| Clostridium perfringens | |
|---|---|
 | |
| Photomicrograph of Gram-positiveClostridium perfringens bacilli | |
Scientific classification | |
| Domain: | Bacteria |
| Kingdom: | Bacillati |
| Phylum: | Bacillota |
| Class: | Clostridia |
| Order: | Eubacteriales |
| Family: | Clostridiaceae |
| Genus: | Clostridium |
| Species: | C. perfringens |
| Binomial name | |
| Clostridium perfringens Veillon & Zuber 1898 Hauduroyet al. 1937 | |
Clostridium perfringens (formerly known asC.welchii, orBacillus welchii) is aGram-positive, bacillus (rod-shaped),anaerobic,spore-formingpathogenic bacterium of the genusClostridium.[1][2]C. perfringens is ever-present in nature and can be found as a normal component of decaying vegetation,marine sediment, theintestinal tract of humans and othervertebrates,insects, andsoil. It has the shortest reportedgeneration time of any organism at 6.3 minutes inthioglycolate medium.[3]
Clostridium perfringens is one of the most common causes offood poisoning in the United States, alongsidenorovirus,Salmonella,Campylobacter, andStaphylococcus aureus.[4] However, it can sometimes be ingested and cause no harm.[5]
Infections induced byC. perfringens are associated with tissuenecrosis,bacteremia, emphysematouscholecystitis, andgas gangrene, which is also known as clostridialmyonecrosis.[6] The specific name,perfringens, is derived from theLatinper (meaning "through") andfrango ("burst"), referring to the disruption of tissue that occurs during gas gangrene.[7] Gas gangrene is caused by alpha toxin, orα-toxin, that embeds itself into the plasma membrane of cells and disrupts normal cellular function by altering membrane structure.[8] Research suggests thatC. perfringens is capable of engaging in polymicrobialanaerobic infections.[9] It is commonly encountered ininfections as a component of the normalflora. In this case, its role in disease is minor.[10]
C. perfringens toxins are a result of horizontal gene transfer of a neighboring cell's plasmids.[11] Shifts in genomic make-up are common for this species of bacterium and contribute to novel pathogenesis.[12] Major toxins are expressed differently in certain populations ofC. perfringens; these populations are organized into strains based on their expressed toxins.[13] This especially impacts the food industry, as controlling this microbe is important for preventing foodborne illness.[12] Novel findings inC. perfringens hyper-motility, which was provisionally thought as non-motile, have been discovered as well.[14] Findings in metabolic processes reveal more information concerningC. perfringens pathogenic nature.[15]
Clostridium perfringens has a stableG+C content around 27 to 28 percent and averagegenome size of 3.5 Mb.[16] Genomes of 56C. perfringens strains have since been made available on theNCBI genomes database for the scientific research community.Genomic research has revealed surprisingly high diversity inC. perfringenspangenome, with only 12.6 percent core genes, identified as the most divergent Gram-positivebacteria reported.[16] Nevertheless,16S rRNA regions in betweenC. perfringens strains are found to be highly conserved (sequence identity >99.1%).[16]
TheClostridium perfringens enterotoxin (CPE)–producing strain has been identified to be a small portion of the overallC. perfringens population (~1-5%) through genomic testing.[17] Advances in genetic information surrounding strain A CPEC. perfringens has allowed techniques such as microbial source tracking (MST) to identify food contamination sources.[17] The CPE gene has been found within chromosomal DNA as well as plasmid DNA. Plasmid DNA has been shown to play and integral role in cell pathogenesis and encodes for major toxins, including CPE.[11]
C. perfringens has been shown to carry plasmid-containing genes forantibiotic resistance. The pCW3 plasmid is the primary conjugation plasmid responsible for creating antibiotic resistance inC. perfringens. Furthermore, the pCW3 plasmid also encodes for multiple toxins found in pathogenic strains ofC. perfringens.[18] Antibiotic resistance genes observed thus far includetetracycline resistance, efflux protein, andaminoglycoside resistance.[19]
Within industrial contexts, such asfood production, sequencing genomes for pathogenic strains ofC. perfringens has become an expanding field of research. Poultry production is impacted directly from this trend as antibiotic-resistant strains ofC. perfringens are becoming more common.[12] By performing a meta-genome analysis, researches are capable to identify novel strains of pathogenic bacterium, such asC. perfringens B20.[12]
Clostridium perfringens is provisionally identified as non-motile. They lack flagella; however, recent research suggests gliding as a form of motility.[20][21]
