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BACTERIAL AGENTS
&
CHEMICAL TOXINS
-By TANUJA TATRARI
“The most probable method for
spread of bio-weapons is aerial
transmission, continuing into water
supplies and food.”
CDC Categories
Category A:
Anthrax
Cholera
Smallpox
Plague
Botulism
Viral hemorrhagic fevers
Category B:
Q-fever
Brucellosis
Glanders
Some toxins
Category C:
Hantavirus
Tick-borne viruses
MDR-TB
BACTERIAL AGENTS
 Bacillus anthracis (spores)  Anthrax
 Yersinia pestis  Plague
 Vibrio cholerae  Cholera
 Clostridium botulinum (toxin)  Botulism
 Brucella spp.  Brucellosis
 Coxiella burnetii  Q-fever
 Burkholderia mallei  Glanders
 Burkholderia pseudomallei  Meliodosis
 Francisella tularensis  Tularemia
 Rickettsia prowazekii  Typhus fever
ANTHRAX as a Bioweapon
 Infectious disease
 AGENT: Bacillus anthracis
• Gram-positive rod
• Sporing
 The bacteria live in soil and usually infect wild and
domestic animals, such as goats, cattle and sheep.
• Anthrax can be created easily in a lab, and
is incredibly durable: Spores of anthrax
bacteria can lie dormant for years before
entering a living host, where they
reactivate and multiply. These
characteristics make anthrax an extremely
dangerous bioterrorism weapon.
PATHOGENESIS
Depending on the route of exposure to B.
anthracis spores, the lesions can be:-
1. Cutaneous anthrax
2. Pulmonary (Inhalational) anthrax
3. Gastrointestinal anthrax
1. INHALATIONAL ANTHRAX
• Due to inhalation of Anthrax spores.
• I.P.: 2-3 days (60days)
• Natural infection is extremely rare
• Spores needs to be <5µm in size to reach the
alveolus.
• Macrophage lyses and destroys some of the
spores.
• Survived spores are transported to the lymph
nodes.
Widened mediastinum and hilar lymphadenopathy
2. GASTROINTESTINAL ANTHRAX
3. CUTANEOUS ANTHRAX
PLAGUE (Black Death) as a Bioweapon
Zoonotic disease
VECTOR: Xenopsylla cheopis (Oriental rat flea)
AGENT: Yersinia pestis
• Gram negative
• Cocco-bacillus
• Non-motile
• Non-sporing bacteria
• Modes of transmission in humans:
i. Bites by fleas especially oriental rat flea
(Xenopsylla cheopis).
ii. Exposure to humans with pneumonic plague.
iii. Handling of infected carcasses.
iv. Scratches or bites from infected domestic
cats.
v. Exposure to aerosols containing plague-
causing bacilli.
• The key to the organism’s virulence is the phenomenon
of “BLOCKAGE”, which aids the transmission of bacteria
by fleas.
CHOLERA as a Bioweapon
 Intestinal infection
 AGENT: Vibrio cholerae
• Gram-negative
• comma-shaped
• motile bacteria.
• Hallmark profuse secretory diarrhoea
• Its antigenic structure consists of a flagellar-H antigen
and a somatic-O antigen.
• The infectious dose depends upon the mode of
administration
i. Ingestion with water= 103 -106
ii. Ingested with food= 102 -104
• V. cholerae O1 and V. cholerae O139
Enterotoxin
promotes the secretion of fluid and
electrolytes into the lumen of the small intestine
DIARRHOEA
CLINICAL PRESENTATION
CHEMICAL TOXINS
BOTULINUM (BO-TOX)
RICIN
STAPHYLOCOCCAL ENTEROTOXIN-B
T-2 MYCOTOXINS
1. BOTULINUM TOXIN (BO-TOX)
Produced by Clostridium botulinum
• Gram-positive
• Rod-shaped
• Anaerobic
• Spore-forming
• Motile bacterium
• with the ability to produce the neurotoxin Botulinum
BOTULINUM
• Most potent toxin known to mankind
• 7 types of Neuro-toxins
• Causes severe flaccid paralytic disease
• Lethal dose: 1.3-2.1 ng/kg in Humans
• No person-to-person transmission
• Multiple cases without common food
source suggests bioterrorism
Botulinum Toxin:
Mechanism of Action
• Site: neuromuscular junction (pre-synaptic)
• Action: binds at acetylcholine release sites to
prevent release
• Effect: muscle weakness (skeletal and cranial
nerve distribution
• Does not cross the blood-brain barrier:
–patients remain alert and afebrile
Botulinum Toxin:
Clinical Findings
• Botulism onset: about 1-3 days
• Cranial nerve palsies early:
– Eye: blurred vision, photophobia, diplopia, ptosis
– Throat: dysarthria, dysphagia
• Skeletal muscle weakness later:
– symmetrical, descending, progressive
– abrupt respiratory failure
RICIN
Potent protein toxin derived from Castor beans
Easily produced / Recently found in France
Inhibits protein synthesis
Causes necrotizing airway lesions:
• Tracheitis
• Bronchitis and Bronchiolitis
• Interstitial pneumonia with ARDS
Inhalation as an aerosol produces severe
respiratory symptoms:
– Day 1: cough, fever, dyspnoea
– Day 2-3: Pulmonary edema, Resp. failure, death
Bioterrorism.ppt medicine bioweapon

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Bioterrorism.ppt medicine bioweapon

  • 2. “The most probable method for spread of bio-weapons is aerial transmission, continuing into water supplies and food.”
