A Microbial Biorealm page on the genus HilbrichS
Higher order taxa
Bacteria; Proteobacteria; Delta/Epsilon subdivision; Campylobacterales; Campylobacteraceae (1)
C. coli, C. concisus, C.curvus, C.fetus subsp. fetus, C. fetus subsp venerealis, C. gracilis, C. helveticus, C.hominis, C. hyointestinalis subsp hyointestinalis, C. hyointestinalis subsp lawsonii, C.jejuni subsp doylei, C. jejuni jejuni, C. lanienae, C.lari, C. mucosalis, C.rectus, C. showae, C. spoterum, C. upsaliensis, B. ureolyticus (9)
Description and significance
Campylobacter is microaerophilic meaning it needs oxygen to survive, but the level of oxygen must be lower than the atmospheric levels. Too much oxygen and the bacterium could be killed. It is spiral in shape, a flagellate, and is very fragile (3,4). Campylobacter can be killed in high levels of oxygen or drying. Most Campylobacter is found within the intestinal tract of animals such as dogs, cats, poultry, swine, cattle, monkeys, rodents, wild birds, and even within humans (4). In humans the bacteria can live and survive without causing illness although often it does. The bacteria cycles through the environment by traveling through the intestinal tracts of animals and exiting the body through feces. The feces is then incorporated into the soil which maintains the low level of oxygen. The animals eat plants and sometimes soil containing the bacteria and the cycle continues. Campylobacter can be found in untreated water that is contaminated with fecal matter and therefore contributes to the cycle of the bacteria (4).
Campylobacter species have varying genomes, but one of the most common species that affects humans and livestock is Campylobacter jejun. Using C. jejuni as an example for the genomic structures, it has a circular chromosome made up of 1.6 million base pairs (10). The large number of base pairs allows for C. jejuni to code for 1,654 proteins that lead to 54 RNA species that are stable (10). The C. jejuni species genome is unusual because there is no insertion sequence or phage- associated sequence within it. Within the genome, there is also very little repetition of sequences, but hypervariable regions have been found (10). The short sequences of homopolymeric nucleotides that are varaible, are often found in regions that code for biosynthesis or for modification to the cell surface structures (10). It is believed that the hypervariability of the short runs is one of C. jejuni's main survival strategy.
Cell structure and metabolism
Campylobacter are microscopic helically-shaped cells. They look to have a "gulled-wing" appearance due to their spiral shape (1). Campylobacter have flagella and are describes as having rapid darting motility due to a long polar flagellum at either one or both ends of the cell. The flagellum is very long, often several times the longer than the length of the cell (1). Motility is slower in a wet environment due to it's sensitivity to levels of oxygen. Campylobacter has an outer covering of lipopolysaccharides due to its Gram negative property (1). The cell surface contains porins that are associated with the peptidoglycan layer as well as adhesive binding proteins. The cells can morph to cocci or elongated cells if left in a prolonged culture, or are exposed to oxygen. Campylobacter produces oxidase and catalase as a result of metabolism (1). It does not utilize carbohydrates for metabolism and are super sensitive to free radicals as well as superoxides (1). Not only are they sensitive to superoxides and free radicals, but also chemical and physical agents.
Campylobacter typically colonizes in the mucous overlying the mucosal surfaces of mammals and birds. The mucous allows the cells to dart about by using their flagella to maintain a colony within a mucosal flow (2,4). Most species of Campylobacter are thermophilic, such as C. jejuni. C. jejuni colonizes in mucous lining in the intestines of birds, specifically the cecum of birds which is roughly 42 degrees Celsius (5). Campylobacter is usually isolated to chickens and other birds and is passed from bird to bird by a common water source, but it can also inhibit other animals that have a lower body temperature or individuals with a weak immune system (4). Although Campylobacter are typically found in their intestinal niches, it can also be found isolated from fecal contamination. The fecal contamination can occur in water and food products like meat and milk causing humans to become infected. Although Campylobacter can be found in other environments, it is mostly found within the intestines of mammals and birds.
Illness caused by Campylobacter is usually caused by the ingestion of a contaminated food product like meat or milk, or by drinking contaminated water. Two of the most common pathologies caused by Campylobacter are Gastroenteritis, also called Campylobacteriosis, and Guillain-Barre Syndrome (GBS) (1). Gastroenteritis is caused primarily by C.jejuni and C. coli but can be attributed to others too. It is an inflammatory bacterial diarrhea which causes damage to the mucosal surface layer of the intestine divisions of the jejenum, ileum, and colon (1). The symptoms are diarrhea, malaise (fatigue), fever, abdominal pain with nausea but no actual vomiting. Onset of the symptoms occur after an incubation period of 1 to 7 days (1). The first symptoms to appear are abdominal cramps and diarrhea. There are also other less common symptoms that can be associated with Gastroenteritis which affect roughly 1/3 the patient population (1). The less common symptoms are prodronal fever, headache, dizziness, myalagia. The symptoms previously mention mimic flu-like symptoms, but will occur within 12-24 hours prior to intestinal symptoms (1). The diarrhea symptoms can range in severity from loose stool, to intense water diarrhea that can account for up to 10 bowl movements a day. Stool may often contain mucous or blood depending on the severity of the case. Normally the symptoms will subside in a few days to a week. Late onset of gastroenteritis can lead to complications such as Guillain-Barre Syndrome. Guillain-Barre Syndrome (GBS) is a reactive autoimmune disease that is self-regulated. GBS is mostly associated with C.jejun (1). GBS targets the Schwann-cells and myelin by causing acute inflammatory demyelinating neuropathy due to a cross reaction (1). The axons of nerve cells may also be targeted by GBS and are affected by molecular mimicry of axonal membranes. Virulence factors of Campylobacter are the following: flagella, endotoxins, adhesins to attach to the mucous layer, and invasins.
