Campylobacter lari is a bacterium that can cause gastroenteritis and other complications in humans and animals. It is less well-known than other Campylobacter species, such as C. jejuni and C. coli. However, studies have reported crucial epidemiological information about C. lari.
Campylobacter lari is the third most common Campylobacter species in humans with gastroenteritis. It has been identified as a cause of reactive arthritis following enteritis, indicating potential complications associated with the infection. The bacterium was isolated from gulls, starlings, mussels, & oysters, among other things. Shellfish contamination is thought to occur via bird reservoirs, resulting in C. lari in certain seafood products.
From 2010 to 2017, state, municipal, and territorial public health officials reported 236 foodborne Campylobacter instances to the Centers for Disease Control and Prevention’s Foodborne Diseases Outbreak Monitoring System, accounting for 2,381 instances. Campylobacter lari is frequently identified in seagulls and other birds, which can be transmitted to humans by contaminated water or food.
Campylobacter lari is frequently found in seagulls and other bird species, serving as a natural reservoir for the bacterium. Transmission to humans can occur via contact with contaminated water or food. Campylobacter lari accounts for approximately 1% to 2% of human campylobacteriosis cases in Europe and North America. However, its prevalence may vary in different regions, with higher occurrence reported in areas such as Japan and Thailand.
Kingdom: Bacteria
Phylum: Proteobacteria
Class: Epsilonproteobacteria
Order: Campylobacterales
Family: Campylobacteraceae
Genus: Campylobacter
Species: Campylobacter lari
Campylobacter lari is a gram-negative bacterium with a distinct spiral or corkscrew shape, characteristic of the Campylobacter genus.
It is a microaerophilic bacterium; it prefers environments with low oxygen levels. The structure of C. lari can exhibit variations in shape, transitioning from its spiral form to more coccoid (spherical), circular, or elongated shapes when exposed to oxygen or cultured for extended periods.
The bacterium is equipped with long flagella that enable motility. These flagella are located at either one end (polar flagellation) or both ends (bipolar flagellation) of the cell. The motility the flagella provides allows C. lari to move in a corkscrew-like manner.
Colony formation of Campylobacter lari typically results in colorless colonies with a diameter ranging from 1.0 -1.5 µm. They have 1602 genes, 1545 of which are protein genes & 57 of which are RNA genes.
Campylobacter lari’s genomic structure consists of a circular, double-stranded DNA molecule with a size of around 1,525,460 base pairs long. This genome comprises many genes that are responsible for various bacterial functions. Notably, three genes, VP1, VP2, & VP3, encode the capsid components. These proteins are involved in developing the bacterium’s outer protein coat.
Campylobacter lari, a species of bacteria, consists of two subspecies: C. lari subsp. lari and C. lari subsp. concheus. The type-strain of C. lari, NCTC 113522, belongs to the subspecies lari. However, various strains of C. lari have been isolated from different sources, including pigs, cattle, dogs, poultry, shellfish, birds, and humans, indicating the broad distribution and potential reservoirs of this bacterium.
The cytolethal distending toxin (cdt), composed of three subunits: cdtA, cdtB, & cdtC, is one significant virulence factor. In eukaryotic cells, this toxin causes cell cycle arrest & apoptosis. The cdtB gene, which produces the toxin’s catalytic component, is found in all Campylobacter isolates, including C. lari.
Another type of virulence factor is adhesion proteins, which allow Campylobacter lari to connect to host cells and tissues, notably the intestinal epithelium. CadF, which binds to fibronectin, FlaA, an essential flagellar protein; & CbpA, which interacts with collagen, are all examples of adhesion proteins. While the cadF and flaA genes are present in all Campylobacter isolates, the cbpA gene may vary between strains.
C. lari uses invasion machinery to infiltrate host cells and avoid detection by the immune system. It contains proteins like CiaB, a type III secretion system component, PldA, a phospholipase that destroys host cell membranes & CsrA, an invasion gene regulator. The presence of the ciaB & pldA genes varies between Campylobacter isolates, but the csrA gene is more prevalent.
C. lari also has a new potential virulence locus termed LicABCD. This locus encodes four proteins with unknown roles, which may be involved in lipooligosaccharide modification or transport. The features of the LicABCD locus can differ between Campylobacter species & strains, contributing to pathogenicity variability.
