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Foundations Exam 3 > Gram+ Rods > Flashcards

Gram+ Rods Flashcards

1
Q

of the Gram+ rods, name 2 non-spore forming species and 3 spore-forming species

A

non-spore forming:
1. Corynebacterium (C. diphtheriae)
2. Listeria monocytogenes

spore-forming:
1. Bacillus (B. anthracis, B. cereus)
2. Clostridial (C. perfringens, C. botulinum, C. tetani)
3. Clostridioides difficile

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2
Q

Where does Corynebacterium diphtheriae come from and how does it spread? (Gram+ rod)

A

humans are only reservoir, spread via respiratory droplets or contact

only clinically significant in areas lacking vaccination, otherwise rare

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3
Q

What is the effect of the exotoxin produced by Corynebacterium diphtheriae? (Gram+ rod)

A

B fragment delivers A by binding to cell membrane proteins CD-9 and Heparin-binding EGF

A toxin ADP-ribosylates elongation factor EF-2 to inactive —> protein synthesis disrupted

just 1 exotoxin molecule completely terminates cell protein synthesis!

[Step 1 note: low iron induces toxin expression, high iron suppresses]

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4
Q

what are the clinical characteristics of infection by Corynebacterium diphtheriae? (Gram+ rod)

A

infects throat/ nasopharynx —> respiratory illness, typically beginning with sore throat

dense/grey layer of cell debris forms pseudomembrane, “bull neck” due to lymphadenopathy

systemic toxin —> myocarditis (major cause of mortality) and neurologic toxicities

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5
Q

how can Corynebacterium diphtheriae be cultured and identified? (Gram+ rod)

A

Tinsdale’s agar: selective medium with potassium tellurite to inhibit respiratory flora

organisms produce black colonies with halos

microscope: “coryneform” (club-shaped)

diagnosis requires confirmation of toxin production

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6
Q

how is Corynebacterium diphtheriae (Gram+ rod) treated?

A

!neutralize toxin! with Diphtheria anti-toxin

Rx: Erythromycin or penicillin

prevention: immunization using inactivated toxin

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7
Q

where does Listeria monocytogenes (Gram+ rod) come from and what populations are especially at risk?

A

only Listeria that infects humans, usually food born (poultry, cheese, ice cream)

very serious for pregnant women, neonates, infants, immunocompromised

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8
Q

how does Listeria monocytogenes (Gram+ rod) invade the body?

A
  1. escape phagolysosome via Listeriolysin O toxin
  2. reorganize actin to create tail and pushes into adjacent cells (direct transfer evades immune response)

facultative intracellular pathogen - immunity is therefore cell-mediated

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9
Q

describe the clinical manifestations of Listeria monocytogenes (Gram+ rod)

A

most commonly mild diarrhea with fever

in at risk populations:
- neonates —> meningitis, septic arthritis
- pregnant women —> flu-like, pre-term delivery
- defects in cell mediated immunity —> generalized infection

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10
Q

how can Listeria monocytogenes (Gram+ rod) be cultured and distinguished?

A

beta-hemolytic with blue-green sheen on blood agar

tumbling motility on LM in hanging drop culture (culture in tube)

can survive with or without oxygen

produces catalase

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11
Q

how is Listeria monocytogenes (Gram+ rod) treated?

A

Ampicillin

prevent with proper food handling (contracted via poultry, cheese, ice cream)

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12
Q

of these spore-forming Gram+ rods, which is an aerobe?
a. Bacillus
b. Clostridia
c. Clostridioides

A

a. Bacillus (B. anthracis, B. cereus) is aerobe

b. Clostridia (C. perfringens, C. tetani, C. botulinum) and (c.) Clostridioides are anaerobes

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13
Q

how is Bacillus anthracis (spore-forming Gram+ rod) contracted?

A

zoonotic (sheep, goats, etc) transmitted to humans via contaminated dust or contact with animal products

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14
Q

what is essential for virulence of Bacillus anthracis (spore-forming Gram+ rod), and what is unique about it?

A

anti-phagocytic capsule composed of proteins (NOT polysaccharides)

essential for full virulence!

[B. anthracis also produces Edema toxin and Lethal toxin, which require protective antigen for cell entry]

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15
Q

what 2 toxins does Bacillus anthracis (spore-forming Gram+ rod) produce, and what do they require?

