Pediatric Diphtheria Follow-up

Updated: May 02, 2019
  • Author: Cem S Demirci, MD; Chief Editor: Russell W Steele, MD  more...
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Further Outpatient Care

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  • Promptly identify close contacts of patients in whom diphtheria is suspected. Tracing of the contacts should begin in the household and can usually be limited to household members and other persons with a history of habitual close contact with the patient.

  • For close contacts, irrespective of their immunization status, the following measures should be taken:

    • Surveillance for 7 days for evidence of disease

    • Culture for C diphtheriae

    • Antimicrobial prophylaxis with oral erythromycin (40-50 mg/kg/d for 7 d; not to exceed 2 g/d) or a single intramuscular injection of penicillin G benzathine (600,000 U for children who weigh < 30 kg and 1.2 million U for children weighing >30 kg and adults)

  • Efficacy of antimicrobial prophylaxis is presumed but not proven. Obtain repeated pharyngeal cultures from contacts proven to be carriers at a minimum of 2 weeks after completion of therapy.

  • Asymptomatic, previously immunized, close contacts should receive a booster dose of a preparation containing diphtheria toxoid (DTaP, DT, Tdap, or Td, depending on age) if they have not received a booster dose of diphtheria toxoid within 5 years. Immunize children in need of the fourth dose.

  • In asymptomatic close contacts who are not fully immunized (defined as having received < 3 doses of diphtheria toxoid) or in whom the immunization status is unknown, active immunization should be undertaken with DTaP, DT, or Td, depending on age.

  • Contacts who cannot be kept under surveillance should receive benzathine penicillin G (not erythromycin), because adherence to an oral regimen is less likely, and a dose of DTaP, DT, Tdap, or Td (depending on age and the person's immunization history).



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  • Serological surveys demonstrated that 20% to more than 50% of adolescents and adults lack immunity to diphtheria toxin in some areas of the United States, with particularly low levels among elderly persons. The only effective control measure against diphtheria is universal immunization with diphtheria toxoid throughout life to provide constant protective antitoxin levels and to reduce indigenous C diphtheriae. Although immunization does not preclude subsequent respiratory or cutaneous carriage of toxigenic C diphtheriae, it decreases local tissue spread, prevents toxic complications, diminishes transmission of the organism, and provides herd immunity when at least 70-80% of a population is immunized. Serum antitoxin concentration of 0.01 IU/mL is conventionally accepted as the minimum protective level, and 0.1 IU/mL provides a definitely protective level.

  • For all indications, diphtheria immunization is administered with tetanus toxoid–containing vaccines. Schedules for immunization against diphtheria are presented annually in the January edition of Pediatrics as a consensus of the American Academy of Pediatrics (AAP), CDC, and American Academy of Family Physicians. [12] Also see the latest edition of the Red Book: Report of the Committee on Infectious Diseases. [13]

  • Travelers to countries with endemic or epidemic diphtheria should have their diphtheria immunization status reviewed and updated when necessary.



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  • Demyelination of nervous tissue is seen in all fatal cases of diphtheria.

    • Frank paralysis occurs in 10-20% of patients and most often involves the muscles of the palate and the hypopharynx, beginning as early as the first 10 days of illness.

    • Difficulty swallowing and nasal speech are often the first indications of neurologic impairment.

    • Involvement of other cranial nerves, which may be delayed until as late as 7 weeks after infection, results in oculomotor paralysis and blurred vision. Diffuse, usually bilateral, motor function deficits resulting from involvement of the anterior horn cells of the spinal cord may be seen as late as 3 months after initial disease, with progression of weakness either from proximal-to-distal regions or, more commonly, from distal-to-proximal regions.

    • Involvement of the phrenic nerve may cause diaphragmatic paralysis at any time between the first and seventh weeks of illness.

    • Elevation of CSF protein levels can be seen and may lead to an erroneous diagnosis of Guillain-Barré syndrome.

    • Recovery from neurologic damage usually is complete in patients who survive.

  • Cardiac complications may arise during the first 10 days of illness or may be delayed until 2-3 weeks after onset, when pharyngeal disease is subsiding. Cardiac involvement is thought to be responsible for 50-60% of deaths associated with diphtheria.

    • The first sign of toxin-induced myocardiopathy is tachycardia disproportionate to the degree of fever.

    • Various dysrhythmias, including first-degree, second-degree, or third-degree heart block; atrioventricular dissociation; and ventricular tachycardia can develop, and congestive heart failure may be a consequence of myocardial inflammation.

    • Echocardiography may reveal dilated or hypertrophic cardiomyopathy.

    • In patients who survive, cardiac muscle regeneration and interstitial fibrosis lead to recovery of normal cardiac function, unless toxic damage has led to a permanent arrhythmia.

  • Airway obstruction by the diphtheritic membrane and peripharyngeal edema combine to pose a risk of death in patients with diphtheria.



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  • For respiratory tract diphtheria, the fatality rate can be set at 10-15%. The prognosis depends on multiple factors, including the virulence of the organism, the patient's age and immunization status, the site of infection, and the timing of administration of the antitoxin. In most diphtheria-related deaths due to complications, mechanical obstruction and cardiac causes are important factors.


Patient Education

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  • Addressing the crucial issue of universal immunization is the most effective guidance regarding education about diphtheria.