  • 5. BACTERIAL AGENTS  Bacillus anthracis (spores)  Anthrax  Yersinia pestis  Plague  Vibrio cholerae  Cholera  Clostridium botulinum (toxin)  Botulism  Brucella spp.  Brucellosis  Coxiella burnetii  Q-fever  Burkholderia mallei  Glanders  Burkholderia pseudomallei  Meliodosis  Francisella tularensis  Tularemia  Rickettsia prowazekii  Typhus fever
  • 6. ANTHRAX as a Bioweapon  Infectious disease  AGENT: Bacillus anthracis • Gram-positive rod • Sporing  The bacteria live in soil and usually infect wild and domestic animals, such as goats, cattle and sheep.
  • 7. • Anthrax can be created easily in a lab, and is incredibly durable: Spores of anthrax bacteria can lie dormant for years before entering a living host, where they reactivate and multiply. These characteristics make anthrax an extremely dangerous bioterrorism weapon.
  • 8.
  • 10. Depending on the route of exposure to B. anthracis spores, the lesions can be:- 1. Cutaneous anthrax 2. Pulmonary (Inhalational) anthrax 3. Gastrointestinal anthrax
  • 11. 1. INHALATIONAL ANTHRAX • Due to inhalation of Anthrax spores. • I.P.: 2-3 days (60days) • Natural infection is extremely rare • Spores needs to be <5µm in size to reach the alveolus. • Macrophage lyses and destroys some of the spores. • Survived spores are transported to the lymph nodes. Widened mediastinum and hilar lymphadenopathy
  • 14. PLAGUE (Black Death) as a Bioweapon Zoonotic disease VECTOR: Xenopsylla cheopis (Oriental rat flea) AGENT: Yersinia pestis • Gram negative • Cocco-bacillus • Non-motile • Non-sporing bacteria
  • 15. • Modes of transmission in humans: i. Bites by fleas especially oriental rat flea (Xenopsylla cheopis). ii. Exposure to humans with pneumonic plague. iii. Handling of infected carcasses. iv. Scratches or bites from infected domestic cats. v. Exposure to aerosols containing plague- causing bacilli.
  • 16. • The key to the organism’s virulence is the phenomenon of “BLOCKAGE”, which aids the transmission of bacteria by fleas.
  • 17.
  • 18.
  • 19.
  • 20. CHOLERA as a Bioweapon  Intestinal infection  AGENT: Vibrio cholerae • Gram-negative • comma-shaped • motile bacteria. • Hallmark profuse secretory diarrhoea • Its antigenic structure consists of a flagellar-H antigen and a somatic-O antigen.
  • 21. • The infectious dose depends upon the mode of administration i. Ingestion with water= 103 -106 ii. Ingested with food= 102 -104
  • 22. • V. cholerae O1 and V. cholerae O139 Enterotoxin promotes the secretion of fluid and electrolytes into the lumen of the small intestine DIARRHOEA
  • 26. 1. BOTULINUM TOXIN (BO-TOX) Produced by Clostridium botulinum • Gram-positive • Rod-shaped • Anaerobic • Spore-forming • Motile bacterium • with the ability to produce the neurotoxin Botulinum
  • 27. BOTULINUM • Most potent toxin known to mankind • 7 types of Neuro-toxins • Causes severe flaccid paralytic disease • Lethal dose: 1.3-2.1 ng/kg in Humans • No person-to-person transmission • Multiple cases without common food source suggests bioterrorism
  • 28. Botulinum Toxin: Mechanism of Action • Site: neuromuscular junction (pre-synaptic) • Action: binds at acetylcholine release sites to prevent release • Effect: muscle weakness (skeletal and cranial nerve distribution • Does not cross the blood-brain barrier: –patients remain alert and afebrile
  • 29. Botulinum Toxin: Clinical Findings • Botulism onset: about 1-3 days • Cranial nerve palsies early: – Eye: blurred vision, photophobia, diplopia, ptosis – Throat: dysarthria, dysphagia • Skeletal muscle weakness later: – symmetrical, descending, progressive – abrupt respiratory failure
  • 30.
  • 31. RICIN Potent protein toxin derived from Castor beans Easily produced / Recently found in France Inhibits protein synthesis Causes necrotizing airway lesions: • Tracheitis • Bronchitis and Bronchiolitis • Interstitial pneumonia with ARDS
  • 32. Inhalation as an aerosol produces severe respiratory symptoms: – Day 1: cough, fever, dyspnoea – Day 2-3: Pulmonary edema, Resp. failure, death