diphtheria(redirected from cutaneous diphtheria)
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An acute infectious disease of humans caused by Corynebacterium diphtheriae. Classically, the disease is characterized by low-grade fever, sore throat, and a pseudomembrane covering the tonsils and pharynx. Complications such as inflammation of the heart, paralysis, and even death may occur due to exotoxins elaborated by toxigenic strains of the bacteria. The upper respiratory tract is the most common portal of entry for C. diphtheriae. It can also invade the skin and, more rarely, the genitalia, eye, or middle ear. The disease has an insidious onset after a usual incubation period of 2–5 days.
The only specific therapy is diphtheria antitoxin, administered in doses proportional to the severity of the disease. Antitoxin is produced by hyperimmunizing horses with diphtheria toxoid and toxin. It is effective only if administered prior to the binding of circulating toxin to target cells. Antibiotics do not alter the course, the incidence of complications, or the outcome of diphtheria, but are used to eliminate the organism from the patient.
Persons with protective antitoxin titers may become infected with diphtheria but do not develop severe disease. Since the 1920s, active immunization with diphtheria toxoid has proved safe and effective in preventing diphtheria in many countries. Diphtheria toxoid is produced by incubating the toxin with formalin. Active immunization requires a primary series of four doses, usually at 2, 4, 6, and 18 months of age, followed by a booster at school entry. See Immunity, Medical bacteriology, Toxin, Vaccination
an acute infectious disease characterized by inflammation, the formation of a tough membrane at the point of introduction of the causative agent of the disease, and a severe general poisoning (intoxication) of the organism.
The causative agent of diphtheria (Corynebacterium diphtheriae) was discovered by the German bacteriologist E. Klebs in 1883 and was isolated in a pure culture by the German bacteriologist F. Löffler. The pathogen is rod-shaped and produces diphtheria exotoxin. The source of infection in diphtheria is a sick person or carrier (a healthy person or a person who has recovered from diphtheria). The diphtheria bacilli are released into the environment with drops of mucus in talking, sneezing, or coughing. Infection occurs when the microbe enters the organism through the mucous membranes of the pharynx, nose, and upper respiratory tracts, and more rarely, through the conjunctiva of the eyes, broken skin, and so forth (the airborne droplet path). The pathogen may also enter through the mouth with food and through various articles such as underwear, clothing, books, and toys. The diphtheria bacillus, having reached the mucous membranes (or the skin), secretes a toxin that causes necrosis (dying) of the epithelium and affection of the blood vessels, with the deposition of a network of fibrin (blood protein) and the formation of a membrane. A general intoxication develops when the toxin reaches the blood. The intoxication predominantly affects the nervous and cardiovascular systems, the adrenals, and kidneys. The incubation period is two to ten days.
In terms of the localization of the process, a distinction is made between diphtheria of the pharynx (the most frequent form), respiratory tract, nose, eyes, ears, external sex organs (in young girls), skin, the umbilicus in the newborn, of wounds, and so forth.
In the localized form of pharyngeal diphtheria the membranes cover the tonsils without extending beyond them, the lymph nodes are moderately enlarged, and the body temperature rises to 38.5°-39° C. Malaise, loss of appetite, and headaches are mildly manifested. In the diffuse form of pharyngeal diphtheria the membranes spread from the tonsils to the mucous membranes of the palatine arches, uvula, and pharynx; general malaise is rather clearly manifested. The toxic form of pharyngeal diphtheria is characterized by a broad lesion of the pharynx; the tonsils are edematous, and their surface is covered by thick membranes of a dirty white color. The process can extend to the nasopharynx and the nasal cavity. Usually, edema of the subcutaneous tissue develops around the enlarged superior cervical lymph nodes. The phenomena of intoxication progressively increase: the heart rhythm is disrupted, swallowing is difficult, and when the process spreads to the respiratory organs, breathing is disrupted. Moreover, during the phenomena of myocarditis in the acute period, nosebleeds are observed. There are stomach pains and diarrhea, and a collapse may occur.
In diphtheria of the respiratory tract, with localization of the process on the mucous membrane of the larynx or the trachea, as a consequence of the formation of membranes, edema, infiltration of the mucous membrane, and spasms of the larynx musculature, respiratory disturbances grow; this is known as diphtheritic croup. The croup is manifested by a “barking” cough, a hoarse voice, even complete aphonia (loss of voice), and acute difficulty in inhaling. With the spread of the process to the bronchi, the severe form of diphtheria, diffuse croup, occurs.
Nasal diphtheria is encountered in young children, and intoxication is not usually observed. Nasal diphtheria is manifested by a unilateral cold with bloody secretions and tends to have an extended course.
Diphtheria of the eyes, ears, external sex organs, digestive tract, skin, and wounds, including the umbilical wound in the newborn, is almost not encountered in modern medical practice.
Complications are noted basically only with the toxic form of diphtheria, particularly if the start of serotherapy is delayed. Collapse develops on the second, third, or fourth day of the illness, and severe myocarditis on the fifth or sixth day. Sometimes peripheral paralyses, paralyses of the cranial nerves, and toxic nephrosis develop; with diphtheritic croup pneumonia develops.
Treatment includes the earliest possible administration of antitoxic antidiphtheric serum, vitamin therapy, and antibacterial therapy. In diphtheritic croup, when there is an increase in the phenomena of disruption of breathing and anoxia, an emergency operation (intubation or tracheotomy) should be performed.
Active immunization plays the basic role in combating diphtheria. In the USSR antidiphtheric inoculations are obligatory for all children. (In the period from the age of five or six months up to 12 years one vaccination and three revaccinations are administered.) Immunization is achieved by adsorbed diphtheria toxoid. Since 1958, in the USSR, inoculations have been administered with the associated preparation (AKDS) which, in addition to the diphtheria toxoid, includes whooping cough vaccine and tetanus toxoid. Due to the active immunization program, the diphtheria morbidity rate in the USSR has declined sharply (by 30.7 times from 1959 through 1966).
Other preventive measures consist in discovering and isolating (hospitalizing) sick persons as quickly as possible. After hospitalization of the sick person, the quarters are disinfected. All persons who have been in contact with the patient are given repeated bacteriological examinations and medical supervision for seven days. Children who have been in contact with sick persons are not allowed to attend children’s institutions (creches, nurseries, schools, and so forth) during this period. The state of children’s specific immunity is checked using the Schick test (named after the Austrian physician B. Schick).
REFERENCESMolchanov, V. I. Difteriia, 2nd ed. Moscow, 1960.
Titova, A. I., and S. Ia. Flekser. Difteriia. Moscow, 1967.
R. N. RYLEEVA and M. IA. STUDENIKIN