| Campylobacter jejuni | |
|---|---|
 | |
Scientific classification | |
| Domain: | Bacteria |
| Kingdom: | Pseudomonadati |
| Phylum: | Campylobacterota |
| Class: | "Campylobacteria" |
| Order: | Campylobacterales |
| Family: | Campylobacteraceae |
| Genus: | Campylobacter |
| Species: | C. jejuni |
| Binomial name | |
| Campylobacter jejuni (Jones and Little, 1931) Veron & Chatelain, 1973 | |
Campylobacter jejuni is a species ofpathogenic bacteria that is commonly associated with poultry, and is also often found in animalfeces. This species of microbe is one of the most common causes offood poisoning in Europe and in the US, with the vast majority of cases occurring as isolated events rather than mass outbreaks. Active surveillance through the Foodborne Diseases Active Surveillance Network (FoodNet) indicates that about 20 cases arediagnosed each year for each 100,000 people in the US, while many more cases are undiagnosed or unreported; the CDC estimates a total of 1.5 million infections every year.[1] The European Food Safety Authority reported 246,571 cases in 2018, and estimated approximately nine million cases of human campylobacteriosis per year in the European Union.[2] In Africa, Asia, and the Middle East, data indicates thatC. jejuni infections areendemic.[3]
Campylobacter is a genus of bacteria that is among the most common causes of bacterial infections in humans worldwide. Campylobacter means "curved rod", deriving from the Greekkampylos(curved) andbaktron (rod). Of its many species,C. jejuni is considered one of the most important from both a microbiological and public health perspective.[4][5]
C. jejuni is commonly associated with poultry, and is also commonly found in animalfeces. Campylobacter is ahelical-shaped, non-spore-forming,Gram-negative,microaerophilic,nonfermenting motile bacterium with a single flagellum at one or both poles,[6] which are also oxidase-positive and grow optimally at 37 to 42 °C.[7][8][9][10] When exposed to atmospheric oxygen,C. jejuni is able to change into a coccal form.[11] This species of pathogenic bacteria is one of the most common causes of humangastroenteritis in the world.Food poisoning caused byCampylobacter species can be severely debilitating, but is rarely life-threatening. It has been linked with subsequent development ofGuillain–Barré syndrome, which usually develops two to three weeks after the initial illness.[12] Individuals with recentC. jejuni infections develop Guillain-Barré syndrome at a rate of 0.3 per 1000 infections, about 100 times more often than the general population.[13] Another chronic condition that may be associated with campylobacter infection isreactive arthritis.[14] Reactive arthritis is a complication strongly associated with a particular genetic make-up. That is, persons who have thehuman leukocyte antigen B27 (HLA-B27) are most susceptible. Most often, the symptoms of reactive arthritis will occur up to several weeks after infection.[4][15]
Campylobacter jejuni was originally namedVibrio jejuni due to its likeness toVibrio spp. until 1963. Seabald and Vernon proposed the genusCampylobacter due to its low levels of guanine and cytosine, non-fermentative metabolism, and microaerophilic growth requirements.[16] The first well recorded incident ofCampylobacter infection occurred in 1938.Campylobacter found in milk caused diarrhea among 355 inmates in two state institutions in Illinois.[16]C. jejuni was first discovered in the small intestines of humans in the 1970s, however, symptoms have been noted since the early 20th century.[17] TheCDC,USDA andFDA collectively identifiedC. jejuni as responsible for over 40% ofbacterial gastroenteritis found inlaboratories as of 1996.[18]
C. jejuni is unable to use sugars as a carbon source, primarily using amino acids for growth instead.[19] The main reasonC. jejuni lacks glycolytic capabilities is a lack ofglucokinase[20] and a lack of the6-phosphofructokinase enzyme to employ theEMP pathway.[16] The four main amino acidsC. jejuni takes in areserine,aspartate,asparagine, andglutamate, which are listed in order of preference.[16] If all of these are depleted, some strains can useproline as well.[16] Either the host or metabolic activity of other gut microbes can supply these amino acids.[19]
