| 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 was discovered in 1891 by Dr. William H. Welch.[1] It was originally known asBacillus aerogenes capsulatus, followed byBacilluswelchii, before the final establishment of its current name.[1]C. perfringens is aGram-positive, bacillus (rod-shaped),anaerobic,spore-formingpathogenic bacterium of the genusClostridium.[2][3]C. perfringens is 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.[4]
Clostridium perfringens is one of the most common causes offood poisoning in the United States, alongsidenorovirus,Salmonella,Campylobacter, andStaphylococcus aureus.[5] However, it can sometimes be ingested and cause no harm.[6]
Infections induced byC. perfringens are associated with tissuenecrosis,bacteremia, emphysematouscholecystitis, andgas gangrene, which is also known as clostridialmyonecrosis.[7] The specific name,perfringens, is derived from theLatinper (meaning "through") andfrango ("burst"), referring to the disruption of tissue that occurs during gas gangrene.[8] 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.[9] Research suggests thatC. perfringens is capable of engaging in polymicrobialanaerobic infections.[10] It is commonly encountered ininfections as a component of the normalflora. In this case, its role in disease is minor.[11]
C. perfringens toxins are a result of horizontal gene transfer of a neighboring cell's plasmids.[12] Shifts in genomic make-up are common for this species of bacterium and contribute to novel pathogenesis.[13] Major toxins are expressed differently in certain populations ofC. perfringens; these populations are organized into strains based on their expressed toxins.[14] This especially impacts the food industry, as controlling this microbe is important for preventing foodborne illness.[13] Novel findings inC. perfringens hyper-motility, which was provisionally thought as non-motile, have been discovered as well.[15] Findings in metabolic processes reveal more information concerningC. perfringens pathogenic nature.[16]
Clostridium perfringens genome is between 2.9 and 4.1 million base pairs.[17] The information on the genome ofC. perfringens is still limited as there is much genetic diversity within this pathogen.[17] It is one of the most variable gram-positive bacteria containing only 12.6 percent core genes that make up the pathogen.[17] Despite the bacteria's diversity across strains,C. perfringens's16S rRNA regions were found to be highly conserved (i.e. nearly identical) across all strains.[17]
The toxin causing food poisoning inClostridium perfringens is the CPE (Clostridium perfringens enterotoxin) cpe gene.[18] Not allClostridium perfringens types have the cpe gene, but all types could include this gene. The cpe gene is located in the plasmid- mediated cpe (p-cpe), or on the chromosomal cpe (c-cpe) strains.[19] The differences in location of the cpe gene give insight into what type of infections could arise. Chromosomal cpe (c-cpe) strains are exclusively isolated from food samples, while p-cpe strains are found in non-food borne samples. c-cpe strains also produce heat resistant spores, while p-cpe strains produce heat sensitive spores.[19] The enterotoxin–producing strain ofClostridium perfringens has been identified to be a small portion of the overallC. perfringens population (~1-5%).[20] Plasmid DNA has been shown to play an integral role in cell pathogenesis and encodes for major toxins, includingClostridium perfringens enterotoxin.[12]
Clostridium perfringens uses horizontal gene transfer. Through the usage ofconjugation,C. perfringens can spread antibiotic resistant genes via plasmids.[21] 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.[22] Antibiotic resistance genes observed thus far includetetracycline resistance, efflux protein, andaminoglycoside resistance.[23]
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.[13]
Clostridium perfringens is provisionally identified as non-motile. They lack flagella; however, recent research suggests gliding as a form of motility in some cultures.[24][25] These hyper-motile variations of the bacteria form due to slight nucleotide polymorphisms and are regulated by various systems such as the CpAL/VirSR system and catabolite control protein A.[25][26] In combination, these regulators help the spread ofC. perfringens by increasing motility in regions of low nutrient densities and increasing toxicity as movement occurs.[26]
In agar plate cultures bacteria with hypermotile variations like SM101 frequently appear around the borders of the colonies. Video imaging of these variants show the formation of long thin filaments that enable motion. The causes of this 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 also display a common trait gene mutations related to cell division.[24]
