Capnocytophaga ochracea

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Higher order taxa

Bacteria; Bacteriodetes; Flavobacteriia; Flavobacteriales; Flavobacteriaceae; Capnocytophaga


NCBI: Taxonomy

Capnocytophaga ochracea

Description and significance

Capnocytophaga ochracea is a gram-negative fusiform-to-rod shaped bacterium that grows in clumps and moves by gliding despite having no flagella (1). This capnophilic aerotolerant anaerobe is found in the oral cavity of humans and contributes to early plaque formation on teeth by being a physical intermediate link between several Streptococcus species and F. nucleatum (2). Dental plaque is associated with periodontal disease and dental caries which is the single most prevalent disease in children (3).

In addition to oral disease, C. ochracea is known to cause sepsis in immunocompromised patients. In immunocompetent patients, intrauterine infections, endocarditis and septic arthritis may occur (4).

Genome structure

The genome of C. ochracea strain VPI 2845 consists of 2,612,925 base pairs all within one circular chromosome (5). It has a GC content of 39.59% which equates to 1,034,404 base pairs. The vast majority of the DNA is found in coding regions, 87.76% (5). There are a total of 2,252 genes of which 2,193 (97.38%) are protein-coding genes, 59 (2.62%) are RNA genes. There are a total of 4 rRNA operons (5). 471 (20.91%) of the genes have transmembrane helices which correlate with C. ochracea’s ecological role in the human oral cavity of plaque formation by binding to several bacteria (5).

Cell structure

C. ochracea are fusiform rods that form confluent colonies with a halo zone, the outer edge of a colony formed because of gliding (1). C. ochracea does not have flagella but it is still motile via a process called gliding in which the cell moves about its longitudinal axis. As cells glide out from the denser center of the colony, the thickness of cells decreases leading to a halo zone (1). Cells growing in a colony structure grow in an end-to-end fashion. Microcolonies ranging between 50-100 cells have been noticed throughout the entirety of the halo zone which is uncommon for gliding prokaryotes (1).

On the cell surface of C. ochracea, there are adhesin sites that allow for coaggregation between C. ochracea and F. nucleatum, Streptococcus and Actinomyces species (6). Simple sugars, such as L-rhamnose, β-methy-D-galactoside, lactose, and α-methy-D-galactoside, are effective inhibitors of C. ochracea-S. sanguis coaggregation. However, L-rhamnose is the most effective inhibitor of C. ochracea from binding with S. sanguis, A. naeslundii, or A. israelii (6).

Metabolic processes

Capnocytophaga ochracea is an aerotolerant anaerobe that requires either an anaerobic environment or 5% CO2 concentration of the gaseous form or 20 mM HCO3- in the hydrated form (7). All strains of C. ochracea are able to ferment glucose, sucrose, maltose and mannose, but most strains ferment amygdalin, fructose, galactose, lactose and raffinose to get an end product of acetate and succinate (5).

C. ochracea transports glucose across the cell membrane by a phosphoenolpyruvate:phosphotransferase system where glucose is converted into two molecules of phosphoenolpyruvate (PEP) by the Embden-Meyer-hof-Parnas pathway (8). Through this pathway, two NADH2 are produced and there is no net gain of ATP. One molecule of PEP goes back to the PEP phosphotransferase system to transport one molecule of glucose across the cell membrane (8). The other molecule of PEP continues to be catabolized via two pathways. One pathway converts PEP into an intermediate, oxaloacetate, by PEP kinase which fixes CO2 to PEP (8). Oxaloacetate is further catabolized into succinate producing ATP and NAD+ in the process. The second pathway converts PEP into pyruvate which generates one ATP. Pyruvate is then broken down into acetate producing another molecule of ATP (8).

The presence of yeast extract can alter the products and intermediates that accumulate in the cytoplasm. In a culture grown without yeast extract, the accumulation of acetate, pyruvate, oxaloacetate, and succinate is observed (8). However, in cultures grown with yeast extract, no pyruvate accumulates resulting in an increase in acetate formation. There also is a two-thirds decrease in oxaloacetate accumulation resulting in an increase of succinate formation (8).