The metabolic pathwaysC. jejuni is capable of include theTCA cycle, anon-oxidative pentose phosphate pathway,gluconeogenesis, andfatty acid synthesis.[21] Serine is the most important amino acid used for growth, brought into the cell bySdaC transport proteins and further broken down intopyruvate by the SdaAdehydratase.[20] Though this pyruvate cannot directly be converted intophosphoenolpyruvic acid (asC. jejuni lacks thissynthetase), the pyruvate can enter the TCA cycle to formoxaloacetic acid intermediates that can be converted to phosphoenolpyruvic acid for gluconeogenesis.[21] This production of carbohydrates is important for the virulence factors ofC. jejuni.[21] The pyruvate created from serine can also be converted toacetyl CoA and be applied to fatty acid synthesis or continue into the TCA cycle to create precursors for other biosynthetic pathways.[21] Aspartate and glutamate are both brought into the cell via Peb1A transport proteins.[20] Glutamate can betransaminated into aspartate, and aspartate can bedeaminated to makefumerate that feeds into the TCA cycle as well.[20] Asparagine is also able to be deaminated into aspartate (which follows the process into the TCA cycle mentioned above).[20] While the amino acids listed above are able to be metabolized,C. jejuni is capable of taking in many of the other amino acids which helps to lower the anabolic cost ofde novo synthesis.[21]
If other sources of carbon are exhausted,C. jejuni can also useacetate andlactate as carbon sources.[20] Acetate is a normal secreted byproduct ofC. jejuni metabolism stemming from the recycling ofCoA, and the absence of other carbon sources can causeC. jejuni to "switch" this reaction to take in acetate for the conversion to acetyl-CoA (catalyzed byphosphate acetyltransferase andacetate kinase enzymes).[20][21] Lactate is a normal byproduct of many fermentative bacteria in the gut, andC. jejuni can take in andoxidize this lactate to supply pyruvate through the activity ofdehydrogenase iron-sulfur enzyme complexes.[20]
The energetic needs of these anabolic pathways are met in multiple ways. Thecytochrome c andquinol terminal oxidases allow forC. jejuni to use oxygen as a terminal electron acceptor for the reduced carriers produced through the TCA cycle (hence whyC. jejuni is considered anobligate microaerophile).[22] The conversion of acetyl-CoA to acetate mentioned above hassubstrate-level phosphorylation take place, giving another form of energy production without the use of microaerophilic respiration.[21]
C. jejuni can use many different electron donors for its metabolic processes, usingNADH andFADH most commonly – thoughC. jejuni uses NADH poorly compared to FADH due to a replacement of genes encoding subunits for NADHdehydrogenases for genes contributing to processes relating to FADH electron donation.[23] Aside from these donors,C. jejuni can turn to products from the host gut microbiota including hydrogen, lactate, succinate, andformate to contribute electrons; formate, for example, is generated through intestinalmixed-acid fermentation.[23] Unlike almost all otherCampylobacter orHelicobacter species,C. jejuni can also accept electrons fromsulfite andmetabisulfite through its cytochrome coxidoreductase system.[23]
While oxygen is mainly used as a terminal electron acceptor,C. jejuni can usenitrate, nitrite, sulfur oxides (such asdimethyl sulfoxide ortrimethylamine N-oxide), or fumarate as terminal electron acceptors as well to survive as a microaerophilic bacterium.[23] Due to oxygen-limited conditions in the common areas of colonization,C. jejuni possesses two separate terminal oxidases with different affinities for oxygen, where the low affinity oxidase can directly retrieve electrons frommenaquinones.[23] The adaptations allowing for multiple electron acceptors help to combat the problem withreactive oxygen species arising from the sole use of oxygen as well;C. jejuni cannot grow under strictly aerobic conditions. EnzymesC. jejuni carries to impede the effects of reactive oxygen species include:superoxide dismutase SodB,alkyl hydroxide reductase AhpC,catalase KatA, andthiolperoxidases Tpx and Bcp.[23]
