Diphtheria in a 7-year-old child in north-eastern Nigeria – management in a resource-poor setting

Introduction

Diphtheria is an acute bacterial infection of the tonsils, pharynx, larynx or nose and, rarely, other mucous membranes and the skin caused by Corynebacterium diphtheria. ¹ Clinical disease is caused by local tissue destruction by severe inflammation as a result of direct tissue invasion by the organism, as well as the distal effect of diphtheria toxin on the heart, kidneys and the peripheral nerves.^2–4 Severe clinical diphtheria is said to be rare in Africa, perhaps as a result of immunity acquired through repeated skin infections by non-toxigenic strains of C. diphtheriae. ⁵

There are four biotypes of toxin producing C. diphtheria – gravis, mitis, intermedius and belfanti. Toxin production is a result of infection of bacteria by corynebacteriophage containing the diphtheria exotoxin gene tox. ⁴ Membranous lesions are rarely produced by non-toxigenic strains, although they may cause a sore throat. Recent studies have shown that non-toxigenic strains of C. diphtheriae may cause infective endocarditis. ⁴ Diphtheria is transmitted through close contact with sufferers or carriers or, rarely, by contact with materials contaminated with discharges from patients. Epidemics can occur in susceptible populations. Waning of vaccine-induced immunity, declining socioeconomic conditions and low immunization coverage are the main drivers of outbreaks of diphtheria.

The incidence of diphtheria has significantly declined over recent decades in many countries as a result of improved sanitation and routine DPT (diphtheria, pertussis and tetanus toxoid) immunization in all children under 5 years old. ⁴ Diphtheria is a vaccine-preventable disease. However, it remains an important disease in many communities in Africa with low immunization coverage. ⁴

Case

A 7-year-old boy living with his grandparents was referred from a primary health care clinic with a 2 week history of nasal quality speech, regurgitation of feeds (fluids) through the nose, hoarseness of the voice, and unstable gait. There was a preceding history of bloody nasal discharge, severe sore throat, mouth ulcers, fever and noisy breathing 2 weeks prior to presentation. However, there was no history of neck swelling (bull neck).

The child was taken to a local primary health care facility, where he was given some drugs including oral antibiotics. At presentation, oral ulcers and bloody nasal discharge were not evident. In addition, no oro-pharyngeal membrane was seen on close examination of the pharynx. Cardiovascular and other systemic examination were essentially normal.

He had not received any of the routine childhood immunization. There was no history of similar illness in his household or neighbourhood. A throat swab for culture and antibiotic sensitivity test was negative for C. diphtheriae.

A diagnosis of clinical diphtheria with neurologic complication was made. He was started on oral erythromycin, nasogastric tube feeding and daily physiotherapy. However, he was not given anti-diphtheria toxin due to its unavailability. He gradually improved and was discharged home after 2 weeks of hospital stay.

The parents were subsequently counselled and the child was started on a routine childhood immunization schedule. The state public health department was notified, following which a team of vaccinators were sent to the area were the child came from and a mop-up DPT immunization was carried on all children 5 years and under living in the locality.

Discussion

Widespread use of DPT under the National Programme on Immunisation (NPI) has significantly contributed to the low incidence of clinical diphtheria in Nigeria over the last two decades or so.

However, the rejection of polio immunization in northern Nigeria over the last few years – following a false rumour that the vaccine was intended to reduce the local population and the current security challenges faced in the region as a result of local Islamist insurgents attacking health care personnel involved in immunization – has drastically affected routine childhood immunization coverage. Consequently, the region has been witnessing an upsurge in the incidence of most of the vaccine-preventable diseases in children, including diphtheria.

The characteristic clinical feature of diphtheria is a reaction to potent exotoxin produced by the organism. ⁴ Absorption of exotoxin results in neurologic and cardiac complications such as myocarditis, heart block and progressive congestive failure.^4,5 The neurological sequelae of diphtheria usually develop late in the disease, that is, about 2–6 weeks after the onset of local symptoms, usually when severe symptoms are resolving, and is as a result of the effect of exotoxin on the myelin sheath and axonal degeneration.^4–6 Neurological complications usually present with features of polyneuropathy that may mimic Gullain-Barré syndrome.^4,5 Available data has shown that about 20% of diphtheria cases develop neurotoxicity. The severity of neurotoxicity is determined by the extent of initial oro-pharyngeal infection. ¹

A diagnosis of diphtheria is confirmed by the isolation and identification of C. diphtheria from infected sites, but cultures are often negative, especially if the patient has received antibiotics.^4–6 Mortality and morbidity in diphtheria is prevented by the prompt administration of diphtheria antitoxin. ⁶ Antitoxin should be given in all suspected cases of diphtheria without waiting for a definitive laboratory confirmation. ⁶ However, because of its unavailability we were unable to give an antitoxin in this case. Diphtheria anti-toxin is the specific treatment for respiratory diphtheria. A test dose is usually given before administration of anti-toxin as the anti-toxin is of equine origin. A single daily dose of anti-toxin (between 20,000 to 100,000 units depending on severity) is given intramuscularly for 14 days. Unfortunately, diphtheria anti-toxin is not available in most centres in Africa. ⁴ Other supportive treatments that are recommended include antibiotics (e.g. penicillin, erythromycin, cephalosporin and tetracycline).^1,7 Antibiotics will stop toxin production and prevent further spread of the organism, but are no substitute for anti-toxins.^6,7 Daily physiotherapy has been shown to improve the recovery from neurological complications in diphtheria. ²

The World Health Organization has recommended prophylactic treatment of carriers with a single dose of benzathine penicillin or a 7--10 day course of oral erythromycin.

Conclusion

Although clinical diphtheria is rare in many parts of the world due to widespread immunization against diphtheria toxin, poor immunization coverage in northern Nigeria may result in an increase of diphtheria cases.