepared foods, this organism can reach levels that cause food poisoning much more quickly than can other bacteria. Meats (especially beef and poultry), meat-containing products (e.g., gravies and stews), and Mexican foods are important vehicles for C. perfringens foodborne illness, although it is also found on vegetable products, including spices and herbs, and in raw and processed foods. Spores of some C. perfringens strains can survive boiling water for an hour or longer in a relatively protective medium (e.g., a cooked-meat medium, <10 minutes for vegetative cells) depending on temperature and food matrix. Hence, C. perfringens can reach levels that cause food poisoning much more quickly than can other bacteria, during cool-down (109-113°F) and storage of prepared foods.
 

Especially beef and poultry are implicated, other meat varieties and meat-containing products such as gravies and stews, as well as Mexican foods are important vehicles for C. perfringens foodborne infections. C. perfringens is also found on vegetable products, including spices and herbs, and in raw and processed foods, where spores of some C. perfringens strains can survive boiling water for an hour or longer in a relatively protective medium e.g., a cooked-meat medium. 

Growth Factors 

Temperature:

Minimum – 10°C Maximum – 47.1°C Optimum (43 – 47°C)

pH:

Minimum – 5 .0 Maximum – 9.0 Optimum (7.2)

Water Activity (aW):

Minimum – 0.93 Maximum – >0.99 Optimum (0.95 – 0.96)

Water Phase Salt:

Maximum – 7%       

 
Disease 
C. perfringens can cause two types of foodborne infections, and the gastroenteritis form is very common and often is mild and self-limiting. However, it may also develop as more severe gastroenteritis depending on the strain, which leads to damage of the small intestine and, potentially, but rarely, fatality. The second form C. perfringens is enteritis necroticans or “pig-bel disease” or characteristic swollen bellies and other severe symptoms, which is rare in the developed world, but more severe than the other form of the infection, and often fatal. As C. perfringens can replicate much more rapidly than most other bacteria that result in the ingestion of a large number of vegetative cells from both infection forms. Hence, C. perfringens will more quickly reach pathogenic levels in contaminated food left unrefrigerated than other bacteria, and the consumers who eat the food may ingest large doses of the bacterium. 

Mortality 

There were an estimated 26 annual deaths in the United, States according to the Centers for Disease Control and Prevention (CDC) and C. perfringens annually accounts for: 

Common gastroenteritis form - A few deaths resulting from diarrhea-induced dehydration and other complications have been reported, and usually were among debilitated or elderly people. 

Pig-bel form (enteritis necroticans) - This disease is often fatal, and it is extremely rare in the U.S. 

 

Infective dose 

Symptoms are caused by ingestion of large numbers of (> 106) vegetative cells or >106 spores/g of food, where toxin production in the digestive tract (or in vitro) is associated with sporulation, which is characterized as a food infection. 

 

Onset 

Symptoms occur about 16 hours after consumption of foods infected with C. perfringens serotypes that are capable of producing the enterotoxin and containing large numbers of (>106) live vegetative cells or (>106) spores. 

Complications 

Complications are rare in the typical, mild gastroenteritis form of the disease, particularly among people under 30 years of age. However, elderly people are more likely to have prolonged or severe symptoms, as are immunocompromised people. The more severe form of the disease may cause necrosis of the small intestine, peritonitis, and septicemia. 

 

Symptoms 

Gastroenteritis form – Common characteristics include watery diarrhea and mild abdominal cramps. 

Pig-bel form (enteritis necroticans) – Abdominal pain and distention, diarrhea (sometimes bloody), vomiting, and patchy necrosis of the small intestine. 

 

Duration 

The milder form of the disease generally lasts 12 to 24 hours, but symptoms may last 1 to 2 weeks in the elderly or infants. 

 

Route of entry 

Oral. 

 

Pathway 

CPE protein usually is released into the intestines when the vegetative cells lyse on completion of sporulation, where this enterotoxin is responsible for clinical presentation in humans. The enterotoxin induces fluid and electrolyte losses from the GI tract, where the principal target organ for CPE is believed to be the small intestine.

 

Pig-bel disease involves the production of the beta toxin, which is highly trypsin-sensitive, where the effects of low gastrointestinal levels of trypsin appear to have contributed to the progression of the disease. It has been demonstrated that when starvation and high levels of potato consumption which generally contain trypsin inhibitor contributed to low levels of this enzyme in the population. 

 
Frequency 

C. Perfringens poisoning is the second most commonly reported foodborne infection in the U.S, which second only to Salmonella when considering bacterial causes of foodborne infection. The CDC estimates that 965,958 domestically acquired cases occur annually in the United States, where there were 34 outbreaks in 2006 included 1,880 cases excluding isolated cases with an average of 50 to 100 people are affected in one outbreak. Many outbreaks probably go unreported, because the implicated foods and patients’ feces are not tested routinely for C. perfringens or its toxin. 
 
Diagnosis 
C. perfringens poisoning is diagnosed by its symptoms and the typical delayed onset of infection, which is confirmed by detection of the toxin in patients’ feces. The presence of exceptionally large numbers of the bacteria in implicated foods or patients’ fecal samples is also used for bacteriological confirmation. 
 
Target Populations 
Institutional settings, where large quantities of food are prepared several hours before serving such as school cafeterias, hospitals, nursing homes, prisons, etc. are the most common circumstance in which C. perfringens poisoning occurs. The young and elderly are the most frequent victims of C. perfringens poisoning, whereas immunocompromised people are at higher risk of severe infection than are others, such as those with HIV/AIDS or undergoing cancer chemotherapy or immunosuppressive drugs for rheumatoid arthritis or other inflammatory conditions.
 
