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Faith's Multisystems module > Micro: toxic shock, Anaerobes, Etc > Flashcards

Micro: toxic shock, Anaerobes, Etc Flashcards

1
Q

What is Toxic Shock Syndrome and what causes it?

A

An acute, systemic illness with FEVER and HYPOTENTION due to a bacterial SUPERANTIGEN. Superantigens cause an overactivation of T cells, leading to capillary storm and eventually tissue damage/multiorgan failure and death.

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2
Q

What organisms typically cause Toxic Shock Syndrome?

A

Staphylcoccus aureus or streptococcus pyogens

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3
Q

What are the types of Staphylcoccal toxic shock syndrome, and what are the key toxins, causes, and common clinical presentation?

A

Menstrual: Associated with retention of high absorbancy tampons: favors TSST-1 production.

Non-menstrual: post-surgical, skin infections, abscess, wounds (burns). Presents with RED skin all over, NOT bacteremic.

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4
Q

Definition of Staphylcoccal toxic shock syndrome?

A
  1. Fever > 102
  2. Hypotention (SBP <90)
  3. Diffuse macular erythoderma
  4. desquamation at 1-2 weeks
  5. 3+ organ systems involved

Do NOT have to isolate staphylcoccus aureus.
negative serology for other organisms (measles, leptospirosis, etc)

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5
Q

Definition of Streptococcal toxic shock syndrome

A
  1. isolation of Streptococcus pyogens from normally sterile site
  2. hypotention (SBP < 90)

AND 2+ of systemic problems such as:
renal insuffciency, coagulopathy, increased liver enzymes, adult respiratory distress syndrome, erythematous macular rash, soft tissue necrosis

Typically presents with PAIN, Skin/Soft tissue infection, and Bacteremia.

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6
Q

How do you treat Toxic Shock Syndrome

A
  1. IV fluids
  2. Through search for site infection: remove foreign bodies/tampon, debridement, drainage of abcesses
  3. antibiotics: vancomycin (MRSA)+ clindamycin (blocks toxin production)
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7
Q

Define endotoxin

A

endotoxins are a poisonous substance that come from within pathogenic organisms

ENDOTOXIN = LPS

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8
Q

What are the components of LPS? What is the toxic part of LPS?

A
  1. O-specific polysaccharide chain (location of variation)
  2. Core glycolipid
    - outer chain
    - inner chain (LIPID A) <= toxic portion of LPS.
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9
Q

How is LPS recognized? What is its use?

A

LPS is a PAMP (Pathogen associated molecular pattern) that will bind to TLR4 a PRR (pattern recognition receptor).

LPS binding to TLR4 will result in activation of the T cell and release of C5a, TNF-a, IL1, and IL6, and may lead to death.

sensing for LPS allows for early detection from bacterial infection and a rapid engagement of an immune response.

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10
Q

Neisseria meningitides - what type of bacteria, how does it appear microscopically?

What are the pathogenic serogroups? Which are covered by vaccines?

A

Gram negative, aerobic, diplocci.

Pathogenic serotypes: A, B, C, X, Y, W135. Vaccines cover only A, X, Y, W135.

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11
Q

What is the meningitis belt?

A

Serogroup A that typically presents during the dry season in Africa

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12
Q

What are the symptoms of meningococcus?

A

Initial symptoms are nonspecific: fever, nausea, vomiting, headache, muscle pains (confused with influenza). Sometimes sore throat (confused with strep pharyngitis).

CLASSIC SYMPTOMS: typically present late in disease before death

  • Hemorrhagic rash (on trunk, lower portions of body: pressure areas bra straps belts etc. petechial => large purpuric/ecchymotic lesions
  • meningismus
  • impaired consciousness
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13
Q

How do survivors of meningococcus look? Do they fully recover?

A

No. Survivors of meningococcus can have some bad sequel - necrosis of distal limps, hearing loss, skin scarring.

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14
Q

Who do you worry about with this bug? Why do doctors worry about it? What about N. Meningitides makes it have this clinical course?

A

Infants, college students, military. It move FAST - can die within 12 hours from presentation.

This is such as fast and dire course because of very high levels of endotoxin release - dramatic increases in cytokines such as TNFa, IL1, IL6, IL8. this is all due to the MEMBRANE BLEBS containing endotoxin from N. meningitides during it’s log growth.

