Diphtheria

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

Diphtheria is an acute pharyngeal or cutaneous infection caused by the toxin-producing Corynebacterium diphtheriae, some strains that 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. The damage of the latter is due to the action of exotoxin. Diagnosis of diphtheria is based on the clinic and is confirmed by culture research. Diphtheria is treated 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 the skin. Corynebacterium diphtheriae strains infected with a beta-phage (carries a gene coding for the formation of a toxin) produce a potent toxin. First, this toxin causes inflammation and necrosis of local tissues, after which the heart, nerves and kidneys are affected.

Humans are the only known reservoir of Corynebacterium diphtheriae. The infection spreads with an air suspension formed by sneezing, by direct contact with oropharyngeal secretions or skin lesions, or, more rarely, with the skin detachable. Most patients become asymptomatic nasopharyngeal carriers. Poor care and public hygiene contribute to the spread of skin diphtheria. In the United States, indigenous people living in endemic foci are in a particularly high risk group.

What are the symptoms of diphtheria?

Symptoms of diphtheria are variable and depend on the place of infection and whether there is toxin production. Most cases of respiratory diphtheria are caused by toxin-producing strains. Most cases of cutaneous diphtheria are due to non-toxin-producing strains. The toxin is poorly absorbed from the surface of the skin, so complications due to the toxin are rare in the cutaneous form of 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 has the first symptoms of diphtheria: moderate intensity of sore throat, dysphagia, minor 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 region of the palatine tonsils. Initially, the membrane can be a white exudate, but usually becomes dirty-gray, fibrinous, and so attached to the tonsils that its removal is accompanied by bleeding from them. Local edema can be expressed in a visually determined increase in the neck (bovine neck), hoarseness, stridor and dyspnea. The membrane can spread to the larynx, trachea and bronchi and cause partial obstruction of the airways, as well as complete obstruction, which leads to sudden death.

Skin lesions usually occur on the limbs. They differ in their appearance and are often indistinguishable from chronic skin pathology (eczema, psoriasis, impetigo). In some cases, protruding ulcers with a grayish coating are formed. Typical pain, soreness, erythema and exudate. In cases where there is exotoxin production, the lesion sites may lose sensitivity. Concomitant nasopharyngeal infection is detected in 20-40% of cases.

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

Damage to the nervous system usually begins within the first week of the disease from bulbar paresis, which leads to dysphagia and nasal regurgitation. Peripheral neuropathy appears in the period from the 3rd to the 6th week of the disease. Neuropathy has both motor and sensory character, but motor disorders predominate. Complete recovery of nervous activity occurs many weeks later.

How is diphtheria diagnosed?

The appearance of the membrane should suggest a diagnosis of diphtheria. Gram staining of the membrane can allow detection of gram-positive bacilli with metochromatic staining. The material for culture testing should be taken under the membrane, or a part of the membrane itself can be taken for examination. The laboratory must be informed that it is necessary to search for Corynebacterium diphtheriae.

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

How is diphtheria treated?

Patients suspected of having diphtheria should be immediately hospitalized in the intensive care unit, to monitor respiratory and cardiac complications. Isolation with respiratory and contact precautions is required. Isolation continues until 2 culture studies taken 24 and 48 hours after antibiotic cancellation are negative.

Diphtheria antitoxin should be administered without waiting for a culture confirmation, since the antitoxin is able to neutralize only the part of the toxin that is not bound to the cells. The use of antitoxin in the cutaneous form of diphtheria, in the absence of evidence of respiratory disease, is of questionable value. The pathological sequence caused by the action of exotoxin is rarely observed in the cutaneous form of diphtheria, however some experts recommend the use of an antitoxin in this form. In the US, the antitoxin should be obtained via CDC. Warning: Diphtheria antitoxin is obtained from horses, so a skin test or conjunctival test should be performed prior to injection to determine sensitivity to the antitoxin. The dose of antitoxin, varying between 20 000 and 100 000 units intramuscularly or intravenously, is determined by the severity of the disease, symptoms and complications. When an allergic reaction to the administration of an antitoxin appears, 0.3 to 1 ml of epinephrine should be injected immediately at a dilution of 1 to 1000 (0.01 ml / kg). The introduction of epinephrine can be subcutaneous, intramuscular or slow intravenous. In patients highly sensitive to antitoxin, the intravenous administration of an antitoxin is contraindicated.

Antibiotics are prescribed to achieve eradication and prevent the spread of infection. They can not replace the antitoxin. Adults can be prescribed either procaine penicillin G 600 000 ED intramuscularly every 12 hours, or erythromycin 250-500 mg orally every 6 hours for 14 days. Children should be assigned either procaine penicillin G at a dose of 12,500-25,000 units / kg every 12 hours intramuscularly, or erythromycin 10-15 mg / kg (maximum 2 g per day) every 6 hours inside or intravenously. Elimination of Corynebacterium diphtheriae is considered complete when, after the completion of the course of antibiotics, no causative agents are found in 2 consecutive culture studies of the materials from the throat and / or nasopharynx (negative results).

Recovery from acute diphtheria is slow, so patients should be advised not to move quickly to active activities. Even normal physical activity can damage a patient recovering from myocarditis.

When the cutaneous form of diphtheria is recommended thorough cleaning of the site of damage with soap and water and the appointment of systemic antibiotics for 10 days.

How is diphtheria prevented?

All people should be vaccinated on time. For children, a diphtheria diphtheria vaccine is used, for adults - DS vaccine. Postponed diphtheria does not guarantee the development of immunity, so people who underwent diphtheria should be vaccinated after recovery. In addition, vaccination updates should be provided to all contact persons, including hospital staff. Protective immunity can be expected no more than 5 years after a booster injection. In those cases when the vaccination status is unknown, it is necessary to carry out vaccination.

It is necessary to examine all close contacts; cultures from the throat and / or nasopharynx should be taken for examination in all contact persons regardless of the vaccination status. Non-diphtheria contact persons should receive erythromycin 250-500 mg orally every 6 hours for adults (10-15 mg / kg for children) for 7 days or a single injection of penicillin G benzathine (600,000 units intramuscularly for those with body weight does not exceed 30 kg, and 1.2 million units are intramuscular for those with a body weight greater than 30 kg .In those cases where the results of laboratory testing are positive, treatment is supplemented with a 10-day course of erythromycin. Time l Carriers should not receive an antitoxin.After 3 days from the start of antibiotic treatment, it is considered safe to return to work, but it is necessary to continue taking the medication.) Repeated culture examination is carried out 2 weeks after antibiotic cancellation .To carriers that can not be monitored, penicillin is prescribed G benzathine, and not erythromycin, which is due to the fact that there is no certainty in the patient's compliance.