Clinical Manifestations

After an incubation of two to four days, colonizing toxigenic diphtheria strains produce toxin locally with initiation of the signs and symptoms of disease (5). In nasal disease, typically seen in infants, the illness appears similar to the common cold but then progresses to a serosanguinous and mucopurulent rhinitis. Excoriation of the nares and upper lip and a white septal pseudomembrane may be seen. Spread of the disease to the pharynx occurs next, causing a sore throat, tonsillitis, low-grade temperature and a white to gray pseudomembrane extending from the tonsils to the posterior pharyngeal pillars and nasopharynx, the most common site for clinical diphtheria. Hoarseness and a barking cough accompany the progression of disease. Laryngeal diphtheria most often develops as an extension of pharyngeal involvement, although occasionally it may be an isolated manifestation of diphtheria. As toxin production continues, there is profound malaise, weakness, cervical lymphadenitis, soft tissue swelling of the neck causing a "bull neck," and occasionally palatine paralysis and upper respiratory obstruction with inspiratory stridor. A small percentage of patients present with malignant or "bull-neck" diphtheria, with extensive pseudomembrane formation, foul breath, massive swelling of the tonsils and uvula, thick speech, cervical lymphadenopathy, striking edematous swelling of the submandibular region and anterior neck, and severe toxicity. Further spread of the disease downward to the larynx, causing worsening hoarseness, dyspnea and inspiratory stridor, and later a tracheo-bronchitis with edema and membrane formation extending along the entire tracheobronchial tree, will often precede respiratory failure.

In mild cases, or those modified by anti-toxin treatment, the membrane is coughed up between the 6th and 10th days, although a sudden and acute airway obstruction may occur from a partially detached piece of membrane. In severe cases, this obstruction is manifested by progressive hypoxia, restlessness, cyanosis, severe prostration, coma, and death. Of note, systemic signs of diphtheria are minimal in laryngeal involvement, due to the poor absorption of the toxin from the laryngeal mucous membrane. In general, however, the laryngeal involvement is associated with tonsillar and pharyngeal diphtheria, resulting in both obstruction and severe toxemia.

In addition to the classic respiratory form of diphtheria, a cutaneous form exists which is associated with the tropics and is prevalent in Southeast Asia. The characteristic, deep, rounded, crater-like lesions are covered with an eschar and take months or years to heal. The lesion acts as a potential reservoir for transmission and spread of the pharyngeal form of the disease. On rare occasions, clinical infection with C. diphtheriae can be seen in other sites such as the ear, conjunctivae, or vagina.

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