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Microbiology > Gram positive Rods > Flashcards

Gram positive Rods Flashcards

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Biology 101 flashcards
1
Q

Corynebacterium diphtheriae

1.) Epidemiology

A

1.) Rare on account of wide vaccination
• Humans are the only reservoir
• Spread by respiratory droplets
Only clinically significant in areas lacking vaccination

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2
Q

Corynebacterium diphtheriae

2.) Pathogenesis

A

Exotoxin composed of fragments A and B
• B facilitates delivery of A to cell interior
• A toxin ADP-ribosylates (bowtie) the elongation factor EF-2 (Accordion)
• ADP-R::EF-2 is inactivated; peptide elongation stops; cell dies

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3
Q

Corynebacterium diphtheriae

3.) Clinical Significance

A

• Infection of the throat and nasopharynx; cervical adenopathy
• Dense, gray debris layer of cell debris forms pseudomembrane (Grey cotton candy w/ plastic covering)
• Cardiac and neurologic toxicities can occur (matador’s blanket is heart shaped)
- Cutaneous disease begins as erythematous pustule, which breaks down to form an ulcer covered with a gray membrane

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4
Q

Corynebacterium diphtheriae

4.) Identification

A
  • Lab identification on selective medium (Tinsdale’s agar)
  • Potassium tellurite is added to inhibit other flora
  • Organism produces black colonies with halos
  • Requires toxin identification
  • Methylene blue staining=polychromatic bands
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5
Q

Corynebacterium diphtheriae

5.) Treatment/Prevention

A

Neutralization of toxin: Diphtheria antitoxin is a horse-derived
hyperimmune antiserum that neutralizes circulating toxin
• 10% get “serum sickness”
• Prompt antibiotic coverage (erythromycin or penicillin)
• Prevention: Immunization using the inactivated toxin

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6
Q

Bacillus anthracis

1.) Epidemiology

A
  • Enzootic disease of world-wide occurrence (sheep, goats, etc)
  • Transmitted to humans by contaminated dust or contact with animal products (wool-sorter’s disease)
  • Veterinary vaccine makes domestic sources rare
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7
Q

Bacillus anthracis

2.) Pathogenesis

A

An*-phagocytic capsule is essential for full virulence
• Produces 3 lethal exotoxins encoded by plasmids
• Edema factor (adenylate cyclase that increase cAMP)
• Lethal toxin (tissue necrosis); protective antigen (cell entry)

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8
Q

Bacillus anthracis

3.) Clinical Significance

A
  • 95% of human cases are cutaneous: painless, swollen pustule with black eschar = “malignant pustule”
  • Sepsis can occur with a 20% mortality if untreated
  • Inhalation of spores can lead to hemorrhagic lymphadenitis with 100% mortality if untreated
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9
Q

Bacillus anthracis

4.) Identification

A
  • Blunt ended bacilli commonly in chains
  • Form endospores- oval and centrally located
  • Blood agar culture: large,grayish,nonhemolytic, nonmotile with an irregular border- facultative or strictly aerobic
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10
Q

Bacillus anthracis

5.) Tx/Prevention

A
  • Cutaneous anthrax: Doxycycline, ciproflaxin erythromycin
  • Multidrug, treatment for inhalation anthrax
  • Aggressive treatment is essential as it is rapidly fatal
  • Prevention: Cell free vaccine available for high risk individuals.
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11
Q

Listeria monocytogenes

1.) Epidemiology

A
  • Listeria monocytogenes is the only species that infects humans
  • Usually foodborne – high contamination rates esp. in poultry
  • Pathogen in pregnant women, neonates, infants & immunocompromised
  • 2500 cases; 27% in pregnant women- 450 deaths; 100 stillbirths
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12
Q

Listeria monocytogenes

2.) Pathogenesis

A
  • Phagocytosed bacteria escape vacuole via membrane damaging toxin
  • Reorganizes actin to create filament tail, pushing the bacterium to allow contact with adjacent cells
  • Direct transfer to adjacent cell evades immune response.
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13
Q

Listeria monocytogenes

3.) Clinical Significance

A

Most common clinical manifestation is diarrhea with fever, N/V
• Meningitis (newborn), bacteremia, septic arthritis can also occur
• Pregnant women can present with “flu-like” symptoms
• Defects in cell-mediated immunity can result in generalized infection

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14
Q

Listeria monocytogenes

4.) Identification

A
  • Blood agar: small beta-hemolytic colony with blue-green sheen
  • Aerobic and facultatively aerobic; non-spore-forming
  • Distinguished from streptococci by morphology, tumbling motility on LM in hanging drop and production of catalase.
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15
Q