Campylobacter lari is a bacterium that, in both humans and animals, can cause gastroenteritis and other issues. C. lari pathogenicity encompasses multiple methods by which the bacteria infect and destroys host tissues. C. lari can colonize the intestinal mucosa using its spiral structure and flagella to penetrate and attach to epithelial cells. Once attached, the bacterium invades the cells & causes damage via a variety of mechanisms. It involves the triggering of apoptosis, or programmed cell death, the breaking of epithelial cell tight junctions, and the activation of inflammatory pathways.
Campylobacter lari can also produce toxins such as cytolethal-distending (CDT). The CDT disrupts the cell cycle & DNA repair pathways, resulting in cell death and tissue damage. C. lari can also change its surface antigens, like lipooligosaccharide (LOS) & capsular polysaccharide (CPS). This change allows the bacterium to elude the host immune system, allowing for long-term infection and possible chronic consequences.
Campylobacter lari can spread from the intestines to the bloodstream and other organs, such as the liver and pancreas. This dissemination can lead to systemic infection and complications such as bacteremia, hepatitis, and pancreatitis. Campylobacter lari can cause autoimmune reactions in some people. It accomplishes this by using its LOS to imitate human gangliosides, forming cross-reactive antibodies. These antibodies assault peripheral nerves by mistake, resulting in Guillain-Barre syndrome.
The human immune system triggers several tasks in combating Campylobacter lari infection. However, research into the precise immunological response to Campylobacter in people needs to be more extensive. Some findings demonstrated significant differences in pro-inflammatory (IL-8, IL-6, IFN-γ) & regulatory (IL-10) cytokines in response to Campylobacter stimulation among individuals. These changes could be attributed to variances in the constitutive expression levels of toll-like receptors (TLRs), which identify pathogen-associated molecular patterns (PAMPs) and initiate an immune response. Previous research using human intestinal epithelial cells has shown that pro-inflammatory cytokines and the secretion of IL-8 & IL-6 are produced in response to Campylobacter activation.
In response to infection, IL-8, released by different cells with TLRs, works as a chemoattractant to recruit immune cells, notably neutrophils. The immune response and the creation of inflammatory mediators are stimulated by IL-6, released by macrophages, T cells, & endothelial cells. These two cytokines, IL-8 & IL-6, are essential in the immune response to Campylobacter infection. However, the experiments only elicited low IFN-γ, a crucial cytokine in the adaptive immune response. According to the research, intestinal epithelial cells are the first to detect Campylobacter cells via their receptors and begin signaling pathways, eventually mobilizing innate immune cells to the site of infection.
The induction of innate immune cells & the activation of different receptor-dependent signaling pathways are critical for bacterial clearance. However, the precise role of immunological components during Campylobacter infection, like cathelicidins, bactericidal permeability-increasing protein molecules, chemokines, inflammasomes, siglec-7 receptors, acute phase protein levels, and T-cell subsets, remains unknown. Understanding these immune responses and filling information gaps will help us better understand human immunity to Campylobacter lari & guide future research efforts.
Campylobacter lari infection can result in various clinical manifestations depending on the individual and the specific strain of the bacteria involved. The most common clinical presentation is an acute gastrointestinal illness characterized by symptoms such as watery or bloody diarrhea, abdominal pain, fever, nausea, and vomiting. Typically, these symptoms develop within 2 to 5 days after ingestion of the bacteria and typically resolve within about a week.
Fever, ranging from 38 to 40°C, is a consistent feature of systemic Campylobacter infection and tends to follow a relapsing or intermittent pattern. Abdominal pain, often localized in the right lower quadrant, and headaches and myalgias (muscle pain) are also frequently reported symptoms. It is important to note that not all Campylobacter infections present with diarrheal illness; some individuals may present with different manifestations, such as subacute bacterial endocarditis (more commonly associated with C. fetus), reactive arthritis, meningitis, or a sluggish fever of unknown origin.
Joint involvement, specifically reactive arthritis, may occur in some cases and often affects a single joint, most commonly the knees. Symptoms of reactive arthritis typically resolve spontaneously within a span of 1 week to several months.
Campylobacter infection is commonly characterized by diarrhea, which can be bloody, accompanied by fever and stomach cramps. Nausea and vomiting may also occur along with the diarrhea. These symptoms generally last for about a week after the initial ingestion of Campylobacter. In some instances, complications may arise from Campylobacter infection, including irritable bowel syndrome, temporary paralysis, arthritis, bacteremia, hepatitis, pancreatitis (inflammation of the pancreas), miscarriage, and Guillain-Barre syndrome (a rare neurological disorder causing weakness and paralysis).
