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Med Bacc > Clostriduim > Flashcards

Clostriduim Flashcards

1
Q

What is the etiology and epidemiology of Clostriduim?

A
  • anaerobic environments
  • spore forming bacilli
  • ubiquitous in soils as well as intestines of humans and non-humans, commonly found in these areas
  • gram-positive
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2
Q

Justinian Kerner

A
  • Ger.Poet and Physician, 1800’s
  • described rod shaped cells (C.botulinum), isolated for spoiled sausage during an outbreak of food poisoning in Wurttemberg, Germany
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3
Q

Emile Van Ermengem

A
  • Belgian
  • Bacteriologist, 1890
  • isolated spore-forming bacilli (C.botulinum) from spoiled cured ham, attributed to food poisoning
  • this would later be wrongly classified as Bacillus botulinus
  • first female research biologist
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4
Q

Ida Bengston

A
  • American Bacteriologist (NIH)
  • in the 1920’s she reclassified Clostridium botulinum
  • classified as anaerobic spore-forming bacilli
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5
Q

Taxonomy of Clostridium:

  1. How many species are there?
  2. What are the ones that are responsible for human disease?
A
  1. the genus contains approx. 100 species
  2. C.botulinum
    • C.tetani
    • C.perfringens
    • C.difficile
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6
Q

Morphology of Clostridium:

A
  • they are spore-forming bacilli
  • gram-positive
  • endospores
  • exopolysaccharide biofilm
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7
Q

More Epidemiology of Clostridium:

  1. Historically, Clostridium is the leading cause of what in soldiers?
  2. How has these wounds declined overtime?
  3. Botulinum and tetanus have also declined overtime, what has caused the decline?
  4. Approx. how many cases per year are there for the two diseases?
A
  1. wound infections in soldiers
  2. advancements in prompt, adequate medical treatments (prophylaxis/antisepsis)
  3. declined in developed nations/ hundreds of cases per year in the U.S., public awareness and widespread immunization are the reasons
  4. 1,000,000 cases per year for each
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8
Q

More questions about Clostridium:

  1. Clostridium can be both _____ and ____.
  2. What are some routs of entry for Clostridium?
  3. What are most Clostridium characterized by?
A
  1. 1 obligate 1.2 opportunistic pathogens
  2. Routs of entry include both ingress (ingestion) and parenteral (wounds)
  3. characterized by acute, toxin-associated infections and are non-invasive
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9
Q

Nosocimial disease in Clostridium:

  1. What species of Clostridium are nosocomial?
  2. How is it transmitted?
A
  1. C.difficile
    • hospital-acquired opportunistis (5000,000 per year in U.S.)
  2. transmitted via fecal-oral route however, carriage rates are low in adults
    - can inhabit the gut asymptotically, low carriage rate, maybe a patient is being treated for MRSA and is on antibiotics
    - antibiotics will clear the MRSA, but the immune diffidence is low, exposed to C.difficile from nurse/doctor via fecal-oral route
    - C.Diff can be established in the gut of patient asymptomatically, he is a new carrier, transmits C.diff disease in the community, came in with one infection but left with another
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10
Q

Fill in the blank: Clostridium infections are associated with a_______- nearly all are ____.

A
  1. broad spectrum of human disease

2. toxin-associated

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11
Q

Answer these questions about Clostridium toxin-associated disease:
1. Neurotoxic clostridium is associated with…?

A
  1. C.tetani

2. C.botulinum

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12
Q

Answer these questions about Clostridium toxin-associated disease:
2. Enterotoxemic and Enteropathogenic clostridia is associated with…?

A
  1. C.perfringens type A-E

2. C.difficile

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13
Q

Answer these questions about Clostridium toxin-associated disease:
3. Histotoxic clostridia is associated with…?

A
  1. C. perfringens and the other ones, whatever
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14
Q

The Big 4! C.perfringens:

1. What does it infect and what does it present as?

A
  1. targets soft tissues of the dermis as well as muscle and organ systems— presents as gas gangrene and cellulitis
  2. attacks the gastrointestinal system— an agent of food poisoning
  3. also presents as narcotizing enteritis, hemorrhagic inflammatory infection of the small bowl, sepsis
    - etiologic symptom, [alpha]-toxin
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15
Q

The Big 4! C.perfringens:

