Coryneform ​Bacteria
By M Borisova, H Coates, K Durber-Stoneman, E Wilcher
Corynebacterium diphtheriae
Kingdom
Phylum
Class
Subclass
Order
Family
Genus
Species
Bacteria
Actinobacteria
Actinobacteria
Actinobacteridae
Actinomycetales
Corynebacteriaceae
Corynebacterium
diphtheriae
Corynebacterium diphtheriae is the bacterium responsible for causing diphtheria. It is usually found in the throat, causing a characteristic pseudomembrane and is (not very invasive). As a result of living in the throat, growth of the bacterium is restricted to external surfaces only in this location, however Corynebacterium diphtheriae causes severe infections because it produces a very potent toxin (Wheelis, 2008). This toxin is secreted by the bacteria into the host cells where it is absorbed into the bloodstream through the mucous membrane. When the toxin enters a host cell, the toxin inhibits protein synthesis for the eukaryotic cell because it alters the necessary elongation factor, EF2 (Greenwood et al., 2012).
Corynebacterium diphtheriae is highly contagious and is mainly spread by aerosol. Diphtheria used to be highly prevalent, but the vaccine DPT has decreased the incidence of infection in developed countries. However the fatality rate is still high in areas where vaccination does not occur (CDC, 2014).
Corynebacterium diphtheriae was not always a pathogenic bacteria. It acquired this ability from phage known as corynephage. The bacterium acquires the tox+ genes from the presence of phage. These genes are controlled by the bacteria and regulated along with iron regulation. When iron levels are low the bacteria will express diphtherial toxin (Trost et al., 2012).
Iron itself is a co-repressor for the tox+ genes, and when present exogenously binds to a repressor molecule; DtxR. When Iron binds to DtxR it activates the molecule which binds to the tox+ genes and prevents transcription. Therefore when iron levels are low the repressor molecule becomes deactivated and transcription of the tox+ genes can occur, causing the production of diphtheria toxin. This happens because Corynebacterium diphtheriae has evolved to recognise that low iron levels in the host is an indication of host response to infection and therefore produces the toxin to weaken the immune response of the host (Murphy, 1996).
Figure 1. Taxonomy of Corynebacterium diphtheriae based on Sayers et al., 2009.
Clinical presentations of diphtheria include: fever, chills, malaise, tachypnea (shallow breathing) and a grey psuedomembrane. This grey pseudomembrane is a thick layer that covers the throat and tonsils, generally leading to hoarseness and a sore throat. This thick pseudomembrane begins to develop within 2-5 days of incubation and will grow to include the pharyngeal walls, tonsils, uvula, and soft palate. In some cases the pseudomembrane can grow in the entire trachea-bronchial tree. This will eventually lead to suffocation because of airway obstruction. A bull-neck appearance may occur which shows a definite area of swelling around the collar and neck. This usually causes issues with swallowing and therefore can cause a lot of issues as a result of this.
Corynebacterium diphtheriae can also cause cutaneous diphtheria. This is another type of diphtheria but this affects the skin. This produces a similar reaction to other bacterial infections: swelling, redness and painful to touch. Not only this but ulcers can occur and these will be covered by a grey membrane. Cutaneous infection is most common in tropical climates or areas where overcrowding is an issue. However, cases of cutaneous diphtheria have occured in the USA.