Campylobacteriosis is an infectious disease caused by bacteria of the genusCampylobacter. In most patients presenting with campylobacteriosis, symptoms develop within two to five days of exposure to the organism and illness typically lasts seven days following onset.[24] Infection withC. jejuni typically results inenteritis, or inflammation of the small intestine, which is characterized by abdominal pain, voluminous diarrhea (often bloody), fever, andmalaise. Individuals infected with this bacteria can experience a prodromal phase of symptoms for the first 1 to 3 days, in which the more severe portion of the disease occurs. The prodromal phase presents with symptoms including rigors, high fever, body aches, and dizziness. Other than the prodromal phase, the acute diarrheal phase of enteritis usually lasts around 7 days, however abdominal pain can persist for weeks afterward.[3] The disease is usuallyself-limiting; however, it does respond toantibiotics. Severe (accompanying fevers, blood in stools) or prolonged cases may requireerythromycin,azithromycin,ciprofloxacin, ornorfloxacin. Fluid replacement viaoral rehydration salts may be needed and intravenous fluid may be required for serious cases.[24] Possible complications of campylobacteriosis includeGuillain–Barré syndrome andreactive arthritis.[3]
C. jejuni is azoonotic disease meaning it is more commonly spread from animals to people than in between humans. People most often contract it by touching something that has been in contact with raw or undercooked chicken in addition to eating or touching poultry that is raw or undercooked.[25] Additionally, it can also be obtained from being in contact with animals or eating undercooked seafood.[25] Thefecal oral route is the most common way it spreads as the bacterium is excreted in animal feces.[26]C. jejuni seldomly causes disease in animals and infections are more common in lower income countries.[27] Deadly infections are not often seen in young adults but rather among the young and elderly.[27] Due to poor sanitation practices in some areas, the bacteria can also be found in ice and water. It is difficult to know the science behind itstransmission due to itssporadic nature.[26][27] The use of antibiotics and other treatments help in slowing and preventing the transmission ofC. jejuni.[26]C. jejuni is afastidiousmicroaerophiles meaning it does need some oxygen to grow, spread, and transmit. However, it is highly adaptable and has adapted to grow in higher concentrations of oxygen.[28]
C. jejuni employs unique strategies to breach theintestinalepithelial layer of itshost cells.[29] It usesproteases, particularlyHtrA, to cleverly disruptcell junctions and temporarily traverse the cells.[29] The membrane-bound proteinFibronectin is a critical binding site forC. jejuni on thebasolateral side of the polarized epithelial cell, facilitating this process.[29] Once inside the cell,C. jejuni leveragesdynein to access theperinuclear space within theClathrin-Coated Vesicle, avoidinglysosomal digestion for up to 72 hours.[29]
To initiate infection,C. jejuni must penetrate the gutenterocytes.[30]C. jejuni releases several different toxins, mainly enterotoxin and cytotoxins, which vary from strain to strain and correlate with the severity of the enteritis (inflammation of the small intestine). During infection, levels of all immunoglobulin classes rise. Of these,IgA is the most important because it can cross the gut wall. IgA immobilises organisms, causing them to aggregate and activate complement, and also gives short-term immunity against the infecting strain of organism.[31] The bacteria colonize the small and large intestines, causing inflammatory diarrhea with fever. Stools contain leukocytes and blood. The role of toxins in pathogenesis is unclear.C jejuni antigens that cross-react with one or more neural structures may be responsible for triggering theGuillain–Barré syndrome.[10]
Hypoacylatedlipopolysaccharide (LPS) fromC. jejuni induces moderateTLR4-mediated inflammatory response in macrophages and suchLPS bioactivity may eventually result in the failure of local and systemic bacterial clearance in patients. At the same time, moderation of anti-bacterial responses may be advantageous for infected patients in clinical practice, since such an attenuatedLPS may not be able to induce severesepsis in susceptible individuals.[32]