Listeria monocytogenes

5.) Tx/Prevention

A

Antibiotics: Ampicillin with short course of gentamicin for synergy in serious infection.
• Prevention with proper food handling

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16
Q

Clostridium perfringens

1.) Epidemiology

A
  • Part of the normal flora of the large intestine, skin, and vagina
  • Spores are found in the soil
17
Q

Clostridium perfringens

2.) Pathogenesis

A

Secretion of exotoxins, enterotoxins and hydrolytic enzymes
• Exotoxin: α Toxin (phospholipase C) lyses ECs, WBCs, RBCs, and platelets
• Enterotoxin (affect intestinal function) alters cell membrane, disrupts ion transport, leads to loss of fluid and proteins; heat-resistant
• Degrada*ve enzymes: DNAse, hyaluronidase, collagenase,proteases

18
Q

Clostridium perfringens

3.) Clinical Significance

A

Myonecrosis occurs when spores are introduced to soft tissue;fermentation of tissue CHO yields gas and rapidly spreading infection
• Anaerobic cellulitis- necrotizing fasciitis
• Food poisoning: no fever; N/D abd pain 8-18H after eating; self-limited
• Enteritis necroticans- rare necrotizing bowel disease
• Clostridial endometritis- complication of incomplete abortion

19
Q

Clostridium perfringens

4.) Identification

A

Large, rod-shaped; non-motile, gram + rods
• Cultured anaerobically on blood agar, grows rapidly and has unique
“double zone” of hemolysis

20
Q

Clostridium perfringens

5.) Tx/Prevention

A
  • Early aggressive surgical treatment with debridement of devitalized tissue
  • Hyperbaric oxygen therapy
  • Penicillin is the antibiotic of choice
21
Q

Clostridium botulinum

1.) Epidemiology

A

Found worldwide in soil and aquatic sediments - spores frequently contaminate vegetables and meat
In a strictly anaerobic environment at neutral or basic pH, organisms germinates and exotoxin produced

22
Q

Clostridium botulinum

2.) Pathogenesis

A

Human disease caused by types A, B and E producing neurotoxic exotoxin
• Toxin is cleaved in axon terminals, light chain blocks acetylcholine release at synapse:: toxin is active at motor neuron endplates
• Flaccid paralysis results

23
Q

Clostridium botulinum

3.) Clinical Significance

A

Classic: food poisoning - difficulty focusing vision, swallowing (CN function)- no fever or sepsis. Bound toxin within nerve terminal is inaccessible.
• Progressive paralysis - leading to resp failure -mortality 15%
• Infant botulism: most common form in US - colonization of large intestine leading to constipation, feeding problems, lethargy- low mortality.
• May come from use of contaminated honey
• Wound botulism: rare - toxin effects at site of injury.

24
Q

Clostridium botulinum

4.) Identification

A

Standard anaerobic identification if isolated from food, stool or sterile site
• Toxin can also be detected – mouse bioassay, EIA

25
Q

Clostridium botulinum

5.) Tx/Prevention

A

Immediate antitoxin - trivalent (A,B,E) horse botulinum immune serum (BIG) or BabyBIG (human serum) plus supportive critical care
• Penicillin
• Infection never results in immunity

26
Q

Clostridium tetani

1.) Epidemiology

A
  • Common in barnyard, garden and other soils
  • Common infection from puncture wounds (e.g. splinter)
  • Immunization and sensitivity to oxygen makes it rare
27
Q

Clostridium tetani

2.) Pathogenesis

A
  • Growth of C. tetani is local but toxin spreads to CNS
  • Single gene product (tetanospasm) cleaved into A and B fragments
  • B fragments delivers A chain to neuron cytoplasm
  • A fragment blocks neurotransmitter release at inhibitory synapses causing severe prolonged muscle spasms
  • A fragment is a protease that cleaves synaptobrevin which abolishes NT release
28
Q

Clostridium tetani

3.) Clinical Significance

A
  • Incubation period from 4 days to several weeks
  • Presents as spastic paralysis ; precipitated by external stimulus
  • Early stages affect jaw muscles (lockjaw)
  • Death (15 - 60%(!)) results from paralysis - respiratory failure
29
Q

Clostridium tetani

4.) Identification

A

Treatment initiated based on clinical presentation - wound is often small and innocuous
• C. tetani has a characteristic morphology (racquet shaped bacillus)

30
Q

Clostridium tetani

5.) Tx/Prevention

A
  • Human tetanus hyperimmune globulin
  • Metronidazole
  • Vent support with trach
  • Immunization with tetanus toxoid; Booster every 10 years recommended.

Microbiology (4 decks)

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