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BMR 605 TEST 2 > Test 2 Bugs 1 Part 2/2 > Flashcards

Test 2 Bugs 1 Part 2/2 Flashcards

1
Q

Define Endospores:

A
  • Metabolically inert and antibiotic resistant.
    • Allows survival in adverse conditions.
  • Calcium dipicolinate dehydrates nucleic acids.
  • Keratin coat protects.
  • Need an autoclave to kill spores.
  • Limited carbon or nitrogen triggers sporulation.
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2
Q

Bacillus anthracis traits

A
  • Aerobes & facultative anaerobes
  • Catalase: Positive
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3
Q

Three types of Bacillus anthracis infections?

A
  • Cutaneous
  • Gastrointestinal
  • Inhalation
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4
Q

Cutaneous anthrax details

A
  • Most human cases
  • Hazard for work with hooved animals, their skins or wools.
  • Process:
    • Traumatic Spore impantation
    • Papule
    • Raised red lesion
    • Painless, black, necrotic eschar with a red, rolled edge.
  • Edema + Lymphadenopathy.
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5
Q

Gastrointestinal anthrax details.

A
  • Rare
  • Spores in contaminated meat
    • GI ulcers + edema.
  • Nausea, fever, abdominal pain, vomiting blood, and diarrhea.
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6
Q

Inhalation anthrax details:

A
  • Woolsorter’s disease
  • Rapid, hemorrhagic lymphadenitis and pneumonia.
  • Exotoxin ⇢ lymph node hemorrhage and edema, hemorrhagic mediastinitis, pulmonary edema, and hemorrhagic pleural effusions. A widened mediastinum is a critical diagnostic feature.
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7
Q

How does Bacillus anthracis to inhibit phagocytosis?

A

Poly-D-glutamate capsule

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8
Q

Anthrax toxin:

Protective antigen (PA)

A

Binds to cells and facilitates entry of lethal factor and/or edema factor.

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9
Q

Anthrax toxin:

Lethal factor (LF)

A

Metalloprotease of MAP kinase (needed of cell signaling, cell division and differentiation) → cell death.

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10
Q

Anthrax toxin:

Edema Factor (EF)

A
  • Calmodulin-activated adenylate cyclase that increases cAMP (changing membrane permeability).
  • Cell water loss → pulmonary/other edema.
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11
Q

Anthrax Toxin details

A
  • Three types:
    • Protective antigen (PA)
    • Lethal factor (LF)
    • Edema factor (EF)
  • Non-toxic individually but form important toxin when combined.
    • PA+LF = Lethal Toxin
    • PA+EF = Edema Toxin
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12
Q

Treatment and prevention of B. anthracis

A
  • Prevention:
    • Vaccination of animal proper disposal of infected.
    • Human Vaccination is limited to those at risk.
  • Treatment
    • Prompt treatment with amoxicillin if penicillin sensitive.
      • Otherwise use Ciprofloxacin
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13
Q

Bacillus cereus natural environment

A

Ubiquitous soil organism found in grains, vegetables, and dairy products.

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14
Q

Bacillus cereus details:

A
  • Most common pathogenic bacilli
  • B. cereus food poisoning
    • Emetic form
      • heat-stable enterotoxin ingested in reheated foods.
      • Rapid onset: 1 to 5 hours after eating toxin-contaminated food.
    • Diarrheal form
      • Heat-labile enterotoxin produced by bacteria multiplying in the GI tract following ingestion of contaminated food.
      • Slow onset: 10 to 15 hours
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15
Q

Listeria: Listeria monocytogenes traits

A
  • Tumbling motility
  • Facultative anaerobes
    • Grow in:
      • Acid
      • High salt
      • Cold temps
  • Grow in cell lining of GI or inside macrophages.
    • Poor CMI (Cell mediated immunity)
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16
Q

Listeria

In adults:

A

Often from contaminated food (undercooked meat, unwashed vegetables, un-pasteurized milk.

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17
Q

Listeria

In neonates:

A

Transplacental or vaginal transmission.

18
Q

Treatment for listeria?

A

Ampicillin

19
Q

Two results of Listeria infection in adults?

A
  • Mild gastroenteritis in the summer.
    • Some people remain fecal carriers
  • Meningitis in immunocompromised (Most common)
    • Renal transplant
    • Newborns
    • Pregnant women
    • those >65 yrs.
20
Q

Two forms of Neonatal listeriosis?

A
  • Granulomatosis infantiseptica: severe in utero infection from Listeria
    • Most babies are stillborn or die soon after birth.
  • Late-onset disease: Acquired at or soon after birth by contact with contaminated body fluids of infected mother.
21
Q

Listeria monocytogenes

Immune avoidance:

A
  • Ingest L. monocytogenes → intestines → uptake into epithelial cells.
  • Listeriolysin forms pores and escapes phagosome before fusion occurs.
  • Multiplies in cells with poor CMI.
22
Q

What are the 4 types of Clostridium and their associated toxins?

A
  1. C. tetani (tetanus)
    1. Tetanus toxin (tetanospasmin)
  2. C. perfringens (wound infection, food poisoning)
    1. Alpha toxin
  3. C. botulinum (botulism)
    1. Botulinum toxin
  4. C. difficile (diarrhea after antibiotic use)
    1. Toxin A = an enterotoxin
    2. Toxin B = a cytotoxin that induces depolymerization of actin & cell cytoskeleton loss.
23
Q

Effect of Tetanus toxin

A

Blocks the release glycine + GABA, which inhibit motor nerve impulses, resulting in spastic paralysis.

