Internal Medicine_Infectious Diseases_2 Flashcards

Bacteria_Strep and Enterococcus_Group A Strep, Group B Strep, Strep pneuomo, Strep viridans, Strep gallolyticus, Enterococcus

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1
Q

Streptococcus agalactiae is colloquially called … ?

A

Group B Streptococcus

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2
Q

What type of bacteria is Streptococcus agalactiae?

A

A gram-positive coccus.

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3
Q

What test is used to differentiate Streptococcus agalactiae from Streptococcus pyogenes?

A

The hippurate hydrolysis test, which is positive for S. agalactiae.

The hippurate hydrolysis test is a biochemical test used to identify bacteria based on their ability to hydrolyze hippurate (N-benzoylglycine) into benzoic acid and glycine. It is particularly useful in differentiating species within the Streptococcus and Campylobacter genera (both positive marked by a purple/blue color).

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4
Q

Streptococcus agalactiae is PYR ( “+” or “-“ )

A

PYR negative

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5
Q

What structural feature protects S. agalactiae from immune defenses?

A

A Polysaccharide capsule.

The Polysaccharide capsule confers virulence.

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6
Q

What is the CAMP test, and how does it help identify S. agalactiae?

A

The CAMP (Christie, Atkins, Munch-Peterson) helps distinguish GBS from other beta-hemolytic streptococci, including group A strep. In the CAMP test, GBS is observed for enhanced hemolysis when it is in close proximity to Staphylococcus aureus, which produces a diffusible factor. This synergistic effect is a characteristic of GBS and helps in its identification.

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7
Q

What type of hemolysis does Streptococcus agalactiae demonstrate on blood agar?

A

Beta-hemolysis (clear zones around colonies).

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8
Q

How can S. agalactiae be distinguished from S. pyogenes in terms of antibiotic sensitivity?

A

S. agalactiae is bacitracin-resistant.

S. pyogenes is bacitracin-sensitive.

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9
Q

What are the three major neonatal infections caused by Streptococcus agalactiae?

A

Neonatal bacterial meningitis.
Neonatal sepsis.
Pneumonia.

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10
Q

Why is S. agalactiae particularly dangerous for neonates?

A

It can colonize the birth canal and be transmitted to the neonate during delivery, leading to severe infections.

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11
Q

When should pregnant women be screened for S. agalactiae colonization?

A

At 35–37 weeks of gestation:
Screen pregnant patients with rectal and vaginal swabs.

Patients with ⊕ culture:
Receive intrapartum penicillin/ampicillin prophylaxis.

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12
Q

What is the prophylactic treatment for S. agalactiae colonization in pregnant women?

A

Intrapartum intravenous penicillin.

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13
Q

What type of hemolysis does Streptococcus pneumoniae exhibit on blood agar?

A

Alpha-hemolysis, producing a greenish discoloration around colonies.

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14
Q

What structural feature protects S. pneumoniae from phagocytosis?

A

Polysaccharide capsule.

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15
Q

How can S. pneumoniae be distinguished from viridans group streptococci in terms of antibiotic sensitivity?

A

S. pneumoniae is optichin-sensitive.

Optochin is a substance used to differentiate between different species of streptococci. Streptococcus pneumoniae is sensitive to optochin, meaning it will inhibit its growth, while viridans group streptococci are resistant and continue to grow in the presence of optochin.

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16
Q

What shape and arrangement are characteristic of S. pneumoniae under a microscope?

A

Lancet-shaped diplococci.

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17
Q

What bile property helps distinguish S. pneumoniae?

A

It is bile-soluble, meaning colonies dissolve in the presence of bile acids.

Streptococcus pneumoniae is bile-soluble, demonstrated by the lysis and disappearance of its colonies on agar upon the addition of bile acids

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18
Q

What are the major infections caused by S. pneumoniae?

A

Meningitis.
Otitis media.
Pneumonia (lobar pneumonia with rust-colored sputum).
Sinusitis.