One of the most important virulence factors ofC. jejuni areflagella. The flagellar protein FlaA has been proven to be one of the abundant proteins in the cell. Flagella are required for motility,biofilm formation, host cell interactions and host colonization. The flagella inC. jejuni can also aid in the secretion intracellular proteins.[19] The production of flagella is energetically costly so the production must be regulated from metabolic standpoint. CsrA is a post-transcriptional regulator that regulates the expression of FlaA by binding toflaA mRNA and is able to repress its translation.CsrA mutant strains have been studied and the mutant strains exhibit dysregulation of 120–150 proteins that are included in motility, host cell adherence, host cell invasion,chemotaxis, oxidative stress resistance, respiration and amino acid and acetate metabolism. Transcriptional and post-transcriptional regulation of flagellar synthesis inC. jejuni enables proper biosynthesis of flagella and it is important for pathogenesis of this bacteria.[33]
C. jejuni employs a highly sophisticated navigation system calledchemotaxis.[29] This system is crucial when the bacterium requires guidance through chemical signals.[29] The chemotaxis system uses specificchemoattractants that direct the bacterium toward areas with a higher concentration of the attractants.[29] The exact nature ofchemoattractants is dependent on the surrounding environmental conditions.[29] Additionally, when the bacterium needs to move away, it usesnegative chemotaxis to move in the opposite direction.[29]
Other important virulence factors ofC. jejuni includethepgl locus, which confers the ability to produceN-linked glycosylation of at least 22 bacterial proteins,[34] at least some of which appear to be important forcompetence, host adherence and invasion.[35]C. jejuni secretesCampylobacter invasive antigens (Cia), which facilitate invasion. The bacteria also produce cytolethal distending toxins that participate in cell cycle control and induction of host cell apoptosis.C. jejuni also exploits different adaptation strategies in which the host factors seem to play a role for pathogenesis of this bacteria.[36]
In the intestines,bile functions as a defensive barrier against colonization byC. jejuni.[37][38] WhenC. jejuni is grown in a medium containing the bile aciddeoxycholic acid, a component of bile, theDNA ofC. jejuni is damaged by a process involvingoxidative stress.[39][37] To survive,C. jejuni cellsrepair this DNA damage by a system employing proteins AddA and AddB that are needed for repair of DNA double-strand breaks.[37]
C. jejuni useshomologous recombination to repair its DNA, facilitated by the AddA and AddB proteins.[37] These proteins replaceRecBCD, which is used in other bacteria likeEscherichia coli.[37] AddA and AddB are crucial fornuclease,helicase, and Chi recognition,[40] which allow for successful homologous recombination.[37]
When AddA and AddB are introduced into a wildC. jejuni variant, an added deletion mutant geneaddAB gene is formed, which repairs DNA damaged byoxidative stress.[37] This inclusion protectsC. jejuni fromdeoxycholate found in bile, allowing for survival.[37] However, the added gene is absent during growth indeoxycholate from 10 to 16 hours and may beup-regulated in response to environmental conditions.[37] Additionally, AddAB proteins enhanceC. jejuni colonization of chicken intestines.[37]
Campylobacter jejuni infection and eventual destruction of host cell cause the release ofchemokines that cause inflammation and activate immune response cells. Inflammatory chemokines such asCXCL1,CCL3/CCL4,CCL2, andCXCL10 are upregulated, further triggering the immune response. The immune response activation is primarily driven by the use of ADP-heptoses to activateALPK1,[41] by aC. jejuni infection[29]
Neutrophil granulocytes usephagocytosis to combatC. jejuni infection, releasingantimicrobial proteins andproinflammatory substances. However,C. jejuni can influence the differentiation process of specific types of neutrophil granulocytes, triggeringhypersegmentation and increased reactivity, which leads to delayedapoptosis and higher production ofreactive oxygen species. In experimental processes,T cells from an immune response only start to grow in number at the inflammation site from the seventh day after infection.[29]
After 11 days of having aCampylobacter jejuni infection, theB lymphocytes in the body increase the production of antibodies that specifically fight againstC. jejuni flagellin.[29] The persistence of these antibodies in the body can last up to one-year post-infection. In this case, the development ofGuillain-Barré syndrome (GBS) is associated with autoimmuneIgG1 antibodies.[29]
