Infant and Wound Botulism

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● causes infections called infant and wound botulism, when the spores germinate in the body
and produce the toxin in vivo.
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● First described in the late 1970s in children between the ages 2 weeks and 6 months who
had ingested spores.
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● The immature state of the neonatal intestine and microbial flora allows the spores to
gain a foothold, germinate, and give off neurotoxin.
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● Wound botulism
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● spores enter a wound or puncture much as in tetanus, but the symptoms are similar to those
of food-borne botulism.

Treatment and Prevention of Botulism

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● testing the:
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● food samples
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● intestinal contents
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● feces
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● infectious botulism is treated with penicillin to control the microbe's growth and
toxin production.
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● People who consume home-preserved food
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● pressure cooker should be tested for accuracy in sterilizing
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● bulging cans or bottles that look or smell spoiled should be discarded, and all home-
bottled foods should be boiled for 10 minutes before eating.
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● Toxin is heat-sensitive and is rapidly inactivated at 100 degrees Celsius
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● Corynebacterium diptheriae
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● straight or somewhat curved rod that tapers at the ends.
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● Chinese characters
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● Epidemiology of Diptheria
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● significant cause of morbidity and mortality
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 ● most cases occur in nonimmunized children from 1-10 years of age living in
crowded, unsanitary conditions.

Pathology of Diptheria

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● exposure results from close contact with the droplets from human carriers
or active infections and occasionally with fomites or contaminated milk.
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● Clinical disease proceeds in two stages:
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● local infection by C. diptheria
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● toxin production and toxemia
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● most common location of primary infection is in the upper respiratory tract (tonsils,
pharynx, and trachea)
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● cutaneous diptheria is usually a secondary infection manifesting as deep, erosive
ulcers that are slow to heal.
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● Usually remain localized at the portal of entry.

Diphtherotoxin and Toxemia

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● cardinal determinant of pathogenecity is the production of diptherotoxin
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● exotoxin is produced only by toxigenic strains of C. diptheriae that carry the structual
gene for toxin production acquired from bacteriophages during transduction.
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● Toxin affects the body in 2 levels:
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● local infection: produces inflammatory reaction
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● sore throat
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● nausea
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● vomiting
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● enlarged cervical lymph nodes
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● severe swelling in the neck
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● fever
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● one life threatening complication, is the pseudomembrane, a greenish-gray film that
develops in the pharynx from the solidification of fluid expressed during inflammation.
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 ● Systemic complication is toxemia, w/c occurs when the toxin is absorbed from the
throat and carried by the blood to certain target organs, primarily the heart and nerves.

Diagnostic methods for the Corynebacteria

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● gray membrane and welling in the throat are somewhat indicative of diptheria

Treatment and Prevention of C. diptheria

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● toxemia are treated with diptheria antitoxin (DAT) derived in horses.
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● Infection is treated with:
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● penicillin
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● erythromycin family
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● bed rest, heart medication, and tracheostomy or bronchoscopy to remove the
pseudomembrane may be indicated.
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● It can be prevented by a series of vaccinations with toxoid, usually given as a part
of a mixed vaccine against tetanus and pertussis (DtaP)
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● currently recommended are three vaccinations starting at 6 to 8 weeks of age,
followed by a booster at 15 months and again at school age.