Campylobacter concisus habitats in the human’s mouth cavity. It travels to the gut and causes severe inflammatory bowel disease. C. concisus is getting common as it is emerging pathogen. But how it spread and about its actual infection sources are not studied well. 

In the last ten years, Campylobacter cases reported are huge. High rates are seen in underdeveloped and some parts of rich nations. The Czech Republic had the worst global rate in 2019, with 215 cases per 100,000 people. Australia and New Zealand also had many cases. 

Outbreaks come from chicken, raw milk, and dirty water. From 2010 to 2017, there were 236 outbreaks in the U.S. tied to Campylobacter contaminated food, and 2,381 people were affected. Campylobacter infects people randomly in undeveloped countries. 

Campylobacter concisus is part of family Campylobacteraceae. It’s spiral or curved shape gives it a corkscrew look because of one or two flagella are arranged. The flagella setup allows the bacteria to move and has has a positive oxidase test. 

C. concisus is around 1 micrometer and the cells are shaped like commas and change shape a bit, looking different from each other. The pleomorphism shows how it can vary in appearance.

C. concisus has two genomospecies with GS1 and GS2. They have differences in their 23S rRNA genes. The genetic difference shows disease in the gut. Genomospecies 2 invades human cells like Caco2 that are epithelial cells from the intestines.

C. concisus has a toxin named Zonnula occludins toxin that damages cell membranes. It also has a surface layer protein from the RTX family (S-layer RTX) that helps it sticks to cells. The surface protein cadF in bacteria attach and grow in the gut and invade cells. A toxin called Cytolethal distending toxin makes C. concisus harmful.

Whole genome studies found that some C. concisus strains have a mutation (GyrA T86I) that makes understanding mechanisms. C. concisus is linked to inflammatory bowel diseases and ulcerative colitis through molecular clues. The csep1 gene with a six nucleotide insertion (csep16 bpi) is in active Crohn’s cases. Having the pSma1 plasmid cause severe ulcerative colitis. 

The csep1 is on the pICON plasmid or the chromosome, show the genetics of C. concisus. The original strain ATCC 33237 is isolated from human gum infections. 

C. concisus lives in the human mouth. It adapts to moist areas of the digestive and reproductive systems. Some strains move to the intestines and contribute to bowel disease. It is found in poultry gut, so transmission from animals to humans is common. The human transmission happens from poultry, sheep and pigs.

In developed nations, drinking unpasteurized milk or eating undercooked poultry causes infection. Human to human spread from fecal or oral contact is possible. Working with farm animals raises the risk of infection. Having stomach acid or taking acid reducing medicines increases susceptibility. 

The exact role of C. concisus in disease is unknown. Some strains move from the mouth to the intestines, causing illness complex. Ongoing research is studying on how C. concisus affects human health. 

The stomach in the body’s first defense against C. concisus. Its acidic environment kill pathogen before they enter the intestines. A safeguarding protein is Secretory IgA synthesized in the gut neutralizes Campylobacter and its toxins. 

The intestines defend against C. concisus in dynamic ways. Peristalsis moves the intestinal muscles. Rhythmic contraction and relaxation are a sweeping motion. It flushes out Campylobacter, not letting them stay too long. Immune cells and dendritic cells destroy invading C. concisus. 

When C. concisus gets into the digestive system, inflammation occurs. Conditions like Crohn’s disease cause swelling from the mouth to the rectum, affecting small and large intestines. Inflammation fight infection, but high reaction damages the gut and cause intestinal disorders. 

C. concisus is present in the human mouth cavity with gained interest due to its link with inflammatory bowel disease.

Those infected with C. concisus have watery diarrhea, sometimes with blood. They feel discomfort, vomit, have belly cramps, and fever. These start 2 to 5 days after contact with the bacteria and last around a week. 

The clinical features of C. concisus infection relate to the gut with diarrhea and stomach issue. The bacteria’s role in inflammatory bowel disease highlights that it contributes to chronic gut inflammation. 

• Culture Test: To identify C. concisus, culture test the bacteria by extracted from stool, or fluids. The warm liking pathogen grows in both high oxygen and low oxygen settings with hydrogen present. Standard tests of hippurate breakdown, & nitrite reduction are used in confirming the species. 

• MALDI-TOF MS Identification: Identifying bacteria through ionization by mass spectrometry is powerful. The test exactly separates C. concisus isolates. Mass spectrometry enables reliable bacterial species identification. 

• Susceptibility Testing: Testing for antibiotic resistance patterns ensures effective treatment management. Examining quinolone resistance uses the Quinolone Resistance Determining Region method. Specific mutations special to C. concisus is useful in its antibiotic suggestions. 

Studies have divided C. concisus to two phenotypically identical genomospecies. It is done by amplified fragment length polymorphisms with housekeeping genes by PCR targeting polymorphisms of the C. concisus 23S rRNA gene. 

Stay away from contaminated dirt, plants, or insects. Wear defensive stuffs and masks. Take care of water safety through boiling or filtration. 

To stop the spreading these infections follow proper hygiene and infection control methods carefully. Handle medical solutions in sterile containers. 

Campylobacter concisus – A New Player in Intestinal Disease – PMC (nih.gov) 

Campylobacter Concisus – an overview | ScienceDirect Topics