In agar plate cultures bacteria with hypermotile variations like SM101 frequently appear around the borders of the colonies. They create long thin filaments that enable them to move quickly, much like bacteria with flagella, according to video imaging of their gliding motion. The causes of the hypermotile phenotype and its immediate descendants were found using genome sequencing. The hypermotile offspring of strains SM101 and SM102, SM124 and SM127, respectively, had 10 and 6 nucleotide polymorphisms (SNPs) in comparison to their parent strains. The hypermotile strains have the common trait of gene mutations related to cell division.[20]
Some strains ofC. perfringens cause various diseases like gas gangrene and myonecrosis. Toxins produced that are required for myonecrosis is regulated by theC. perfringens Agr-like (CpAl) system through the VirSR two-component system. The CpAL/VirSR system is a quorum sensing system encoded by other pathogenic clostridia. Myonecrosis starts at the infection site and involves bacteria migrating deeper via gliding motility. Researchers investigated if the CpAL/VirSR system regulates gliding motility. The study demonstrated that the CpAL/VirSR regulatesC. perfringens gliding motility. Additionally, the study suggests that gliding bacteria in myonecrosis have increased transcription of toxin genes.[21]
There are two methods ofgenetic manipulation via experimentation that have been shown to cause genetic transformation inC. perfringens.
The first report of transformation inC. perfringens involvedpolyethyleneglycol-mediated transformation ofprotoplasts. The transformation procedure involved the addition of the plasmid DNA to the protoplasts in the presence of high concentrations ofpolyethylene glycol. During the first protoplast transformation experiment, L-phase variants ofC. perfringens were generated bypenicillin treatment in the presence 0.4m sucrose. After the transformation procedure was completed, all of the transformed cells were still in the form of L-phase variants. Reversion to vegetative cells was not obtained, but it was observed that autoplasts (protoplasts derived fromautolysis) were able to be regenerated to produce rods with cell walls and could be transformed withC. perfringens plasmid DNA.[22]
Electroporation involves the application of a high-voltage electric field to vegetative bacteria cells for a very short period. This technique resulted in major advances in genetic transformation ofC. perfringens, due to the bacteria often displaying itself as a vegetative cell or as dormant spores in food.[23] The electric pulse creates pores in the bacterial cell membrane and allows the passive influx of DNA molecules.[24]
C. perfringens is an aerotolerant anaerobe bacterium that lives in a variety of environments including soil and human intestinal tract.[15]C. perfringens is incapable of synthesizing multiple amino acids due to the lack of genes required for biosynthesis.[15] Instead, the bacterium produces enzymes and toxins to break down host cells and import nutrients from the degrading cell.[15]
C. perfringens has a complete set ofenzymes forglycolysis andglycogen metabolism. In the fermentation pathway,pyruvate is converted intoacetyl-CoA bypyruvate-ferredoxin oxidoreductase, producingCO2 gas and reducedferredoxin.[25] Electrons from the reduced ferredoxin are transferred to protons by hydrogenase, resulting in the formation of hydrogen molecules (H2) that are released from the cell along withCO2. Pyruvate is also converted tolactate bylactate dehydrogenase, whereas acetyl-CoA is converted intoethanol,acetate, andbutyrate through various enzymatic reactions, completing theanaerobic glycolysis that serves as a potential main energy source forC. perfringens.C. perfringens utilizes a variety of sugars such asfructose,galactose,glycogen,lactose,maltose,mannose,raffinose,starch, andsucrose, and various genes forglycolytic enzymes. The amino acids of these various enzymes and sugar molecules are converted topropionate throughpropionyl-CoA, which results in energy production.[25]
Membrane-damaging enzymes, pore-forming toxins, intracellular toxins, and hydrolytic enzymes are the functional categories into whichC. perfringens' virulence factors may be divided. These virulence factor-encoding genes can be found on chromosomes and large plasmids.[13]
The human gastrointestinal tract is lined withintestinal mucosa that secretemucus and act as a defense mechanism against pathogens, toxins, and harmful substances. Mucus is made up ofmucins containing severalO-linked glycanglycoproteins that recognizes and forms a barrier around microbes, preventing them from attaching to endothelial cells and infecting them.[26][27]C. perfringens can secrete differentcarbohydrate-active enzymes (CAZymes) that aid in degrading mucins and other O-glycans within the intestinal mucosa. These enzymes include: Sialidases, Hexosaminidases, Galactosidases, and Fucosidases belonging to variousglycoside hydrolase families.[27]