Campylobacter infections often precedeGBS, indicating thatmolecular mimicry between the bacteria and host nervous tissues may be the underlying cause.[29]C. jejuni, the most common causative agent of humancampylobacteriosis, can survive in the gut for several days but does not establish a long-term infection due to its low replication rate, which is incompatible with a persistent bacterial presence.[29] The bacteria-induced apoptosis of infected gut cells results in the rapid clearance of thepathogen, which likely contributes to the self-limiting nature of the disease.[29]
Campylobacter jejuni is commonly associated with poultry, and it naturally colonises thedigestive tract of many bird species. All types of poultry and wild birds can become colonized with campylobacter. One study found that 30% of Europeanstarlings in farm settings inOxfordshire, United Kingdom, were carriers ofC. jejuni. It is also common in cattle, and although it is normally a harmlesscommensal of the gastrointestinal tract in these animals, it can causecampylobacteriosis in calves. It has also been isolated fromwombat andkangaroo feces, being a cause of bushwalkers'diarrhea. Contaminated drinking water and unpasteurized milk provide an efficient means for distribution. Contaminated food is a major source of isolated infections, with incorrectly prepared meat and poultry as the primary source of the bacteria.[42] Moreover, surveys show that 20 to 100% of retail chickens are contaminated. This is not overly surprising, since many healthy chickens carry these bacteria in their intestinal tracts and often in high concentrations, up to 108 cfu/g.[43] The bacteria contaminate the carcasses due to poor hygiene during the slaughter process. Several studies have shown increased concentrations of campylobacter on the carcasses after the evisceration.[44][43] Studies have investigated the chicken microbiome to understand how, why and when campylobacter appears within the chicken gut.[45] The impact of industrial system production systems on the chicken gut microbiome and campylobacter prevalence has also been investigated.[46]
Raw milk is also a source of infections. The bacteria are often carried by healthy cattle and by flies on farms. Unchlorinated water may also be a source of infections. However, properly cooking chicken, pasteurizing milk, and chlorinating drinking water kill the bacteria.[47] While salmonella is transmitted vertically in eggs, campylobacter is not. Therefore, consumption of eggs does result in human infection from campylobacter.[48]
Local complications of campylobacter infections occur as a result of direct spread from the gastrointestinal tract and can includecholecystitis,pancreatitis,peritonitis, and massivegastrointestinal hemorrhage. Extraintestinal manifestations of campylobacter infection are quite rare and may include meningitis, endocarditis, septic arthritis, osteomyelitis, andneonatal sepsis.Bacteremia is detected in <1% of patients with campylobacter enteritis and is most likely to occur in patients who are immunocompromised or among the very young or very old.[49] Transient bacteremia in immunocompetent hosts withC. jejuni enteritis may be more common but not detected because the killing action rapidly clears most normal human serotypes, and blood cultures are not routinely performed for patients with acute gastrointestinal illness.[50]
Serious systemic illness caused by campylobacter infection rarely occurs, but can lead to sepsis and death. The case-fatality rate for campylobacter infection is 0.05 per 1000 infections. For instance, one major possible complication thatC. jejuni can cause isGuillain–Barré syndrome, which induces neuromuscular paralysis in a sizeable percentage of those who suffer from it. Over time, the paralysis is typically reversible to some extent; nonetheless, about 20% of patients with GBS are left disabled, and around 5% die.[4][15] In March 2025, India reported 300 GBS cases; while only about one in 1000 individuals infected with C. jejuni develops GBS, India had more than 1000 C. jejuni outbreaks during 2024 and it is suspected that that a specific strain of C.jejuni with neurotoxic potential has been circulating.[51]
Another chronic condition that may be associated with campylobacter infection isreactive arthritis, which is strongly associated with a particular genetic make-up. That is, persons who have thehuman leukocyte antigen B27 (HLA-B27) are most susceptible. Most often, the symptoms of reactive arthritis will occur up to several weeks after infection.[4][15]
