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.