Current Research and or Application to Biotechnology
One recent article about Campylobacter is that garlic contains a compound which has been linked with killing C. jejuni, the most common species that causes Gastroenteritis (8). It can be accomplished using garlic compound concentration levels of over 100 lower than those found in two popular antibiotics. This means that garlic can be used to reduce the risk of illness due to Campylobacter by making kitchens cleaner and safer. In order to find the compound, diallyl sulfide's ability was tested as well as two commonly used antibiotics, ciprofloxin and erythromycin (8). All three were tested on their ability to eliminate C. jejuni in biofilms and in cells in vitro (8). The results of the test showed that the garlic compound of diallyl sulfide was able to eliminate two different strains of C. jejuni much faster than the antibiotic compounds (8). While the antibiotic compounds needed a minimum inhibitory concentration (MIC) of 16 and 8 mg/L and 16 and 4 mg/L for the different strains, the garlic compound had a MIC of 0.04mg/L, much lower than the antibiotic compound (8). This new finding could make food safer by using it during food preparation and even in packaging of some food goods. The garlic compound may even extend the shelf life by eliminating Campylobacter formation. Another recent article claimed that acid found in the stomach may prime Campylobacter for intestinal infections. With the known fact that Campylobacter infections occur in the intestine, this means that the bacteria must somehow adapt to the acidic environment of the stomach to pass through to it's ideal niche. The researchers of the article found that not only does the Campylobacter survive, but it also adapts in order to do so (6). The stomach has a pH level varying from 2 to 7 and food can be stored there for up to one hour, so in order for Campylobacter to survive, it must take this variables into consideration (6). During the researchers investigation they found that Campylobacter down regulates activity of gene regulating of metabolism and cell division, but up regulates activity of the set of genes needed to express and make flagella needed for movement (6). While they slow down normal cell processes, the acid shock will trigger motility of the cell. In order to prove that acid shocked Campylobacter has a better survival rate, researchers attempted to introduce acid shocked and unexposed Campylobacter into epithelial cells from mouse gut (6). It appeared that the acid shocked cells were better prepared for invading than the unexposed. The last example of recent finding of Campylobacter was an article about the decline of Campylobacteriosis, but Guillain-Barre Syndrome still being significant. The study came from New Zealand which has one of the highest claimed incidences of Campylobacteriosis (7). Although the number of claims is dropping, new cases of GBS are still a common finding among these patients. They found that hospitalizations for camyplobacteriosis increased the risk 320 fold for further hospital admission for GBS in the following months (7). Although many patients do recover from the symptoms of paralysis and need for intensive care, roughly 3% die in New Zealand from GBS (7). Because of the severity of GBS, a Campylobacter infection should never be treated as just a stomach bug.
1. "BSCI 424 Pathogenic Microbiology -- Campylobacter." BSCI 424 Pathogenic Microbiology -- Campylobacter. Web. 06 May 2012. <http://www.life.umd.edu/classroom/bsci424/pathogendescriptions/Campylobacter.htm>
2. "Campylobacter." - Vermont Department of Health. Web. 06 May 2012. <http://healthvermont.gov/prevent/campylobacter/Campylobacter.aspx>.
3."Campylobacter." Centers for Disease Control and Prevention. Centers for Disease Control and Prevention, 20 July 2010. Web. 06 May 2012. <http://www.cdc.gov/nczved/divisions/dfbmd/diseases/campylobacter/>.
4. "Campylobacter Questions and Answers." Campylobacter Questions and Answers. Web. 06 May 2012. <http://www.fsis.usda.gov/Fact_Sheets/Campylobacter_Questions_and_Answers/index.asp>.
5. Dworkin, Martin M., and Stanley Falkow. Proteobacteria: Delta and Epsilon Subclasses, Deeply Rooting Bacteria. New York, NY: Springer, 2006. Print.
6. "Exposure to Stomach Acid Primes Campylobacter for Intestinal Infection." News from the Institute of Food Research. Web. 6 May 2012. <http://news.ifr.ac.uk/2012/04/exposure-to-stomach-acid-primes-campylobacter-for-intestinal-infection/>.
7. McMillan, Virginia. "Campylobacteriosis Declining but Guillain-Barré Syndrome Still Significant Outcome." NZdoctor.co.nz. 08 Feb. 2012. Web. <http://www.nzdoctor.co.nz/news/2012/february-2012/>.
8. "MedWire News - Infectious Diseases - Garlic Compound Effective against Campylobacter Jejuni." MedWire News - Infectious Diseases - Garlic Compound Effective against Campylobacter Jejuni. Web. 6 May 2012. <http://www.medwire-news.md/43/99149/Infectious_Diseases/Garlic_compound_effective_against_Campylobacter_jejuni.html>.
9. Nachamkin, Irving, and Martin J. Blaser. Campylobacter. Washington, D.C.: ASM, 2000. Print.
10. "Supplemental Content." National Center for Biotechnology Information. U.S. National Library of Medicine. Web. 10 May 2012. <http://www.ncbi.nlm.nih.gov/pubmed/10688204>
Edited by student of Dr. Lynn M Bedard, DePauw University http://www.depauw.edu