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COPY FDN3 By Nathan and Minnie > Gram Positive Bacteria > Flashcards

Gram Positive Bacteria Flashcards

1
Q

Which compounds determine the pathogenicity of Staphylococcus aureus?

A
  • Toxic shock syndrome toxin 1 (TSST-1)
  • Staphylococcal enterotoxins A-E, G-I
  • Exfoliatin (exfoliative toxin)
  • Alpha toxin (alpha-hemolysin)
  • Panton-Valentine leukocidin (PVL)
  • Coagulase
  • Protein A
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2
Q

Why are Staphylococcal enterotoxins A-E and G-I relevant?

How do they exert their effects?

Why are they hard to kill?

A

Cause staphylococcal food poisoning and toxic shock syndrome

Superantigens

Act directly on neural receptors in upper GI tract, stimulating vomiting center in brain to cause vomiting 2-5 hrs after ingestion

Resistant to boiling for 30 minutes and digestive enzymes

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3
Q

What kind of toxin is alpha-toxin from Staphylococcus aureus?

What kind of factor alpha-toxin an example of?

A

Pore-forming toxin

(inserts into lipid bilayers of mammalian cells, forms pores, causes cell death and tissue destruction)

Hemolysin

(lyses RBCs when bacteria are grown on blood agar plates, thought to lyse other types of cells during infections or disrupt intercellular junctions in epithelial barriers)

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4
Q

What is the function of coagulase from Staphylococcus aureus?

How does it work?

A

polymerizes fibrin to form clots, block neutrophils

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5
Q

What is the function of Protein A from Staphylococcus aureus?

How does it work?

A

Prevents antibody-mediated immune clearance

Binds to Fc portion of IgG molecules

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6
Q

What clinical diseases does Staphylococcus aureus cause?

A
  • Joint and bone infections
  • Endocarditis
  • Toxic shock syndrome
  • Staphylococcal food poisoning
  • Scalded skin syndrome
  • Skin and soft tissue infections
  • Hospital-acquired infections (nosocomial)
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7
Q

What are the symptoms of toxic shock syndrome from Staphylococcus aureus?

What tends to occur upon resolution of toxic shock syndrome?

What is this illness most associated with?

What is this illness also associated with?

Are blood cultures positive or negative?

A

High fever, vomiting, diarrhea, sore throat, muscle pain, rash, hypotension or shock that can lead to organ failure

Desquamation of skin, especially digits

Most common cause: tampon use (strains that colonize vagina and produce TSST-1)

Wound infections (S. aureus enterotoxins or TSST-1 are the cause)

Blood cultures are negative

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8
Q

What is the difference between a furuncle and a carbuncle?

A

Furuncles are boils, most of which begin with the blockage of hair follicle or sweat gland that subsequently becomes infected

Carbuncles are multiple abscesses formed after infection spreads from a furuncle

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9
Q

How can you differentiate Staphylococcus aureus from streptococci using a lab test?

A

Staphylococcus aureus is catalase positive

Streptococci are catalase negative

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10
Q

How can you differentiate Staphylococcus aureus from Staphylococcus epidermidis and Staphylococcus saprophyticus on a lab test?

A

Staphylococcus aureus is coagulase positive

Staphylococcus epidermidis and Staphylococcus saprophyticus are coagulase negative

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11
Q

Enterococci are [Gram, shape]

A

Enterococci are Gram-positive cocci

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12
Q

Which species of Enterococci are medically important?

Which is more common?

Which is more resistant to antimicrobials?

A

Enterococcus faecalis and E. faecium

E. faecalis is more common

E. faecium is more resistant to antimicrobials

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13
Q

Describe the treatment strategy for Enteroccoci

A
  • Penicillin/ampicillin (usually w/ aminoglycosides)
  • If resistant to penicillin/ampicillin, use vancomycin
  • If resistant to vancomycin, use linezolid or daptomycin
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14
Q

What procedure is important to order after Streptococcus gallolyticus infection? Why?

A

Colonoscopy to rule out colon cancer

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15
Q

How are streptococci grouped?