Immunocompromised individuals, like those with HIV infection or who have undergone organ transplantation, are at a higher risk of developing these complications. Additionally, Campylobacter can occasionally spread to the bloodstream in people with weakened immune systems, leading to severe and potentially life-threatening infections.
The diagnosis of Campylobacter lari infection can be achieved through various laboratory tests.
Culture method: It is the gold standard method for diagnosing Campylobacter lari from stool samples. Selective media such as charcoal cefoperazone deoxycholate agar or Skirrow’s medium are inoculated with the stool sample to perform a culture. The plates are then incubated under specific microaerobic conditions, typically 5% oxygen, 10% carbon dioxide, and 85% nitrogen, at 42°C for 48 hours. Colonies typically appear as small, round, and gray to translucent colonies. These colonies are examined for characteristics, including morphology, Gram staining, oxidase reaction, catalase reaction, hippurate hydrolysis, and nitrate reduction. Additionally, the ability of the colonies to grow at different temperatures, precisely 25°C and 37°C, can help distinguish C. lari from other closely related Campylobacter species, such as C. jejuni and C. coli.
Polymerase chain reaction (PCR): It is a rapid and sensitive method for detecting and differentiating Campylobacter lari. It involves extracting DNA from the stool sample and amplifying specific genes of the bacterium using targeted primers. The amplified products can be detected using gel electrophoresis, hybridization probes, or real-time fluorescence, allowing for accurate identification.
Serology: Another diagnostic approach detects antibodies against Campylobacter lari in the patient’s serum. This blood test utilizes techniques such as enzyme-linked immunosorbent assay (ELISA) or immunofluorescence assay (IFA) to measure the levels of immunoglobulins (IgM, IgG, or IgA) specific to Campylobacter lari antigens. Serology is useful for epidemiological studies and can assist in diagnosing chronic or extraintestinal infections.
Regular and thorough handwashing with water & soap, especially before handling food, after restroom usage, and after contact with animals or their feces.
Campylobacter lari can be found mainly in birds & often animals. Implementing effective animal management methods, like keeping farms clean and sanitary, disposing of waste properly, and managing the spread of pathogens in animal populations, can help lower the risk of transmission.
Campylobacter lari is frequently spread via contaminated food, particularly poultry products. It is critical to handle & prepare food safely to avoid bacterial contamination. It involves appropriately cooking chicken to kill bacteria, minimizing cross-contamination between cooked and raw foods, maintaining excellent hygiene while handling food, & storing perishable products at suitable temperatures.
Campylobacter lari – microbewiki (kenyon.edu)
Campylobacter Lari – an overview | ScienceDirect Topics
Campylobacter lari is a bacterium that can cause gastroenteritis and other complications in humans and animals. It is less well-known than other Campylobacter species, such as C. jejuni and C. coli. However, studies have reported crucial epidemiological information about C. lari.
Campylobacter lari is the third most common Campylobacter species in humans with gastroenteritis. It has been identified as a cause of reactive arthritis following enteritis, indicating potential complications associated with the infection. The bacterium was isolated from gulls, starlings, mussels, & oysters, among other things. Shellfish contamination is thought to occur via bird reservoirs, resulting in C. lari in certain seafood products.
From 2010 to 2017, state, municipal, and territorial public health officials reported 236 foodborne Campylobacter instances to the Centers for Disease Control and Prevention’s Foodborne Diseases Outbreak Monitoring System, accounting for 2,381 instances. Campylobacter lari is frequently identified in seagulls and other birds, which can be transmitted to humans by contaminated water or food.
Campylobacter lari is frequently found in seagulls and other bird species, serving as a natural reservoir for the bacterium. Transmission to humans can occur via contact with contaminated water or food. Campylobacter lari accounts for approximately 1% to 2% of human campylobacteriosis cases in Europe and North America. However, its prevalence may vary in different regions, with higher occurrence reported in areas such as Japan and Thailand.
