Diphtheria

Diphtheria (diphtheria, suffocating disease) is an acute anthroponotic infectious disease with an aerosol mechanism of transmission of the pathogen, characterized by predominant damage to the oropharynx and respiratory tract with the development of fibrinous inflammation at the site of introduction of the pathogen and toxic damage to the cardiovascular system, nervous system and kidneys.

Diphtheria is an acute pharyngeal or skin infection caused by the toxin-producing Corynebacterium diphtheriae, some strains of which are capable of producing exotoxin. Symptoms of diphtheria are either nonspecific skin infections or pseudomembranous pharyngitis, accompanied by secondary damage to the myocardium and nervous tissue. Damage to the latter is caused by the action of the exotoxin. Diagnosis of diphtheria is based on the clinical picture and confirmed by a culture study. Treatment of diphtheria is with antitoxin and penicillin or erythromycin. Vaccination in childhood should be routine.

ICD-10 codes

• A36. Diphtheria.
  • A36.0. Diphtheria of the pharynx.
  • A36.1. Diphtheria of the nasopharynx.
  • A36.2. Diphtheria of the larynx.
  • A36.3. Diphtheria of the skin.
  • A36.8. Other diphtheria.
  • A36.9. Diphtheria, unspecified.

What causes diphtheria?

Diphtheria is caused by Corynebacterium diphtheriae, which infects the nasopharynx (respiratory diphtheria) or skin. Strains of Corynebacterium diphtheriae infected with betaphage (carries a gene encoding toxin production) produce a potent toxin. This toxin first causes inflammation and necrosis of local tissues, then damages the heart, nerves, and kidneys.

Humans are the only known reservoir for Corynebacterium diphtheriae. Infection is spread by aerosols generated by sneezing, by direct contact with oropharyngeal secretions or skin lesions, or, less commonly, by cutaneous secretions. Most patients become asymptomatic nasopharyngeal carriers. Poor nursing care and public hygiene contribute to the spread of cutaneous diphtheria. In the United States, native-born residents of endemic areas are at particularly high risk.

What are the symptoms of diphtheria?

Symptoms of diphtheria vary depending on the site of infection and whether toxin is produced. Most cases of respiratory diphtheria are caused by toxin-producing strains. Most cases of cutaneous diphtheria are caused by non-toxin-producing strains. The toxin is poorly absorbed from the skin, so complications due to the toxin are rare in cutaneous diphtheria.

Diphtheria has an incubation period that usually lasts 2-4 days and a prodromal period that lasts 12-24 hours. After this, the patient develops the first symptoms of diphtheria: moderate sore throat, dysphagia, low-grade fever, and tachycardia. Nausea, vomiting, sneezing, headache, and fever are more common in children. If diphtheria is caused by a toxin-producing strain, a characteristic membrane appears in the tonsil area. Initially, the membrane may be a white exudate, but it usually becomes dirty gray, fibrinous, and so attached to the tonsils that its removal is accompanied by bleeding from them. Localized edema may manifest itself as a visually defined enlargement of the neck (bull neck), hoarseness, stridor, and dyspnea. The membrane can extend into the larynx, trachea, and bronchi, causing partial airway obstruction or complete obstruction, resulting in sudden death.

Skin lesions usually occur on the extremities. They vary in appearance and are often indistinguishable from chronic skin pathology (eczema, psoriasis, impetigo). In some cases, protruding ulcers with a grayish coating are formed. Pain, tenderness, erythema and exudate are typical. In cases where there is exotoxin production, the damaged areas may lose sensitivity. Concomitant nasopharyngeal infection is detected in 20-40% of cases.

Myocarditis most often develops between the 10th and 14th days of illness, but may occur any time from the 1st to the 6th week of illness. Minor ECG changes are found in 20-30% of patients, but atrioventricular block, complete heart block, and ventricular arrhythmias may occur, which are often associated with high mortality. Acute heart failure may also develop.

Damage to the nervous system usually begins during the first week of the disease with bulbar paresis, which leads to dysphagia and nasal regurgitation. Peripheral neuropathy appears between the third and sixth weeks of the disease. Neuropathy is both motor and sensory in nature, but motor impairments predominate. Complete recovery of nervous activity occurs many weeks later.

