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By
Isha R
BOTULISM
CONTENTS
 Etiology
 Pathogenesis
 Clinical manifestations
 Types
 Lab diagnosis
 Treatment
 prevention
Etiology
Botulism is a rare,life -threatening disease characterized
by cranial nerve palsies and descending flaccid
paralysis.
Clostridium botulinum is a gram-positive spore-forming obligate
anaerobic bacilli. It produces a powerful toxin called botulinum
toxin, which causes botulism. Rare strains of Clostridium
butyricum and Clostridium baratii also produce neurotoxins.
Pathogenesis
Seven distinct serotypes of neurotoxins (A through G) are well
characterized; serotypes A, B, E, and F reportedly cause disease in
humans. The neurotoxins are encoded by bont gene.
The neurotoxins are metalloproteases composed of a light chain
and a heavy chain. The light chain has catalytic activity, and the
heavy chain contains a translocation domain and a receptor-
binding domain.
The receptor- binding domain of the heavy chain mediates the
neurospecific binding of neurotoxins, which leads to its
internalization within endocytic compartments.
Heavy chain of the toxin binds to acetylcholine receptors on
presynaptic membranes of motor neurons of the peripheral
nervous system. It does no affect the CNS
Light chain causes proteolysis of several proteins involved in the
release of acetylcholine. Inhibition of acetylcholine release at the
synapse, results in flaccid paralysis.
Clinical manifestations
The manifestations of botulism are due to decreased
acetylcholine in cranial nerve and parasympathetic nerve
terminals.
Manifestations appear after an incubation period of 18-36 hours;
which include:
- Diplopia
-dysphasia
-dysarthria
-descending symmetric flaccid paralysis of voluntary muscles
-reduced deep tendon reflexes
-constipation
-respiratory muscle paralysis, may lead to death.
There is no sensory or cognitive deficits
Ocular findings are caused by extraocular muscle paralysis due
to palsies of cranial nerves III, IV, and VI.
Oral and nasal regurgitation of foods or beverages is caused by
cranial nerve IX palsy.
Types
a. Food-borne botulism
b. Wound botulism
c. Infant botulism
d. Adult intestinal botulism
e. Iatrogenic botulism
f. Inhalational botulism
Food-borne botulism: It results from consumption of foods
contaminated with preformed botulinum toxin
Most common source: Homemade improperly canned or fermented
food and beverages
Wound botulism: It results from contamination of wounds with C.
botulinum spores. It presents like food- borne botulism except for
absence of gastrointestinal features.
It can be recurrent in injection drug users (e.g. mes to convert black
tar heroin.
Infant botulism: It is the most common type; accounts for 75% of
total cases. It results from ingestion of contaminated food (usually
honey) with spores of C.botulinum in children ≤1 year of age.
Spores germinate in the intestine releasing the toxin
Manifestations include inability to suck and swallow, weakened
voice, ptosis, floppy neck, and extreme weakness (hence called
floppy child syndrome).
Adult intestinal botulism: Rarely, in
patients with suppressed normal flora, the colonized clostridial
spores may germinate producing toxin; as in infant botulism
Iatrogenic botulism: It results from injection of overdose of the
toxin while used for therapeutic purpose
Inhalational botulism: Aerosolization of spores may occur as in act
of bioterrorism
Lab diagnosis
Diagnosis of botulism includes isolation of the bacilli and
demonstration of the toxin.
Gram staining of smears made from suspected food or feces-reveals
gram-positive, non-capsulated bacilli with subterminal, oval, bulging
spores It is motile by peritrichate flagella
Isolation: Culture is done on blood agar or Robertson's cooked meat
(RCM) broth. In RCM broth, they can be by fun either proteolytic and
saccharolytic; turning the meat particles into black and pink
respectively
Growth on culture media may be confirmed by Gram by c
staining and biochemical tests or by automated methods such as
MALDI-TOF. Serotyping is done with type specific antisera
Treatment
Treatment for botulism consists of two components:
meticulous monitoring and supportive care, including
admittance to the intensive care unit when indicated, and
administration of botulinum antitoxin, the only specific therapy
for botulism, as quickly as possibleas paralysis from botulism
can be rapidly progressive.
The antitoxin prevents the progression of paralysis but
does not reverse existing paralysis
: It should be administered immediately on clinical suspicion,
without waiting for laboratory confirmation. Earlier the
administration, better is the cure rate because antitoxin can
neutralize the unbound free toxin molecules. However, once toxin
binds to nerve endings, antitoxin has no role
Prevention
Because most foodborne botulism cases are caused by home-
canned or home-preserved foods, the prevention of foodbome
botulism depends mainly on proper preparation and preservation
that ensures the destruction of spores .
Wound botulism largely affects people who inject drugs,
especially black tar heroin. Using safe injection practices may
help prevent wound botulism and many other infections, such as
HIV and hepatitis C virus infections. Thus, educating injection
drug users on the prevention of wound botulism and other
infections is vital in protecting their health.
Honey is the only food that has been identified as an
epidemiologically associated reservoir of spores of neurotoxin
producing species of Clostridium. Honey should not be fed to
infants <1 year of age.
