Clinical manifestations:
C. diphtheria is usually not an invasive organism. Clinical manifestations are related with both the local and systemic effect of the diphtheria toxin. The toxin is accountable for local tissue destruction and in the formation of membrane. Diphtheria is categorized into numerous clinical types, based on the site of disease.(1) Respiratory diphtheria:
C. diphtheria infects mainly the upper respiratory tract, where the organism colonizes the mucosal surface of the nasopharynx and multiplies locally with no bloodstream invasion. Following an incubation period of generally 2-5 days, the illness starts steadily with malaise, anorexia, sore throat, and fever.
Locally, toxin induces tissue necrosis, leukocyte response and creation of a hard, adherent pseudomembrane composed of a mixture of fibrin, dead cells and bacteria. The membrane is strongly adherent and bleeding takes place upon attempts to eliminate it.
(2) Pharyngeal diphtheria:
The membrane generally starts to form on the tonsils or posterior pharynx. In more rigorous cases it can spread progressively over the pharyngeal wall, fauces and the soft palate all the mode to the bronchi. This is termed as pharyngeal diphtheria.(3) Laryngeal diphtheria:
Since the membrane spreads the patients might develop important edema of the submandibular regions and the anterior neck with the lymphadenopathy, providing them a characteristic ‘bull neck appearance’. In severe situations the neck edema might extend past the clavicles into the chest, accompanied by the erythema. Laryngeal diphtheria can take place as an outcome of membrane extension. It exists with hoarseness, strider and dyspnoea, and airway barrier.(4) Systemic effect:
The disease might progress, when sufficient toxins enter the blood-stream, causing harsh prostration, striking pallor, fast pulse, stupor and coma. Such effects might consequence in death in a week of onset of symptoms. The absorbed toxin can too cause delayed damage at far-away sites. The most often affected organs are the heart (i.e., myocarditis) and the cranial nerves. Such complications might take place from 1 to 12 weeks after disease onset.(5) Cutaneous diphtheria:
Cutaneous diphtheria frequently appears as a secondary infection of a prior wound. Primary cutaneous diphtheria starts as a tender pustule and expands to an oval punched-out ulcer with a membrane and edematous rolled borders. The skin infections might differ in severity, though toxin-induced complications are generally uncommon.(6) Local infections:
C. diphtheria might also cause local infections like conjunctivitis, vulvovaginitis, and primary or secondary otitis media.
Asymptomatic nasopharyngeal infection with C. diphtheria is more common than clinical disease. The length of carriage averages 10 days, though chronic carriers might shed the organism for 6 months or more. Antibiotic treatment is efficient in terminating shedding.
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