Kingdom: Bacteria
Phylum: Proteobacteria
Class: Epsilonproteobacteria
Order: Campylobacterales
Family: Campylobacteraceae
Genus: Campylobacter
Species: Campylobacter lari
Campylobacter lari is a gram-negative bacterium with a distinct spiral or corkscrew shape, characteristic of the Campylobacter genus.
It is a microaerophilic bacterium; it prefers environments with low oxygen levels. The structure of C. lari can exhibit variations in shape, transitioning from its spiral form to more coccoid (spherical), circular, or elongated shapes when exposed to oxygen or cultured for extended periods.
The bacterium is equipped with long flagella that enable motility. These flagella are located at either one end (polar flagellation) or both ends (bipolar flagellation) of the cell. The motility the flagella provides allows C. lari to move in a corkscrew-like manner.
Colony formation of Campylobacter lari typically results in colorless colonies with a diameter ranging from 1.0 -1.5 µm. They have 1602 genes, 1545 of which are protein genes & 57 of which are RNA genes.
Campylobacter lari’s genomic structure consists of a circular, double-stranded DNA molecule with a size of around 1,525,460 base pairs long. This genome comprises many genes that are responsible for various bacterial functions. Notably, three genes, VP1, VP2, & VP3, encode the capsid components. These proteins are involved in developing the bacterium’s outer protein coat.
Campylobacter lari, a species of bacteria, consists of two subspecies: C. lari subsp. lari and C. lari subsp. concheus. The type-strain of C. lari, NCTC 113522, belongs to the subspecies lari. However, various strains of C. lari have been isolated from different sources, including pigs, cattle, dogs, poultry, shellfish, birds, and humans, indicating the broad distribution and potential reservoirs of this bacterium.
The cytolethal distending toxin (cdt), composed of three subunits: cdtA, cdtB, & cdtC, is one significant virulence factor. In eukaryotic cells, this toxin causes cell cycle arrest & apoptosis. The cdtB gene, which produces the toxin’s catalytic component, is found in all Campylobacter isolates, including C. lari.
Another type of virulence factor is adhesion proteins, which allow Campylobacter lari to connect to host cells and tissues, notably the intestinal epithelium. CadF, which binds to fibronectin, FlaA, an essential flagellar protein; & CbpA, which interacts with collagen, are all examples of adhesion proteins. While the cadF and flaA genes are present in all Campylobacter isolates, the cbpA gene may vary between strains.
C. lari uses invasion machinery to infiltrate host cells and avoid detection by the immune system. It contains proteins like CiaB, a type III secretion system component, PldA, a phospholipase that destroys host cell membranes & CsrA, an invasion gene regulator. The presence of the ciaB & pldA genes varies between Campylobacter isolates, but the csrA gene is more prevalent.
C. lari also has a new potential virulence locus termed LicABCD. This locus encodes four proteins with unknown roles, which may be involved in lipooligosaccharide modification or transport. The features of the LicABCD locus can differ between Campylobacter species & strains, contributing to pathogenicity variability.
Campylobacter lari is a bacterium that, in both humans and animals, can cause gastroenteritis and other issues. C. lari pathogenicity encompasses multiple methods by which the bacteria infect and destroys host tissues. C. lari can colonize the intestinal mucosa using its spiral structure and flagella to penetrate and attach to epithelial cells. Once attached, the bacterium invades the cells & causes damage via a variety of mechanisms. It involves the triggering of apoptosis, or programmed cell death, the breaking of epithelial cell tight junctions, and the activation of inflammatory pathways.
Campylobacter lari can also produce toxins such as cytolethal-distending (CDT). The CDT disrupts the cell cycle & DNA repair pathways, resulting in cell death and tissue damage. C. lari can also change its surface antigens, like lipooligosaccharide (LOS) & capsular polysaccharide (CPS). This change allows the bacterium to elude the host immune system, allowing for long-term infection and possible chronic consequences.
Campylobacter lari can spread from the intestines to the bloodstream and other organs, such as the liver and pancreas. This dissemination can lead to systemic infection and complications such as bacteremia, hepatitis, and pancreatitis. Campylobacter lari can cause autoimmune reactions in some people. It accomplishes this by using its LOS to imitate human gangliosides, forming cross-reactive antibodies. These antibodies assault peripheral nerves by mistake, resulting in Guillain-Barre syndrome.