Sialidases, also called neuraminidases, function to breakdown mucin byhydrolyzing the terminal sialic acid residues located within the protein through the process ofdesialylation.C. perfringens has three sialidases belonging toglycoside hydrolase family 33 (GH33): NanH, NanI, and NanJ. All strains ofC. perfringens encode for at least one of these enzymes.[27][28]
C. perfringens can secrete NanI and NanJ through secretion signalpeptides located on each protein. Research suggests that NanH operates in the cytoplasm ofC. perfringens, as it does not contain a secretion signal peptide. NanH contains only a catalytic domain, whereas NanI and NanJ contain acatalytic domain and additionalcarbohydrate-binding modules (CBMs) to aid in catalytic activity. Located on their N-terminals, NanI contains CBM40, whereas NanJ contains both CBM40 and CBM32. Based on studies analyzing the three-dimensional structure of NanI, itsactive site has a pocket-like orientation that aids in the removal of sialic acid residues from sialomucins in the intestinal mucosa.[27]
The mucus layer consists of intestinal mucin glycans, glycolipids, and glycoproteins that containhexosamines, such asN-acetylglucosamine (GlcNAc) andN-acetylgalactosamine (GalNAc).C. perfringens encodes for eighthexosaminidases that break down hexosamines in the mucus. These hexosaminidases belong to four glycoside hydrolase families: GH36, GH84, GH89, and GH123.[27]
C. perfringens encodes for AagA (CpGH36A) andCpGH36B inglycoside hydrolase family 36 (GH36): AagA removes GalNAc from O-glycans, andCpGH36B is expected to have a similar structure to AagA, but specificities on its function are unknown. NagH, NagI, NagJ, and NagK, belonging to glycoside hydrolase family 84 (GH84), cleave terminal GlcNAc residues using a substrate-assisted digestion mechanism. AgnC (CpGH89), belonging toglycoside hydrolase family 89 (GH89), both cleaves GlcNAc from the ends of mucin glycans and acts on gastric mucin. Belonging to glycoside hydrolase family 123 (GH123),CpNga123 cleaves GalNAc, but research suggests that it only breaks down glycans taken up byC. perfringens due to the absence of a secretion signal peptide.[27]
C. perfringens has fourgalactosidases that belong to theglycoside hydrolase family 2 (GH2):CpGH2A,CpGH2B,CpGH2C, andCpGH2D. Research suggests that these enzymes are effective at breaking down core mucin glycan structures with the ability to bindgalactose using CBM51. However, minimal research exists on the specific functioning of galactosidases inC. perfringens.[27]
Fucose monosaccharides are located on the terminal ends of core O-linked glycans.C. perfringens encodes for three fucosidases that belong to two glycoside hydrolase families: Afc1 and Afc2 inglycoside hydrolase family 29 (GH29), and Afc3 in glycoside hydrolase family 95 (GH95). Afc3 contains a C-terminal CBM51 and is the only fucosidase that contains a carbohydrate-binding module inC. perfringens. Fucosyl residues tend to cover the ends of glycans and protect them against enzymatic digestion, so research suggests that the ability of fucosidases to cleave complex and diverse fucosyl linkages is due to long-term adaptations inC. perfringens that persisted within close range of mucins.[27]
There are five major toxins produced byClostridium perfringens. Alpha, beta, epsilon and enterotoxin are toxins that increase a cells permeability which causes an ion imbalance while iota toxins destroy the cell's actin cytoskeleton.[29] On the basis of which major, "typing" toxins are produced,C. perfringens can be classified into seven "toxinotypes", A, B, C, D, E, F and G:[30]
Toxin Type | Alpha | Beta | Epsilon | Iota | Enterotoxin | NetB | Notes |
|---|---|---|---|---|---|---|---|
| A | + | - | - | ||||
| B | + | + | - | - | |||
| C | + | + | - | +/- | - | ||
| D | + | - | + | - | +/- | - | |
| E | + | - | + | +/- | - | ||
| F | + | - | + | - | |||
| G | + | - | + |
Alpha toxin (CPA) is a zinc-containing phospholipase C, composed of two structural domains, which destroy a cell's membrane. Alpha toxins are produced by all five types ofC. perfringens. This toxin is linked togas gangrene of humans and animals. Most cases of gas gangrene has been related to a deep wound being contaminated by soil that harborsC. perfringens.[29][32]
Beta toxins (CPB) are a protein that causes hemorrhagicnecrotizing enteritis andenterotoxaemia in both animals (type B) and humans (type C) which leads to the infected individual's feces becoming bloody and their intestines necrotizing.[29]Proteolytic enzymes, such as trypsin, can break down CPB, making them ineffective. Therefore, the presence of trypsin inhibitors in colostrum makes CPB especially deadly for mammal offspring.[33]