A

By hemolysis

Alpha hemolysis: partial hemolysis, greenish tint (viridans, pneumoniae)

Beta hemolysis: complete hemolysis, clear color; Group A, Group B, Group D groups based on cell wall carbohydrate antigens (pyogenes, agalactiae)

(Note: Group D usually has gamma hemolysis) (grp D is gallolyticus)

Gamma hemolysis: Group D; no hemolysis

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16
Q

Describe Streptococcus pneumoniae

(Hemolysis, growth, clinical significance)

A
  • Alpha-hemolytic
  • Grows as diplococci on gram-stained specimen
  • Causes pneumonia, other respiratory tract infections
  • Virulence factors
    • Capsule: Prevents phagocytosis
    • Pneumolysin: degrades hemoglobin to a green pigment
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17
Q

What is the most clinically relevant group B streptococcus?

(Hemolysis, clinical significance)

A

Streptococcus agalactiae

Beta-hemolytic

  • Causes neonatal sepsis, meningitis
  • Colonizes the vagina; passed to the newborn during delivery
  • Women who are GBS (+) are treated with penicillin or vancomycin prior to delivery
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18
Q

Describe the appropriate course of treatment for a Streptococcus pyogens infection

A
  • Penicillin = treatment of choice
    • Most strains are sensitive
  • If STSS
    • Treat with penicillin + clindamycin (inhibits SPE production)
    • Give IVIG: Contains aintbodies against toxins
  • If necrotizing fasciitis
    • Treat with penicillin + clindamycin (inhibits SPE production)
    • Surgical debridement necessary
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19
Q

List the relevant toxins associated with Streptococcus pyogenes

A
  • Streptolysin (SLO)
  • M Protein
  • Streptococcal pyogenic endotoxins (SPEs)
  • Streptokinase
  • C5a Peptidase
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20
Q

List the clinical diseases associated with Streptococcus pyogenes

A
  • Streptococcal pharyngitis
  • Scarlet Fever
  • Streptococcal Toxic Shock Syndrome (STSS)
  • Necrotizing fasciitis
  • Impetigo
  • Cellulitis
  • Rheumatic Fever
  • Post-streptococcal glomerulonephritis (PSGN)
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21
Q

Describe the relevant clinical findings of post-streptococcal glomerulonephritis (PSGN)

A
  • Onset 2 weeks after the initial S. pyogenes infection
    • Early treatment of strep throat does not prevent PSGN (vs for rheumatic fever it would)
  • Damage due to accumulation of SLO antibodies/antigens in the kidney
  • Can follow pharyngitis OR soft tissue infection
  • Associated with edema, hypertension, hematuria, proteinuria
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22
Q

How is rheumatic fever diagnosed?

A

Use JONES criteria

  • J - Joints (polyarthritis)
  • O - Heart problems (think of the O as a heart shape)
  • N - Nodules (subcutaneous)
  • E - Erythema marginatum (rash w/thick red border)
  • S - Sydenham’s chorea (rapid involuntary movements, especially in hands and face)

Look for SLO antibodies as evidence of a recent S. pyogenes infection

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23
Q

Describe the effects of streptococcal pyogenic endotoxins (SPEs)

A

SPEA, SPEC (super antigens, carried on phage) -> Scarlet Fever, STSS

SPEB (protease, cleaves tissue proteins) -> Necrotizing fasciitis

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24
Q

How would you differentiate between TSS and STSS?

A

TSS: Caused by Staphylococcus aureus

  • Rash
  • Associated with tampon use

STSS: Caused by Streptococcus pyogenes

  • No rash
  • Not associated with tampon use
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25
Q

What is streptokinase?

Why is it significant?

A

Streptokinase is virulence factor associated with streptococcus pyogenes

It causes lysis of fibrilin clots by converting plasminogen to plasmin

  • Bad: causes bacteria to spread
  • Good: Therapeutic uses in lysing coronary artery clots in acute myocardial infarction
26
Q

What is C5a peptidase?

What does it do?

A

A virulence factor associated with Streptococcus pyogenes

It is an extracellular enzyme that cleaves C5a (a complement component)

  • This prevents the recruitment of phagocytes to bacteria
27
Q

Bacillus spp. are [metabolic, Gram stain, shape, important characteristc]

A

Bacillus spp. are aerobic Gram-positive rods that form spores

28
Q

Bacillus anthracis is a [metabolic, Gram stain, shape, features of growth, important characteristic]

A

Bacillus anthracis is aerobic Gram-positive rods that grows in chains (bamboo rods/box cars) and forms spores

29
Q

What are the determinants of pathogenicity of Bacillus anthracis?

Where are they found?

A
  • Anthrax toxin (an AB toxin)
  • Capsule composed of poly-D-glutamic acid

Both found on a plasmid

30
Q

How do A-B toxins work?

