Infection caused by Corynebacterium diphtheriae results in a toxin mediated illness causing an acute demyelinating polyneuropathy.
Usually it affects the oropharynx and larynx and causes palatal paralysis in more than 10% of cases.
Commonly associated with nasal speech, nasal regurgitation, perioral numbness, diplopia, anisocoria, ptosis, mydriasis, dysphagia, weakness of the tongue, and sternocleidomastoid muscle weakness.
Later in the course of the disease a generalize peripheral neuropathy develops with sensory, motor, and autonomic features.
Associated with a characteristic swollen neck, sometimes referred to as “bull neck”.
Caused by Corynebacterium diphtheriae, a facultative anaerobic, Gram-positive bacterium.
Characterized by sore throat, low grade fever, and an adherent pseudomembrane on the tonsils, pharynx, and/or nasal cavity.
A milder form can be restricted to the skin.
Myocarditis occurs in about 20% of cases.
Peripheral neuropathy occurs in about 10% of cases.
A contagious disease spread by direct physical contact or from aerosolized secretions of infected individuals.
Essentially eradicated in industrialized nations through vaccination.
The diphtheria–pertussis–tetanus (DPT) vaccine is recommended for all school-age children in the U.S., and boosters of the vaccine are recommended for adults, since the benefits of the vaccine decrease with age without constant re-exposure.
The diphtheria–pertussis–tetanus (DPT) vaccine is particularly recommended for those traveling to areas where the disease has not been eradicated.
Symptoms usually begin two to seven days after infection and include fever of 38°C or above, chills, fatigue, bluish skin coloration, sore throat, hoarseness, cough, headache, difficulty or painful swallowing, dyspnea, foul-smelling bloodstained nasal discharge,lymphadenopathy, cardiac arrhythmias, myocarditis, and cranial and peripheral nerve palsies.
C. diphtheriae toxin is produced only when infected with a bacteriophage that encodes genetic information into the bacteria.
Diphtheria toxin is a single, 60,000 molecular weight protein composed of two peptide chains, fragment A and fragment B, held together by a disulfide bond.
Fragment B gains the toxin entry into the host cell by binding to the EGF-like growth factor (HB-EGF) on the cell surface.
It is to internalized within an endosome and split by a trypsin-like protease into its individual A and B fragments, with release of fragment A into the cell’s cytoplasm.
Fragment A inhibits the synthesis of proteins in the affected cells.
Laboratory criteria for the diagnosis of diphtheria includes identification of Corynebacterium diphtheriae from a gram stain or throat culture from a clinical specimen,
Histopathologic diagnosis via a stain called “Albert’s Stain”.
Empirical treatment should generally be started in a patient in whom suspicion of diphtheria is high.
Patients with severe neck adenopathy may require intubation or a tracheotomy.
Abnormal cardiac rhythms can occur, and can lead to heart failure.
Can cause paralysis of the eye, neck, throat, or respiratory muscles.
Patients with severe disease are hospitalized and given a diphtheria antitoxin.
Antitoxin does not neutralize toxin that is already bound to tissues.
Delay in the administration of antitoxin is associated with increased in mortality, and treatment should be based on clinical clinical diagnosis, and should not await laboratory confirmation.
Antibiotics are not affective in healing local infection.
Antibiotics are used in patients or carriers to eradicate C. diphtheriae and prevent its transmission.
Recommended antibiotics include: Metronidazole, erythromycin, or procaine penicillin, while patients with allergies to penicillin G or erythromycin can use rifampin or clindamycin.
Diptheria toxin can lead to potentially life-threatening complications of the heart and kidneys.
Fatality rates between 5% and 10% occur in adults, and in children under five years and adults over 40 years, the fatality rate may be as much as 20%.
Outbreaks, though very rare, still occur.