Epsilon toxin (ETX) is a protein produced by type B and type D strains ofC. perfringens. This toxin is currently ranked the third most potent bacterial toxin known.[34] ETX causesenterotoxaemia in mainly goats and sheep, but cattle are sometime susceptible to it as well. An experiment using mice found that ETX had an LD50 of 50-110 ng/kg.[35] The excessive production of ETX increases the permeability of the intestines. This causes severe edema in organs such as the brain and kidneys.[36]
The very low LD50 of ETX has led to concern that it may be used as a bioweapon. It appeared on theselect agent lists of the US CDC and USDA, until it was removed in 2012. There are no human vaccines for this toxin, but effective vaccines for animals exist.[37]
Iota toxin (ITX) is a protein produced by type E strains ofC. perfringens. Iota toxins are made up of two, unlinked proteins that form a multimeric complex on cells. Iota toxins prevent the formation of filamentous actin. This causes the destruction of the cells cytoskeleton which in turn leads to the death of the cell as it can no longer maintain homeostasis.[38]
This toxin (CPE) causes food poisoning. It alters intracellular claudin tight junctions in gut epithelial cells. This pore-forming toxin also can bind to human ileal and colonic epithelium in vitro and necrotize it. Through the caspase-3 pathway, this toxin can cause apoptosis of affected cells. This toxin is linked to type F strains, but has also been found to be produced by certain types of C, D, and E strains.[39]
TpeL is a toxin found in type B, C, and G[40] strains. It is in the sameprotein family asC. difficile toxin A.[41] It does not appear important in the pathogenesis of types B and C infections, but may contribute to virulence in type G strains. It glycosylates Rho andRas GTPases, disrupting host cell signaling.[40]
Tissuenecrosis,bacteremia, emphysematouscholecystitis, andgas gangrene, also known as clostridialmyonecrosis, have been linked to infections associated withC. perfringens.[8] Research suggests thatC. perfringens is capable of engaging in polymicrobialanaerobic infections.[42]
Clostridium perfringens is a common cause of food poisoning in the United States.C. perfringens produces spores, and when thesespores are consumed, they produce a toxin that causes diarrhea. Foods cooked in large batches and held at unsafe temperatures (between 40 °F and 140 °F) are the source ofC. perfringens food poisoning outbreaks. Meats such as poultry, beef, and pork are commonly linked toC. perfringens food poisoning.[43]C. perfringens can proliferate in foods that are improperly stored due to the spore's ability to survive normal cooking temperatures. The type A toxin ofC. perfringens, also known as the CPA is responsible for food poisoning.[44]
Clostridium perfringens is the most common bacterial agent forgas gangrene.[45] Gas gangrene is induced byα-toxin that embeds itself into the plasma membrane of cells and disrupts normal cellular function by altering membrane structure.[8] Some symptoms include blisters, tachycardia, swelling, and jaundice.[45]
C. perfringens is most commonly known for foodborne illness but can translocate from a gastrointestinal source into the bloodstream which causesbacteremia.C. perfringens bacteremia can lead to toxin-mediated intravascular hemolysis and septic shock.[46] This is rare as it makes up less than 1% of bloodstream isolates but is highly fatal with a reported mortality rate of 27% to 58%.[47]
Clostridium perfringens food poisoning can also lead to another disease known as enteritis necroticans orclostridial necrotizing enteritis, (also known as pigbel); this is caused byC. perfringens type C. This infection is often fatal. Large numbers ofC. perfringens grow in the intestines and secrete exotoxin. This exotoxin causes necrosis of the intestines, varying levels of hemorrhaging, and perforation of the intestine. Inflammation usually occurs in sections of the jejunum, midsection of the small intestine.[48]Perfringolysin O (pfoA)-positiveC. perfringens strains were also associated with the rapid onset ofnecrotizing enterocolitis in preterm infants.[49]
A strain ofC. perfringens might be implicated inmultiple sclerosis (MS) nascent (Pattern III) lesions.[50] Tests inmice found that two strains of intestinalC. perfringens that produced epsilon toxins (ETX) caused MS-like damage in the brain, and earlier work had identified this strain ofC. perfringens in a human with MS.[51][52] MS patients were found to be 10 times more likely[53] to be immune-reactive to the epsilon toxin than healthy people.[54] Greatly increased rates of gut colonization by type B and DC. perfringens are seen in MS patients.[55]
Tissue gas occurs whenC. perfringens infects corpses. It causes extremely accelerated decomposition and can only be stopped byembalming the corpse. Tissue gas most commonly occurs to those who have died from gangrene, largedecubitus ulcers, necrotizing fasciitis or to those who had soil, feces, or water contaminated withC. perfringens forced into an open wound.[56]
