Chapter 3Infectious Diseases Related To Travel
Tejpratap S. P. Tiwari
Diphtheria is caused by toxigenic strains of Corynebacterium diphtheriae biotype mitis, gravis, intermedius, or belfanti. The bacteria produce an exotoxin that, if absorbed in the bloodstream, may damage nerves and organs such as the heart and kidneys.
MODE OF TRANSMISSION
Humans are the only known reservoir of C. diphtheriae. Person-to-person transmission occurs through oral or respiratory droplets, close physical contact, and rarely, by fomites. Cutaneous diphtheria is common in tropical countries, and contact with discharge from skin lesions may transmit infection in these environments.
Diphtheria is found worldwide; countries with endemic diphtheria are shown in Table 3-01. During the 1990s, large epidemics occurred in the newly independent states of the former Soviet Union. More recently in the Americas, diphtheria outbreaks have occurred in Haiti and the Dominican Republic. Diphtheria is uncommon in industrialized countries because of longstanding routine use of DTP (diphtheria and tetanus toxoids and pertussis vaccine). Diphtheria is rare in the United States; the last case occurred in an elderly traveler returning from Haiti in 2003. Diphtheria causes significant illness and death in developing countries where vaccination coverage is low.
Symptomatic infection is extremely rare in adequately immunized people, even though active immunization with diphtheria toxoid does not prevent colonization or transient carriage of C. diphtheriae. Higher risk of acquiring disease and potentially life-threatening complications are possible in inadequately immunized or unimmunized travelers to countries with endemic diphtheria.
Table 3-01. Countries with endemic diphtheria
|Africa||Algeria, Angola, Egypt, Eritrea, Ethiopia, Guinea, Niger, Nigeria, Sudan, Zambia, and other sub- Saharan countries|
|Americas||Bolivia, Brazil, Colombia, Dominican Republic, Ecuador, Haiti, and Paraguay|
|Asia/South Pacific||Bangladesh, Bhutan, Burma (Myanmar), Cambodia, China, India, Indonesia, Laos, Malaysia, Mongolia, Nepal, Pakistan, Papua New Guinea, Philippines, Thailand, and Vietnam|
|Middle East||Afghanistan, Iran, Iraq, Saudi Arabia, Syria, Turkey, and Yemen|
|Europe||Albania, Armenia, Azerbaijan, Belarus, Estonia, Georgia, Kazakhstan, Kyrgyzstan, Latvia, Lithuania, Moldova, Russia, Tajikistan, Turkmenistan, Ukraine, and Uzbekistan|
The incubation period is 2–5 days (range, 1–10 days). Affected anatomic sites include the mucous membrane of the upper respiratory tract (nose, pharynx, tonsils, larynx, and trachea [respiratory diphtheria]), skin (cutaneous diphtheria), or rarely, mucous membranes at other sites (eye, ear, vulva). Nasal diphtheria can be asymptomatic or mild, with a blood-tinged discharge.
Respiratory diphtheria has a gradual onset and is characterized by a mild fever (rarely >101°F [38.3°C]), sore throat, difficulty swallowing, malaise, loss of appetite, and if the larynx is involved, hoarseness. The hallmark of respiratory diphtheria is a pseudomembrane that appears within 2–3 days of illness over the mucous lining of the tonsils, pharynx, larynx, or nares and that can extend into the trachea. The pseudomembrane is firm, fleshy, grey, and adherent, and it will bleed after attempts to remove or dislodge it. Fatal airway obstruction can result if the pseudomembrane extends into the larynx or trachea, or if a piece of it becomes dislodged.
In severe respiratory diphtheria, cervical lymphadenopathy and soft-tissue swelling in the neck give rise to a “bull-neck” appearance. Systemic complications, including myocarditis and polyneuropathies, can result from absorption of diphtheria toxin from the infection site. However, cutaneous and nasal diphtheria are localized and rarely associated with systemic toxicity. The case-fatality ratio of respiratory diphtheria is 5%–10%.
A presumptive diagnosis is usually based on clinical features. Diagnosis is confirmed by isolating C. diphtheriae from culture of nasal or throat swabs or membrane tissue. Toxin production is confirmed by performing a modified Elek test. PCR assays can also be performed on isolates, swabs, or membrane specimens to rapidly confirm the presence of the tox gene responsible for production of diphtheria toxin, but the test is available only in research or reference laboratories.
Patients with respiratory diphtheria require hospitalization to monitor response to treatment and manage complications. Equine diphtheria antitoxin (DAT) is the mainstay of treatment and is administered after specimen testing, without waiting for laboratory confirmation. In the United States, DAT is available to physicians under a Food and Drug Administration–approved investigational new drug protocol by contacting CDC at 770-488-7100.
An appropriate antibiotic (erythromycin or penicillin) should be used to eliminate the causative organisms, stop exotoxin production, and reduce communicability. Supportive care (airway, cardiac monitoring) is required. Antimicrobial prophylaxis (erythromycin or penicillin) is recommended for close contacts of patients.
