BOTULISM

PRESENTED BY
GHISING, ASTAK
UV GULLAS COLLEGE OF MEDICINE
 ETIOLOGY AND PATHOGENESIS
• Seven serologically distinct serotypes of botulinum toxin (A through
G) have been confirmed. Botulinum toxin is produced by four
recognized species of clostridia: Clostridium botulinum and rare
strains of Clostridium argentinense, Clostridium baratii, and
Clostridium butyricum.

• All these species are anaerobic gram-positive spore-forming

organisms. The spores survive environmental conditions and ordinary
cooking procedures.
• Food-borne botulism is caused by consumption of foods contaminated
with botulinum toxin; no confirmed host-specific factors are involved
in the disease.
• Wound botulism is caused by toxin produced from germinating C.
botulinum spores that contaminate an abscess or a wound.
• Infant botulism is caused by toxin produced in situ by toxigenic
clostridia colonizing the intetine of children.
• Adult intestinal-colonization botulism, a rare form that is poorly
understood, is believed to have a pathology similar to that of infant
botulism but occurs in adults; typically, patients have some anatomic
or functional bowel abnormality or have recently used antibiotics that
may help toxigenic clostridia compete more successfully against the
normal bowel microbiota.
• Regardless of how exposure occurs, botulinum neurotoxin enters the
vascular system and is transported to peripheral cholinergic nerve
terminals, including neuromuscular junctions, postganglionic
parasympathetic nerve endings, and peripheral ganglia. Botulinum
toxin is a zinc-endopeptidase protein of ~150 kDa, consisting of a 100-
kDa heavy chain and a 50-kDa light chain. Steps in neurotoxin activity
include (1) heavy-chain binding to nerve terminals, (2) internalization
in endocytic vesicles, (3) translocation of the light chain to cytosol,
and (4) light-chain serotype-specific cleavage of one of several
proteins involved in the release of the neurotransmitter acetylcholine.
Inhibition of acetylcholine release by any of the seven toxin serotypes
results in characteristic flaccid paralysis.
 CLINICAL PRESENTATION
• The clinical syndrome of botulism consists of bilateral cranial-nerve
palsies that may progress to respiratory compromise, a bilateral
descending flaccid paralysis of voluntary muscles, and even death.
• The incubation period from ingestion of contaminated food to onset
of symptoms in food-borne botulism is usually 8–36 h but can be as
long as 10 days and is dose dependent. Incubation periods of 4–17
days have been documented in wound botulism associated with
accidental injury.
• Pupillary reflexes may be depressed, and fixed or dilated pupils are
sometimes noted. Autonomic symptoms such as dizziness, dry mouth, and
“sore throat” are common.
• Weakness descends from the head, often rapidly, to involve the neck, arms,
thorax, and legs; weakness and some cranial nerve deficits can be
asymmetric.
• Deep tendon reflexes typically are normal or may progressively disappear.
Paresthesias, while rare, have been reported. Ataxia, which has sometimes
been reported, manifests not as cerebellar ataxia but rather as gait
problems due to weakness or visual issues.
• The absence of cranial nerve palsies makes botulism highly unlikely, as does
a lack of cranial nerve deficits at the onset of illness.
• Nausea, vomiting, and abdominal pain may precede or follow the onset of
paralysis in food-borne botulism.
• Cranial nerve deficits may manifest as some of the following: diplopia,
dysarthria, dysphonia, ptosis, ophthalmoplegia, facial paralysis, and
impaired gag reflex.
• Infants with botulism typically present with a reduced ability to suck
and swallow, constipation, weakened voice, ptosis, sluggish pupils,
hypotonia, lethargic appearance, and floppy FIGURE 148-1 Artist’s
rendition of an adult with mild botulism. The patient has ptosis and
facial paralysis manifested as lethargy and expressionless facies. The
patient is fully alert. As in adults, illness can progress to generalized
flaccidity and respiratory compromise.
 DIFFERENTIAL DIAGNOSIS
The illnesses most commonly considered in the differential diagnosis of
adult botulism cases include
• Guillain-Barré syndrome (GBS),
• Myasthenia gravis, stroke syndromes,
• Eaton-Lambert syndrome,
• Tick paralysis,
• Less likely considerations are tetrodotoxin poisoning, shellfish
poisoning, diphtheria, and tetanus
• Botulism is sometimes confused with other illnesses because a
neurologic examination is not adequately performed, particularly
when a patient presents with symptoms that do not immediately
indicate a neurologic illness—e.g., respiratory symptoms.

• A thorough history and a meticulous physical examination can

effectively eliminate many alternative diagnoses, but a workup for
other diagnoses should not delay treatment with botulinum antitoxin.
 DIAGNOSTIC WORK - UP
• Botulism is confirmed in specialized public health laboratories by
demonstration of toxin in clinical specimens (e.g., serum, stool, gastric
aspirate, and sterile-water enema samples) or in samples of ingested foods.
• Isolation of toxigenic clostridia from stool also provides evidence of
botulism.
• Wound cultures yielding the organism are highly suggestive in symptomatic
cases.
• The universally accepted method for confirmation of botulism is the mouse
bioassay; no testing available in hospital or other clinical laboratories (e.g., a
blood culture or culture-independent diagnostic test) can detect botulinum
toxin or C. botulinum.
 TREATMENT
• The cornerstones of treatment for botulism are meticulous intensive care
and administration of botulinum antitoxin. Because antitoxin is most
beneficial early in the course of clinical illness, it should be administered
empirically and before the time-consuming workup for other illnesses or
laboratory confirmation is complete.
• Persons of all ages in whom botulism is suspected should be hospitalized
immediately so that signs of respiratory failure.
• Botulinum antitoxin can limit the progression of illness because it
neutralizes toxin molecules in the circulation that have not yet bound to
nerve endings. However, antitoxin does not reverse existing paralysis,
which may take weeks to improve.
• In wound botulism, suspect wounds and abscesses should be cleaned,
debrided, and drained promptly. The role of penicillin and
metronidazole in treatment and decolonization is unclear.
• Person-to-person transmission of botulism does not occur. Universal
precautions are the only infection-control measures required during
inpatient care. Patients with botulism can acquire health care–
associated infections, deep venous thromboses, and other ailments
that occur among patients who are hospitalized and immobile for
long periods.