Clostridium perfringens infections can lead to various clinical manifestations, ranging from mild gastrointestinal symptoms to life-threatening conditions. The most common presentation is food poisoning, characterized by acute abdominal pain, diarrhea, and, in some cases, vomiting, typically occurring 6 to 24 hours after the ingestion of contaminated food. Unlike many other foodborne illnesses, fever is usually absent. Symptoms are usually self-limiting and resolve within 24 to 48 hours; however, severe dehydration can occur in cases of significant fluid loss. Symptoms of dehydration include dry mouth, decreased urine output, dizziness, and fatigue. Severe symptoms such as diarrhea that persists for more than 48 hours, the inability to keep fluids down, or signs of severe dehydration may necessitate medical attention.[57] Most people are able to recover fromC. perfringens food poisoning without treatment. However, people who experience diarrhea are usually instructed to drink water or rehydration solutions.[58]
Gas gangrene caused byClostridium perfringens is characterized by severe symptoms, including intense pain at the injury site, fever, rapid heart rate, sweating, and anxiety. The affected area may show signs of swelling, discoloration (ranging from pale to dark red or purplish), and large, discolored blisters filled with foul-smelling fluid. As the toxins spread, skin and muscle tissue are rapidly destroyed, leading to large areas of dead tissue, gas pockets under the skin (crepitus), and possiblerenal failure due to red blood cell destruction.Sepsis andseptic shock may also occur, which can be fatal.[59]
Necrotizing enteritis caused byClostridium perfringens presents with a wide range of symptoms, which can vary in severity. The clinical signs range from mild diarrhea to more severe manifestations such as intense abdominal pain, vomiting, bloody stools, and even septic shock. In the most serious cases, the infection can lead to death.[60]
The diagnosis ofClostridium perfringens food poisoning relies on laboratory detection of the bacterium or its toxin in either a patient’s stool sample or contaminated food linked to the illness. A positive stool culture would have growth of at least 10 cfu/g of C.perfringens. Stool studies includeWBCs,ova, and parasites in order to rule out other potentialetiologies.ELISA testing is used to detect the CPA toxin. DiagnosingC. perfringens food poisoning is relatively uncommon for several reasons.[61] Most individuals with this foodborne illness do not seek medical care or submit a stool sample for testing, and routine testing forC. perfringens is not typically performed in clinical laboratories. Additionally, public health laboratories generally conduct testing for this pathogen only in the event of an outbreak.[62]
The diagnosis of gas gangrene typically involves several methods to confirm the infection. Imaging techniques such asX-rays,CT scans, orMRIs can reveal gas bubbles or tissue changes indicative of muscle damage. Additionally, bacterial staining or culture of fluid taken from the wound helps identifyClostridium perfringens and other bacteria responsible for the infection. In some cases, abiopsy is performed, where a sample of the affected tissue is analyzed for signs of damage or necrosis.[59]
The diagnosis of clostridial necrotizing enteritis is primarily based on the patient's clinical symptoms, which can include severe abdominal pain, vomiting, and bloody diarrhea. Additionally, confirmation of the presence ofClostridium perfringenstype C toxin in stool samples is crucial for accurate diagnosis.[60]
Clostridium perfringens is responsible for an estimated 966,000 cases annually, or about 10.3% of all foodborne illnesses in which a pathogen is identified. Transmission typically occurs when food contaminated withC. perfringens spores is consumed, allowing the bacteria to produce a toxin in the intestines that causes diarrhea. Outbreaks are often associated with foods cooked in large batches, such as poultry, meat, and gravy, and held at unsafe temperatures between 40-140 °F, which allows the bacteria to thrive. These outbreaks tend to occur in settings where large groups are served, such as hospitals, school cafeterias, prisons, nursing homes, and catered events. In most cases,C. perfringens infection causes mild symptoms, including watery diarrhea and mild abdominal cramps, with symptoms typically appearing 8 to 12 hours after consuming contaminated food and resolving within 24 hours. About 90% of affected individuals recover without seeking medical attention, usually within two days. However, vulnerable groups such as the elderly, young children, and immunocompromised individuals face a higher risk of severe complications like dehydration, which can lead to more serious illness or, in rare cases, death. Each year,C. perfringens infections result in approximately 438 hospitalizations and 26 deaths, accounting for 0.8% of foodborne illness-related hospitalizations and 1.9% of associated deaths. Outbreaks are most common in November and December, coinciding with holiday foods like turkey and roast beef. The economic burden ofC. perfringens is significant, estimated at $342.7 million annually, including $53.2 million in medical costs, $64.3 million in productivity loss, and $225 million related to fatalities.[63][64]