The toxins that are required for some diseases caused byC. perfringens, such as myonecrosis, are regulated by theC. perfringens Agr-like (CpAl) system through the VirSR two-component system. This CpAL/VirSR system acts as a quorum sensing system encoded by other pathogenic clostridia. Studies have demonstrated that this CpAL/VirSR system also regulatesC. perfringens gliding motility. This multifunctionality of the CpAL/VirSR system represents a relationship in which motility is positively and directly related to an increasing toxin production, worsening infection strength as the pathogen spreads.[25]
Studies have also demonstrated a correlation between glucose levels and motility rates ofClostridium perfringens. As glucose levels rise, through the repression of pilT and pilD, genes that help type IV pili formation, through catabolite control protein A, gliding motility was observed to decrease. This relationship allows forC.perfringens to help spread from areas of low sugar concentration, such as the human gut, into other regions worsening infections.[26]
There are two methods ofgenetic manipulation via experimentation that have been shown to causegenetic transformation inC. perfringens, the first being Protoplast transformation and second Electroporation. The first method involves the variations ofC. perfringens with compromised cell wall while the second utilizes electricity and vegetative versions ofC. perfringens.
The first report of transformation inC. perfringens involvedpolyethyleneglycol-mediated transformation ofprotoplasts, bacteria whose cell wall has been removed. This transformation procedure involved the addition of plasmid DNA to the protoplasts in the presence of high concentrations ofpolyethylene glycol. Initial protoplast transformation experiments utilized, L-phase variants, cell wall deficient versions, ofC. perfringens viapenicillin treatment in the presence 0.4m sucrose. However, after the transformation procedure was completed, all of the transformed cells were stuck in the form of L-phase variants, unable to regenerate cell wall. In contrast, it was observed that autoplasts, protoplasts derived fromautolysis (the natural degradation of bacterial cell walls through the use of the bacteria's own enzymes), were able to regenerate and produce rods with cell walls as well as be transformed withC. perfringens plasmid DNA.[27]
Electroporation involves the application of a high-voltage electric field to vegetative bacteria cells for a very short period of time. 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.[28] The electric pulse creates pores in the bacterial cell membrane and allows the passive influx of DNA molecules. This method was found to be more efficient than the previously stated protoplast transformation due to the simpler procedure and greater yields.[29]
C. perfringens is an aerotolerant anaerobe bacterium that lives in a variety of environments including soil and human intestinal tract.[16]C. perfringens is incapable of synthesizing multiple amino acids due to the lack of genes required for biosynthesis.[16] Instead, the bacterium produces enzymes and toxins to break down host cells and import nutrients from the degrading cell.[16]
C. perfringens has a complete set ofenzymes forglycolysis andglycogen metabolism. In the fermentation pathway,pyruvate is converted intoacetyl-CoA bypyruvate-ferredoxin oxidoreductase, producingcarbon dioxide gas and reducedferredoxin.[30] 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.[30]
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.[14]
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.[31][32]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.[32]
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. These three sialidases are typically encoded by all strains ofC. perfringens.[32][33]
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.[32]
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.[32]
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.[32]
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.[32]
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.[32]
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.[34] 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:[35]
Toxin Type | Alpha | Beta | Epsilon | Iota | Enterotoxin | NetB | ||
|---|---|---|---|---|---|---|---|---|
| A | + | - | - | - | - | - | ||
| B | + | + | + | - | - | - | ||
| C | + | + | - | - | +/- | - | ||
| D | + | - | + | - | +/- | - | ||
| E | + | - | - | + | +/- | - | ||
| F | + | - | - | - | + | - | ||
| G | + | - | - | - | - | + |
C. perfringens alpha toxin is the bacterium’s major virulence factor and the major cause ofgas gangrene, a myonecrotic disease.[34] Alpha toxin is produced by all five types ofC. perfringens. It has phospholipase C and sphingomyelinase activities, through which it hydrolyzes phospholipids in eukaryotic cell membranes.[37] The hydrolysis of phospholipids in the membrane can lead to hemolysis and necrosis of muscle cells.[38]
Alpha toxin structure is composed of two domains: the N-terminal domain (1-250 residues) and the C-terminal domain (251-370 residues). The N-domain consists of a zinc-containing catalytic site for the degradation of phospholipids, while the C-domain is responsible for membrane binding in lipid bilayers.[38]
