Campylobacter jejuni
Campylobacter jejuni | |
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Scientific classification | |
Domain: | Bacteria |
Phylum: | Campylobacterota |
Class: | "Campylobacteria"
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Order: | Campylobacterales |
Family: | Campylobacteraceae
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Genus: | Campylobacter |
Species: | C. jejuni
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Binomial name | |
Campylobacter jejuni (Jones et al., 1931) Veron & Chatelain, 1973
|
Campylobacter jejuni is a species of
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 Greek kampylos (curved) and baktron (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
History
Campylobacter jejuni was originally named Vibrio jejuni due to its likeness to Vibrio spp. until 1963. Seabald and Vernon proposed the genus Campylobacter due to its low levels of guanine and cytosine, non-fermentative metabolism, and microaerophilic growth requirements.[16] In 1886 a pediatrician, Theodor Escherich, observed Campylobacters from diarrhea samples of children.[17] The first isolation of C. jejuni was in Brussels, Belgium, from stool samples of a patient with diarrhea.[17] The first well recorded incident of Campylobacter infection occurred in 1938. Campylobacter found in milk caused diarrhea among 355 inmates in two state institutions in Illinois.[16]
Metabolism
C. jejuni is unable to utilize sugars as a carbon source, primarily using amino acids for growth instead.[18] The main reason C. jejuni lacks glycolytic capabilities is a lack of glucokinase[19] and a lack of the 6-phosphofructokinase enzyme to employ the EMP pathway.[20] The four main amino acids C. jejuni takes in are serine, aspartate, asparagine, and glutamate, which are listed in order of preference.[20] If all of these are depleted, some strains can use proline as well.[20] Either the host or metabolic activity of other gut microbes can supply these amino acids.[18]
The metabolic pathways C. jejuni is capable of include the TCA cycle, a non-oxidative pentose phosphate pathway, gluconeogenesis, and fatty acid synthesis.[21] Serine is the most important amino acid used for growth, brought into the cell by SdaC transport proteins and further broken down into pyruvate by the SdaA dehydratase.[19] Though this pyruvate cannot directly be converted into phosphoenolpyruvic acid (as C. jejuni lacks this synthetase), the pyruvate can enter the TCA cycle to form oxaloacetic acid intermediates that can be converted to phosphoenolpyruvic acid for gluconeogenesis.[21] This production of carbohydrates is important for the virulence factors of C. jejuni.[21] The pyruvate created from serine can also be converted to acetyl 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.[19] Glutamate can be transaminated into aspartate, and aspartate can be deaminated to make fumerate that feeds into the TCA cycle as well.[19] Asparagine is also able to be deaminated into aspartate (which follows the process into the TCA cycle mentioned above).[19] 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 of de novo synthesis.[21]
If other sources of carbon are exhausted, C. jejuni can also utilize acetate and lactate as carbon sources.[19] Acetate is a normal secreted byproduct of C. jejuni metabolism stemming from the recycling of CoA, and the absence of other carbon sources can cause C. jejuni to "switch" this reaction to take in acetate for the conversion to acetyl-CoA (catalyzed by phosphate acetyltransferase and acetate kinase enzymes).[19][21] Lactate is a normal byproduct of many fermentative bacteria in the gut, and C. jejuni can take in and oxidize this lactate to supply pyruvate through the activity of dehydrogenase iron-sulfur enzyme complexes.[19]
The energetic needs of these anabolic pathways are met in multiple ways. The cytochrome c and quinol terminal oxidases allow for C. jejuni to use oxygen as a terminal electron acceptor for the reduced carriers produced through the TCA cycle (hence why C. jejuni is considered an obligate microaerophile).[22] The conversion of acetyl-CoA to acetate mentioned above has substrate-level phosphorylation take place, giving another form of energy production without the use of microaerophilic respiration.[21]
Disease
Pathogenesis
To initiate infection, C. jejuni must penetrate the gut
Hypoacylated
One of the most important virulence factors of C. jejuni are flagella. 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 in C. jejuni can also aid in the secretion intracellular proteins.[28] 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 to flaA 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 in C. jejuni enables proper biosynthesis of flagella and it is important for pathogenesis of this bacteria.[29]
Other important virulence factors of C. jejuni are the ability to produce N-linked glycosylation of more than 30 proteins. These proteins are important for the bacteria colonization, adherence and invasion. C. jejuni secretes Campylobacter invasive antigens (Cia) which facilitates the motility. The bacteria produces also 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.[30]
Sources
Campylobacter jejuni is commonly associated with
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.[36] Campylobacter is not, in contrast to Salmonella, transmitted vertically into eggs and therefore humans do not get infected by consuming eggs.[citation needed]
Possible complications