Clostridial necrotizing enteritis is rare in the United States; typically, it occurs in populations with a higher risk. Data show that of the 9.4 million cases of foodborne illness in the United States each year, only about 11% are caused byClostridium perfringens.[65] "Risk factors forenteritis necroticans include protein-deficient diet, unhygienic food preparation, sporadic feasts of meat (after long periods of a protein-deficient diet), diets containing large amounts oftrypsin inhibitors (sweet potatoes), and areas prone to infection of the parasiteAscaris (produces a trypsin inhibitor). This disease is contracted in populations living in New Guinea, parts of Africa, Central America, South America, and Asia.[48]
Risk factors for gas gangrene include severe injuries, abdominal surgeries, and underlying health conditions such ascolon cancer, diseases of the blood vessels,diabetes, anddiverticulitis. However, the most common way to get gas gangrene is through a traumatic injury. In the United States, there is only about 1000 cases of gas gangrene per year. When addressed with adequate care, gas gangrene has a mortality rate of 20-30% but has a mortality rate of 100% if left untreated.[66]
On May 7, 2010, 42 residents and 12 staff members at a Louisiana (USA) state psychiatric hospital were affected and experienced vomiting, abdominal cramps, and diarrhea. Three patients died within 24 hours. The outbreak was linked to chicken which was cooked a day before it was served and was not cooled down according to hospital guidelines. The outbreak affected 31% of the residents of the hospital and 69% of the staff who ate the chicken. How many of the affected residents ate the chicken is unknown.[67]
In May 2011, a man died after allegedly eating food contaminated with the bacteria on atransatlanticAmerican Airlines flight. The man's wife and daughter were suing American andLSG Sky Chefs, the German company that prepared the inflight food.[68]
In December 2012, a 46-year-old woman died two days after eating a Christmas Day meal at a pub inHornchurch,Essex, England. She was among about 30 people to fall ill after eating the meal. Samples taken from the victims containedC. perfringens. The hotel manager and the cook were jailed for forging cooking records relating to the cooking of the turkey.[69]
In December 2014, 87-year-old Bessie Scott died three days after eating a church potluck supper inNackawic,New Brunswick, Canada. Over 30 other people reported signs of gastrointestinal illness, diarrhea, and abdominal pain. The province's acting chief medical officer says,Clostridium perfringens is the bacteria [sic] that most likely caused the woman's death.[70]
In October 2016, 66-year-old Alex Zdravich died four days after eating an enchilada, burrito, and taco at Agave Azul inWest Lafayette, Indiana, United States. Three others who dined the same day reported signs of foodborne illness, which were consistent with the symptoms and rapid onset ofC. perfringens infection. They later tested positive for the presence of the bacteria, but the leftover food brought home by Zdravich tested negative.[71][72]
In November 2016, food contaminated withC. perfringens caused three individuals to die, and another 22 to be sickened, after aThanksgiving luncheon hosted by a church inAntioch, California, United States.[73]
In January 2017, a mother and her son sued a restaurant inRochester, New York, United States, as they and 260 other people were sickened after eating foods contaminated withC. perfringens. "Officials from the Monroe County Department of Public Health closed down the Golden Ponds after more than a fourth of its Thanksgiving Day guests became ill. An inspection revealed a walk-in refrigerator with food spills and mold, a damaged gasket preventing the door from closing, and mildew growing inside."[74]
In July 2018, 647 people reported symptoms after eating at aChipotle Mexican Grill restaurant inPowell, Ohio, United States. Stool samples tested by theCDC tested positive forC. perfringens.[75]
In November 2018, approximately 300 people in Concord,North Carolina, United States, were sickened by food at a church barbecue that tested positive forC. perfringens.[76]