  1. Where can C.perfringens become established and what can it do once established?
  2. What does multiplication and toxin production lead to?
A
  1. it can become established in anaerobic wounds, it impaired blood supply due to trauma and occlusion favors growth
  2. multiplication and toxin production (collagenases, lipases, proteases and hemolysins) leads to rapid tissue necrosis
    - prognosis is grim and infections can be fatal
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16
Q

Connect the presentation to the bacteria and the toxin that causes it:

  1. C.perfringens?
  2. C.botulinum?
  3. C.tetani?
  4. C.difficile?
A
  1. C.perfringens—- gas gangrene, cellulitis, food poisoning, narcotizing enteritis and sepsis (alpha toxin)
  2. C.botulinum—botulism (botulinum toxin, BoNT)
  3. C.tetani—- tetanus (tenanospasmin, TeNT)
  4. C.difficile—pseudomembranous colitis ( ToxA/ToxB)
17
Q

Answer these questions regarding Clostridium toxins:

1. The difference between all of the big 4 is determined by what?

A
  1. production of toxin
18
Q

Answer these questions regarding Botulinum toxin:

  1. What toxin is botulinum caused by and what are its clinical symptoms?
  2. What are the 3 forms of botulism and what do they do in the body?
A
  1. Botulism is caused by the bacteria C.botulinum neurotoxin (BoNT), causes a symmetrical, descending paralysis, death is due to cardiac/pulmonary failure
  2. there are 3 forms of Botulism
    • Adult– caused by ingestion of preformed toxin;toxinosis
    • Infant– replication and toxin production in the intestine
    • Wound botulism– replication and toxin production in wounds
19
Q

Answer these questions regarding Botulinum toxin:

  1. How deadly is BoNT? How many BoNT toxins are there and which one has the highest mortality?
  2. BoNT disseminates in the blood and lymphatics to do what?
  3. What type of dichain does BoNT have?
  4. What are the 3 functional domains of the dichain?
A
  1. very potent toxin, the lethal dose (LD50) >40ng, at least 8 immunogenetically distinct BoNT toxins, Only [A, B, E] are clinically relevant, Mortality highest for A, this id due to receptor affinity
  2. to cranial and then to peripheral nervous tissues
  3. large A-B dichain (ca 150kDa) neurotoxin
  4. Heavy C-terminal chain (Hc)— neurospecific binding
    • Heaby N-terminal chain (Hn)—- translocation of HL
    • Light chain (Lc)– is a protease
20
Q

Explain the mechanism for BoNT:

A
  1. Neurospecific binding of BoNT and receptor-mediated endocytosis is achieved by HC domain
  2. BoNT will then bind to SNAP-25 (synaptosomal-associated protein receptors) on neurons, this will result in receptor-mediated endocytosis
  3. The Hn domain will then fuse with the endosome membrane to form the HL domain (a pore-like translocation domain), this domain is moved through the pore into the host cell cytoplasm
  4. Normal neuromuscular junctions? host SNARE proteins deliver synaptic vesicles that have acetylcholin to the synaptic cleft
  5. the LC protease subunit of BoNT cleaves SNARE proteins, this prevents delivery of synaptic vesicles to the junction, leads to muscle fibers to become paralyzed
21
Q

Answer these questions about TeNT:

  1. What neurotoxin causes tetanus and what are its clinical symptoms?
  2. How does C.tetani enter its host and what does it do one entered through the host? What can this lead to?
A
  1. tetanus is caused by C.tetani tetanospasmin (TeNT), clinical symptoms are trismus (lockjaw), extreme muscle rigidity, painful spasms (opisthotonos), one inside the host it will replicate and produce TeNT
  2. it enters its host parenterally through breaks in the skin [ dog/pig bite, gunshot, dirty needles, barbed wire, puncture wounds form nails], this can eventually lead to cardiac/pulmonary failure
22
Q

Answer these questions about TeNT:

  1. What type of dichain does TeNT have? Is TeNT as toxic as BoNT?
  2. What does TeNT interfere with in the body?
  3. What is GABA?
A
  1. TeNT has a A-B dichain, similar structure to BoNT, it is however less toxic (LD50– 100ng)
  2. it interferes with the delivery of y-amino butyric acid (GABA) neurotransmitter to neuromuscuar junctions in nerve synapses
  3. GABA is an inhibitory neurotransmitter, it blocks the release of acetylcholin (muscle contraction) at neurotransmitter junctions
23
Q

Explain the mechanism for TeNT pathogenesis:

A
  1. TeNT light chain (Lc) protease targets the SNARE protein synaptobrevin, this normally delivers GABA containing inhibitory vesicles to the junction
  2. this will lead to spasms, muscle rigidity, convulsion, death
  3. Tetanus toxin prevents the release of glycine and GABA, prevents relaxation of muscles
24
Q

What is the main difference between TeNT and BoNT?