An estimated 2 million cases of campylobacter enteritis occur annually, accounting for 5–7% of cases of gastroenteritis.[52] Campylobacter has a large animal reservoir, with up to 100% of poultry, including chickens, turkeys, and waterfowl, having asymptomatic intestinal infections. The major reservoirs ofC. fetus are cattle and sheep. More than 90% of campylobacter infections occur during the summer months due to undercooked meats from outdoor cooking.[3] Nonetheless, the incidence of campylobacter infections has been declining. Changes in the incidence of culture-confirmedCampylobacter infections have been monitored by the Foodborne Diseases Active Surveillance Network (FoodNet) since 1996. In 2010, campylobacter incidence showed a 27% decrease compared with 1996–1998. In 2010, the incidence was 13.6 cases per 100,000 population, and this did not change significantly compared with 2006–2008.[53][54]
In 2020, there were around 120,000 cases ofC. jejuni infection, which showed a decline of about 25.4% compared to the previous year.[29] However, theCOVID-19 pandemic may have influenced this decrease, and its statistical significance is yet to be determined.[29]C. jejuni infections tend to peak in July, which could be linked to the rise in temperature worldwide.[29] This pattern is associated with an increased reflection rate of the bacteria, which needs further investigation to establish any potential correlations.[29]
Campylbacter jejuni infections are extremely common worldwide, although exact figures are not available. New Zealand reported the highest national rate, which peaked in May 2006 at 400 per 100,000 population.[1][54]C. jejuni infection is a significant global health issue, with infection rates ranging from 0.3 to 2.9%.[29] It is a widespread infection that affects individuals of all ages but is more prevalent indeveloping countries.[29] In these areas,diarrhea is the most common clinical presentation, and it has a severe impact on children.[29]
Campylobacter is more frequently isolated in males than females, and homosexual men appear to have a higher risk of infection by atypical campylobacter-related species such asHelicobacter cinaedi andHelicobacter fennelliae.[54]
Campylobacter infections can occur in all age groups. Studies show a peak incidence in children younger than 1 year and in people aged 15–29 years. The age-specific attack rate is highest in young children. In the United States, the highest incidence ofCampylobacter infection in 2010 was in children younger than 5 years and was 24.4 cases per 100,000 population.[53] Community based studies done in developing countries show about 60,000 out of every 100,000 children under five years old are affected by campylobacter infections.[3] However, the rate of fecal cultures positive for campylobacter species is greatest in adults and older children.[54]
Diagnostic tests are available to identify campylobacter infections, including those caused byC. jejuni.[3] Thestool culture is considered thegold standard for diagnosingC. jejuni,[55][better source needed] and selective culture techniques are used to distinguish it from other variants.[3] Stool cultures are grown at 42 degrees Celsius in an atmosphere of 85% N2, 10% CO2, and 5% O2, asC. jejuni requires these conditions due to beingthermophilic andmicroaerophilic.[56] A final diagnosis from a stool sample requires agram stain or phase contrast microscopy.[55]
Aside from stool cultures,C. jejuni can be detected usingenzyme immunoassay (EIA) orpolymerase chain reaction (PCR).[3] These methods are more sensitive than stool cultures, but PCR tends to be the most sensitive especially in children and developing countries.[57]
Campylobacter infections tend to be mild, requiring only hydration and electrolyte repletion while diarrhea lasts. Maintenance of electrolyte balance, not antibiotic treatment, is the cornerstone of treatment for campylobacter enteritis. Depending on the degree of dehydration, alternate measures may be taken includingparenteral methods of hydration.[58][59] Indeed, most patients with this infection have a self-limited illness and do not require antibiotics at all; however, they may be the best form of treatment in more severe cases of infection.