24
Q

Effect of Alpha Toxin

A

Fermentation of muscle carbohydrates which produces gas.

25
Q

Effect of Botulinum toxin

A

Acts on myoneural junctions, blocking the release of acetylcholine → flaccid paralysis.

26
Q

Effect of Toxin A and B.

A
  • Toxin A: Mucosal injury and hemorrhagic necrosis.
  • Toxin B: Cytotoxin, that induces depolymerization of actin and cytoskeleton loss.
27
Q

C. tetani Infection

A
  • Paralysis begins in jaw (trismus/lock-jaw, risus sardonicus) and descends into large muscle groups (back arching).
  • Death from paralysis of throat & respiratory muscles.
28
Q

C. tetani

Prevention and treatment

A
  • Vaccines: Tetanus toxoid vaccines DTaP, Tdap, DT, Td.
  • Treatment: Wound debridement
    • Metronidazole; tetanus immune globulin
    • Benzos or neuromuscular blockers until toxin wears off.
29
Q

C. perfringens

Infections

A
  • Wound infection: results in Gas gangrene (anaerobic cellulitis), clostridial myonecrosis.
  • Food poisoning: watery diarrhea, late onset 8-24 hrs after ingestion. No vomiting. Resolves in 24h.
    • Since toxin is not preformed such as in S. aureus/ B. cereus, onset is delayed.
30
Q

C. botulinum

Infection

A
  • Foodborne botulism:
    • Produced in poorly canned vegetables.
      • 12-48hrs after meal.
    • Neurological, not GI
  • Infant botulism
    • Spores ingested in dust or honey.
    • Results in Floppy baby syndrome.
  • Wound botulism: similar to food botulism.
  • Treatment:
    • Antitoxin blocks circulating toxin, but cannot effect that already in the nerves.
31
Q

C. difficile

Infection

A
  • Environmental - spores transferred to patients.
  • Endogenous ~5% of adults carry it.
    • Anti-biotics allow it to overgrow other bacteria.
      • Pseudomembrane formation (white-yellow plaques).
  • Treatment: Metronidazole; oral vancomycin
    • Stool transplant or surgery in severe cases.
32
Q

Corynebacterium diphtheriae

Details

A
  • Catalase: positive
  • aerobic
  • Human is reservoir host.
  • Can be grown on Loeffler coagulated serum medium; tellurite medium.
  • Spread: Respiratory droplets or skin contact.
33
Q

Cornebacterium diphtheria: explain how while normally present can turn pathogenic.

A

C. diphtheria only creates toxin (A-B toxin) when the bacteria is infected by corynephage beta through lysogenic conversion (transduction).

No phage = no toxin = no disease.

34
Q

Describe Respiratory Diphtheria:

A
  • 2-6 days incubation
  • Toxin absorbed and disseminated → myocarditis, cardiac dysfunction, and laryngeal nerve palsy.
    • Death from respiratory obstruction or cardiac failure.
35
Q

Describe Cutaneous diphtheria:

A

Acquired by skin contact, forming nonhealing ulcer, toxin can cause systemic effects.

36
Q

Corynebacterium diphtheria

Vaccines

A

Diphtheria toxoid vaccines: DTaP, Tdap, DT, Td.

37
Q

Gardenerlla: Gardnerella vaginalis

Details:

A
  • Main organism in bacterial vaginosis.
    • Disease is the most common vaginal infection.
    • Occurs due to disruption of normal flora.
      • Lactobacillus maintains acidic environment.
    • Tested by positive amine test
      • Fishy smell
  • “clue cells” help differentiate it from Trichomonas vaginalis.
  • Due to low inflammatory changes, it is a vaginosis rather than a vaginitis.
  • Treatment of choice is metronidazole.
38
Q

Cutibacterium (Propionibacterium) acnes

Details:

A
  • Gram+ and normally found on skin.
  • Lives on glycerol from sebum.
  • Acne
    • Cutibacterium produce lipases which digest sebum but also release proinflammatory fatty acids, results in pustule or nodule formation (comedones).
  • Treatment: Benzoyl peroxide and vitamin a (to reduce keratin production)
39
Q

Actinomyces: Actinomyces israelii

A
  • Anaerobe
  • Bacilli, to branched, filamentous forms (looks like fungi).
  • Normal mucosal flora in gingival crevices, the female genital tract and gastrointestinal tract.
  • Endogenous infection from trauma that compromises tissue blood flow allows penetration.
  • Cervicofacial (“lumpy jaw” from tooth extraction), thoracic, abdominal, or pelvic abscesses (interuterine device)
    • Can result in hard yellow microcolonies (sulfur granules). Brain abscesses occur. Often misdiagnosed as neoplasms.
40
Q

Nocardia Details:

A
  • Obligate aerobe
  • Partially acid-fast (have mycolic acid in cell wall)
  • Catalase: Positive
  • Urease: Positive
41
Q

3 types of Nocardia infection and details:

A
  • Pulmonary nocardiosis
    • Inhalation
    • In patients with low WBC or CD4+
    • Not contagious
  • Immunocompetent patients: Cutaneous or subcutaneous infections
    • Ulcers & Cellulitis.
  • Rare other infections
    • Brain abscesses
    • Bacteremia

BMR 605 TEST 2 (10 decks)

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