In 2021, a foodborne illness outbreak inHomer, Alaska, affected approximately 80 employees of South Peninsula Hospital and was traced to Cubano sandwiches served during staff meals. TheAlaska Department of Health and Social Services identified the likely cause asC. perfringens. No hospitalizations were reported, and the outbreak was contained to hospital staff. Such localized outbreaks are considered uncommon in Alaska when not tied to a national foodborne incident.[77]
PreventingClostridium perfringens contamination and growth involves careful food handling, proper cooking, and appropriate storage practices. Most foods, especially beef and chicken, can be protected by cooking them to the recommended internal temperatures. Using a kitchen thermometer is the most reliable way to check that meats reach safe cooking temperatures. As a general rule, food should be avoided if it smells, tastes, looks off, or has been left out at unsafe temperatures for a long period of time.[78]
C. perfringens spores can multiply within a temperature range of 59 °F (15 °C) to 122 °F (50 °C).[79] To prevent bacterial growth, leftovers should be refrigerated within two hours of preparation, with their temperature chilled down to below 40 °F (4 °C). Large portions of food that contain meat, should be divided into smaller containers before refrigeration to ensure even cooling. Before serving leftovers, they should be reheated to at least 165 °F (74 °C) to destroy any bacteria that may have grown during storage.[78]
High-risk foods, such as canned vegetables, smoked or cured meats, and salted or smoked fish, require additional attention. Improper processing or storage can allow bacteria to grow and produce dangerous toxins. Signs of contamination, such as unusual odors, changes in texture, or bulging cans (also known as "bombage"), indicate food spoilage and should be disposed.[80]
Preventinggas gangrene involves taking precautions to avoid bacterial infections. Healthcare providers follow strict protocols to prevent infections, including those caused byClostridium perfringens. To reduce the risk of gas gangrene, individuals should clean wounds thoroughly with soap and water and seek medical attention for deep or uncleanable wounds. It is also essential to monitor injuries for changes in skin condition or the onset of severe pain. Wearing protective gear when engaging in activities like biking or motorcycling can help prevent injury. Additionally, working with healthcare providers to manage underlying conditions that affect circulation or weaken the immune system can further reduce the risk of infection.[59]
The treatment ofClostridium perfringens infections depends on the type and severity of the condition. For severe infections, such asgas gangrene (clostridial myonecrosis), the primary approach involves surgical debridement of the affected area. This procedure removes devitalized tissue where bacteria grow, which limits the spread of the infection.Antimicrobial therapy is usually started at the same time, with penicillin being the most commonly used drug.[81] However,C. perfringens shows different resistance patterns with about 20% of strains being resistant to clindamycin, and 10% being resistant to metronidazole.[82]C. perfringens is often more susceptible to vancomycin when compared to other pathogenicClostridia, making it an alternative option for treatment in some cases.[81]
Therapies, such ashyperbaric oxygen therapy (HBOT), may also be used for severe clostridial tissue infections. HBOT increases oxygen delivery to infected tissues, creating an environment that inhibits the growth of anaerobic bacteria likeC. perfringens. While not commonly used, HBOT can be beneficial in certain cases.[83]
For foodborne illness caused byC. perfringens, treatment is typically unnecessary. Most people who suffer from food poisoning caused byC. perfringens usually fight off the illness without the need of any antibiotics. Extra fluids should be drank consistently until diarrhea dissipates.[84]
C. perfringens has shown increasingmultidrug resistance, particularly in strains from humans and animals. High resistance levels were found with antibiotics such as tetracycline, erythromycin, and sulfonamides. Genetic factors, misuse of antibiotics, and bacterial evolution are the cause of this issue. This highlights the importance of finding new treatment strategies.[85]
Multilocus Sequence Typing (MLST) andWhole Genome Sequencing (WGS) have been used to find the genetic diversity ofC. perfringens. These methods have identified 195 distinct sequence types grouped into 25 clonal complexes from 322 genomes. Phylogenetic groups were also found in multiple different hosts and environmental sources. This highlights the bacteria's transmission potential and adaptability across species.[86]
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