Diphtheria Causes Throat Infection Biology Essay

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Diphtheria is an infectious upper respiratory disease mainly caused by the toxin of Corynebacterium diphtheriae bacteria. C. diphtheria is living in mouth, nose and skins of the infected person. This disease is characterized by sore throat, low fever, and adherent membrane on tonsil. Usually it affects the throat and nose and in more serious cases, it can affect the heart and nerves. It is a contagious disease spread by direct physical contact or respiratory droplets from the throat through coughing and sneezing of an infected person. The toxin production is due to specific viruses that carrying the genetic information for toxin (tow gene) which infects the bacillus [2].

Corynebacterium diphtheria: Corynebacteria are Gram-positive, rod-shaped, aerobic, non-motile, bacteria classified as Actinobacteria. Corynebacteria are related phylogenetically to actinomycetes and mycobacteria. They have the characteristic of forming irregular or V-shaped arrangements in normal growth. The genus Corynebacterium consists of a diverse group of bacteria including plant and animal pathogens. Some corynebacteria are part of the normal life of humans, finding a suitable niche in virtually every anatomic site, especially the skin and nares. A very popular and widely known bacterium is Corynebacterium diphtheriae which causes the disease Diphtheria [4]. The main symptoms of the diphtheria are:-

The bacteria can invade any of the mucous membranes and have 2-5 days incubation time. The diphtheria infection occurs in different parts of the body and varies in severity of pain. The most common site of infection is the tonsils, pharynx, and sometimes it may invade the nasal tissues, larynx and skin. Pharyngeal, laryngeal and tonsillar diphtheria are more severe as compare to other type of diphtheria because more amount of toxins are absorbed by blood serum. The pseudomembrane is a fibrin network infected with multiplying C. diphtheriae cells which grows over a necrotic lesion on the epithelial cells on the surface of the throat. The consequences of this membrane may be severe if the membrane will grow up to much extent which blocks the air ways in throat [3].

The outcome of the disease depends on how much toxin is absorbed into the bloodstream. The toxin has degenerative effects on the heart, muscles, spleen, nerves, liver and kidneys. In the most severe cases, an infected person will develop myocarditis (inflammation of heart muscle) or neuritis (damage in nerves), which leads to heart failure and local paralysis most commonly of the soft palate [2].


Usually all the strains of C. diphtheriae don�t have toxic because the gene for diphtheria toxin (DT) is not found in the genome of bacteria. DT gene is actually located on the genome of a corynephage (virus), a certain type of prophage. The toxinogenicity of Corynebacterium diphtheriae is depending upon the phage that has a functional gene for the toxin protein. Usually all phages doesn�t carry the DT gene tox, so it is possible for a C. diphtheriae bacterium to undergo lysogenic conversion or be infected by a prophage, without producing the diphtheria toxin [1].

C. Diphtheria produces the diphtheria toxin as a single protein. Technically this DT is a proenzyme, because it is cleaved by bacterial proteases into two fragments, A (molecular weight 21,150) and B (molecular weight 39,000). Fragment A is the sole source of toxicity of DT and is catalytically active. Fragment B have no enzymatic activity and is less stable than the active fragment A. After entering the toxin into the host cell each fragment plays different roles. Diphtheria toxin enters the host cell by binding to the extracellular EGF domain of the heparin-binding epidermal growth factor precursor (HB-EFG precursor). This binding initiates a hydrophobic domain of the fragment B to form a channel across the membrane through which fragment A can pass into the cytoplasm. Fragment B contains the transmembrane and receptor-binding domains of the toxin, which remains on the plasma membrane [1].

DT is an ADP-ribosyl (ADPR) transferase. The toxicity of DT comes from blocking protein synthesis in the host cell by inactivating EF-2 or cellular elongation factor. EF-2 is an essential part of the process of translation. Fragment A is free in the cytoplasm and catalyzes the reaction as below:

EF-2 + NAD+ --> ADPR-EF-2 + nicotiamide + H+

This above reaction forms a covalent bond between ADPR and EF-2 that blocks the functional site which interacts with RNA in translation, and consequentially stopping all protein synthesis at a particular ribosome.

The structural gene of DT is in the phage chromosome and the expression of this gene is controlled by DtxR gene on the corynebacterium diphtheriae chromosome. Usually expression of tox gene is inhibited by negative feedback from the DTxR gene product. The levels of iron in the surrounding tissue environment have a significant effect on the expression of DTxR and consequentially on DT production. Low levels of iron inhibit the expression of DTxR which helps in stopping the negative feedback loop inhibiting tox gene expression. If the corynebacterium diphtheriae bacteria are grown under certain severe iron-deficient conditions, DT protein can make up about 5% of all protein being synthesized. In other words, iron acts as a co-repressor with DTxR to prevent the expression of DT production [3].