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Diphtheria is an acute
disease that results from a localized infection and a systemic toxemia
caused by exotoxin -producing strains of Corynebacterium diphtheriae.
The name is derived from the
Greek words koryne
(club) and
diphtheria
(leather), the latter referring to the grey membrane at the site of
infection.
Diphtheria is amenable to virtually
complete eradication by routine immunization with diphtheria toxoid.
Even in medically advanced, however,
diphtheria may occur when immunization procedures breakdown because of
war or complacency. An important epidemic occurred in Texus in
1970.
The low-grade endemicity of diphtheria
depends on the occurrence of toxigenic Corynebacterium diphtheriae in
the nasopharynges of a small number (fewer than 1%) of asymptomatic
human carriers.
Transmission to nonimmune individuals
usually occurs by the respiratory route.
In diphtheria, unlike food poisoning or
tetanus, a parasitic relationship exists between the causative
microorganism, C diphtheriae, and its host.
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(Dr Tsutsumi)
Clinical
Presentation:
Diphtheria is a composite of a local
inflammation and a systemic intoxication.
Toxin produced locally by toxogenic
strains of C. diphtheriae is responsible for an inflammatory reaction
on body surface at the site of infection (usually the oral pharynx,
from which the process often extends to the nose or larynx).
Occasionally the tracheal, esophageal,
or gastric mucosa is involved as well.
Less commonly, but particularly in the
tropics, cutaneous trauma or burns may be the site of diphtheria.
The umbilical cord (in diphtheria
neonatorum), the genital tract, and the conjuctivae are rare sites.
Unlike streptococcal tonsilitis,
diphtheria is often insidious in onset and may be preceded by 2 to 3
days of listlessness, malaise, and headache before local symptoms
occur.
Cervical adenopathy seems out of
proportion to the pharyngeal lesion.
Soon small gray or white patches of
exudates appear on the pharyngeal mucosa, usually over the tonsils.
These enlarge and coalesce and, with
the accumulation of blood, become gray or black.
This exudate constitutes the
characteristic diphtheritic membrane, which consists of leukocytes and
numerous bacteria enmeshed in a dense network of fibrin.
The epithelial surface becomes necrotic
and densely adherent to the overlying membrane ; this adherence
explains why raw bleeding points are exposed when the membrane is
forcibly removed.
If particularly extensive, the local
process may produce mechanical respiratory obstruction, stridor, and
even asphyxiation.
The local inflammatory process and its
mechanical consequences are less important in the evolution of
diphtheria than is the profound toxemia that characterizes the
infection.
Diphtheria toxin, produced by C.
diphtheriae in response to infection of that organism by a specific
bacteriophage, is a potent inhibitor of cellular protein synthesis.
It is readily absorbed from the point
of production into the blood stream, and its effects are noted in many
organs and systems throughout the body.
Clinically apparent weakness or
paralysis of limbs is rare. Neuropathic manifestations of diphtheria
are usually temporary and disappear within 2 or 3 months if the
patient survives.
Organs
involved:
Lymph Node:
The lymphoid tissues both in
regional lymph nodes and systemically (as in the spleen) undergo
hyperplasia with the development of prominent germinal centers that
are often centrally necrotic.
Heart:
Diphtheria toxin is
particularly toxic to the myocardium.
In the early stages, interstitial
edema, cloudy swelling of myocardial fibers, and the accumulation of
fine cytoplasmic granules of lipid are seen microscopically.
Later these changes become widespread
and are more severe.
Myocardial fibers eventually undergo
necrosis, and a focal interstitial myocarditis with exudation of
mononuclear cells occurs.
Cardiac involvement, either acutely in
the form of cardiovascular collapse or as an arrhythmia or more
chronically in the form of congestive heart failure, is the most
common threat to life in diphtheria.
Kidney:
A
nonspecific, nonsuppurative interstitial nephritis is frequent in
diphtheria and is believed to be responsible for the proteinuria often
observed. The renal lesion usually resolves completely in patients who
recover.
Liver:
The liver
is characteristically enlarged, hepatocytes exhibit cloudy swelling
and less commonly focal necrosis.
Nerves:
Diphtherial
toxin has a special affinity for peripheral nerves. Toxic effects are
manifested in degeneration or even destruction of myelin sheaths. Axis
cylinders undergo swelling and rarely necrosis. The paralytic effects
of diphtheritic neuropathy are often sharply localized. Paralysis of
the voluntary muscles of the palate may produce a peculiar nasal
quality of the voice and a tendency to regurgitate fluids through the
nose.
Hypopharynx:
Hypopharyngeal
involvement may lead to aspiration pneumonia.
Eye:
Involvement of extraocular muscles may produce diplopia, and
involvement of the ciliary body may result in defective visual
accommodation.
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