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Diphtheria Slide

Diphtheria is caused by Corynebacterium diphtheriae and produces a toxin that can cause myocarditis, polyneuropathy, and other systemic issues. It is characterized by a pseudomembrane forming in the throat and neck swelling. Treatment involves diphtheria antitoxin and antibiotics. Vaccines like DTaP and Tdap can prevent diphtheria.

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7K views11 pages

Diphtheria Slide

Diphtheria is caused by Corynebacterium diphtheriae and produces a toxin that can cause myocarditis, polyneuropathy, and other systemic issues. It is characterized by a pseudomembrane forming in the throat and neck swelling. Treatment involves diphtheria antitoxin and antibiotics. Vaccines like DTaP and Tdap can prevent diphtheria.

Uploaded by

andre andre
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd
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diphtheria

 Definition: Diphtheria is a nasopharyngeal and


skin infection caused by Coryne-bacterium
diphtheriae.
 Some strains produce diphtheria toxin, which
can cause myocarditis, polyneuropathy, and
other systemic toxicities.
 The toxin is associated with the formation of
pseudomembranes in the pharynx during
respiratory infection.
Etiology :
 C. Diphtheriae, gram-positive,
unencapsulated,
 non-motile, nonsporulating rod.
 The bacteria often form clusters of parallel
arrays (palisades) in culture, referred to as
Chinese characters.
 C. diphtheriae is a club-shaped, gram-
positive, unencapsulated, non-motile,
nonsporulating rod. The bacteria often
form clusters of parallel arrays (palisades)
in culture
Clinical Features Respiratory Diphtheria

 Upper respiratory tract illness due to C.


diphtheriae typically has a 2- to 5-day
incubation period.
 Clinical diagnosis is based on the constellation
of sore throat; low-grade fever; and a
tonsillar, pharyngeal, or nasal
pseudomembrane.
 Unlike that of GAS pharyngitis, the
pseudomembrane of diphtheria is tightly
adherent; dislodging the membrane usually
causes bleeding.
Clinical Features Respiratory Diphtheria

Occasionally, weakness, dysphagia, headache,


and voice change are the initial
manifestations.
Massive swelling of the tonsils anc "bull-neck"
diphtheria resulting from submandibular and
paratracheal ederr.i can develop.
This illness is further characterized by foul
breath, thick speech and stridorous breathing.
Complications

 Respiratory tract obstruction due to swelling and sloughing of


pseudomembrane
 Myocarditis (dysrhythmia, dilated cardiomyopathy) is seen in
almost one-quarter of hospitalized pts; those who die usually
do so within 4 or 5 days
 Neurologic manifestations may appear during the first 2
weeks of illness They begin with dysphagia and nasal
dysarthria and progress to cranial nerve involvement,
including weakness of the tongue and facial numbness.
 Respiratory and abdominal muscle weakness may follow.
Several weeks_ later, a generalized sensorimotor
polyneuropathy with prominent autonom-ic dysfunction
(including hypotension) may occur.
 Most survivors improve gradually
Diagnosis
 A definitive diagnosis is based on
compatible clinical findings isolation of C.
diphtheriae from local lesions or its
identification by histhology.
 Nonselective media and appropriate
selective media must be used.
 Diphtheria antitoxin is the most important
component of treatment and should be
given as soon as possible.
 Because antitoxin is produced in horses,
current protocol includes a test dose to
rule out immediate-type hypersensitivity.
 Pts who exhibit hypersensitivity should be
desensitized before receiving a full dose.
 Treatment to prevent trans mission to contacts is
administered for 14 days; the recommended options
are (1) procaine penicillin G (600,000 U DVI every 12 h
in adults; 12,500-25,000U/: kg IM every 12 h in
children) until the pt can take oral penicillin V (125-250
mg qid); or (2) erythromycin (500 mg IV every 6 h in
adults; 40-50 mg/kg per day IV in 2-4 divided doses in
children) until the pt can take oral erithromycin (500
mg qid).
 Rifampin and clindamycin are other options. Culture
should document eradication of the organism 1 and 14
days after completion of antibi-otic therapy. Supportive
care and isolation should be instituted.
Prognosis

 Risk factors for death include bull-neck


diphtheria, myocarditis with ventricular
tachycardia, atrial fibrillation, complete heart
block, an age of >60 years or <6 months,
alcoholism, extensive pseudomembrane
elongation, and laryngeal, tracheal, or
bronchial involvement.
 The interval between onset of local disease
and antitoxin administration also predicts
outcome
Prevention
 DTaP (diphtheria and tetanus toxoids and acellular
pertussis vaccine adsorbed) is recommended for
primary immunization of children up to age 7
years.
 Tdap (tetanus toxoid with reduced diphtheria
toxoid and acellular pertussis) is recommended as
the booster vaccine for children 11-12 years old
and as the catch-up vaccine for children 7-10 and
13-18 years old.
 Td (tetanus and diphtheria toxoids) is
recommended for routine booster use in adults at
10-year intervals or for tetanus-prone wounds.
When >10 years have elapsed since the last
Prevention
Td dose, adults 19-64 years old should receive a
single dose of Tdap.
Close contacts of pts with respiratory diphtheria
should have throat specimens cultured for C.
diphtheri-ae, should receive a 7- to 10-day course
of oral erythromycin or one dose of benzathine
penicillin (1.2 mU for persons >6 years old;
600,000 U for children <6 years old), and should
receive vaccine if immunization status is
uncertain.

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