C. ochracea is found in the human oral cavity where it takes part in plaque biofilm formation. It is an early colonizer of pellicle which is a layer of salivary glycoproteins on the surface of a tooth and helps to protect the tooth from decay (9). However, 18 genera of bacteria frequently participate in coaggregation and adhere to the pellicle directly or to other bacteria to form a plaque (9).

C. ochracea is capable of both adhering to other bacteria utilizing adhesins and other bacteria binding to its receptors (6). C. ochracea binds to 16 members of the genera Actinomyces, Rothia, and Streptococcus. There are two types of adhesin sites on C. ochracea, an L-rhamnose sensitive site and an N-acetylneuraminic acid (NeuAc) sensitive site (6). Under normal conditions, S. sanguis and A. naeslundii bind to L-rhamnose sensitive adhesin sites located on the 155 K Mr polypeptide; however, the addition of L-rhamnose will inhibit coaggregation between C. ochracea and either of these two bacteria (10). A. israelii binds to both the L-rhamnose sensitive sites as well as the NeuAc site. Addition of only L-rhamnose or NeuAc partially inhibits coaggregation of A. israelii and C. ochracea, but the combined addition of both L-rhamnose and NeuAc significantly inhibits coaggregation (6).

In C. ochracea aggregation with F. nucleatum, the former releases a soluble component that enhances biofilm formation by the latter (11). It also has been noted that L-lysine strongly inhibits coaggregation between these two bacteria (11).


As stated above, C. ochracea plays a key role in the initial formation of dental plaques. Within this plaque, it is one of the bacteria that actually causes periodontitis (4). However, C. ochracea causes much more severe infections once it enters the bloodstream, usually via periodontal abscess, periodontitis, or ulcerations. C. ochracea infections are most common in immunocompromised patients and can lead to sepsis, purpura fulminanas and gangrene (4). In immunocompromised patients there is a mortality rate between 14%-43% (12). C. ochracea also causes infections immunocompetent patients such as intrauterine infections, endocarditis, peritonitis and septic arthritis (4).

Current Research

A case study released in 2007 described the first case of C. ochracea leading to severe sepsis, multisystem organ failure and purpura fulminans in an immunocompetent host (4). The patient had an uncomplicated dental extraction, but two weeks after the procedure he developed severe abdominal pain as well as a temperature of 102 °F. A few hours later, he developed purpura on his ears, feet, hands and trunk. Soon after the appearance of purpura fulminans, he developed respiratory failure and oliguric renal failure which required mechanical ventilation and hemodialysis respectively. The purpura fulminans progressed into gangrene in his lower legs and fingers, forcing the patient to undergo bilateral below the knee and phalanges amputation.

An article released in 2009 sequenced the genome of Capnocytophaga ochracea type strain VPI 2845 utilizing Sanger and 454 sequencing platforms. The research found that C. ochracea is composed of a single circular chromosome consisting of 2,612,925 base pairs (5). DNA coding regions compromise 87.76% of the total DNA that encodes 2,252 genes. The genome has a GC content of 39.59% (5). There are 59 RNA genes and 4 rRNA operons. There are 471 genes that have transmembrane helices (5).

An article published in 2012 investigated biofilm formation between Fusobacterium nucleatum and Capnocytophaga ochracea utilizing visual assay. It was determined that the addition of ethylenediamine tetraacetic acid, N-acetyl-D-galactosamine or lysine inhibit coaggregation between these two bacteria (11). Heating or treating F. nucleatum cells with proteinase K affected coaggregation, but identical treatment of C. ochracea cells did not, suggesting that a proteinase K-sensitive and thermolable proteinaceious component of F. nucleatum is involved in adhesion with a cell surface component on C. ochracea. Biofilm formation by F. nucleatum is enhanced by the addition of culture supernatant of or co-culture with C. ochracea (11). But, NaOH is not involved in the signaling pathway to enhance biofilm formation. C. ochracea releases a diffusible signaling molecule which stimulates biofilm formation by F. nucleatum (11). Autoinducer-2 is involved in this signaling pathway (11).