Streptococcus pneumoniae is a leading cause of meningitis, otitis media, pneumonia, and sinusitis (Use the acronym MOPS).

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19
Q

What virulence factor allows S. pneumoniae to evade immune defenses?

A

IgA protease, which cleaves IgA antibodies.

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20
Q

Which population is particularly susceptible to S. pneumoniae infections due to its capsule?

A

Patients with sickle cell disease.

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21
Q

What are the treatment options for S. pneumoniae?

A

First-line:
Penicillin or amoxicillin

For sensitivity to penicillin:
Macrolides (e.g., azithromycin or clarithromycin)

For resistant strains:
Ceftriaxone

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22
Q

What vaccines are recommended for S. pneumoniae?

A

For young children and at-risk adults and seniors:
PCV (pneumococcal conjugate vaccine)

For at risk children and adults who have had PCV:
PPSV23 (pneumococcal polysaccharide vaccine)

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23
Q

What type of hemolysis do viridans group streptococci exhibit on blood agar?

A

Alpha-hemolysis, similar to S. pneumoniae.

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24
Q

How can viridans group streptococci be distinguished from S. pneumoniae?

A

Viridans streptococci are optichin-resistant.

They are bile-insoluble (colonies persist in bile).

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25
Q

What structural feature do viridans streptococci lack, differentiating them from S. pneumoniae?

A

A capsule.

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26
Q

What infections are caused by viridans streptococci?

A

Dental caries: (S. mutans and S. sanguinis).

Infective endocarditis: Often in damaged heart valves (especially the mitral valve).

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27
Q

What substance produced by viridans streptococci aids in adherence to teeth and damaged heart valves?

A

Dextrans, which bind to fibrin-platelet aggregates.

Viridans group streptococci utilize dextrans (insoluble extracellular polysaccharides) to adhere to tooth enamel and fibrin-platelet aggregates on damaged heart valves, potentially leading to dental plaque and infective endocarditis, respectively. Viridans group streptococci have a propensity to adhere to previously damaged heart valves when they establish an infection that can result in subacute bacterial endocarditis. This adherence occurs particularly in the presence of damaged or abnormal valve surfaces, such as those seen in the mitral valve.

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28
Q

Which particular viridans group causes endocarditis?

A

S. sanguinis

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29
Q

Which particular viridans groups cause dental caries?

A

S. sanguinis, S. mutans and S. mitis

30
Q

What type of bacteria is Streptococcus pyogenes?

A

It is a gram-positive coccus that forms chains or pairs.

31
Q

What is the main virulence factor of Streptococcus pyogenes that helps evade the immune system?

A

A hyaluronic acid capsule.

32
Q

What type of hemolysis does Streptococcus pyogenes demonstrate on blood agar?

A

Beta-hemolysis, creating clear zones around colonies.

33
Q

How can Streptococcus pyogenes be differentiated from other streptococci?

A

It is bacitracin-sensitive and PYR-positive.

Streptococcus agalactiae is bacitracin resistant and PYR-negative.

34
Q

What are some pyogenic infections caused by Streptococcus pyogenes?

A

Impetigo: Honey-crusted skin lesions.
Pharyngitis (strep throat): Erythematous and inflamed throat.
Cellulitis and erysipelas: Skin infections with erythema.

35
Q

What toxins does Streptococcus pyogenes produce, and what conditions do they cause?

A

Pyrogenic exotoxins (SPE): Cause scarlet fever and toxic shock syndrome (TSS).
SpeB: Causes necrotizing fasciitis (flesh-eating bacteria).

36
Q

What are the hallmark symptoms of scarlet fever?

A

Acute period:
* Fever after a 2 to 5 incubation period.
(including malaise, headache, chills and myalgia)

  • Strawberry tongue.
  • Pharyngitis with tonsillar exudates
    (enlarged cervical lymph nodes)

Exanthem Phase
* Desquamative “sandpaper” rash 12-48 hours after fever onset
(non-blanching maculopapular rash)

  • Rash normally is sparing of the palms and soles but can appear a week later.
37
Q

What is toxic shock syndrome (TSS) caused by Streptococcus pyogenes?

