Corynebacterium diphtheriae are irregular-shaped (pleomorphic), aerobic, Gram-positive bacilli responsible for the disease diphtheria that attacks only human hosts. Both toxin-producing and non-toxin-producing strains of C. diphtheriae can adhere to and colonize the mucosal tissues of the upper respiratory tract. Transmission is generally person-to-person via airborne droplets. Sometimes, these people can appear healthy, but are still contagious. The disease results solely from the exotoxin produced rather than from the bacteria directly. It takes only one molecule of diphtheria toxin to kill a cell in the human heart or nervous system. Each bacterium can produce 5,000 such molecules every hour.
The name Diptheria comes from the Greek word ‘dipthera,’ meaning leather, referring to the tough, gray, mucousy membrane that blocks the victim’s throat. The Spanish called it ‘garrotillo,’ referring to the executioner’s implement – a string around the neck, tightened by twisting a stick. As a result of this disease, tracheotomies were first used during the epidemic in Naples in 1610. An epidemic in New Hampshire in 1735 claimed about 1,000 lives, 900 of which were children. Diptheria is thought to be the illness that caused the death of George Washington in 1799. By the mid-19th century, the microbes seemed to have developed a more potent strain because the death toll started to mount substantially.
The bacterium was finally identified in 1883. A few years later, it was known to produce poisons called exotoxins. The microbes responsible for producing the disease are infected with viral parasites called lysogenic bacteriophages. The gene that directs the production of the diphtheria toxin is carried by the bacteriophage (known as beta corynephage); and the toxin, therefore, is produced only by those corynephage that contain that particular gene and does not come from the C. diphtheriae bacterium directly. Without the bacteriophage, C. diphtheriae would not be the dangerous microbe that it is. Other members of the same genus may occasionally be infected with beta corynephage and can produce the diphtheria toxin, but that occurs only in very rare circumstances.
The toxin prevents protein synthesis. At first, no damage is noted until the host cells start dying because of a lack of newly synthesized proteins. As the dead cells accumulate, the bacteria produce more toxin; and the area of destruction expands. The incubation period ranges from several days to a week before clinical symptoms appear. Lesions begin to appear at the back of the throat and look like a thick fibrous membrane that is filled with trapped host cells and bacteria. This membrane is known as a pseudomembrane and adheres firmly to the epithelial surfaces. As the disease progresses, this membrane spreads upward into the nasopharyngeal tissues and/or downward into the larnyx and trachea, often obstructing the airway, resulting in suffocation of the patient. The lesions are generally superficial and rarely penetrate into deeper tissues. However, on rare occasions, the toxin can produce necrosis of such internal organs as the liver, kidneys, and adrenal glands. Another notable symptom includes the swelling of the lymph nodes in the neck, often referred to as a “bull neck.”
The most frequent and dangerous damage done by the toxin is to the heart and central nervous system (CNS), often resulting in death. The disease may linger for many weeks because of the damage of the CNS, and varying levels of paralysis may occur as a result. In areas of poor sanitation, diphtherial skin lesions can occur; and the toxin produced is the same as in the throat. Recovery from diphtheria often takes six months, which does not necessarily mean that the bacteria has been eliminated from the body. Many of those who have recovered continue to be healthy carriers for prolonged periods of time.
Diphtherial sores on the skin are contagious and occur mainly in tropical countries where overcrowding and sanitary problems occur. The rash caused by the skin diphtheria looks very much like impetigo and can also cause a nasal discharge and excoriated skin around the nose.
Diphtheroids are the result of a phage that has infected a diphtheria bacterium. They are known to occasionally cause endocarditis and sepsis in immunocompromised patients. One of these is known as JK (the other is C.xerosis) which produces a life-threatening disease with a mortality rate as high as 75%. Usually found in patients with artificial valves or IV catheters, the organism is very resistant to most antibiotics. Two species, C. haemolyticum and C. ulcerans, can cause pharyngitis with symptoms similar to those produced by Group A strep. C. pseudotuberculosis can cause a tuberculosis-like illness. A cousin to C. diphtheria is C. glutamicum (used also to manufacture MSG, or monosodium glutamate).
Vaccinations have greatly reduced the number of cases. Those who do contract the disease are often ones who have never been immunized or the elderly who have lost their immune status. As with all vaccines, there is controversy surrounding its manufacture and use. Diphtheria vaccine is part of the tetanus-whooping cough vaccination (DPT) given, starting in infancy, but it does not give lifelong immunity requiring a booster shot every ten years.
Passive immunization is given with an antitoxin to those who are suspected of having the disease already. In addition, penicillin, or erythromycin, is given, not only to stop further growth of the bacteria, but also to prevent the patient from becoming a carrier after recovery. A procedure known as the Schick test is used to determine whether a person is susceptible to the diphtheria bacterium.