Biomedical Engineering Reference
In-Depth Information
Diplopia, dysphonia, dysarthria, and dysphagia
occur, followed by a symmetric, descending,
progressive weakness of the extremities along with
weakness of the respiratory muscles. Other symp-
toms may include nausea and vomiting. The patient
is alert, oriented, and afebrile. Additional neuro-
logic findings may include a diminished gag reflex,
facial paresis, tongue weakness, and nystagmus.
Respiratory failure due to paralysis of respiratory
muscles may cause death of the patient [1,5].
Therapy should be continued for 60 days (IV and
po combined).
A licensed vaccine is available and is admin-
istered as a 0.5ml SC dose at 0, 2, and 4 weeks
and then at 6, 12, and 18 months. Boosters are
given yearly to those at ongoing risk of exposure.
Anthrax vaccination is not recommended for the
general public. Post-exposure prophylaxis (PEP)
against inhalational anthrax is accomplished with
ciprofloxacin 500mg (10-15mg/kg) po bid for
60 days, or doxycycline 100mg (2.2mg/kg) po
bid. Exposed individuals may receive three doses
of vaccine (at 0, 14, and 28 days), potentially
enabling a shortened 30-day course of antimi-
crobials. If penicillin sensitivity is established,
PEP can be switched to penicillin V 500mg po
q6h (40-80mg/kg/day divided q6h in children),
or amoxicillin 500mg po q8h (40-80mg/kg/day
divided q8h in children) [2,3,4,5,9,11,13].
4.2.3 Diagnosis
The diagnosis of botulism is largely clinical. A
mouse-neutralization assay can provide confirma-
tion [5].
4.2.4 Differential Diagnosis
The differential diagnosis of botulism includes
myasthenia gravis and the Lambert-Eaton myas-
thenic syndrome, but these conditions are rarely
fulminant and lack autonomic features. Guillain-
Barré syndrome and other acute inflammatory
polyneuropathies should also be included among
differential diagnostic possibilities, but these enti-
ties seldom begin with cranial nerve dysfunction.
Polio patients generally present with fever and
asymmetric flaccid paralysis. Magnesium intoxi-
cation, diphtheria, organophosphate poisoning, and
brain stem infarction may be mistaken for botulism
intoxication [5].
4.2 Disease: Botulism Intoxication
4.2.1 Causative Agent
Clostridium botulinum
is an anaerobic Gram-
positive sporulating bacillus that may produce any
of seven neurotoxins (Types A-G). Illness occurs
between 1-5 days following exposure to botulinum
toxin, dependent upon the toxin dose and the condi-
tion of the individual [5].
4.2.2 Clinical Description
The concurrent inception of cranial nerve palsies
and descending paralysis may alert clinicians to
the diagnosis of botulism. Fever is absent, neuro-
logic manifestations are symmetric, the patient
remains responsive, the heart rate is normal or
slow in the absence of hypotension, and sensory
deficits are absent, except for diploplia. Inhaled
botulinum toxin is clinically similar to foodborne
botulism, although the time of onset of paralytic
symptoms may be longer than for foodborne cases.
Initial symptoms include ptosis, generalized weak-
ness, lassitude, and dizziness. Diminished saliva-
tion with extreme mouth dryness may contribute to
a sore throat. With the progression of the disease,
more severe motor symptoms begin to appear.
4.2.5 Medical Management
Supportive care and prolonged nursing may be
necessary for treatment. Suspected cases should
be monitored for respiratory compromise using
forced expiratory volume measurements. Intuba-
tion and ventilatory assistance may be required
in the event of respiratory failure. Tracheotomy
may also be required. A trivalent (types A, B,
and E) botulinum antitoxin (of equine origin)
is used in the treatment of foodborne botulism.
Administration should begin at the first indica-
tion of possible intoxication, in the absence of
horse serum sensitivity. A botulism toxoid (inac-
tivated toxin) vaccine offering immunity to toxin