THANK YOU

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Everything You Need to Know About Botulism

  • 2. CONTENTS  Etiology  Pathogenesis  Clinical manifestations  Types  Lab diagnosis  Treatment  prevention
  • 3. Etiology Botulism is a rare,life -threatening disease characterized by cranial nerve palsies and descending flaccid paralysis. Clostridium botulinum is a gram-positive spore-forming obligate anaerobic bacilli. It produces a powerful toxin called botulinum toxin, which causes botulism. Rare strains of Clostridium butyricum and Clostridium baratii also produce neurotoxins.
  • 4. Pathogenesis Seven distinct serotypes of neurotoxins (A through G) are well characterized; serotypes A, B, E, and F reportedly cause disease in humans. The neurotoxins are encoded by bont gene. The neurotoxins are metalloproteases composed of a light chain and a heavy chain. The light chain has catalytic activity, and the heavy chain contains a translocation domain and a receptor- binding domain. The receptor- binding domain of the heavy chain mediates the neurospecific binding of neurotoxins, which leads to its internalization within endocytic compartments.
  • 5. Heavy chain of the toxin binds to acetylcholine receptors on presynaptic membranes of motor neurons of the peripheral nervous system. It does no affect the CNS Light chain causes proteolysis of several proteins involved in the release of acetylcholine. Inhibition of acetylcholine release at the synapse, results in flaccid paralysis. Clinical manifestations The manifestations of botulism are due to decreased acetylcholine in cranial nerve and parasympathetic nerve terminals.
  • 6. Manifestations appear after an incubation period of 18-36 hours; which include: - Diplopia -dysphasia -dysarthria -descending symmetric flaccid paralysis of voluntary muscles -reduced deep tendon reflexes -constipation -respiratory muscle paralysis, may lead to death. There is no sensory or cognitive deficits Ocular findings are caused by extraocular muscle paralysis due to palsies of cranial nerves III, IV, and VI.
  • 7. Oral and nasal regurgitation of foods or beverages is caused by cranial nerve IX palsy. Types a. Food-borne botulism b. Wound botulism c. Infant botulism d. Adult intestinal botulism e. Iatrogenic botulism f. Inhalational botulism
  • 8. Food-borne botulism: It results from consumption of foods contaminated with preformed botulinum toxin Most common source: Homemade improperly canned or fermented food and beverages Wound botulism: It results from contamination of wounds with C. botulinum spores. It presents like food- borne botulism except for absence of gastrointestinal features. It can be recurrent in injection drug users (e.g. mes to convert black tar heroin. Infant botulism: It is the most common type; accounts for 75% of total cases. It results from ingestion of contaminated food (usually honey) with spores of C.botulinum in children ≤1 year of age.
  • 9. Spores germinate in the intestine releasing the toxin Manifestations include inability to suck and swallow, weakened voice, ptosis, floppy neck, and extreme weakness (hence called floppy child syndrome). Adult intestinal botulism: Rarely, in patients with suppressed normal flora, the colonized clostridial spores may germinate producing toxin; as in infant botulism Iatrogenic botulism: It results from injection of overdose of the toxin while used for therapeutic purpose Inhalational botulism: Aerosolization of spores may occur as in act of bioterrorism
  • 10. Lab diagnosis Diagnosis of botulism includes isolation of the bacilli and demonstration of the toxin. Gram staining of smears made from suspected food or feces-reveals gram-positive, non-capsulated bacilli with subterminal, oval, bulging spores It is motile by peritrichate flagella Isolation: Culture is done on blood agar or Robertson's cooked meat (RCM) broth. In RCM broth, they can be by fun either proteolytic and saccharolytic; turning the meat particles into black and pink respectively
  • 11. Growth on culture media may be confirmed by Gram by c staining and biochemical tests or by automated methods such as MALDI-TOF. Serotyping is done with type specific antisera Treatment Treatment for botulism consists of two components: meticulous monitoring and supportive care, including admittance to the intensive care unit when indicated, and administration of botulinum antitoxin, the only specific therapy for botulism, as quickly as possibleas paralysis from botulism can be rapidly progressive. The antitoxin prevents the progression of paralysis but does not reverse existing paralysis
  • 12. : It should be administered immediately on clinical suspicion, without waiting for laboratory confirmation. Earlier the administration, better is the cure rate because antitoxin can neutralize the unbound free toxin molecules. However, once toxin binds to nerve endings, antitoxin has no role Prevention Because most foodborne botulism cases are caused by home- canned or home-preserved foods, the prevention of foodbome botulism depends mainly on proper preparation and preservation that ensures the destruction of spores .
  • 13. Wound botulism largely affects people who inject drugs, especially black tar heroin. Using safe injection practices may help prevent wound botulism and many other infections, such as HIV and hepatitis C virus infections. Thus, educating injection drug users on the prevention of wound botulism and other infections is vital in protecting their health. Honey is the only food that has been identified as an epidemiologically associated reservoir of spores of neurotoxin producing species of Clostridium. Honey should not be fed to infants <1 year of age.