TABLE 1 Diphtheria Key Points Overview

Preventable, acute toxin-mediated disease caused by Corynebacterium diphtheriae Currently rare in most developed nations after the implementation of vaccination Pathophysiology of C. diphtheria

Aerobic and facultative anaerobic Gram-positive bacilli Exists exclusively on human mucous membranes and skin

Potent exotoxin is synthesized by some strains after 2-4 days of incubation, taken up by cells and inhibiting protein synthesis, causing necrosis with formation of a tough pseudomembrane of leukocytes, dead host cells, fibrin, and erythrocytes, which may precipitate airway obstruction Symptomatology (by location of infection)

Nasal—typically infants, serosanguinous and mucopurulent rhinitis, excoriation of the nares and upper lip, and a white septal pseudomembrane may be seen Pharynx—pharyngitis, 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 Larynx—worsening hoarseness, dyspnea and inspiratory stridor, and later a tracheobronchitis Malignant or "bull-neck" diphtheria—extensive pseudomembrane formation, halitosis, massive swelling of the tonsils and uvula, thick speech, cervical lymphadenopathy, striking edematous swelling of the submandibular region and anterior neck, and severe toxicity Toxin production accompanied by profound malaise, weakness, cervical lymphadenitis, cervical soft tissue swelling causing a "bull neck," and occasionally palatine paralysis and upper respiratory obstruction with inspiratory stridor Cutaneous—associated with tropics, prevalent in Southeast Asia. The characteristic, deep, rounded, crater-like lesions are covered with an eschar and take months or even years to heal Diphtherial neuropathy usually involves the cranial nerves, causing diplopia, slurred speech, and dysphagia Diagnosis

Isolation on specialized growth media including potassium tellurite (Tinsdale agar) to inhibit other oral flora

Treatment is reserved for patients carrying toxigenic strains, identified by streaking of the organism and controls on toxin-antibody impregnated paper and observing for immunoprecipitation lines PCR may also be used to detect toxin genes Treatment

Removal of membrane by direct laryngoscopy or bronchoscopy may be necessary to prevent or alleviate airway obstruction Diphtheria antitoxin must be delivered promptly to prevent myocarditis, neuritis, or death, after administration of intradermal skin test for horse serum sensitivity Penicillin G or erythromycin antibiotic course, with repeated nasopharyngeal cultures to confirm eradication of carrier state Bed rest for 12 days to prevent sudden cardiac death from myocarditis Strict isolation Prognosis

Mortality rate reported from most series varies from 5% to 10% Vaccinated patients experience a mild illness

Abbreviation: PCR, polymerase chain reaction.

The diphtheria organisms remain in the superficial layers of the respiratory mucosa and induce a local inflammatory reaction. The potent exotoxin released by the organism is taken up by cells and inhibits protein synthesis, causing necrosis. Initially, a gray exudate of dead host cells and white blood cells forms, which is easily removed. After the addition of fibrin and red blood cells, the tough gray-brown pseudomembrane is produced; this is difficult to remove, and bleeds after such attempts. Subsequently, bacterial superinfection may occur with Staphylococcus aureus and Streptococcus pyogenes.

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