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Illness Bacteria And death owing to suffocation may occur unless the oxygen lack is corrected by intubation or tracheotomy. The soluble toxin is carried in the general circulation to susceptible organs such as the heart and cranial or peripheral nerves. Cardiac failure may be the result of specific necrotic in-jury to the myocardium or it may be secondary to peripheral circulatory disturbances. The cranial or peripheral nerve involvement is presumably due to the direct action of the toxin on the nerve cells.
The explanation of the relatively selective action of the toxin remains obscure. Aside from the striking, picture of the local lesion, the pathologic changes noted in fatal cases of diphtheria are relatively nonspecific. Grossly, the heart, liver, kidneys, and adrenal glands may show degenerative changes characterized microscopically by necrosis, fatty infiltration, and parenchymatous degeneration. Clinical Manifestations. Diphtheria is characterized by a relatively short incubation period —one to four days on average, with an Outside limit of one week. The clinical manifestations depend, first, upon the severity of the process (which may show every gradation between a mild, nearly inapparent infection and a highly malignant progressive one), and, second, upon the anatomic location of the primary lesion.
The more important clinical types are faucial (or tonsillar), nasopharyngeal, and laryngeal. Extra-respiratory forms of the disease such as ocular, aural, and cutaneous diphtheria do occur, but in general, are of less importance. in faucial diphtheria the process is limited essentially to the tonsillar area. The onset is abrupt and is characterized by moderate fever, chilliness, general malaise, and mild sore throat. Swallowing is relatively painless. The pharynx is moderately injected and dull red. The pseudo-membrane first appears as a thick gelatinous exudate confined to one tonsil. This spreads to the other tonsil and thickens to give the typical dirty white or grayish-yellow diphtheritic membrane. If the pseudomembrane is forcibly removed, a raw, bleeding surface is exposed beneath, over which the membrane rapidly forms anew.
Tonsillar swelling is usually present, and frequently there is some enlargement of the cervical lymph nodes. If the tonsils are absent, the membrane may be less characteristic. Often the process spreads to involve the uvula and soft palate, which become edematous. If the process remains limited to the tonsillar area, the clinical 2 tKv• he. so mild that a definite diagnosis can be made only by isolation or the organism. Nasopharyngeal diphtheria represents a spread of the original process from the faucial area to the uvula, soft palate, posterior pharyngeal wall, and nasal mucosa. The membrane covering these areas presents a dirty yellow appearance; in some instances, it invades the anterior' nares and protrudes through the external opening.
Illness Bacteria Occasionally the middle ear may be invaded as well. There is considerable faucial edema and usually a serosanguineous nasal discharge. Enlargement of the cervical lymph nodes is almost invariably present; the swelling may be so severe as to deserve the name bull neck. A characteristic diphtheritic odor is usually present as well as pallor and cyanosis. Toxemia is the rule, and the patient is almost always prostrated. Oliguria, albuminuria, weak, rapid pulse, and high fever are prominent features. If recovery ensues, sequelae are common. This form of the disease should not be confused with anterior nasal diphtheria, in which the disease process is limited to the anterior nares, which is a relatively benign process with minimal toxicity, and which is important chiefly because of its epidemiologic implications.
Laryngeal diphtheria usually results from the spread of infection downward from the nasopharynx, although the primary lesion may be in the larynx itself. It is a particularly dangerous form of the disease, because the membrane and accompanying edema produce mechanical obstruction of the airway, giving rise to the classic diphtheria croup. The first symptoms are hoarseness, dyspnea, and a characteristic brassy cough. As the obstruction increases, dyspnea becomes more severe, and ultimately cyanosis appears together with aphonia and expiratory and inspiratory stridor. As bronchial secretions accumulate behind the obstruction, the accessory muscles of respiration are brought into play, and the spasmodic attacks of severe dyspnea gradually become frequent and persistent.
Unless the airway is restored by intubation or tracheotomy, death by suffocation ensues. Rarely the process involves the bronchial tree as well. Extrarespiratory diphtheria. Although diphtheria is usually a disease of the upper respiratory tract, other parts of the body may be the site of primary or secondary diphtheritic lesions., Thus, wounds, sores, and abrasions of the skin may become secondarily infected. During World War II several skin infections occurred among men serving in the tropics. These took the form of chronic, nonhealing ulcers that developed at the site of minor abrasions. Over time, a dirty grayish membrane appeared. The majority of these infections yielded mitis strains on culture. The relatively low percentage of sequelae suggests that the absorption of toxin from such wounds was not great, although some were accompanied by polyneuritis (see below).
The Illness Bacteria fact that antitoxin alone usually gave disappointing results in these cutaneous cases raises the possibility that many of these so-called “tropical sores” had a complex etiology. Ocular diphtheria is a rare form of the disease; the conjunctivae are chiefly involved. Diagnosis. The presumptive diagnosis of diphtheria must be made on clinical grounds without waiting for laboratory confirmation since the early specific therapy of the disease is paramount. The cardinal features pointing to the diagnosis are (1) comparatively painless pharyngitis involving the tonsils (or tonsillar beds) and frequently the uvula and soft palate as well; (2) a relative lack of