A
  • BoNT leads to the blockage of the release of acetychlorine, prevents muscle relaxation
  • TeNT leads to uncontrolled release of acetylcholine, stopping muscle contraction
25
Q

Answer these questions about C.Difficile:

  1. Where is C.diff found naturally?
  2. What type of antibiotics permits intestinal growth?
A
  1. C.diff is found naturally in the intestinal microbiota in a small percentage of healthy adults, it is also found naturally in the environment
  2. Broad spectrum antibiotic therapy can permit intestinal growth
26
Q

Answer these questions about TcdA/TcdB in C.diff:

  1. Some strains of C.diff produce varying amounts of certain enterotoxins. What are these enterotoxins and what are their clinical symptoms?
  2. Both TcdA/TcdB are what? And what can this cause?
A
  1. C.diff produces varying amounts of enterotoxin ToxA (TcdA) and cytotoxin ToxB (TcdB), the main clinical symptoms are secretory diarrhea and inflammation, determined by sequelae of psudomembraneous colitis
  2. both are cytotoxic, this causes disruption of the actin cytoskeleton and tight junctions, this will later lead to fluid accumulation and destruction of intestinal epithelium
27
Q

TcdA/TcdB question:

1. What are the four functional domains of TcdA and TcdB?

A
  1. GTD– glucosyltransferase
  2. APD– autoprotease
  3. Delivery–translocation
  4. CROPS– receptor binding, [combined repetitive oligopeptides] domain
28
Q

Explain the TcdA pathogenesis:

A
  1. TcdA binds to CROPS receptors, internalized by receptor-mediated endocytosis
  2. Delivery/translocation domain fuses with endosome membrane
  3. GTD domain is then translocated through the delivery domain, then released into the host cytoplasm
  4. GTD glucosylates Rho family GTPases– altering signal transduction and causing dysregulation of cytoskeleton, Tj loosening and inducing apoptosis
  5. TcdA/B cytotoxicity and immune-stimulation leads to psudomembrane formation and colitis in the large bowl
29
Q

Answer these questions about diagnosis of Clostridium:

  1. Diagnosis of wound infections is based on what?
  2. C.diff diagnosis is based on symptoms in conjugation with antibiotic chemotherapy. What does a colonoscopy show?
  3. Early diagnosis is important. Why is this?
A
  1. wound infections (C.perfringens) based on clinical syndrome, direct microscopic exam with gran reaction/culture of wound exudates
  2. C.diff diagnosis, culture from stool, colonoscopy is required for diagnosis of psudomembranous colitis
  3. various diseases share similar symptoms on tetanus (C.tetani) and botulism (C.botulinum) [rabies, meningitis, stroke, overdose], early diagnosis is crucial for positive prognosis
30
Q

Answer these questions about diagnosis of Clostridium:

  1. What would be included in a C.botulinum diagnosis?
  2. What CDC/FDA test can show the presence of C.botulinum?
A
  1. diagnosis includes brain scans, nerve conduction (NCS) examination of spinal fluid (spinal tap), validate by detection of BoNT in serum and exudates
  2. approved an ELISA immunoassay for lab conformation of BoNT [A, B, E, F] directly from clinical samples
31
Q

Answer these questions about prevention of Clostridium:

  1. What can prevent food-bore botulism?
  2. Are there any vaccines for any of the bacterial types?
  3. What can help with the prevention of C.diff infection?
A
  1. adequate food preservation methods, heat all canned food before eating
  2. toxoid-based vaccines against tetanus, DTaP and TdaP
  3. prudent practice in prescribing broad-spectrum antibiotics for high-risk patients, patient isolation, environment decontamination could mitigate further nosocomial spread
32
Q

Answer these questions about therapy of Clostridium:

  1. What is botulism treated with? What do the antibodies do to BoNT?
  2. What antibiotics can be used for C.diff? What about probiotics? Reoccurring infections?
A
  1. treated with antibody immunotherapy- HBAT- composed of antibodies that are able to neutralize BoNT in tissues
  2. for C.diff, metronidazole, vancomysin, fidaxomicin, probiotics/immunotherapy limited in efficacy, reoccurring infections lead to the use of fecal microbiota transplantation

Med Bacc (4 decks)

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