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.[34]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.[39]
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.[40] 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.[41] The excessive production of ETX increases the permeability of the intestines. This causes severe edema in organs such as the brain and kidneys.[42]
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.[43]
Iota toxin 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.[44]
This enterotoxin causes food poisoning. It alters intracellular claudin tight junctions in gut epithelial cells. This spore-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.[45]
TheClostridium perfringens enterotoxin gene is known to express during sporulation, whenC. perfringens is under nutrient deficient condition. The symptoms of food poisoning often occur when the heat resistant spores of type AClostridium perfringens enterotoxin-producing strains survive through improper cooking, then germinate the food through sporulation, causing the pathogen to then multiply into a large number of vegetative cells. Once ingested and present inside the intestinal wall, the vegetative cells start to produce enterotoxin, and follow by the cells lysing to excrete the enterotoxin into the body to then affect the host.[46]
Necrotic enteritis B-like(NetB) toxin encodes for a protein that has virulence factors that affect avian intestinal tissue, causing the illness known asnecrotizing enteritis. This toxin has been mostly found in the intestines of chickens and has known to damage the lining of the intestinal tract. Some symptoms can akin to diarrhea, reduced appetite, "Turkish Towel"(describing the appearance of a thick yellowish or greenish pseudomembrane that covers the intestinal lining of avian species), and abrupt death.[47] NetB toxin works by forming pores that help find cholesterol-free regions. These regions facilitate the entry of ions such as Na+, Cl-. and Ca2+, which allow for the cells of the intestinal lining to lyse, damaging the entirety of the intestinal walls and lining.[48]
TpeL is a toxin found in type B, C, and G[49] strains. It is in the sameprotein family asC. difficile toxin A.[50] 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.[49]
Perfringolysin O (PFO) is a pore-forming haemolytic toxin belonging to thecholesterol-dependent cytolysin (CDC) family. It holds the ability to bindcholesterol in host cell membranes to form pores. While most strains ofC. perfringens contain thepfoA gene, some lineages have been shown to have a reduced presence of it, such as lineage V in infant-associated strains. Lack of thepfoA gene corresponds with reduced virulence. PFO can potentially contribute to the pathogenesis of diseases such as myonecrosis, necrotizing enterocolitis, haemorrhagic enteritis in calves, andsepticaemia in humans, including preterm infants.[51]
Food poisoning,gas gangrene,clostridial necrotizing enteritis,bacteremia, tissuenecrosis, emphysematouscholecystitis, and more illnesses/diseases have been linked to infections associated withC. perfringens.[9] Research also suggests thatC. perfringens is capable of engaging in polymicrobialanaerobic infections.[52]
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.[53]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.[54]
Food poisoning is 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.[55] 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.[56]
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."[57]
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.[58]
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.[59]
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.[60]
Clostridium perfringens is the most common bacterial agent forgas gangrene, also known as clostridialmyonecrosis.[61] Gas gangrene is induced byα-toxin that embeds itself into the plasma membrane of cells and disrupts normal cellular function by altering membrane structure.[9]
Some symptoms include pain at the injury site, blisters, swelling, discoloration, tachycardia, fever, and jaundice.[61] Discoloration ranges from pale to dark red or purplish, and the blisters are large and 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 possible renal failure due to red blood cell destruction. Sepsis and septic shock may also occur, which can be fatal.[62]
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.[63]
Symptoms cover a wide range and 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.[64]
Perfringolysin O (pfoA)-positiveC. perfringens strains were also associated with the rapid onset ofnecrotizing enterocolitis in preterm infants.[51]
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.[65] 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%.[66]
A strain ofC. perfringens might be implicated inmultiple sclerosis (MS) nascent (Pattern III) lesions.[67] 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.[68][69] MS patients were found to be 10 times more likely to be immune-reactive to the epsilon toxin than healthy people.[70] Greatly increased rates of gut colonization by type B and DC. perfringens are seen in MS patients.[69]
