Corynebacterium diphtheria: Morphology and Identification, Pathogenesis, Pathology, Clinical Findings, Diagnostic Laboratory Tests, Treatment, Epidemiology, Prevention, and Control.

Question 1

Morphology and identification

Answer 1

Corynebacterium diphtheriae is a gram-positive, non-motile, non-spore-forming rod with a characteristic club-shaped or ‘Chinese letter’ (palisading) arrangement. It contains metachromatic granules (Babes-Ernst granules) that stain with methylene blue. It grows on Loeffler’s medium (enhances granule visibility) and Tellurite agar (produces black colonies due to tellurite reduction). Toxin production can be confirmed by Elek test (in vitro toxin detection by immunodiffusion), PCR for tox gene, or cell culture cytotoxicity assays.

Question 2

Pathogenesis

Answer 2

Pathogenicity depends on the production of diphtheria toxin, an exotoxin encoded by a tox gene carried by a lysogenic bacteriophage (β-phage). The toxin inhibits protein synthesis by ADP-ribosylation of elongation factor 2 (EF-2), causing cell death. Only toxigenic strains cause disease. The local infection is usually limited to the throat, but the toxin can disseminate systemically, damaging the heart, nerves, and kidneys.

Question 3

Pathology

Answer 3

The toxin causes necrosis of mucosal epithelial cells and an inflammatory exudate composed of fibrin, leukocytes, and dead cells, forming a tough grayish pseudomembrane tightly adherent to the mucosa. Removal can cause bleeding. Systemic absorption of toxin leads to myocarditis, demyelination of nerves (particularly cranial nerves), and renal damage.

Question 4

Clinical findings

Answer 4

Classic respiratory diphtheria begins with sore throat, malaise, low-grade fever, and cervical lymphadenopathy (‘bull neck’). A gray pseudomembrane forms on the tonsils, pharynx, or larynx and may obstruct airways. Systemic complications include myocarditis (arrhythmias, heart failure), peripheral neuritis (cranial nerve palsies, especially soft palate paralysis), and nephropathy. Cutaneous diphtheria presents with chronic ulcers covered by gray membrane. Carriers may be asymptomatic but spread the organism.

Question 5

Diagnostic laboratory tests

Answer 5

Diagnosis includes: 1) Gram stain and methylene blue stain of throat swab showing gram-positive rods with metachromatic granules. 2) Culture on Loeffler’s or Tellurite medium. 3) Elek test to detect toxin production. 4) PCR to detect tox gene. 5) Schick test (historical): intradermal injection of toxin to assess immunity (positive = susceptible).

Question 6

Treatment

Answer 6

Begin treatment immediately—do not wait for lab confirmation. Administer diphtheria antitoxin (horse serum) to neutralize circulating toxin. Give antibiotics: erythromycin or penicillin to eradicate bacteria and prevent transmission. Supportive care includes airway management, monitoring for myocarditis and neuritis. Isolation of the patient is essential until cultures are negative.

Question 7

Epidemiology

Answer 7

Diphtheria is transmitted by respiratory droplets or direct contact. Humans are the only reservoir. Asymptomatic carriers play a key role in transmission. It is rare in countries with effective vaccination programs but still occurs in areas with low immunization coverage or lapses in booster doses. Cutaneous diphtheria is more common in tropical climates.

Question 8

Prevention and control

Answer 8

Prevention relies on vaccination with diphtheria toxoid, given in combination vaccines (DTaP for children, Tdap/Td boosters for adolescents and adults). Immunity wanes over time—boosters every 10 years are recommended. In outbreak settings, close contacts should receive prophylactic antibiotics and booster doses. Carriers may be treated with antibiotics to eliminate colonization.