Local complications of Campylobacter infections occur as a result of direct spread from the gastrointestinal tract and can include
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 that C. jejuni can cause is Guillain–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. Another chronic condition that may be associated with Campylobacter infection is
Epidemiology
Frequency
United States
An estimated 2 million cases of Campylobacter enteritis occur annually, accounting for 5–7% of cases of gastroenteritis.[38] Campylobacter organisms have a large animal reservoir, with up to 100% of poultry, including chickens, turkeys, and waterfowl, having asymptomatic intestinal infections. The major reservoirs of C. fetus are cattle and sheep. More than 90% of Campylobacter infections occur during the summer months due to undercooked meats from outdoor cooking.[39] Nonetheless, the incidence of Campylobacter infections has been declining. Changes in the incidence of culture-confirmed Campylobacter 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.[40][41]
International
Campylbacter jejuni infections are extremely common worldwide, although exact figures are not available. New Zealand reported the highest national campylobacteriosis rate, which peaked in May 2006 at 400 per 100,000 population.[1][41]
Sex
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 as Helicobacter cinaedi and Helicobacter fennelliae.[41]
Age
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 of Campylobacter infection in 2010 was in children younger than 5 years and was 24.4 cases per 100,000 population.[40] 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.[39] However, the rate of fecal cultures positive for Campylobacter species is greatest in adults and older children.[41]
Evaluation
Campylobacter infections can be diagnosed through stool culture, enzyme immunoassay, or PCR. However, enzyme immunoassay and PCR are both higher in sensitivity than stool culture. Selective culture techniques are used in stool culture to isolate C. jejuni.[39]
Treatment
Patients with Campylobacter infection should drink plenty of fluids as long as the diarrhea lasts to maintain hydration. Patients should also get rest. If they cannot drink enough fluids to prevent dehydration or if the symptoms are severe, medical help is indicated. In more severe cases, certain antibiotics can be used and can shorten the duration of symptoms if given early in the illness.[40] Moreover, maintenance of electrolyte balance, not antibiotic treatment, is the cornerstone of treatment for Campylobacter enteritis. Indeed, most patients with this infection have a self-limited illness and do not require antibiotics at all. Nevertheless, antibiotics should be used in specific clinical circumstances. These include high fevers, bloody stools, prolonged illness (symptoms that last >1 week), pregnancy, infection with HIV, and other immunocompromised states.[15]
Prevention
Some simple food-handling practices can help prevent Campylobacter infections.[1]
- Cook all poultry products thoroughly. Make sure that the meat is cooked throughout (no longer pink) and any juices run clear. All poultry should be cooked to reach a minimum internal temperature of 165 °F (74 °C).
- Wash hands with soap before preparing food.
- Wash hands with soap after handling raw foods of animal origin and before touching anything else.
- Prevent cross-contamination in the kitchen by using separate cutting boards for foods of animal origin and other foods and by thoroughly cleaning all cutting boards, countertops, and utensils with soap and hot water after preparing raw food of animal origin.
- Do not drink unpasteurized milk or untreated surface water.
- Make sure that people with diarrhea, especially children, wash their hands carefully and frequently with soap to reduce the risk of spreading the infection.
- Wash hands with soap after contact with pet feces.
Genome
The genome of C. jejuni strain NCTC11168 was published in 2000, revealing 1,641,481
Initial transposon mutagenesis screens revealed 195 essential genes, although this number is likely to go up with additional analysis.[45]
Natural genetic transformation
C. jejuni is naturally competent for genetic transformation.
DNA repair
In the intestinal environment, bile functions as a defensive barrier against colonization by C. jejuni.[47][48] When C. jejuni is grown in a medium containing the bile acid deoxycholic acid, a component of bile, the DNA of C. jejuni is damaged by a process involving oxidative stress.[49][47] To survive, C. jejuni cells repair this DNA damage by a system employing proteins AddA and AddB that are needed for repair of DNA double-strand breaks.[47]
Laboratory characteristics
Characteristic | Result |
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Growth at 25 °C | − |
Growth at 35–37 °C | + |
Growth at 42 °C | + |
Nitrate reduction | + |
Catalase test
|
+ |
Oxidase test | + |
Growth on MacConkey agar | + |
Motility (wet mount) | + |
Glucose utilization | − |
Hippurate hydrolysis
|
+ |
Resistance to nalidixic acid | − |
Resistance to cephalothin
|
+ |
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"
See also
References
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External links
- Campylobacter jejuni genomes and related information at PATRIC, a Bioinformatics Resource Center funded by NIAID
- Current research on Campylobacter jejuni at the Norwich Research Park Archived 2017-06-14 at the Wayback Machine
- Type strain of Campylobacter jejuni at BacDive - the Bacterial Diversity Metadatabase