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Infection > Lecture 2.2: Toxins > Flashcards

Lecture 2.2: Toxins Flashcards

1
Q

What is a Toxin?

A

• Substances that contribute to pathogenicity
• Major Virulence factor
• Chemicals produced by pathogens that harm tissues
• Chemicals that trigger host immune responses that cause damage
• Do not produce infection

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2
Q

What is Toxigenicity?

A

It is the ability to produce a toxin

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3
Q

What is Toxaemia?

A

It is the presence of toxin in the host’s blood

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4
Q

What is a Toxoid?

A

AN inactivated toxin used in a vaccine

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5
Q

What are Antitoxins?

A

Antibodies against a specific toxin

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6
Q

What are the 2 Type of Toxins?

A

Exotoxins and Endotoxins

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7
Q

Exotoxins

A

• Extracellular: Mostly soluble proteins secreted by bacteria
• Secreted by Gram Positive and Negative Bacteria
• Highly Specific
• High Potency
• Denatured
• Local Action
• Extremely Lethal

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8
Q

Endotoxins

A

• Lipopolysaccharides (LPS) & Structural components
• Secreted by Gram Negative Bacteria
• Released by lysis
• Low specificity
• Low potency
• Not Denatured
• Act on remote sites

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9
Q

What are the 3 ways Exotoxins can cause harm?

A

• Signalling at host cell membranes (type I)
• By damaging membranes (type II)
• By entering target cells and directly altering function (type III)

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10
Q

What are the 3 Classes of Toxins?

A

• Neurotoxin
• Enterotoxin
• Superantigens

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11
Q

What is Toxic Shock Syndrome caused by?

A

It is caused by either staphylococcus or streptococcus bacteria that produce TSST-1 Toxin

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12
Q

What are Symptoms of Toxic Shock Syndrome? (9)

A

• High fever
• Low blood pressure
• Headache
• Rapid heartbeat
• Nausea and vomiting
• Muscle pain
• Malaise and confusion
• Rashes on the soles and palms
• Peeling of the skin

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13
Q

What is the Mode of Action of Superantigens/Type 1 Toxins?

A

• They can interact with a large number of different CD4+ T cells
• This results in the promiscuous activation of T cells that secrete IL-2
• Leading to a chain reaction of cytokine synthesis
• Which terminates in the production TNF-α & IL-1
(• Similar to gram negative septic shock)

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14
Q

What is Staphylococcal Scalded Skin Syndrome (SSSS) caused by?

A

• It is caused by group II coagulase-positive staphylococci
• Mainly S.aureus

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15
Q

What are Symptoms of Staphylococcal Scalded Skin Syndrome (SSSS)?

A

• Fever
• Redness
• Bullae
• Skin Exfoliation

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16
Q

What is Gas Gangrene caused by?

A

The release of toxins by Clostridium species

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17
Q

What are the Symptoms of Gas Gangrene?

A

• The site of infection becomes inflamed
• May become a bronze or blue-black colours
• Odorous fluid may seep from the wound
• The fluid may look fizzy or frothy due to the presence gas produced from
fermentation of glucose

18
Q

What is the mortality rate of Gas Gangrene?

A

• Due to traumatic gas gangrene occurs in approximately 25% of cases
• In non-traumatic cases, mortality occurs 67-100% of the time

19
Q

How does Diagnosis of Non-Traumatic Gas Gangrene occur? (3)

A

Analysis of Symptoms

Necrosis of the muscles and gas production may be viewed through MRI and CT scan

Fluids from the wound may be cultured to determine if both anaerobic Clostridium and other aerobic species are present

20
Q

How does Diagnosis of Traumatic Gas Gangrene occur? (3)

A

Analysis of Symptoms

In traumatic cases, and if the infected muscle is visible, it will appear grey, green and purple in colour

In traumatic cases, and if the infected muscle is visible, it will appear grey, green and purple in colour

21
Q

How do you treat Gas Gangrene?

A

• Draining the wound
• Removal of infected tissues to prevent the
spreading of infection
• Implementation of antibiotics
• Hyperbaric Oxygen Therapy

22
Q

Characteristics of Clostridia Bacteria

A

• Large
• Gram Positive
• Bacilli
• Strictly Anaerobic
• Spore Forming
• Fermentative

23
Q

Species of Clostridia Bacteria

A

• C.perfringes
• C.difficile
• C.tetani
• C.botulinum

24
Q

What are 2 components of A-B Toxins?

A

A: Active
B: Binding

25
Q

Examples of A-B Toxins

A

• Cholera toxin produced by Vibrio cholera (Cholera)
• A-B neurotoxin produced by Clostridium botulinum (Botulism)
• Tetanospasmin, A-B neurotoxin produced by Clostridium tetani (Tetanus)

26
Q

General Mechanism of Action of A-B Toxins (4 Steps)

A
  1. Bacterium produces and releases exotoxins
  2. B component of exotoxin binds to host cell receptor, and exotoxin enters cell
  3. A component of exotoxin alters cell function by inhibiting protein synthesis
  4. B component is released from the cell
27
Q

What is Botulism?

A

Botulism is poisoning that is due to Clostridium botulinum toxin

28
Q

What causes Botulism?

A

Botulism can occur when neurotoxin is produced in vivo by C. botulinum

Or when preformed neurotoxin is acquired in an external source such as if the toxin is ingested, injected, or inhaled

29
Q

What part of the body is affected in Botulism?

A

It affects the peripheral nerves

30
Q

Symptoms of Botulism? (11)

A

• No Fever
• Symmetric cranial nerve palsies
• Symmetric descending muscle weakness
• Flaccid paralysis without sensory deficits
• Tachycardia
• Nausea & Vomiting
• Slurred Speech
• Problems urinating
• Dry mouth
• Abdominal distention
• Drooping eyelids

31
Q

Treatment of Botulism

A

Treatment is with support and antitoxin

32
Q

What are the 3 Types of Botulism?

A

• Wound botulism
• Infant botulism (the most common form)
• Adult enteric botulism (rare)

33
Q

What is the Mechanism of Action of the Botulinum Toxin?

A

It inhibits the release of acetylcholine

34
Q

What is Tetanus? What causes it?

A

Tetanus is acute poisoning from a neurotoxin produced by Clostridium tetani

35
Q

How long is incubation period of Tetanus?

A

The incubation period ranges from 2 to 50 days (average, 5 to 10 days)

36
Q

Symptoms of Tetanus (5)

A

• Opisthotonus
• Intermittent tonic spasms of voluntary muscles
• Spasm of the masseters accounts for the name lockjaw
• Fever and sweating.
• Changes in blood pressure and fast heart rate

37
Q

Treatment of Tetanus

A

Human tetanus immune globulin and intensive support

38
Q

Mode of Action of Tetanus (7)

A

• The toxin enters peripheral nerve endings, binds there irreversibly
• Travels retrograde along the axons and synapses
• Ultimately enters the central nervous system
• Release of inhibitory transmitters from nerve terminals is blocked
• Unopposed muscle stimulation by acetylcholine & general tonic spasticity
• Usually with superimposed intermittent tonic seizures
• Once bound, the toxin cannot be neutralised

39
Q

Worldwide Mortality Rate of Tetanus

A

50%

40
Q

Mortality Rate of Tetanus in Untreated Adults

A

15 to 60%

Infection (21 decks)

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