A
  1. Edema toxin: adenylate cyclase, increase in cAMP —> widespread leak of fluid from capillaries
  2. Lethal toxin —> tissue necrosis

both require protective antigen for cell entry

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16
Q

what are the clinical manifestations of Bacillus anthracis (spore-forming Gram+ rod) infection?

A

mostly cutaneous - painless, swollen pustule with black eschar (“malignant pustule”), sepsis if untreated

inhalation of spores —> hemorrhagic mediastinitis (100% mortality without treatment)

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17
Q

how can Bacillus anthracis (spore-forming Gram+ rod) be cultured and how does it appear morphologically?

A

non-hemolytic on blood agar with “comma shape” colonies

blunt-ended in chains with centrally-located endospores - appearance of bamboo

facultative or strictly aerobic

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18
Q

how is Bacillus anthracis (spore-forming Gram+ rod) treated? specify for cutaneous and inhalation anthrax

A

cutaneous anthrax: Doxycycline, ciproflaxin, erythromycin

inhalation anthrax: Ciprofloxacin + clindamycin

aggressive and fast treatment

prevention: cell-free vaccine available for high risk individuals

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19
Q

where does Bacillus cereus (aerobic Gram+ rod, spore-forming) infection come from?

A

food born (think “cereal”)

*intoxication rather than infection

emetic form associated with spore-contaminated rice

20
Q

Of Clostridia (obligate anaerobe Gram+ rods, spore-forming), which of these species is invasive?
a. C. tetani
b. C. botulinum
c. C. perfringens

A

c. C. perfringens - invasive

C. tetani and C. botulinum are toxin-forming

*note that all these species synthesize potent exotoxins

21
Q

what genus of bacteria does this describe?
- spore-forming
- obligate anaerobes
- form endospores
- synthesize potent exotoxins
- produce large, raised colonies on blood agar
- single or double zones of hemolysis
- can ferment sugar or digest proteins

A

Clostridia: Gram+ rod

22
Q

where can Clostridium perfringens (spore-forming Gram+ rod) be found?

A

normal flora of large intestine, skin, vagina

spores found in soil

*note Clostridium are obligate anaerobes (damaged by oxygen) and can ferment sugar or digest protein

23
Q

what is the purpose of alpha toxin of Clostridium perfringens (spore-forming Gram+ rod)?

A

alpha toxin (phospholipase C): lyses WBCs, RBCs, platelets

also produces heat-resistant enterotoxin (loss of fluids, proteins), degradative enzymes (DNAase, hyaluronidase, collagenase, protease)

24
Q

what are the clinical characteristics of Clostridium perfringens (spore-forming Gram+ rod) infection?

A

myonecrosis when spores introduced to soft tissue - fermentation yields gas, gas gangrene, life-threatening

food poisoning: no fever, self-limited

clostridial endometritis: complication of incomplete abortion

25
Q

how is Clostridium perfringens (spore-forming Gram+ rod) cultured?

A

anaerobically on blood agar - unique double zone of hemolysis (complete + partial ring of hemolysis)

26
Q

how is Clostridium perfringens (spore-forming Gram+ rod) treated?

A

early aggressive debridement of devitalized tissue, hyperbaric oxygen therapy, combo antibiotics

27
Q

where is Clostridium botulinum (spore-forming Gram+ rod) found?

A

soil, aquatic sediments, spores in vegetables and meat (especially home-canned) - most cases due to toxin ingestion (food poisoning)

produce toxin in anaerobic and neutral/basic pH environment —> toxin is what causes disease

(“toxin-forming” type of Clostridia, versus invasive)

28
Q

how does Clostridium botulinum (spore-forming Gram+ rod) cause disease?

A

via neurotoxic exotoxin - cleaves SNARE proteins that allow vesicle docking and NT release

light chain blocks Ach release (toxin is active at neuron end plates) —> flaccid paralysis

affects skeletal muscle and parasympathetic nervous system

[recall that somatic/skeletal muscle and parasympathetic nerves have Ach presynaptically, and all postsynaptic are Ach]

29
Q

how does Botulism, caused by Clostridium botulinum (spore-forming Gram+ rod), present?

(not in infants or from wounds)

A

botulism —> loss of somatic motor nerves and parasympathetic motor nerves (toxin affects somatic and parasympathetic nerves)

symmetric neurological deficits - double vision, difficulty swallowing, flaccid paralysis (progressive, can lead to respiratory failure), ptosis, pupillary dilation, loss of intestinal peristalsis, etc

preserved cognitive responsiveness and sensation

Dyplopia, Dysarthria, Dysphagia, Dyspnea

30
Q

what is the most common form of Botulism in the US?