A

Fragment B (binding) binds to surface of cells and transports Fragment A into cells

Fragment A (active) has activity that damages cell

31
Q

What kind of toxin is anthrax toxin?

Describe the structure of anthrax toxin

A

A-B toxin

Actually two toxins that share the same B subunit

A subunit: edema factor (adenylate cyclase, increase cAMP)

and lethal factor (cleaves host kinases, lyse/inactivate immune cells)

B subunit: protective antigen (forms pore for A subunit entry)

32
Q

How does cutaneous anthrax occur?

Describe the symptoms of cutaneous anthrax

How does cutaneous anthrax resolve?

A

Spores introduced into skin through cuts or abrasion exposed to contaminated carcasses or through fly bites

Small red papule enlarges to form an ulcer w/ blackened necrotic eschar surrounded by expanding zone of edema, painless, may be surrounded by small satellite vesicles

Spontaneously resolves

33
Q

How does inhalation anthrax (Woolsorters’ disease) occur?

Describe the symptoms of inhalation anthrax

What disease does inhalation anthrax resemble?

How does inhalation anthrax resolve?

A

Spores inhaled often during handling of contaminated hides, hair, or wool

Fever, shortness of breath, hypotension

Resembles the flu

Death

(large hemorrhagic mediastinal lymph nodes are common, organisms sometimes seen on blood smear)

34
Q

What is a telltale symptom of inhalation anthrax on xray?

A

Widened mediastinum

35
Q

How is Bacillus anthracis treated?

A
  • Sensitive to penicillin
  • Ciprofloxacin and doxycycline are recommended due to concerns about weaponized strains resistant to penicillin
  • Second agent added for inhalational anthrax (rifampin, vancomycin, pencillin, clarithromycin)
  • Raxibacumab and oblitoxaximab for inhalational anthrax
36
Q

Listeria monocytogenes are [Gram stain, metabolic, shape, intra/extracellular]

A

Listeria monocytogenes are Gram-positive facultatively anaerobic rod-shaped bacteria that are facultatively intracellular

also beta-hemolytic, catalase positive, and has tumbling motility

37
Q

What clinical diseases does Listeria monocytogenes cause?

A
  • Asymptomatic or influenza-like illness in pregnant women (but can cause abortion, premature delivery, bacteremia)
  • Neonatal disease (early or late onset)
  • Mengitis in elderly or immunocompromised individuals
38
Q

Corynebacteria diptheriae is a [metabolic, Gram stain, shape, distinctive morphology]

A

Corynebacteria diptheriae are aerobic Gram-positive bacilli that can have an irregular swelling at one end (club shape) under certain growth conditions

39
Q

How is Corynebacteria diptheriae maintained in humans?

What are the hosts for Corynebacteria diptheriae?

A

Asymptomatic carriage in immune humans

Humans are the only host

40
Q

What type of toxin is diphtheria toxin?

What carries diphtheria toxin?

A

Both A-B toxin and ADP-ribosylating toxin

Carried on integrated bacteriophage

41
Q

List examples of ADP-ribosylating toxins

A
  • Diphtheria toxin of Corynebacteria diptheriae
  • Exotoxin A of Pseudomonas aeruginosa
  • Cholera toxin of Vibrio cholerae
  • Heat labile toxin of Escherichia coli
  • Pertussis toxin of Bordetella pertussis
42
Q

What is a prominent indicator of diphtheria?

A

Thick grey adherent pseudomembrane observed on mucosa of oropharynx, palate, nasopharynx, nose, or larynx

(composed of necrotic cell debris, fibrin, and blood cells that accumulate after cell damage caused by diphtheria toxin)

43
Q

How is Corynebacteria diptheriae diagnosed on lab test?

A
  • Gram stain of smears: bacteria lie in clusters at acute angles (Chinese letter) or parallel groups (palisade)
  • Gray to black colony on specialized medium containing tellurite that inhibits growth of most upper respiratory bacteria
44
Q

How is Corynebacteria diptheriae treated?

A
  • Horse antisera against diphtheria toxin
  • Patients monitored for respiratory or cardiac failure
  • Antibiotics given to prevent spread of infection, not to increase rate of healing in people who have receive antitoxin (macrolides, penicillin G, rifampicin, clindamycin)
  • Close contacts should be cultured and given vaccination booster if required
45
Q

What organism usually causes an infection where a pus-filled abscess or furuncle is present?

A

Staphylococcus spp.

