Diphtheria

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Pathogenesis and Pathophysiology. Diphtheria is an acute infectious disease caused by the bacteria Corynebacterium diphtheria. Diphtheria is transmitted by respiratory droplets from infected persons or asymptomatic carriers. There are two forms, oropharyngeal and cutaneous, and the incubation period is from 1 to 4 days. The bacteria affects the respiratory tract and often the heart, kidneys, and nervous system as well. In the immediate area of the infection, usually the nose and throat, the bacteria produce

TABLE 39-6 -- BOTANICAL TOXINS

Plant

Chemical

Mechanism of Toxicity

Physiological Changes

Amanita muscaria mushroom (flyagarue)

Ibotenic acid

Activates NMDA reeeptors

Marked depolanzation with excitation and exeOEtotoxicity

Clitobyte stcromelalga

Acromelic acid

Activates kainic acid receptors

Spasms, excitation, seizures

mushroom

Museanne

Activates cholinergic parasympathetic endings

Severe sweating, salivation, and hypertension

Cycad

Beta-N-Methyl-amino-l-alanine (BMAA)

Aetivates NMDA reeeptors

Associated with ALS-Guamanian PD-dementia complex

Chiekpea Lathyrus

Beta-N-Oxalyl-amino-l-alanine (BOAA)

Aets as an agonist of AMPA receptors in spinal neurons

Induces spastic paralysis of lower limbs termed neurolathynsm

Betel nut

Arecoline

Stimulates parasympathetic receptors and callses CNS arousal

Excitation, salivation, slowed heart rate

Henbane

Seopl)lamine

Antagollizes muscarinic cholinergic receptors

Rapid heart rate, sedation and confusion, dilated pupils

Deadly nightshade, Jimson weed

Atropine

Antagonizes museannie cholinergic receptors

Rapid heart rate, sedation and confusion, dilated pupils

NMDA, N-methyl D-aspartate; ALi, amyotrophic latera selerosis PD, Parkinson's disease AMPA, alpha-amino-3 hydroxy-5-methyl-4-isoxazoleproprionic acid

a toxin that causes tissue damage and can spread via the bloodstream to other organs. Muscle and myelin are preferentially affected by this powerful exotoxin. Neurological symptoms result from either direct damage to muscle and peripheral nerve or from indirect damage caused by hypoxia and airway obstruction. Fortunately, the exotoxin does not penetrate the blood-brain barrier, and therefore the CNS is not directly affected. U Pathological signs include demyelinization of the ganglia of the peripheral nerves, especially the node of Ranvier, and the cranial and somatic nerves.

Epidemiology and Risk Factors. Diphtheria is now rare in many parts of the world owing to immunization. Potential risk factors for this disease are lack of immunization, crowding, and poor hygiene. In the United States, only five cases of diphtheria were reported in 1991. However, because of a drop in routine child immunizations in the U.S.S.R., a diphtheria epidemic that included more than 50,000 cases was reported in 1993 and 1994.

Clinical Features and Associated Findings. The clinical course follows a predictable pattern. Between the fifth and twelfth days of the illness the initial symptoms are sore throat, fever, a gray to black throat membrane, nasal voice, regurgitation, and dysphagia. At about this time the trigeminal, facial, vagus, and hypoglossal cranial nerves may be affected. In approximately half the patients who have postdiphtheria neurological dysfunction, ocular involvement and paralysis of accommodation were noted in the second or third week. Mononeuropathies can also occur within 2 weeks of onset, and further peripheral neuropathy, predominantly sensory polyneuropathy, or proximal motor neuropathy extending distally is characteristic in the sixth and seventh weeks of the illness. Sometimes toxic encephalopathy, consisting of a change in mental status, drowsiness, and possibly convulsions, is seen.

Differential Diagnosis and Evaluation. The diagnosis must be based on the clinical history and clinical presentation. Physical examination may show a characteristic gray membrane in the throat, enlarged lymph glands, and swelling of the neck and larynx. In patients with a clinical picture of Guillain-Barre syndrome with visual blurring and palatal involvement, a diagnosis of diphtheria should be questioned. Diphtheric polyneuropathy can be distinguished from all other polyneuropathies by the early bulbar symptoms, unique ciliary paralysis, and subacute evolution of a delayed symmetrical sensorimotor peripheral polyneuropathy. Diagnostic testing should include Gram's stain of the infected membrane, a throat culture, and an electrocardiogram (ECG), which will show evidence of myocarditis.

Management. There is no specific treatment for the neurological symptoms of diphtheria. Treatment generally involves administration of antitoxin within 48 hours of the earliest signs of infection, rest, and maintenance of proper airway and cardiac function. All contacts of the infected person should be immunized, since protective immunity is not present longer than 10 years after the last vaccination. Diphtheria is preventable through immunization at the age of 3 months. Booster doses at 1 year and before the child enters school are suggested.

Prognosis. The death rate is 10 percent. If the patient does not expire because of respiratory distress or cardiac failure, he or she stabilizes and slowly recovers completely. Therefore, activities should be slowly resumed.

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