The human immune system triggers several tasks in combating Campylobacter lari infection. However, research into the precise immunological response to Campylobacter in people needs to be more extensive. Some findings demonstrated significant differences in pro-inflammatory (IL-8, IL-6, IFN-γ) & regulatory (IL-10) cytokines in response to Campylobacter stimulation among individuals. These changes could be attributed to variances in the constitutive expression levels of toll-like receptors (TLRs), which identify pathogen-associated molecular patterns (PAMPs) and initiate an immune response. Previous research using human intestinal epithelial cells has shown that pro-inflammatory cytokines and the secretion of IL-8 & IL-6 are produced in response to Campylobacter activation.
In response to infection, IL-8, released by different cells with TLRs, works as a chemoattractant to recruit immune cells, notably neutrophils. The immune response and the creation of inflammatory mediators are stimulated by IL-6, released by macrophages, T cells, & endothelial cells. These two cytokines, IL-8 & IL-6, are essential in the immune response to Campylobacter infection. However, the experiments only elicited low IFN-γ, a crucial cytokine in the adaptive immune response. According to the research, intestinal epithelial cells are the first to detect Campylobacter cells via their receptors and begin signaling pathways, eventually mobilizing innate immune cells to the site of infection.
The induction of innate immune cells & the activation of different receptor-dependent signaling pathways are critical for bacterial clearance. However, the precise role of immunological components during Campylobacter infection, like cathelicidins, bactericidal permeability-increasing protein molecules, chemokines, inflammasomes, siglec-7 receptors, acute phase protein levels, and T-cell subsets, remains unknown. Understanding these immune responses and filling information gaps will help us better understand human immunity to Campylobacter lari & guide future research efforts.
Campylobacter lari infection can result in various clinical manifestations depending on the individual and the specific strain of the bacteria involved. The most common clinical presentation is an acute gastrointestinal illness characterized by symptoms such as watery or bloody diarrhea, abdominal pain, fever, nausea, and vomiting. Typically, these symptoms develop within 2 to 5 days after ingestion of the bacteria and typically resolve within about a week.
Fever, ranging from 38 to 40°C, is a consistent feature of systemic Campylobacter infection and tends to follow a relapsing or intermittent pattern. Abdominal pain, often localized in the right lower quadrant, and headaches and myalgias (muscle pain) are also frequently reported symptoms. It is important to note that not all Campylobacter infections present with diarrheal illness; some individuals may present with different manifestations, such as subacute bacterial endocarditis (more commonly associated with C. fetus), reactive arthritis, meningitis, or a sluggish fever of unknown origin.
Joint involvement, specifically reactive arthritis, may occur in some cases and often affects a single joint, most commonly the knees. Symptoms of reactive arthritis typically resolve spontaneously within a span of 1 week to several months.
Campylobacter infection is commonly characterized by diarrhea, which can be bloody, accompanied by fever and stomach cramps. Nausea and vomiting may also occur along with the diarrhea. These symptoms generally last for about a week after the initial ingestion of Campylobacter. In some instances, complications may arise from Campylobacter infection, including irritable bowel syndrome, temporary paralysis, arthritis, bacteremia, hepatitis, pancreatitis (inflammation of the pancreas), miscarriage, and Guillain-Barre syndrome (a rare neurological disorder causing weakness and paralysis).
Immunocompromised individuals, like those with HIV infection or who have undergone organ transplantation, are at a higher risk of developing these complications. Additionally, Campylobacter can occasionally spread to the bloodstream in people with weakened immune systems, leading to severe and potentially life-threatening infections.
The diagnosis of Campylobacter lari infection can be achieved through various laboratory tests.
Culture method: It is the gold standard method for diagnosing Campylobacter lari from stool samples. Selective media such as charcoal cefoperazone deoxycholate agar or Skirrow’s medium are inoculated with the stool sample to perform a culture. The plates are then incubated under specific microaerobic conditions, typically 5% oxygen, 10% carbon dioxide, and 85% nitrogen, at 42°C for 48 hours. Colonies typically appear as small, round, and gray to translucent colonies. These colonies are examined for characteristics, including morphology, Gram staining, oxidase reaction, catalase reaction, hippurate hydrolysis, and nitrate reduction. Additionally, the ability of the colonies to grow at different temperatures, precisely 25°C and 37°C, can help distinguish C. lari from other closely related Campylobacter species, such as C. jejuni and C. coli.