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15
Q

What serious complication can occur with N. Meningitides?

A

Waterhouse-Friderichsen syndrome: infarcted adrenal glands.

Symptoms: shock, cutaneous purpuric lesions, acute hemorrhagic necrosis of adrenal glands.

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16
Q

How is N. Meningitides spread? What is the 3 ft rule?

A

N. meningitides main reservoir is humans in the nasopharynx. It is spread through respiratory droplets especially in confined quarters (3-ft barrier - incidence of N. meningitides decreases if soldiers beds were 3 ft apart).

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17
Q

What risk factors increases chances of getting N. Meningitides?

A

Terminal complement component deficiency (C5-9)*

Others: asplenia, other upper respiratory tract infections, variations of mannose-binding lectin, cigarette smoking.

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18
Q

How do you diagnose N. Meningitides?

A

Gold standard: culture from blood/CSF
Gram stain for gram - dipplococci
latex agglutination on CSF or urine
PCR (investigational)

*in meningococcal sepsis, gram stain of a punch biopsy of skin lesions is more sensitive (72%) than gram stain of CSF (22%) - and you get the results faster

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19
Q

Treatment of N. Meningitides

A

Antibiotics for 10-14 days

  • penicillin
  • *third generation cephalosporins (ceftriaxone) esp when there is PCN resistance
  • tx shock with fluids, vasopressors, ICU care
  • steroids?
20
Q

Prevention (if you were in close contact with someone with N. Meningitides - kissing, CPR, prolonged contact)

A

rifampin x2 days
IM ceftriaxone once
ciprofloxacin once (except in children)

Vaccination - MPSV4 (conjugated to diptheria toxoid) or MCV4
treats against serogroups A, C, Y, and W-135

21
Q

What are the characteristics of a strict anaerobe?

A
  • Can’t use O2
  • Unable to break down H2O2 (no catalase except in Bacteroides)
  • In presence of O2, toxic superoxide anions accumulate (no superoxide dismutase except in Bacteroides)
22
Q

What are the three key features of anaerobic bacterial infections?

  • where do they come from?
  • how many present in a bacterial infection?
  • clinical presentation?
A
  1. Anaerobes displaced from normal flora (skin, oral cavity, gut, female genital tract) into deeper sites can cause disease. Also trauma.
    - Brain abscesses typically involve anaerobic bacteria
  2. Multiple bugs usually present: polymicrobial - may facilitate anaerobic microenvironment.
  3. Foul smell!!!
23
Q

Clostridium: Gram stain? Spore/non spore? cocci/rod? anaerobe/aerobes? anything else?

Clostridia: define microscopic features of C. tetani, Gas gangrene clostridia, and C. botulinum

A

Gram + Spore forming rod anaerobe
-> spore looks like a dark circle within a circle within a circle

C. tetani: looks like tennis rackets ==o
Gas gangrene clostridia: rod ====
C. botulinum: =o=

24
Q

Which clostridia is the most common cause of invasive clostridial infections? Where is it found, what does it make that makes it clinically unique?

A

Clostridia Perfringens. Spores are found in the soil, organisms in the intestinal tract. It is highly metabolically active = makes lots of GAS => GAS GANGRENE

lecithinase/a-hemolysin - a phospholipase that kills cells and hemolyzes RBC in vitro and in vivo (unique!!). This leads to MUSCLE NECROSIS (no neutrophils, tissue blue/black)

25
Q

What are the lab findings of clostridia perfringens? How do you culture, what is unique about it etc

A

C. perfringens has lecithinase = causes lysis of RBC and will digest egg yolk in agar. also causes STORMY FERMENTATION in milk.

26
Q

Actinomyces: Gram +/-? spore/nonspore? cocci/rods? anaerobe/aerobe?

A

Gram + non-spore forming rod anaerobe forms chains

27
Q

How does Actinomyces grow in culture that’s unique? clinical feature?

A

looks like a TOOTH on agar: colony molar appearance. Clinically, it forms macro colonies that resembles GRAINS OF SAND that can be seen in abscesses and sinus tracts => SULFUR GRANULES

28
Q

What is the typical past medical history of a patient with actinomyces?