  1. Poirier, T. P., S. J. Tonelli, and S. C. Holt. "Ultrastructure of Gliding Bacteria: Scanning Electron Microscopy of Capnocytophaga Sputigena, Capnocytophaga Gingivalis, and Capnocytophaga Ochracea." Infection and Immunity 26.3 (1979): 1146-158. Ncbi.
  2. Kapke, Paul A., Albert T. Brown, and Thomas T. Lillich. "Carbon Dioxide Metabolism by Capnocytophaga Ochracea: Identification, Characterization, and Regulation of a Phosphoenolpyruvate Carboxykinase." Infection and Immunity 27.3 (1980): 756-66. Ncbi.
  3. Peterson, Scott N., Erik Snesrud, Jia Liu, Ana C. Ong, Mogens Kilian, Nicholas J. Schork, and Walter Bretz. "The Dental Plaque Microbiome in Health and Disease." Ed. Sarah K. Highlander. PLoS ONE 8.3 (2013): 1-10.
  4. Desai, Sima S., Rebecca A. Harrison, and Melissa D. Murphy. "Capnocytophaga Ochracea Causing Severe Sepsis and Purpura Fulminans in an Immunocompetent Patient." Journal of Infection 54.2 (2007): 107-09.
  5. Mavrommatis, Konstantinos, Sabine Gronow, and Philip Hugenholtz. "Complete Genome Sequence of Capnocytophaga Ochracea Type Strain (VPI 2845)." Standards in Genomic Science 1.2 (2009): 101-09. Ncbi.
  6. Weiss, Ervin I., Jack London, Paul E. Kolenbrander, Angelika S. Kagermeier, and Roxanna N. Andersen. "Characterization of Lectinlike Surface Components on Capnocytophaga Ochracea ATCC 33596 That Mediate Coaggregation with Gram-positive Oral Bacteria." Infection and Immunity 55.5 (1987): 1198-292.Ncbi.
  7. Gilligan, Peter H., L. R. McCarthy, and Brenda K. Bissett. "Capnocytophaga Ochracea Septicemia." Journal of Clinical Microbiology 13.4 (1981): 643-45. Ncbi.
  8. Calmes, Robert, G. W. Rambicure, W. Gorman, and Thomas T. Lillich. "Energy Metabolism in Capnocytophaga Ochracea." Infection and Immunity 29.2 (1980): 551-60. Ncbi.
  9. Kolenbrander, Paul E., and Jack London. "Adhere Today, Here Tomorrow: Oral Bacterial Adherence." Journal of Bacteriology 175.11 (1993): 3247-251. Ncbi.
  10. Weiss, E.i., I. Eli, B. Shenitzki, and N. Smorodinsky. "Identification of the Rhamnose-sensitive Adhesin of Capnocytophaga Ochracea ATCC 33596." Archives of Oral Biology 35 (1990): 127-30.
  11. Okuda, Tamaki, Katsuji Okuda, Eitoyo Kokubu, Tomoko Kawana, Atsushi Saito, and Kazuyuki Ishihara. "Synergistic Effect on Biofilm Formation between Fusobacterium Nucleatum and Capnocytophaga Ochracea." Anaerobe 18.1 (2012): 157-61.
  12. Forlenza, Susanw., Michaelg. Newman, Alleni. Lipsey, Stuarte. Siegel, and Uzy Blachman. "Capnocytophaga Sepsis: A Newly Recognised Clinical Entity In Granulocytopenic Patients." The Lancet 315.8168 (1980): 567-68.

Edited by [Jason Pan], student of Jennifer Talbot for BI 311 General Microbiology, 2014, Boston University.