Antibiotic treatment forCampylobacter infections is usually not required nor recommended. Antibiotics are limited for treating high-risk patients including immunocompromised and older individuals. Severe cases exhibiting symptoms such as bloody stools, fever, severe abdominal pain, pregnancy, infection with HIV, and prolonged illness (symptoms that last > 1 week) may also require treatment by antibiotics which can help to shorten the duration of the symptoms.[3][15][53] It is advisable to treat these infections withmacrolide antibiotics, such aserythromycin orazithromycin. Erythromycin is inexpensive and limits toxic exposure to patients, however resistance rates are reportedly increasing; its use is continued however, as resistance rates remain below 5%.[60] Azithromycin usage is increasing due to various drug characteristics, including its once-a-day dosage, tolerability by patients, decreased relation toInfantile hypertrophic pyloric stenosis (IHPS), and less negative symptoms; this is comparative to erythromycin.Fluoroquinolones are another source of treatment, however resistance rates of bacteria to this type of antibiotic is greatly increasing.[60]
Fluoroquinolones were first approved as a treatment for campylobacter infections in 1986, and were later U.S. Food and Drug Administration (FDA) approved in 1996, so as to control infections in poultry flocks. The CDC began monitoring campylobacter in 1997 in the National Antimicrobial Resistance Monitoring System (NARMS). Data from NARMS indicatedciprofloxacin, a fluoroquinolone, had microbial resistance rates of 17% in 1997–1999, which further increased to 27% in 2015–2017.[60] On September 12, 2005, the FDA suspended the use of all fluoroquinolones in poultry production, and the prevalence of campylobacter strains that are fluoroquinolone resistant in poultry flocks, poultry products, production facilities, and human infections became vital to monitor; this was in an effort to determine if the fluoroquinolone ban led to a reduction in the antibiotic-resistant strains.[61] A presence of drug-resistance to ciprofloxacin has been observed in isolate studies, as well as significant drug-resistance among campylobacter to the antibioticsnalidixic acid andtetracyclines. There is a low rate of resistance toerythromycin, the preferred source of antibiotic treatment for campylobacter infections, however resistant strains have been detected in many countries among sources of the origin of food from farm animals.[62]
Some simple food-handling practices can help prevent campylobacter infections.[1]
| Characteristic | Result |
|---|---|
| Growth at 25 °C | − |
| Growth at 35–37 °C | + |
| Growth at 42 °C | + |
| Nitrate reduction | + |
| Catalase test | + |
| Oxidase test | + |
| Growth onMacConkey agar | + |
| Motility (wet mount) | + |
| Glucose use | − |
| Hippurate hydrolysis | + |
| Resistance tonalidixic acid | − |
| Resistance tocephalothin | + |
Under light microscopy,C. jejuni has a characteristic "sea-gull" shape as a consequence of its helical form. Campylobacter is grown on specially selective "CAMP"agar plates at 42 °C, the normal avian body temperature, rather than at 37 °C, the temperature at which most other pathogenic bacteria are grown. Since the colonies areoxidase positive, they usually only grow in scanty amounts on the plates.Microaerophilic conditions are required for luxurious growth. A selective blood agar medium (Skirrow's medium) can be used. Greater selectivity can be gained with an infusion of a cocktail of antibiotics:vancomycin,polymixin-B,trimethoprim, andactidione (Preston's agar),[63] and growth undermicroaerophilic conditions at 42 °C.
The genome ofC. jejuni strain NCTC11168 was published in 2000, revealing 1,641,481base pairs (30.6% G+C) predicted to encode 1,654proteins and 54 stableRNA species. The genome is unusual in that virtually noinsertion sequences orphage-associated sequences and very fewrepeat sequences are found. One of the most striking findings in the genome was the presence of hypervariable sequences. These shorthomopolymeric runs ofnucleotides were commonly found in genes encoding the biosynthesis or modification of surface structures, or in closely linked genes of unknown function. The apparently high rate of variation of these homopolymeric tracts may be important in the survival strategy ofC. jejuni.[64] The genome was re-annotated in 2007 updating 18.2% of product functions.[65] Analysis also predicted the firstpathogenicity island inC. jejuni among select strains, harbouring the bacteria'sType VI secretion system and putative cognate effectors.[66]
Initialtransposon mutagenesis screens revealed 195essential genes, although this number is likely to go up with additional analysis.[67]
C. jejuni is naturally competent for genetic transformation.[68]Natural genetic transformation is a sexual process involving DNA transfer from one bacterium to another through the intervening medium, and the integration of the donor sequence into the recipient genome byhomologous recombination.C. jejuni freely takes up foreign DNA harboring genetic information responsible forantibiotic resistance.[68] Antibiotic resistance genes are more frequently transferred in biofilms than betweenplanktonic cells (single cells that float in liquid media).[69]
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