A

infant botulism: constipation, lethargy, hypotonia

associated with honey

caused by Clostridium botulinum (spore-forming Gram+ rod)

31
Q

how is Clostridium botulinum (spore-forming Gram+ rod) infection diagnosed?

A

by detecting the toxin (not the organism), either in serum/stool/leftover food

32
Q

how is Clostridium botulinum (spore-forming Gram+ rod) infection treated?

A

immediate antitoxin! Botulinum toxin is super potent

infection never results in immunity

33
Q

where is Clostridium tetani (spore-forming Gram+ rod) found and contracted?

A

barnyard, garden, other soils

common infection from puncture wounds (spores need to be deeply inoculated into tissue because C. tetani is strictly anaerobic)

34
Q

what causes illness by Clostridium tetani (spore-forming Gram+ rod)? how does it present?

A

toxin-producing type of Clostridium - growth of bacteria is local but neurotoxin spreads to CNS

single gene product (tetanospasm) cleaved into A and B fragments - B delivers A into neuron cytoplasm

A fragment blocks GABA or glycine release at inhibitory synapses —> spastic paralysis, lockjaw, autonomic hyperactivity, respiratory failure

[incubation period 4 days to several weeks]

35
Q

how does paralysis caused by Clostridia botulinum compare to that caused by Clostridia tetani? explain why these differences occur

A

C. botulinum: Botulinum toxin blocks Ach release at somatic and parasympathetic motor nerve terminals —> flaccid paralysis

C. tetani: Tetanus toxin blocks GABA/glycine release at inhibitory synapses —> spastic paralysis (disinhibition of motor nerves)

36
Q

what is the shape of Clostridium tetani?

A

Clostridium tetani: spore-forming Gram+ rod, obligate anaerobic

racquet-shaped bacillus

37
Q

what is recommended regarding immunization against Clostridium tetani (spore-forming Gram+ rod)?

A

immunization with tetanus toxoid + booster every 10 years

can also give tetanus immune globulin if no history of immunization with toxoid (or ineffective immune system)

infection does not confer immunity because lethal dose is lower than immunogenic dose

38
Q

what bacteria species does this describe?
- spore-forming
- strictly anaerobic
- aggressive nosocomial pathogen
- causes antibiotic-associated colitis
- minor component of GI flora

A

Clostridioides difficile: anaerobic Gram+ rod, spore-forming

spores acquired via fecal-oral route but doesn’t typically germinate until antibiotic use disrupts normal GI flora

associated with use of proton pump inhibitors (decreased acid production in stomach = more spore survival)

39
Q

what do the toxins of Clostridioides difficile (Gram+ rod, spore-forming) do?

A

produce Toxin A and B: glycosylate/inactive Rho family proteins —> damage epithelial cells, producing pseudomembrane

toxin levels correspond to severity of disease

40
Q

what is the clinical manifestation of Clostridioides difficile (Gram+ rod, spore-forming) infection?

A

Clostridioides difficile is toxin-producing (rather than invasive), so illness is due to Toxin A and B (inactive Rho proteins)

causes watery diarrhea following antibiotic therapy (disrupts GI flora, allowing C. difficile germination)

“antibiotic-associated colitis” with high WBC count and sepsis

41
Q

how is Clostridioides difficile (Gram+ rod, spore-forming) diagnosed?

A

hard to culture, very sensitive to oxygen (anaerobic)

pseudomembranes in large intestine, antigen detection in stool

NAAT (nucleic acid amplification test) used to detect gene that encodes Toxin B

42
Q

what type of Gram+ bacteria grow as branching filaments? (2)

A

Nocardia: aerobic (N. asteroides)

Actinomyces: anaerobic (A. israelii)

43
Q

where is Nocardia asteroides (branching Gram+) found, how is it transmitted, and where does it infect the body?

A

exogenous: soil, water

transmitted via respiratory route, contamination of skin lesion

infects lung, brain

44
Q

where is Actinomyces israelii (branching Gram+) found, how is it transmitted, and where does it infect the body?

A

endogenous: normal flora

transmitted via endogenous source

infects oral cavity, abdomen, female GU tract

45
Q

what is the typical clinical manifestation of infection with either Nocardia asteroides or Actinomyces israelii?

A

tend to cause abscesses - masses of bacteria in pus are yellow (“sulfur granules”)

culture required to identify species

Foundations Exam 3 (28 decks)

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