Polymerase chain reaction (PCR): It is a rapid and sensitive method for detecting and differentiating Campylobacter lari. It involves extracting DNA from the stool sample and amplifying specific genes of the bacterium using targeted primers. The amplified products can be detected using gel electrophoresis, hybridization probes, or real-time fluorescence, allowing for accurate identification.
Serology: Another diagnostic approach detects antibodies against Campylobacter lari in the patient’s serum. This blood test utilizes techniques such as enzyme-linked immunosorbent assay (ELISA) or immunofluorescence assay (IFA) to measure the levels of immunoglobulins (IgM, IgG, or IgA) specific to Campylobacter lari antigens. Serology is useful for epidemiological studies and can assist in diagnosing chronic or extraintestinal infections.
Regular and thorough handwashing with water & soap, especially before handling food, after restroom usage, and after contact with animals or their feces.
Campylobacter lari can be found mainly in birds & often animals. Implementing effective animal management methods, like keeping farms clean and sanitary, disposing of waste properly, and managing the spread of pathogens in animal populations, can help lower the risk of transmission.
Campylobacter lari is frequently spread via contaminated food, particularly poultry products. It is critical to handle & prepare food safely to avoid bacterial contamination. It involves appropriately cooking chicken to kill bacteria, minimizing cross-contamination between cooked and raw foods, maintaining excellent hygiene while handling food, & storing perishable products at suitable temperatures.
Campylobacter lari – microbewiki (kenyon.edu)
Campylobacter Lari – an overview | ScienceDirect Topics
Campylobacter lari is a bacterium that can cause gastroenteritis and other complications in humans and animals. It is less well-known than other Campylobacter species, such as C. jejuni and C. coli. However, studies have reported crucial epidemiological information about C. lari.
Campylobacter lari is the third most common Campylobacter species in humans with gastroenteritis. It has been identified as a cause of reactive arthritis following enteritis, indicating potential complications associated with the infection. The bacterium was isolated from gulls, starlings, mussels, & oysters, among other things. Shellfish contamination is thought to occur via bird reservoirs, resulting in C. lari in certain seafood products.
From 2010 to 2017, state, municipal, and territorial public health officials reported 236 foodborne Campylobacter instances to the Centers for Disease Control and Prevention’s Foodborne Diseases Outbreak Monitoring System, accounting for 2,381 instances. Campylobacter lari is frequently identified in seagulls and other birds, which can be transmitted to humans by contaminated water or food.
Campylobacter lari is frequently found in seagulls and other bird species, serving as a natural reservoir for the bacterium. Transmission to humans can occur via contact with contaminated water or food. Campylobacter lari accounts for approximately 1% to 2% of human campylobacteriosis cases in Europe and North America. However, its prevalence may vary in different regions, with higher occurrence reported in areas such as Japan and Thailand.
Kingdom: Bacteria
Phylum: Proteobacteria
Class: Epsilonproteobacteria
Order: Campylobacterales
Family: Campylobacteraceae
Genus: Campylobacter
Species: Campylobacter lari
Campylobacter lari is a gram-negative bacterium with a distinct spiral or corkscrew shape, characteristic of the Campylobacter genus.
It is a microaerophilic bacterium; it prefers environments with low oxygen levels. The structure of C. lari can exhibit variations in shape, transitioning from its spiral form to more coccoid (spherical), circular, or elongated shapes when exposed to oxygen or cultured for extended periods.
The bacterium is equipped with long flagella that enable motility. These flagella are located at either one end (polar flagellation) or both ends (bipolar flagellation) of the cell. The motility the flagella provides allows C. lari to move in a corkscrew-like manner.
Colony formation of Campylobacter lari typically results in colorless colonies with a diameter ranging from 1.0 -1.5 µm. They have 1602 genes, 1545 of which are protein genes & 57 of which are RNA genes.
Campylobacter lari’s genomic structure consists of a circular, double-stranded DNA molecule with a size of around 1,525,460 base pairs long. This genome comprises many genes that are responsible for various bacterial functions. Notably, three genes, VP1, VP2, & VP3, encode the capsid components. These proteins are involved in developing the bacterium’s outer protein coat.
Campylobacter lari, a species of bacteria, consists of two subspecies: C. lari subsp. lari and C. lari subsp. concheus. The type-strain of C. lari, NCTC 113522, belongs to the subspecies lari. However, various strains of C. lari have been isolated from different sources, including pigs, cattle, dogs, poultry, shellfish, birds, and humans, indicating the broad distribution and potential reservoirs of this bacterium.