PREVENTIVE MEASURES FOR TRAVELERS
For protection against diphtheria, all travelers should be up-to-date with diphtheria toxoid vaccine before departure. Diphtheria toxoid is not manufactured as a monovalent vaccine but is available in pediatric (D) and adult formulations (d) that are combined with other vaccines such as tetanus toxoid (DT, Td), tetanus toxoid and acellular or whole-cell pertussis antigens (DTaP, DTwP, Tdap), or as a DTwP/DTaP combination with other antigens (such as hepatitis B, inactivated poliovirus vaccines, or Haemophilus influenzae type b vaccine).
In the United States, infants and children aged <7 years are vaccinated with diphtheria toxoid in combination with tetanus toxoid and acellular pertussis vaccine (DTaP) according to the routine childhood immunization schedule recommended by the ACIP (see Chapter 7, Vaccine Recommendations for Infants and Children). Immunization for infants and children aged <7 years consists of 5 doses of DTaP vaccine. The first 3 doses are usually given at ages 2, 4, and 6 months, followed by booster doses at ages 12–18 months and 4–6 years (see Table 7-02).
Adolescents aged 11–18 years should receive a dose of Tdap instead of Td for booster immunization against tetanus, diphtheria, and pertussis if they have completed the recommended childhood DTwP/DTaP vaccination series (see Table 7-03). Adults aged 19–64 years who have not previously received Tdap should receive a single dose of age-appropriate Tdap to replace a single dose of Td for active booster immunization against tetanus, diphtheria and pertussis. Adults aged ≥65 years who have or who anticipate having close contact with an infant aged <12 months and who have not previously received Tdap should receive a single dose of Tdap to protect against pertussis and reduce the likelihood of transmission; all other adults aged ≥65 years who have not previously received Tdap may be given a single dose of Tdap instead of Td. Thereafter, routine booster doses with Td should be given to all adults every 10 years to maintain seroprotection against diphtheria, as well as tetanus. This booster is particularly important for travelers who will live or work with local populations in countries where diphtheria is endemic.
Adolescents and adults who have never been immunized against pertussis, tetanus, or diphtheria, who have incomplete immunization, or whose immunity is uncertain should follow the catch-up schedule established for Td/Tdap. Tdap can be substituted for any of the Td doses in the series.
- American Academy of Pediatrics. Diphtheria. In: Pickering LK, Baker CJ, Long SS, McMillan JA, editors. Red Book: 2009 Report of the Committee on Infectious Diseases. 28th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2009. p. 280–83.
- Bisgard KM, Hardy IR, Popovic T, Strebel PM, Wharton M, Chen RT, et al. Respiratory diphtheria in the United States, 1980 through 1995. Am J Public Health. 1998 May;88(5):787–91.
- CDC. Availability of diphtheria antitoxin through an investigational new drug protocol. MMWR Morb Mortal Wkly Rep. 2004;53(19):413.
- CDC. Diphtheria acquired by US citizens in the Russian Federation and Ukraine—1994. MMWR Morb Mortal Wkly Rep. 1995 Mar 31;44(12):237, 43–4.
- CDC. Fatal respiratory diphtheria in a US traveler to Haiti—Pennsylvania, 2003. MMWR Morb Mortal Wkly Rep. 2004 Jan 9;52(53):1285–6.
- CDC. Updated recommendations for use of tetanus toxoid, reduced diphtheria toxoid and acellular pertussis (Tdap) vaccine from the Advisory Committee on Immunization Practices, 2010. MMWR Morb Mortal Wkly Rep. 2011 Jan 14;60(1):13–5.
- Farizo KM, Strebel PM, Chen RT, Kimbler A, Cleary TJ, Cochi SL. Fatal respiratory disease due to Corynebacterium diphtheriae: case report and review of guidelines for management, investigation, and control. Clin Infect Dis. 1993 Jan;16(1):59–68.
- Galazka A. The changing epidemiology of diphtheria in the vaccine era. J Infect Dis. 2000 Feb;181 Suppl 1:S2–9.
- Kretsinger K, Broder KR, Cortese MM, Joyce MP, Ortega-Sanchez I, Lee GM, et al. Preventing tetanus, diphtheria, and pertussis among adults: use of tetanus toxoid, reduced diphtheria toxoid and acellular pertussis vaccine recommendations of the Advisory Committee on Immunization Practices (ACIP) and recommendation of ACIP, supported by the Healthcare Infection Control Practices Advisory Committee (HICPAC), for use of Tdap among health-care personnel. MMWR Recomm Rep. 2006 Dec 15;55(RR-17):1–37.
- Wharton M, Vitek CR. Diphtheria toxoid. In: Plotkin SA, Orenstein WA, editors. Vaccines. 4th ed. Philadelphia: WB Saunders; 2004. p. 211–28.
- World Health Organization. WHO vaccine-preventable diseases monitoring system: 2009 global summary. Geneva: WHO; 2009. Available from: http://www.who.int/immunization/documents/WHO_IVB_2009/en/index.html.
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