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Infectious Diseases > T14: Toxin Associated infections > Flashcards

T14: Toxin Associated infections Flashcards

1
Q

Differentiate between an exotoxin and an endotoxin

A

Endotoxin= not secreted. Exotoxin= Secreted

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2
Q

List 4 examples of exotoxins

A
  1. Enterotoxins
  2. Neurotoxins
  3. Cytotoxins
  4. Superantigens (pyrogenic exotoxins)
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3
Q

What do pyrogenic exotoxins do?

A

Massive stimulation of the immune system

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4
Q

Describe 2 effects of exotoxins

A
  1. Damage cell wall/ membrane

2. Affect intracellular processes/ structures

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5
Q

A-B Toxins

  • What type of toxins are these? (endo or Exo)
  • What do A and B stand for?
  • List 5 examples of A-B toxins
A
  • Exotoxins
  • A= active component, B= binding component
  • Cholera, Diphtheria, Anthrax, Pertussis, Shigella, S. aureus
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6
Q

State whether this refers to endo or exotoxin:

- component of Gram - cell wall

A

Endotoxin

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7
Q

State whether this refers to endo or exotoxin:

- Gram + and Gram -

A

Exotoxin

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8
Q

State whether this refers to endo or exotoxin:
- Lipid and polysaccharides (core or variable) are responsible for the toxic activity and causes systemic effects due to immune system stimulation

A

Endotoxin

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9
Q

How do endotoxins work?

A

Endothelial damage» fibrinolysis» vascular permeability» vasodilation
DIC» septic shock

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10
Q

DIPHTHERIA: Corynebacterium diphtheriae

  • How is it spread? (airborne, contact, droplet, etc.)
  • How is the diagnosis made?
  • How do we manage it?
A
  • Droplet spread
  • Dx on culture
  • Give anti-toxin (low access in SA), penicillin + supportive management
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11
Q

Name the toxin that:

Has high affinity for heart and neurological structures

A

Diphtheria

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12
Q

Name the toxin that:

Classically presents as Pharyngitis with grey-white membrane

A

Diphtheria

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13
Q

What do we give to prevent Diphtheria at 6w, 10w, 14w

A

DTap/ IPV/Hib

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14
Q

At which ages do we give Td (Diftavax) booster

A

6 + 12 years

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15
Q

Anthrax (Bacillus anthracis) has a toxin complex consisting of 3 proteins- what are these and what of they do?

A
  1. Protective antigen- bings to macrophage receptor
  2. Oedema factor- blocks adenyl cyclase
  3. Lethal factor- vascular permeability
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16
Q

There are 3 types of anthrax presentations, depending on the mode of transmission. Explain these presentations

A
  1. Respiratory anthrax- inhalation of spore/ wool fibers» causes pulmonary hemorrhage and hemodynamic collapse (resp failure)
  2. GIT anthrax: ingestion of contaminated meat from animals that dies of anthrax» hemorrhagic diarrhea
  3. Cutaneous anthrax» inoculation of skin» malignant pustule. 10% fatal- spread to the blood
17
Q

Describe the following pertaining anthrax

  1. Dx
  2. Rx
  3. Prevention
A
  1. Inform lab (contanimants)
  2. Penicillin, doxycycline, ciprofloxacin
  3. Vaccinate animals and give toxoid in high-risk occupations- vets/ leather or wool industry
18
Q

Name the species that cause gad gangrene

A

Clostridium perfrigens
Clostridium septicum
Clostridium histolyticum

19
Q

What is the source of clostridium spp. and how does it get to the body?

A

Soil, human and animal feces and it infects contaminated wounds with poor blood supply and severe tissue damage

20
Q

Name the clostridial toxins that are :

  1. Cytotoxic
  2. Cause tissue breakdown
A
  1. Lecithinase

2. Hyaluronidase, collagase, proteinases

21
Q

Due to the rapid spread of infection in gas gangrene, how do patients present?

A

With acute pain

22
Q

Describe the sequelae of toxemia of clostridium (in gas gangrene) species

A

Toxemia» massive hemolysis» renal failure» death

23
Q

Describe the following pertaining to gas gangrene

  1. Diagnosis
  2. Treatment
  3. Prevention
A
  1. Culture of tissue/ exudate, blood culture
  2. Resus, early surgical debridement, amputation? and A/B covering gram + and -
  3. Clean wounds and debride early
24
Q

BOTULISM

  1. Name the cause of botulism
  2. What type of exotoxin is this and how does it work?
  3. What is the source of the cause of botulism?
  4. Describe transmission
A
  1. Clostridium botulinim
  2. Neurotoxin- prevents ACh release at the NMJ
  3. Spores found in the soil, animals, environment
  4. Ingestion of contaminated food, wound infection with spores (IVDU)
25
Q

BOTULISM- describe the following

  1. Clinical presentation
  2. Therapy
  3. Prevention
A
  1. Symmetrical descending flaccid paralysis
  2. polyvalent antitoxin, ICU, ventilation
  3. Heat sterilization of food when preserved/ canned (the toxin is heat-labile)
26
Q