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.[71]
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.[72] 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.[73]
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.[62]
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.[64]
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.[74] 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 and 140 °F, which allows the bacteria to thrive. 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.[74] 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.[74][75]
C. perfringens spores can multiply within a temperature range of 59°F (15°C) to 122°F (50°C).[76] 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.[77] Canned vegetables, smoked or cured meats, and salted or smoked fish, require additional attention.[78]
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 difficult to clean wounds. It is also essential to monitor injuries for changes in skin condition or the onset of severe pain. Additionally, working with healthcare providers to manage underlying conditions that affect circulation or weaken the immune system can further reduce the risk of infection.[62]
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.[79] However,C. perfringens shows different resistance patterns with about 20% of strains being resistant to clindamycin, and 10% being resistant to metronidazole.[80]C. perfringens is often more susceptible to vancomycin when compared to other pathogenicClostridia, making it an alternative option for treatment in some cases.[79]
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.[81]
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 drunk consistently until diarrhea dissipates.[82]
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.[83]
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.[84]
While the majority of research of pathogenicC. perfringens has been on avian species, there is some research into aquatic species. Previous research into aquatic species containing the bacterium has shown that spores ofC. perfringens were detected in the sludge where fish and shellfish live, explaining that it should theoretically be possible to contaminate aquatic species. In this new research, it is found that out of 141 fish and healthy aquatic samples, there were 80 positive samples ofC. perfringens, of which 26 samples of raw clam were tested and 22 were found to have a positive result, and 15 samples were cooked clam and 14 were found to be positive for theC. perfringens pathogen.[85]
The Clostridium perfringens bacterium is the second leading cause of food-borne illness in the United States(causing about 1 million illnesses annually). The bacterium has free rein through multiple mediums, such as soil, waterways, feces, sewage, in the intestinal tract of humans and animals, and even in/on food such as uncooked beef and poultry. This adaptation allows for the microbe to infect human and animal host populations alike.[48]
Infested livestock can result in a reduced availability of viable meat, eggs, milk, produce, and other valuable resources. This loss of agriculture and livestock could cause a significant economic loss and would impact food security.[86]
C. perfringens has the ability to sporulate, which allows for the microbe to survive in extreme and harsh conditions. This includes exposure to extreme temperatures, pH, and antimicrobials/other sterilant types.[86]The spores ofClostridium perfringens have been proposed as useful conservative indicators of human sewage-derived fecal contamination and surrogates for other environmentally stable pathogens because they are both specific to sewage contamination and environmentally stable.C. perfringens spores meet many of the key criteria for an ideal fecal-indicator organism: they are unique to fecal sources, commonly present in sewage, and consistently linked to human waste.[87] Studies have shown that aC. perfringens level above 10 CFU/100 ml can have adverse health effects on humans.[88]
According to a study examine the number of isolate genomes ofC. perfringens around the world, it was found that the countries with the greatest variety of different genomes were USA and China, with 595 and 553 isolated genomes respectively.[86] Across 195 countries and 1,898 isolated genomes in total, it was found that the continents with the most variety ofC. perfringens genomes were The Americas, Asia, and Australia.[86]
| Adulterants,food contaminants | |
|---|---|
| Food additives | |
| Intestinal parasites,parasitic disease | |
| Microorganisms | |
| Pesticides | |
| Preservatives | |
| Sugar substitutes | |
| Toxins,poisons,environment pollution | |
| Food fraud | |
| Food processing | |
| Food contamination incidents |
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| Regulation,standards,watchdogs | |
| Institutions |
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| Related topics | |