(Especially S. aureus)

Staph is coagulase (+). Coagulase converts fibrinogen to fibrin, which forms a barrier around the furuncle

46
Q

Which gram-positive bacteria have available vaccines?

A
  • Corynebacterium diphtheriae
  • Bacillus anthraces
  • Clostridium tetani
47
Q

Which bacteria is this?

A

Bacillus anthracis

Gram (+), rod-shaped bacteria that grows in chains

48
Q

Clostridium tetani is a [Gram stain, metabolic, shape distinctive morphology]

A

Clostridium tetani is a gram (+), obligate anaerobe bacillus that forms terminal spores that exist in large reservoirs in soil

49
Q

What kind of wounds may become infected with Clostridium tetani?

A

Deep puncture wounds

The bacteria is an obligate anaerobe; the spores must reach a part of the body where the is no oxygen in order to germinate

50
Q

Clostridium botulinum is a [Gram stain, metabolic, shape, distinctive morphology]

A

Clostridium botulinum is a Gram (+) obligate anaerobe bacillus that forms subterminal spores. It is found is soil, ponds, lakes, and on plants

51
Q

What is the difference between tetanus toxin and botulism toxin?

A

Their targets;

Tetanus toxin targets inhibitory neurons in the CNS (renshaw cells), inhibiting GABA and glycine release

Botulinum toxin targets motor neurons in the CNS, inhibiting ACh release

52
Q

How is infant botulism different from food-borne botulism?

A

Infant botulism: ingestion of spores

Food-borne botulism: ingestion of the pre-formed toxin

Spores cannot germinate in the adult intestine, but they can germinate in the infant’s; this leads to toxin production and infant botulism

53
Q

How is botulism prevented?

A

No vaccine is available

Thoroughly cook canned foods/practice proper canning techniques

Don’t feed honey to infants <12 months

54
Q

What are the major differences between botulism and tetanus infections?

A

Type of paralysis

  • Tetanus = increased muscle tone
  • Botulism = no muscle tone

Method of contracting the disease

  • Tetanus = puncture wound
  • Botulism = canned food, wound, honey (infant)

Treatment

  • Tetanus = Human tetanus immunoglobulin, penicillin or metronidazole
  • Botulism = Trivalent equine antitoxin, respiratory support
55
Q

Which individuals are most likely to be infected with Nocardia?

A

Anyone with deficient cell-mediated immunity. This includes patients with…

  • Lymphoma
  • Transplants
  • Glucocorticoid use
  • Men (more susceptible than women
56
Q

What are the 3 diseases caused by Nocardia?

A

Pulmonary nocardiosis

CNS nocardiosis

Transcutaneous nocardiosis

57
Q

How is a Nocardia infection diagnosed?

A
  • The organism is present in large numbers in lesions
  • Truly gram (+)
  • Stains partially acid-fast on Kinyoun or Carbol Fuchsin
  • Catalase (+)
  • Urease (+)
  • Organisms are culturable on blood agar
    • Grows as characteristic filamentous structures
    • But may take 2 weeks for colonies to be visible
58
Q

How is a Nocardia infection treated?

A

Choice: Trimethoprim/sulfamethoxazole

Alternative: Minocycline, amikacin

Brain abscesses may need to be drained, debridement may be necessary

59
Q

Actinomyces israeli is a [Gram stain, metabolic, shape distinctive morphology]

A

Actinomyces israeli is a gram (+), obligate anaerobe that grows in filamentous rods that resemble fungus

It is part of the normal flora of the mouth, GI tract, and female genital tract

60
Q

What are the major differences between Nocardia spp. and Actinomyces israeli?

A

Metabolism

  • Nocardia = obligate aerobe
  • A. israeli = obligate anaerobe

Staining

  • Nocardia stains partially acid fast
  • A. israeli does not
61
Q

How is an Actinomyces israeli infection diagnosed?

A

Organism seen in gram-stained sulfur granules

  • The granules themselves are diagnostic of Actinomyces israeli infection
  • The organism will grow from cultures
  • If sulfur granules are not present, it may just be part of normal flora
  • Not acid fast (distinguishes from Nocardia)
62
Q

Describe Clostridioides difficile

[Gram stain, metabolism, shape]

A

Clostridioides difficile, aka C. diff is a gram-positive, anaerobic bacillus

Note: Spore forming, like other Clostridioides spp.

COPY FDN3 By Nathan and Minnie (12 decks)

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