The cytolethal distending toxin (cdt), composed of three subunits: cdtA, cdtB, & cdtC, is one significant virulence factor. In eukaryotic cells, this toxin causes cell cycle arrest & apoptosis. The cdtB gene, which produces the toxin’s catalytic component, is found in all Campylobacter isolates, including C. lari.
Another type of virulence factor is adhesion proteins, which allow Campylobacter lari to connect to host cells and tissues, notably the intestinal epithelium. CadF, which binds to fibronectin, FlaA, an essential flagellar protein; & CbpA, which interacts with collagen, are all examples of adhesion proteins. While the cadF and flaA genes are present in all Campylobacter isolates, the cbpA gene may vary between strains.
C. lari uses invasion machinery to infiltrate host cells and avoid detection by the immune system. It contains proteins like CiaB, a type III secretion system component, PldA, a phospholipase that destroys host cell membranes & CsrA, an invasion gene regulator. The presence of the ciaB & pldA genes varies between Campylobacter isolates, but the csrA gene is more prevalent.
C. lari also has a new potential virulence locus termed LicABCD. This locus encodes four proteins with unknown roles, which may be involved in lipooligosaccharide modification or transport. The features of the LicABCD locus can differ between Campylobacter species & strains, contributing to pathogenicity variability.
Campylobacter lari is a bacterium that, in both humans and animals, can cause gastroenteritis and other issues. C. lari pathogenicity encompasses multiple methods by which the bacteria infect and destroys host tissues. C. lari can colonize the intestinal mucosa using its spiral structure and flagella to penetrate and attach to epithelial cells. Once attached, the bacterium invades the cells & causes damage via a variety of mechanisms. It involves the triggering of apoptosis, or programmed cell death, the breaking of epithelial cell tight junctions, and the activation of inflammatory pathways.
Campylobacter lari can also produce toxins such as cytolethal-distending (CDT). The CDT disrupts the cell cycle & DNA repair pathways, resulting in cell death and tissue damage. C. lari can also change its surface antigens, like lipooligosaccharide (LOS) & capsular polysaccharide (CPS). This change allows the bacterium to elude the host immune system, allowing for long-term infection and possible chronic consequences.
Campylobacter lari can spread from the intestines to the bloodstream and other organs, such as the liver and pancreas. This dissemination can lead to systemic infection and complications such as bacteremia, hepatitis, and pancreatitis. Campylobacter lari can cause autoimmune reactions in some people. It accomplishes this by using its LOS to imitate human gangliosides, forming cross-reactive antibodies. These antibodies assault peripheral nerves by mistake, resulting in Guillain-Barre syndrome.
The human immune system triggers several tasks in combating Campylobacter lari infection. However, research into the precise immunological response to Campylobacter in people needs to be more extensive. Some findings demonstrated significant differences in pro-inflammatory (IL-8, IL-6, IFN-γ) & regulatory (IL-10) cytokines in response to Campylobacter stimulation among individuals. These changes could be attributed to variances in the constitutive expression levels of toll-like receptors (TLRs), which identify pathogen-associated molecular patterns (PAMPs) and initiate an immune response. Previous research using human intestinal epithelial cells has shown that pro-inflammatory cytokines and the secretion of IL-8 & IL-6 are produced in response to Campylobacter activation.
In response to infection, IL-8, released by different cells with TLRs, works as a chemoattractant to recruit immune cells, notably neutrophils. The immune response and the creation of inflammatory mediators are stimulated by IL-6, released by macrophages, T cells, & endothelial cells. These two cytokines, IL-8 & IL-6, are essential in the immune response to Campylobacter infection. However, the experiments only elicited low IFN-γ, a crucial cytokine in the adaptive immune response. According to the research, intestinal epithelial cells are the first to detect Campylobacter cells via their receptors and begin signaling pathways, eventually mobilizing innate immune cells to the site of infection.
The induction of innate immune cells & the activation of different receptor-dependent signaling pathways are critical for bacterial clearance. However, the precise role of immunological components during Campylobacter infection, like cathelicidins, bactericidal permeability-increasing protein molecules, chemokines, inflammasomes, siglec-7 receptors, acute phase protein levels, and T-cell subsets, remains unknown. Understanding these immune responses and filling information gaps will help us better understand human immunity to Campylobacter lari & guide future research efforts.