Food Analysis 

Standard bacteriological culturing methods are applied to determine the C. perfringens in implicated foods and feces of patients, and the serological assays are used for detecting enterotoxin in the feces of patients and for testing the ability of strains to produce toxin. Further identifications are carried out using PCR based methods in modern identification techniques. 

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

Common Foodborne Pathogens - VIII

Shigella spp. Risk Profile

Shigella infection (shigellosis) is an intestinal infection caused by a family of bacteria known as shigella. Shigella is very contagious and the main sign of shigella infection is diarrhea with blood, which is caused by Shigella sonnei, S. boydii, S. flexneri, and S. dysenteriae. Shigellae are Gram-negative, non-motile, non-spore-forming, rod-shaped bacteria. Some strains produce enterotoxins and Shiga toxin, where the latter is very similar to the toxins produced by E. coli O157:H7. Humans are the only host of Shigella, but it has also been isolated from higher primates and it is frequently found in water polluted with human feces. 

Shigellae are very sensitive to environmental conditions die rapidly and heat-sensitive, hence do not survive the pasteurization and cooking temperatures. Shigella species are tolerant to low pH and are able to transit the harsh environment of the stomach. These pathogens can grow in low pH foods, such as some fruits and vegetables, or survive on produce commodities packaged under vacuum or modified atmosphere and can also survive in water, with a slight decrease in numbers.
 
Growth Factors

Temperature:

            Minimum – 6.1°C     Maximum – 47.1°C 

pH:

Minimum – 4.8         Maximum – 9.3        

Water Activity (aW):

Minimum – 0.96       Maximum – -            

Water Phase Salt:

Maximum – 5.2%    

 
Disease

The infection caused by Shigella is shigellosis and also called bacillary dysentery, where diarrhea may range from watery stool to severe, life-threatening dysentery. All Shigella spp. can cause acute, bloody diarrhea, and can spread rapidly through a population under unsanitary conditions with mass populations. S. dysenteriae type 1 causes the most severe disease and is the only serotype that produces the Shiga toxin, which may be partially responsible for cases in which hemolytic uremic syndrome (HUS) develops. On the other hand, S. sonnei produces the mildest form of shigellosis, which is usually watery diarrhea; S. flexneri and S. boydii infections can be either mild or severe.
 

Mortality

The disease usually is self-limiting in healthy people, although some strains are associated with fatality rates as high as 10-15%.

 

Infective dose

As few as 10 to 200 cells can cause disease, depending on the age and condition of the host.

 

Onset

Eight to 50 hours.

 

Complications

The disease usually consists of self-limiting diarrhea in healthy people and the symptom includes fever and stomach cramps, but severe cases, which tend to occur primarily in immunocompromised or elderly people and young children, are associated with mucosal ulceration, rectal bleeding, and potentially drastic dehydration. Potential sequelae of shigellosis include reactive arthritis and hemolytic uremic syndrome.

 

Symptoms

May include abdominal pain; cramps; diarrhea; fever; vomiting; blood, pus, or mucus in stools; tenesmus (straining during bowel movements).

 

Duration

Uncomplicated cases usually resolve in 5 to 7 days. Most of the time, the illness is self-limiting. In some circumstances, antibiotics are given, such as trimethoprim-sulfamethoxazole, ceftriaxone, or ciprofloxacin.

 

Route of entry

The fecal-oral route is the primary means of human-to-human transmission of Shigella. However, the contamination of foods is often due to an infected food handler with poor personal hygiene.

 

Pathway

The disease is caused when Shigella cells attach to, and penetrate, colonic epithelial cells of the intestinal mucosa and they multiply intracellularly while spreading into contiguous epithelial cells, resulting in tissue destruction.

 
Frequency

According to the US Centers for Disease Control and Prevention (CDC), there are about 15,000 domestically acquired foodborne infections of laboratory-confirmed isolates are reported each year, with estimates of actual occurrence ranging from 24,511 to 374,789 cases (average of 131,243) and about 31% of them estimated to be foodborne. Nonetheless, most of the foodborne infections are caused by 31 different pathogens, where Shigella is ranked as the sixth most frequent cause after norovirus, Salmonella species, Clostridium perfringens, Campylobacter, and Staphylococcus aureus. Shigellosis appears to follow seasonal variations, and the highest incidences generally occur during the warmer months of the year in developed countries.
  
Diagnosis
Diagnosis is by serological or molecular identification of cultures isolated from the stool, but Shigella may be more difficult to cultivate if stool samples are not processed within a few hours. However, cultivating Shigella spp is relatively difficult and depends on the amount of time within which stool or food samples are collected and processed. In terms of growth, shigellae are not particularly fastidious in their requirements and, in most cases, the organisms are routinely cultivated in the laboratory, on artificial media.
 
Target Populations
Everyone in the community is susceptible to shigellosis, but children 1 to 4 years old, the elderly, and the immunocompromised are most at risk to some degree. Further, Shigellosis is very common among people with AIDS and AIDS-related complex.
 
Food Analysis

A molecular-based method (PCR) that targets a multi-copy virulence gene has been developed and implemented by the FDA. Improvements in the bacterial isolation method continue as Shigellae remain a challenge to isolate from foods. The window for collecting and processing Shigella from foods, for cultivation, maybe days rather than hours, as is the case with stool, depending on the food matrix and storage conditions, such as temperature. Shigella species can be outgrown by the resident bacterial populations found in foods, which may reflect the usual low numbers of the organism present in foods, or a very large number of non-Shigella bacteria in some foods. The physiological state of the pathogen at the time of analysis may be another factor that reduces the chance of isolating Shigella from foods. Environmental conditions could affect its ability to either grow or survive in any food matrix.

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