How is diphtheria diagnosed?

The appearance of a membrane should suggest the diagnosis of diphtheria. Gram staining of the membrane may reveal gram-positive bacilli with metachromatic staining. Material for culture should be taken from beneath the membrane, or a portion of the membrane itself may be removed for examination. The laboratory should be notified to search for Corynebacterium diphtheriae.

Cutaneous diphtheria should be suspected when a patient develops skin lesions during a breakthrough of respiratory diphtheria. A smear or biopsy should be sent for culture.

How is diphtheria treated?

Patients suspected of having diphtheria should be admitted immediately to an intensive care unit for monitoring of respiratory and cardiac complications. Isolation with respiratory and contact precautions is required. Isolation is continued until 2 cultures taken 24 and 48 hours after stopping antibiotics are negative.

Diphtheria antitoxin should be given without waiting for culture confirmation because the antitoxin can neutralize only the noncellular toxin. Use of antitoxin in cutaneous diphtheria without evidence of respiratory disease is of questionable value. Pathologic sequelae due to exotoxin are rare in cutaneous diphtheria, but some experts recommend use of antitoxin in this form. In the United States, antitoxin must be obtained from the CDC. Caution: Diphtheria antitoxin is derived from horses; a skin or conjunctival test should be performed before injection to determine susceptibility to the antitoxin. The dose of antitoxin, which ranges from 20,000 to 100,000 units given intramuscularly or intravenously, is determined by the severity of the disease, symptoms, and complications. If an allergic reaction to the administration of antitoxin occurs, 0.3 to 1 ml of epinephrine should be administered immediately in a 1:1000 dilution (0.01 ml/kg). Epinephrine may be administered subcutaneously, intramuscularly, or slowly intravenously. In patients who are highly sensitive to the antitoxin, intravenous administration of the antitoxin is contraindicated.

Antibiotics are given to achieve eradication and prevent dissemination of the infection. They cannot replace the antitoxin. Adults can be given either procaine penicillin G 600,000 units intramuscularly every 12 hours or erythromycin 250-500 mg orally every 6 hours for 14 days. Children should be given either procaine penicillin G 12,500-25,000 units/kg every 12 hours intramuscularly or erythromycin 10-15 mg/kg (maximum 2 g daily) every 6 hours orally or intravenously. Corynebacterium diphtheriae is considered eradicated when 2 consecutive throat and/or nasopharyngeal cultures are negative after completion of the antibiotic course.

Recovery from acute diphtheria is slow, so patients should be advised not to resume vigorous activity too quickly. Even normal physical activity can be harmful to a patient recovering from myocarditis.

For cutaneous diphtheria, it is recommended to thoroughly clean the affected area with soap and water and prescribe systemic antibiotics for 10 days.

How is diphtheria prevented?

All people should be vaccinated on time. For children, the diphtheria vaccine DPT is used, for adults - DS vaccine. Having had diphtheria does not guarantee the development of immunity, so people who have had diphtheria should be vaccinated after recovery. In addition, all contacts, including hospital staff, should receive vaccination updates. Protective immunity can be expected for no more than 5 years after a booster injection. In cases where the vaccination status is unknown, vaccination should be carried out.

All close contacts should be tested; throat and/or nasopharyngeal cultures should be taken from all contacts regardless of vaccination status. Asymptomatic contacts of diphtheria should receive erythromycin 250-500 mg orally every 6 hours for adults (10-15 mg/kg for children) for 7 days or a single dose of penicillin G benzathine (600,000 units intramuscularly for those weighing 30 kg or less and 1.2 million units intramuscularly for those weighing more than 30 kg). If laboratory tests are positive, treatment is supplemented with a 10-day course of erythromycin. Patients should be closely monitored during treatment. Carriers should not receive antitoxin. It is considered safe to return to work after 3 days of antibiotic therapy, but continued medication should be taken. Repeat cultures should be performed 2 weeks after stopping antibiotics. Carriers who cannot be monitored are given penicillin G benzathine rather than erythromycin. This is because there is no confidence in patient compliance.