A

Actinomycosis is typically a chronic suppurative and granulomatous disease of the CERVIO-FACIAL - typically appears in patients with POOR ORAL HYGIENE or after invasive dental surgery, or in thoracic or abdominal areas.

  • typically requires TISSUE injury to begin infection (neglected gum hygiene)
29
Q

What is the clinical buzz word for Actinomyces presentation?

Treatment?

A

LUMPY JAW - typically from an infected tooth that travels down a sinus tract and pops out of the jaw.

Surgery for injured tissue, long term HIGH DOSE PENICILLIN

30
Q

Propionibacterium: Gram +/-? spore/nonspore? cocci/rods? anaerobe/aerobe?

What is the typical presentation?

A

Gram + non spore rod anaerobic.

ACNE. Can also cause infection of prosthetic devices.

31
Q

Bacteroides fragilis: where is it typically found? What type of infection does it cause? What is its main virulence factor?

A

Typically found in the female genital tract and colon.

Can cause abscess formation (typically intraabdominal), however is usually in a mixed infection

Polysaccharide capsule = anti-phagocytic.

32
Q

Bacteroides fragilis: Gram +/-? spore/nonspore? cocci/rods? anaerobe/aerobe? Other unique features?

A

Gram - non spore rod anaerobe (but is aero tolerant because it creates catalase and superoxide dismutase).

33
Q

Bacteroides fragilis: how do you culture that defines it as bactericides fragilis?

A
  • Grows in bile (bile-esculin agar): grows BLACK

- b-lactamase +

34
Q

What are some of the virulence factors of anaerobes? Are anaerobes innately invasive?

A

Virulence factors:
- digestive enzymes
- physical properties (polysaccharide capsules!)
- synergism: creates ideal anaerobic environment/blocks host defense
Especially with facultative organisms

No - anaerobes are NOT innately invasive.

34
Q

What are some of the virulence factors of anaerobes? Are anaerobes innately invasive?

A

Virulence factors:
- digestive enzymes
- physical properties (polysaccharide capsules!)
- synergism: creates ideal anaerobic environment/blocks host defense
Especially with facultative organisms

No - anaerobes are NOT innately invasive.

35
Q

What are some key facts about anaerobic infections above the waist?

A

These are primarily related to DENTITION
sinuses are in close proximity to dentition: can have decreased 02 concentration due to obstruction in respiratory infections = perfect for anaerobe infection!

typically SENSITIVE to most antibiotics!

35
Q

What are some key facts about anaerobic infections above the waist?

A

These are primarily related to DENTITION
sinuses are in close proximity to dentition: can have decreased 02 concentration due to obstruction in respiratory infections = perfect for anaerobe infection!

typically SENSITIVE to most antibiotics!

36
Q

What are some key facts about anaerobic infections below the waist?

A

These are typically due to GI or WOMEN GU normal flora

Typically more RESISTANT to antibiotics.

36
Q

What are some key facts about anaerobic infections below the waist?

A

These are typically due to GI or WOMEN GU normal flora

Typically more RESISTANT to antibiotics.

37
Q

What 4 classes of antibiotics are specific for anaerobes?

A

Penicillins
Carbapenems
Clindamycin
Metronidazole

37
Q

What 4 classes of antibiotics are specific for anaerobes?

A

Penicillins
Carbapenems
Clindamycin
Metronidazole

38
Q

Best method to treat anaerobic infections?

A

HEAL WITH STEEL
remove devitalized tissue/pus and expose remaining tissue to oxygen and good perfusion.

Use antibiotics secondary.

38
Q

Best method to treat anaerobic infections?

A

HEAL WITH STEEL
remove devitalized tissue/pus and expose remaining tissue to oxygen and good perfusion.

Use antibiotics secondary.

39
Q

How do you treat Appendicitis? Do you ever culture?

A

NO CULTURE - way too many organisms. Treat empirically with:

Ampicillin, Gentamicin, Clindamycin

Surgical drainage, debridement, tissue/organ removal

39
Q

How do you treat Appendicitis? Do you ever culture?

A

NO CULTURE - way too many organisms. Treat empirically with:

Ampicillin, Gentamicin, Clindamycin

Surgical drainage, debridement, tissue/organ removal

Faith's Multisystems module (12 decks)

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