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Campylobacter jejuni
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Campylobacter jejuni
Campylobacter jejuni is a species of pathogenic bacteria that is commonly associated with poultry, and is also often found in animal feces. This species of microbe is one of the most common causes of food 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 are diagnosed 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. 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. In Africa, Asia, and the Middle East, data indicates that C. jejuni infections are endemic.
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.
C. jejuni is commonly associated with poultry, and is also commonly found in animal feces. Campylobacter is a helical-shaped, non-spore-forming, Gram-negative, microaerophilic, nonfermenting motile bacterium with a single flagellum at one or both poles, which are also oxidase-positive and grow optimally at 37 to 42 °C. When exposed to atmospheric oxygen, C. jejuni is able to change into a coccal form. This species of pathogenic bacteria is one of the most common causes of human gastroenteritis in the world. Food poisoning caused by Campylobacter species can be severely debilitating, but is rarely life-threatening. It has been linked with subsequent development of Guillain–Barré syndrome, which usually develops two to three weeks after the initial illness. Individuals with recent C. jejuni infections develop Guillain-Barré syndrome at a rate of 0.3 per 1000 infections, about 100 times more often than the general population. Another chronic condition that may be associated with campylobacter infection is reactive arthritis. Reactive arthritis is a complication strongly associated with a particular genetic make-up. That is, persons who have the human leukocyte antigen B27 (HLA-B27) are most susceptible. Most often, the symptoms of reactive arthritis will occur up to several weeks after infection.
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. 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. C. jejuni was first discovered in the small intestines of humans in the 1970s, however, symptoms have been noted since the early 20th century. The CDC, USDA and FDA collectively identified C. jejuni as responsible for over 40% of bacterial gastroenteritis found in laboratories as of 1996.
C. jejuni is unable to use sugars as a carbon source, primarily using amino acids for growth instead. The main reason C. jejuni lacks glycolytic capabilities is a lack of glucokinase and a lack of the 6-phosphofructokinase enzyme to employ the EMP pathway. The four main amino acids C. jejuni takes in are serine, aspartate, asparagine, and glutamate, which are listed in order of preference. If all of these are depleted, some strains can use proline as well. Either the host or metabolic activity of other gut microbes can supply these amino acids.
The metabolic pathways C. jejuni is capable of include the TCA cycle, a non-oxidative pentose phosphate pathway, gluconeogenesis, and fatty acid synthesis. 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. 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. This production of carbohydrates is important for the virulence factors of C. jejuni. 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. Aspartate and glutamate are both brought into the cell via Peb1A transport proteins. Glutamate can be transaminated into aspartate, and aspartate can be deaminated to make fumerate that feeds into the TCA cycle as well. Asparagine is also able to be deaminated into aspartate (which follows the process into the TCA cycle mentioned above). 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.
If other sources of carbon are exhausted, C. jejuni can also use acetate and lactate as carbon sources. 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). 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.
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). 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.
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Campylobacter jejuni
Campylobacter jejuni is a species of pathogenic bacteria that is commonly associated with poultry, and is also often found in animal feces. This species of microbe is one of the most common causes of food 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 are diagnosed 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. 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. In Africa, Asia, and the Middle East, data indicates that C. jejuni infections are endemic.
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.
C. jejuni is commonly associated with poultry, and is also commonly found in animal feces. Campylobacter is a helical-shaped, non-spore-forming, Gram-negative, microaerophilic, nonfermenting motile bacterium with a single flagellum at one or both poles, which are also oxidase-positive and grow optimally at 37 to 42 °C. When exposed to atmospheric oxygen, C. jejuni is able to change into a coccal form. This species of pathogenic bacteria is one of the most common causes of human gastroenteritis in the world. Food poisoning caused by Campylobacter species can be severely debilitating, but is rarely life-threatening. It has been linked with subsequent development of Guillain–Barré syndrome, which usually develops two to three weeks after the initial illness. Individuals with recent C. jejuni infections develop Guillain-Barré syndrome at a rate of 0.3 per 1000 infections, about 100 times more often than the general population. Another chronic condition that may be associated with campylobacter infection is reactive arthritis. Reactive arthritis is a complication strongly associated with a particular genetic make-up. That is, persons who have the human leukocyte antigen B27 (HLA-B27) are most susceptible. Most often, the symptoms of reactive arthritis will occur up to several weeks after infection.
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. 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. C. jejuni was first discovered in the small intestines of humans in the 1970s, however, symptoms have been noted since the early 20th century. The CDC, USDA and FDA collectively identified C. jejuni as responsible for over 40% of bacterial gastroenteritis found in laboratories as of 1996.
C. jejuni is unable to use sugars as a carbon source, primarily using amino acids for growth instead. The main reason C. jejuni lacks glycolytic capabilities is a lack of glucokinase and a lack of the 6-phosphofructokinase enzyme to employ the EMP pathway. The four main amino acids C. jejuni takes in are serine, aspartate, asparagine, and glutamate, which are listed in order of preference. If all of these are depleted, some strains can use proline as well. Either the host or metabolic activity of other gut microbes can supply these amino acids.
The metabolic pathways C. jejuni is capable of include the TCA cycle, a non-oxidative pentose phosphate pathway, gluconeogenesis, and fatty acid synthesis. 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. 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. This production of carbohydrates is important for the virulence factors of C. jejuni. 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. Aspartate and glutamate are both brought into the cell via Peb1A transport proteins. Glutamate can be transaminated into aspartate, and aspartate can be deaminated to make fumerate that feeds into the TCA cycle as well. Asparagine is also able to be deaminated into aspartate (which follows the process into the TCA cycle mentioned above). 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.
If other sources of carbon are exhausted, C. jejuni can also use acetate and lactate as carbon sources. 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). 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.
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). 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.
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