Campylobacter lari infection can result in various clinical manifestations depending on the individual and the specific strain of the bacteria involved. The most common clinical presentation is an acute gastrointestinal illness characterized by symptoms such as watery or bloody diarrhea, abdominal pain, fever, nausea, and vomiting. Typically, these symptoms develop within 2 to 5 days after ingestion of the bacteria and typically resolve within about a week.
Fever, ranging from 38 to 40°C, is a consistent feature of systemic Campylobacter infection and tends to follow a relapsing or intermittent pattern. Abdominal pain, often localized in the right lower quadrant, and headaches and myalgias (muscle pain) are also frequently reported symptoms. It is important to note that not all Campylobacter infections present with diarrheal illness; some individuals may present with different manifestations, such as subacute bacterial endocarditis (more commonly associated with C. fetus), reactive arthritis, meningitis, or a sluggish fever of unknown origin.
Joint involvement, specifically reactive arthritis, may occur in some cases and often affects a single joint, most commonly the knees. Symptoms of reactive arthritis typically resolve spontaneously within a span of 1 week to several months.
Campylobacter infection is commonly characterized by diarrhea, which can be bloody, accompanied by fever and stomach cramps. Nausea and vomiting may also occur along with the diarrhea. These symptoms generally last for about a week after the initial ingestion of Campylobacter. In some instances, complications may arise from Campylobacter infection, including irritable bowel syndrome, temporary paralysis, arthritis, bacteremia, hepatitis, pancreatitis (inflammation of the pancreas), miscarriage, and Guillain-Barre syndrome (a rare neurological disorder causing weakness and paralysis).
Immunocompromised individuals, like those with HIV infection or who have undergone organ transplantation, are at a higher risk of developing these complications. Additionally, Campylobacter can occasionally spread to the bloodstream in people with weakened immune systems, leading to severe and potentially life-threatening infections.
The diagnosis of Campylobacter lari infection can be achieved through various laboratory tests.
Culture method: It is the gold standard method for diagnosing Campylobacter lari from stool samples. Selective media such as charcoal cefoperazone deoxycholate agar or Skirrow’s medium are inoculated with the stool sample to perform a culture. The plates are then incubated under specific microaerobic conditions, typically 5% oxygen, 10% carbon dioxide, and 85% nitrogen, at 42°C for 48 hours. Colonies typically appear as small, round, and gray to translucent colonies. These colonies are examined for characteristics, including morphology, Gram staining, oxidase reaction, catalase reaction, hippurate hydrolysis, and nitrate reduction. Additionally, the ability of the colonies to grow at different temperatures, precisely 25°C and 37°C, can help distinguish C. lari from other closely related Campylobacter species, such as C. jejuni and C. coli.
Polymerase chain reaction (PCR): It is a rapid and sensitive method for detecting and differentiating Campylobacter lari. It involves extracting DNA from the stool sample and amplifying specific genes of the bacterium using targeted primers. The amplified products can be detected using gel electrophoresis, hybridization probes, or real-time fluorescence, allowing for accurate identification.
Serology: Another diagnostic approach detects antibodies against Campylobacter lari in the patient’s serum. This blood test utilizes techniques such as enzyme-linked immunosorbent assay (ELISA) or immunofluorescence assay (IFA) to measure the levels of immunoglobulins (IgM, IgG, or IgA) specific to Campylobacter lari antigens. Serology is useful for epidemiological studies and can assist in diagnosing chronic or extraintestinal infections.
Regular and thorough handwashing with water & soap, especially before handling food, after restroom usage, and after contact with animals or their feces.
Campylobacter lari can be found mainly in birds & often animals. Implementing effective animal management methods, like keeping farms clean and sanitary, disposing of waste properly, and managing the spread of pathogens in animal populations, can help lower the risk of transmission.
Campylobacter lari is frequently spread via contaminated food, particularly poultry products. It is critical to handle & prepare food safely to avoid bacterial contamination. It involves appropriately cooking chicken to kill bacteria, minimizing cross-contamination between cooked and raw foods, maintaining excellent hygiene while handling food, & storing perishable products at suitable temperatures.
Campylobacter lari – microbewiki (kenyon.edu)
Campylobacter Lari – an overview | ScienceDirect Topics
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