TETANUS

  1. Name the causative organism
  2. Tetanus toxin is also a neurotoxin (like botulinum toxin): Name this toxin and explain how it works
  3. How does tetanus get to humans?
  4. Describe the clinical picture
  5. True or false: diagnosis is made by culture
A
  1. Clostridium tetani
  2. Toxospasmin- It blocks the normal inhibition of UMN over LMN» causing increased tone and spastic paralysis
  3. Contamination of wounds with spores from the environment (dust/ soil)&raquo_space; spores germinate in the wounds with poor blood supply (anaerobic)
  4. Lockjaw, muscle spasms. Sympathetic nerves: tachycardia, fluctuating Bp
  5. False= culture is impossible. Dx= clinical
27
Q

TETANUS

  1. Describe the management of a patient presenting with tetanus
  2. What preventative measures are there in place for tetanus?
  3. Name 2 types of tetanus prophylaxis
  4. Describe tetanus prophylaxis for clean, minor wounds vs dirty wounds.
A
  1. ICU support, give antitoxin (Ig), metronidazole, and wound debridement
  2. Give TT (tetanus toxoid) to pregnant women in LEDCs, Td given at 6 + 12 yo to boost immunity. Hygienic birth practices and daily disinfection of umbilical stump
  3. TIG (tetanus antitoxin) and TT (tetanus toxoid)
  4. Clean, minor wounds= No TIG. TT is always given except if completed TT course and booster at 6+ 12 within the past 5 years. Dirty wounds= TIG + TT- Except if completed a course of TT and booster within the 5 past years
28
Q

TOXIC SHOCK SYNDROME

  1. What kind of exotoxins are these?
  2. Name the 2 causative organisms and where they work
  3. What is the mechanism of these toxins?
  4. And with that said - describe the clinical presentation
  5. Describe the management of these patients
A
  1. Pyrogenic exotoxins
  2. S. aureus (enterotoxin) and Staphylococcus pyogenes (Erythrogenic toxin)
  3. They are potent stimulators of T-lymphocytes&raquo_space; uncontrolled cytokine release
  4. Fever, conjunctivitis, headache, sore throat, vomiting and diarrhea, strawberry tongue, erythematous skin rash, hypotension, multiorgan failure, shock (Bacteraemia is rare)
  5. IV fluids, supportive, removal of infected focus, antimicrobial Rx
29
Q

SCARLET FEVER

  1. What is the causative organism?
  2. Describe the clinical presentation
  3. What treatment do you give for scarlet fever?
  4. What are the complications of scarlet fever?
A
  1. Group B beta-streptococcus
  2. Pharyngitis and erythematous skin rash (Erythrogenic toxin)
  3. Give penicillin or a macrolide
  4. Peritonsillar abscess, otitis media, septicemia, myocarditis, rheumatic fever, glomerulonephritis
30
Q

CLOSTRIDIUM DIFFICILE

  1. Classify this bacteria (Gram and shape)
  2. In terms of clinical presentation, there is a whole range of presentations. Describe the following
    - Mild
    - Moderate
    - Severe
    - Fulminant
  3. True or false- Toxin A and B independently cause disease
A
  1. Gram + spore-forming bacillus
  2. Mild- Diarrhea and no colitis; Moderate- Diarrhoea and colitis; Severe: moderate plus high WCC, serum Cr, Fever, hypoalbumin; fulminant: toxic megacolon
  3. True
31
Q

CLOSTRIDIUM DIFFICILE

  1. List 3 risk factors for clostridium difficile
  2. How is C. difficile diagnosed?
  3. How is C. difficile treated?
  4. Describe the prevention of C. difficile
A
  1. Hospitalisation; Antibiotic use (cephalosporines, fluoroquinolones, clindamycin) and old age
  2. Detection of toxin and NAAT (nucleic acid detection)
  3. Rx= metronidazole and if severe, vancomycin
  4. Antibiotic stewardship, hand hygiene, clean environment, more clinical awareness
32
Q

WHOOPING COUGH

  • Name the toxins involved here
  • Name the causative orgnism
  • If a patient has whooping cough, what are your differentials?
  • Explain how you would go about proving the diagnosis objectively
  • Describe the management
A
  • Tracheal cytotoxin and pertussis cytotoxin
  • Bordetella pertussis
  • Viral: adenovirus, parainfluenza, RSV, mycoplasma pneumonia
  • I would need to inform labs about Bodertella (special media) after taking a nasopharyngeal swab. Some labs do PCR
  • Oxygen, ventilation, IV rehydration, and 14 days of erythromycin (or azithromycin or clarithromycin)
    It is a notifiable disease
33
Q

BORDETELLA PERTUSSIS

  • What are the complications of Bordetella pertussis
  • What precautions do you take for pertussis?
  • Explain how PEP is given in: asymptomatic vs coughing contacts
  • When are we at the highest risk for pertussis?
  • Explain prevention
  • What does DTap-IPV/Hib protect against?
A
  • Bordetella pneumonia, hypoxia encephalopathy, seizures, secondary bacterial infections (OM, pneumonia). Pressure effects (pneumothorax, epistaxis, subconjunctival hemorrhage, subdural hematoma)
  • Droplet and standard precautions
  • If asymptomatic- no Rx. If symptomatic= give Rx for pertussis and investigate other causes
  • When pt is coughing, talking, sneezing, and during procedures: suctioning, nebulization
  • DTap-IPV/ Hib. Immunization is not lifelong (wanes 4-8 years later)
  • Diphtheria, Tetanus, acellular pertussis, inactivated polio vaccine, Hib

Infectious Diseases (8 decks)

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