Diphtheria, Diphtheria

Office of Laboratory Security, Public Health Agency of Canada Corynebacterium diphtheriae Material Safety Data Sheet. January 2000.

Historically quite common, diphtheria has largely been eradicated in industrialized nations through widespread vaccination. In the United States for example, there were 52 reported cases of diphtheria between 1980 and 2000; between 2000 and 2007 there were only five cases as the DPT ( DiphtheriaPertussisTetanus ) vaccine is recommended for all school aged children. Boosters of the vaccine are recommended for adults since the benefits of the vaccine decrease with age without constant re-exposure; they are particularly recommended for those traveling to areas where the disease has not been eradicated.

It was named after its inventor, Bla Schick (18771967), a Hungarian-born American pediatrician. A massive five-year campaign was coordinated by Dr. Schick. As a part of the campaign, 85 million pieces of literature were distributed by Metropolitan Life Insurance Company with an appeal to parents to "Save your child from diphtheria." A vaccine was developed in the next decade, and deaths began declining in earnest in 1924.

The toxin binds to EGF-like domain of Heparin-binding EGF-like growth factor (HB-EGF) through fragment B and is internalized with HB-EGF by receptor-mediated endocytosis. The low pH in the late endosomes induce pore formation by fragment B as well as catalyses the release of catalytic fragment A into the cytosol. Diphtheria toxin catalyzes the ADP-ribosylation of, and inactivates, the elongation factor eEF-2.

The toxin then transfers an ADP-ribose from NAD + to a diphthamide residue, a modified histidine (amino acid), which is found within the EF-2 protein. EF-2 is needed for translocation of tRNA from the A-site to the P-site of the ribosome during translation. The ADP-ribosylation is reversible by administering high concentrations of nicotinamide, one of the reaction products http://www.textbookofbacteriology.net/diphtheria_3.html.

These symptoms are caused by the toxin released by the bacterium. Low blood pressure may develop in these patients. Longer-term effects of the diphtheria toxin include cardiomyopathy and peripheral neuropathy (sensory type).

Signs of cutaneous diphtheria infection develop an average of seven days after the appearance of the primary skin disease.

People in this stage should seek immediate medical attention, as obstruction in the throat may require intubation or a tracheotomy. Abnormal cardiac rhythms can occur early in the course of the illness or weeks later, and can lead to heart failure. Diphtheria can also cause paralysis in the eye, neck, throat, or respiratory muscles. Patients with severe cases will be put in a hospital intensive care unit (ICU) and be given a diphtheria anti-toxin. Since antitoxin does not neutralize toxin that is already bound to tissues, delaying its administration is associated with an increase in mortality risk. Therefore, the decision to administer diphtheria antitoxin is based on clinical diagnosis, and should not await laboratory confirmation.

Source: Wikipedia > Diphtheria