Clinical classification by localization
Depending on where the inflammation develops and how pronounced the toxic syndrome is, diphtheria is divided into several major groups.
- Oropharyngeal diphtheria. This is the most common variant. According to severity, it is subdivided into:
- Localized forms: catarrhal, islet, or membranous.
- Generalized (spread) form: the fibrinous deposit extends beyond the tonsils.
- Toxic forms: from mild subtoxic to toxic grades I, II, III, and extremely severe hypertoxic.
- Respiratory diphtheria (croup). Classified by the level of involvement:
- Localized croup (only the larynx is affected).
- Generalized croup (larynx and trachea).
- Descending croup (inflammation extends down into the bronchi).
- Nasal diphtheria. May present in a catarrhal-ulcerative or membranous form.
- Rare localizations. Involvement of the oral mucosa, esophagus, genitals, and cutaneous diphtheria (in the area of wounds) can occur.
- Combined forms. Simultaneous involvement of several anatomical areas.
Classification of bacterial carriage
Against the background of established antitoxic and antibacterial immunity, bacterial carriage may develop. It occurs in convalescents and in individuals who have not had diphtheria (practically healthy or having ENT pathologies).
According to the duration of the course, the following types of carriage are distinguished:
- Transitory: the pathogen is isolated once.
- Short-term: lasts up to 2 weeks.
- Moderate duration: lasts up to 1 month.
- Prolonged and recurrent: lasts over 1 month.
- Chronic: the pathogen persists in the body for more than 6 months.
ICD-10 categorization
The International Classification of Diseases codes the disease under the category A36:
- A36.0 — pharyngeal diphtheria;
- A36.1 — nasopharyngeal diphtheria;
- A36.2 — laryngeal diphtheria;
- A36.3 — cutaneous diphtheria;
- A36.9 — unspecified form.
Specific organ lesions are coded with A36.8 (other diphtheria). These include the conjunctival form (H13.1), diphtheritic myocarditis (I41.0), and polyneuritis (G63.0).
Types of local inflammation
The clinical picture directly depends on the type of epithelium on which the pathogen multiplies.
- Diphtheritic inflammation. Forms on stratified squamous epithelium (oropharynx). The epithelium is tightly fused with the underlying connective tissue, which is why the fibrinous deposit holds firmly and does not detach for a long time.
- Croupous inflammation. Occurs on prismatic and columnar secreting epithelium (larynx, trachea, bronchi). Due to the loose connection with the tissues, the fibrinous membrane quickly detaches as a single cast. This creates an immediate threat of airway obstruction and asphyxia.
Pathomorphological changes in internal organs
Toxic forms of the infection lead to systemic damage to the body:
- Heart: hemorrhages appear under the epicardium. Myolysis is characteristic in the acute stage. In a prolonged course, fatty degeneration of the myocardium and proliferation of connective tissue occur (“tiger heart of diphtheria”). The heart chambers dilate, the muscle becomes flabby, and thrombus formation is possible.
- Nervous system: predominantly affects peripheral nerves and autonomic ganglia located close to the oropharynx (vagus, phrenic nerves). Parenchymatous neuritis develops (myelin breakdown with preserved axis cylinders), which determines the reversibility of paralyses.
- Kidneys and adrenal glands: necrotizing nephrosis occurs in the kidneys (up to massive cortical necroses), and hemorrhages and disappearance of lipids occur in the adrenal glands.
- Lymph nodes: regional nodes are plethoric, enlarged, with foci of necrosis and hemorrhages visible on cross-section.
Briefly: answers to topical questions
What are the clinical criteria (edema boundaries) for dividing toxic oropharyngeal diphtheria into grades I, II, and III?
The severity grade of toxic oropharyngeal diphtheria is determined by the spread of subcutaneous tissue edema. The materials describe the boundaries for grades II and III, while grade I is not described:
- Toxic diphtheria grade II — dense edema extends to the base of the neck.
- Toxic diphtheria grade III — edema extends below the clavicles (sometimes reaching the base of the xiphoid process), and in bedridden patients, it spreads to the face, the back of the neck, and the back.
Which complications of diphtheria are considered early and which are late?
Specific complications of diphtheria are divided into early and late according to the time of onset.
- Early complications — pathology of target organs occurring during the tonsillitis period of the disease. For myocarditis, it is specifically indicated: early myocarditis develops from the 4th day of the illness and is the most severe. Infectious-toxic shock in severe forms of oropharyngeal diphtheria develops in the first days of the disease.
- Late complications — late myocarditis, the onset of which spans 3–4 weeks; subsequently, severe polyneuropathies develop in toxic diphtheria. With the progressive worsening of moderate-to-severe toxic forms, ITS (infectious-toxic shock) may develop at a later stage.
To remember the forms of respiratory diphtheria (croup), use the “ladder” rule: inflammation descends strictly from top to bottom. First is localized croup (larynx only), one step lower is generalized (larynx + trachea), and at the very bottom is descending (involving the bronchi).
Class and exam questions
Why are paralyses in diphtheria reversible?
The toxin causes parenchymatous neuritis, in which only the myelin sheath is destroyed, while the axon cylinder of the nerve fiber remains intact. This preserves the potential for regeneration of nervous system elements.
What is the main difference between diphtheritic and croupous inflammation?
Diphtheritic inflammation occurs on stratified squamous epithelium, where the deposit is tightly fused to the tissue. Croupous inflammation develops on the columnar epithelium of the respiratory tract: the membrane lies loosely there and can easily detach as a cast, causing asphyxia.
What does the term «diphtheritic tiger heart» mean?
This is the macroscopic picture of cardiac involvement in prolonged diphtheria. It is caused by fatty degeneration of the myocardium and abundant development of connective tissue, which gives the heart muscle a characteristic mottled appearance.
What else to study on this topic
- Characteristics of tonsillitis syndrome in diphtheria
- Mechanisms of formation of antitoxic immunity
- Features of localized forms of oropharyngeal diphtheria
- Pathogenesis of adrenal damage in toxic forms
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