Diphtheria is an acute, toxin-mediated disease caused by the bacterium orynebacterium diphtheriae. Toxin production (toxigenicity) occurs only when the bacillus is itself infected (lysogenized) by a specific virus (bacteriophage) carrying the genetic information for the toxin (tox gene). Only toxigenic strains can cause severe disease.
Simplified version: The diphtheria is a bacteria, and a virus called a bacteriophage, inserts itself into the diphtheria bacteria, and takes over the bacterial genes to make toxin. The Diphtheria bacteria isn’t the problem. It’s whether the bacteriophage that converts the bacterial genes into a toxin is around or not. That is the determinant of clinical disease, not the presence of the bacteria.
You can pick up diphtheroids anywhere. Diphtheria is still around as it is ubiquitous. Clinical disease is more likely to been seen in poverty stricken areas, because it’s a toxin-mediated disease, and more likely to be seen where people have insufficient vitamin C and other micronutrients. . Even when the bacteriophage is around, many people might carry diphtheria or even be infected, but rarely get clinical diphtheria. The toxin can’t be produced in the presence of iron. So people who have iron deficiency are more likely to have clinical diphtheria.
Circulation of toxigenic strains of C. diphtheriae persists in parts of both developed and developing countries where diphtheria is not being reported. For example, a focus of toxigenic C. diphtheriae was found in South Dakota in 1996 with molecular analysis of strains suggesting local persistence since the 1970s; and a recent serological study in rural Kenya showed high diphtheria immunity among unvaccinated persons, suggesting continued circulation.
Eradication is not currently feasible because preliminary evidence suggests that circulation of toxigenic C. diphtheriae might persist, even in populations with fairly high childhood immunization coverage, and might be difficult to detect; and sustainable reservoirs for the toxin gene might exist in nonhuman mammals. Future feasibility depends on understanding prevention of continued circulation and evidence that circulation of the toxin gene in the animal reservoirs is not sustained indefinitely.
Seven factors could hinder eradication: the phage carrying the toxin gene can occasionally be found in nondiphtheria Corynebacterium species infecting animals (this may represent an ineradicable reservoir for reintroduction of toxin gene into non-toxigenic C. diphtheriae strains); infection with a toxigenic strain can either be direct or in situ by a phage carrying the toxin gene, infecting a commensal non-toxigenic C. diphtheriae strain; an asymptomatic carrier state exists, even among immune persons, and circulation appears to be able to continue under some settings, even in populations with fairly high childhood immunization rates; immunity to diphtheria is not life-long (a minimum of three doses is required for effective primary immunization, and periodic booster doses are required throughout adult life to maintain protective titres — in addition, immune persons are not distinguishable from susceptible persons except by serological or Schick testing; in countries with low incidence, both the clinician and the laboratory can easily miss the diagnosis of diphtheria, and empirical antibiotic treatment can prevent recovery of the organism; limited epidemiological, clinical, and laboratory expertise is available on diphtheria; and political will may be lacking because the disease burden is low in developed countries and is perceived to be relatively low in developing countries.
You can develop natural immunity to Diphtheria without being vaccinated. It was clearly shown in Russia because they found that the key to fighting diphtheria had nothing to do with antibodies but with production of interferon. The people who got diphtheria in Russia were vaccinated with twice the number of doses but the CDC conveniently overlooked this fact.
“Thymomegalia is registered in every third child in some regions [of Russia].” In this paper the authors confirm that after DPT-immunization of the children with thymomegalia the anti-diphtheria antibodies is not being produced at all or in an insufficient quantity.”
(Ref: Kuz’menko L. G., Arziamova V. V. Nedostatochnost’ produktsii protivodifteriinyh antitel u detei s timomegaliei pri immunizatsii vaktsinoi AKDS (The insufficiency of the anti-diphtheria antibodies production after immunization with DPT vaccine) Detskie infektsii (Children infections), 2004, 2(7), с. 24-26.)
Yet, we are told that it’s very important for immunodeficient children who can’t make antibodies to have these vaccines. But what use is the antitoxin antibodies from vaccines if immunodeficient kids can’t make antibodies? It makes no sense.
Thymomegalia is registered in every third child in some regions [of Russia]. In this paper the authors confirm that after DPT-immunization of the children with thymomegalia the anti-diphtheria antibodies is not being produced at all or in an insufficient quantity.
It is known that DPT vaccination even in healthy children not only produces a specific immune response, but causes the allergic reorganization in the body, lowers the specific resistance… The children with modified reactivity from the high-risk groups react to DPT-vaccination by the long-term suppression of resistance, by developing postvaccinal complications, by defective immune response, by high morbidity… It was demonstrated the DPT-vaccinations (from the first to the third shot) in the most children with thymomegalia of the 1st grade by their first year of life caused the complicated course of the vaccinal process, namely allergic complications, acute respiratory diseases, the lack or inferior immune reaction to diphtheria or pertussis toxins and enlarging the thymus up to 2nd-3rd grade. The result of the three shots was the factual absence of immunity to whooping cough, low anti-diphtheria and high anti-tetanus… immunity.”
(Ref: Adishcheva N. I. Kliniko-immunologicheskie pokazateli vaktsinal’nogo protsessa AKDS u detei s uvelicheniem timusa I stepeni (Clinical-immunological characteristics of the vaccinal process in children with 1st grade thymomegalia Abstract of PhD thesis. Tomsk, 1996, pp. 2 and 24.)