Written by MicroDok

Corynebacterium diphtheriae is a Gram-positive, non-spore forming, aerobic, rod-shaped and motile bacterium that causes diphtheria, an upper respiratory tract illness. They are pleomorphic organisms exhibiting different characteristic morphological shapes including V-shapes, irregular shapes and club-shapes. C. diphtheriae and other species in the genera Corynebacteria grow on the mucous membrane of the upper respiratory tract, skin, nares and wounds of humans. C. diphtheriae is an airborne bacterial pathogen that is resistant to drying, and can be transmitted in human populations via nasal secretions. C. diphtheriae is a toxin-producing bacterium that produces diphtheria toxin, an exotoxin that propagates the pathogenicity of the bacterium in vivo.


C. diphtheriae causes both local and systemic infections in humans. Local infections can occur in the tonsils, nose, conjunctiva and the pharynx while systemic infections may affect the kidneys, cardiac muscles of the heart, adrenal glands and the liver cells. Following the invasion of C. diphtheriae into the body through the respiratory route, the bacterium becomes deposited on the local tissues of the throat and tonsils. C. diphtheriae harbours the β prophage that contains the tox gene responsible for the production of diphtheria toxin. β prophage is a temperate bacteriophage, and it is what controls the production of diphtheria toxin by C. diphtheriae. Diphtheria toxin contains two domains: the A and B domains.

After production, diphtheria toxin become absorbed by the damaged mucous membranes of the tonsils and throat, and this leads to destruction of epithelial cells coupled with an inflammatory reaction, all of which culminates to the formation of a grayish-white exudates called pseudomembrane that surrounds the tonsils, larynx and pharynx. Pseudomembrane is a lesion that contains cells of C. diphtheriae and damaged host cells, and the manifestation of pseudomembrane on the tonsils, larynx and pharynx can eventually result in suffocation due to blockage of air passage. Swelling of the lymph nodes in the neck region can also occur, and profuse bleeding can ensue following the clinical attempt to remove the pseudomembrane. Death can occur if left untreated. Clinical signs and symptoms of diphtheria may include fever, cough, and discharge of thick mucopurulent secretions from the nares.


Laboratory diagnosis of C. diphtheriae infection is mainly dependent on identification of the pathogen from clinical specimens including throat and nose swabs. Physical examination of the throat and tonsil regions of infected patients for pseudomembrane appearance also aids diagnosis. Specimens are examined microscopically by Gram staining for the detection of beaded heads of C. diphtheriae containing metachromatic granules. Bacterial culture in Loeffler serum medium and Tellurite blood agar are used for the primary isolation of C. diphtheriae from nose and throat swabs. PCR tests and serological tests including ELISA can also be used to diagnose the infection.   

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Illustration of the rod shaped morphology of C. diphtheriae  in a Gram stain. C. diphtheriae forms beaded heads containing metachromatic granules when stained and viewed under the microscope.

C. diphtheriae  growing on blood agar.


The antibiotics used for treating diphtheria include penicillin, erythromycin, clindamycin, gentamicin and vancomycin. Diphtheria antitoxin which counters the effect of diphtheria toxin in vivo can also be used in severe diphtheria infections. Early treatment of diphtheria using antibiotics and antitoxin will help to eliminate and neutralize the toxigenicity of the pathogen.


The control and prevention of diphtheria is largely dependent on sustained massive immunization of susceptible individuals using the diphtheria, tetanus and pertussis (DTaP) vaccine. This approach will help to maintain a high level of active immunity in terms of herd immunity in a population and drastically reduce the spread and distribution of toxin-producing C. diphtheriae in a particular geographical area.


Prescott L.M., Harley J.P and Klein D.A (2005). Microbiology. 6th ed. McGraw Hill Publishers, USA.

Madigan M.T., Martinko J.M., Dunlap P.V and Clark D.P (2009). Brock Biology of Microorganisms, 12th edition. Pearson Benjamin Cummings Inc, USA.

Balows A, Hausler W, Herrmann K.L, Isenberg H.D and Shadomy H.J (1991). Manual of clinical microbiology. 5th ed. American Society of Microbiology Press, USA.

Barrett   J.T (1998).  Microbiology and Immunology Concepts.  Philadelphia,   PA:  Lippincott-Raven Publishers. USA.

Basic laboratory procedures in clinical bacteriology. World Health Organization (WHO), 1991. Available from WHO publications, 1211 Geneva, 27-Switzerland.

Murray P.R, Baron E.J, Jorgensen J.H., Pfaller M.A and Yolken R.H (2003). Manual of Clinical Microbiology. 8th edition. Volume 1. American Society of Microbiology (ASM) Press, Washington, D.C, U.S.A.

Murray P.R, Baron E.J, Jorgensen J.H., Pfaller M.A and Yolken R.H (2003). Manual of Clinical Microbiology. 8th edition. Volume 2. American Society of Microbiology (ASM) Press, Washington, D.C, U.S.A.

Murray P.R., Rosenthal K.S., Kobayashi G.S., Pfaller M. A. (2002). Medical Microbiology. 4th edition. Mosby Publishers, Chile.


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