A

A superantigen-mediated condition characterized by high fever, rash, and shock.

38
Q

What are two major post-infectious complications of Streptococcus pyogenes?

A

Rheumatic fever.
Post-streptococcal glomerulonephritis (PSGN).

39
Q

Rheumatic fever is a type ____ hypersensitivity reaction

A

II

40
Q

What is the pathogenesis of rheumatic fever?

A

Cross-reactivity between M protein and human tissues, leading to molecular mimicry. It confers resistance to phagocytosis and plays a role in the pathogenesis of the immunologic sequela that lead to rheumatic heart disease and glomerulonephritis. Protein M shares a sequence homology with human cardiac myosin.

Streptolysin O lyses red blood cells and immune cells, aiding in immune evasion.

Streptokinase do converts plasminogen to plasmin, facilitating fibrin degradation and tissue invasion.

DNases produced by Streptococcus pyogenes degrade host DNA, helping the bacteria evade immune defenses.

41
Q

What are the JONES criteria for diagnosing acute rheumatic fever?

A

2 Major or 1 Major with 2 Minor

Major:
J: Joints (migratory polyarthritis).
♡: Carditis (pancarditis).
N: Nodules (subcutaneous).
E: Erythema marginatum (ring-shaped rash).
S: Sydenham chorea (involuntary movements).

Minor:
Fever, Elevated ESR, Polyarthalgias, Prolonged PR interval

42
Q

When does the sequella of Group A Streptococcus tend to show clinical signs after an acute infection?

A

2 to 4 weeks

Acute rheumatic fever (ARF) is a noninfectious complication of S. pyogenes infection (e.g., tonsillopharyngitis) and can manifest with fever, skin lesions, and elevated ESR. However, the symptoms of ARF typically develop 2–4 weeks after S. pyogenes infection and the skin lesions seen in ARF are subcutaneous nodules and erythema marginatum.

43
Q

What is the long term sequella of rheumatic fever?

A

Mitral value disease (mitral regurgitation and stenosis)

44
Q

Mitral ________ occurs in the early period of rheumatic fever sequella.

A

mitral regurgitation.

45
Q

Mitral ________ occurs in the early period of rheumatic fever sequella.

A

mitral stenosis.

46
Q

What is the management for rheumatic fever?

A

ECHO, EKG, Antibiotics, and NSAIDs for joint pain.

47
Q

What antibiotic is preferred for rheumatic fever and how is this managed?

A

Prophylaxis
Penicillin G IM for 4 weeks, Penicillin V PO daily, or Azithromycin PO daily

With carditis and valve disease until 40 years old or for 10 years
With just carditis until 21 years old or for 10 years
Without carditis until 21 years old or for 5 years

48
Q

What are the hallmark features of Post-streptococcal glomerulonephritis (PSGN)?

A

Nephritic syndrome

Hematuria (cola-colored urine; dysmorphic RBCs in urine; RBC casts).
Edema and face puffiness (proteinuria < 3.5 g/day).
Hypertension.
Azotemia.

49
Q

When do features of Post-streptococcal glomerulonephritis (PSGN) present following acute infection with Group A streptococcus?

A

2 weeks following skin or respiratory tract infection.

50
Q

What are the common lab findings for Post-streptococcal glomerulonephritis (PSGN)?

A

High Antistreptolysin O titer, Low Complement titer, or High DNase B titer

Enlarged Glomeruli and hypercellular growth on light microscope.
Granular appearance on immunofluorescence.
Subepithelial humps of IgG and C3 on electron microscope.

51
Q

Does early antibiotic treatment reduce the risk of PSGN?

A

No, but it significantly reduces the risk of rheumatic fever.

52
Q

Does streptococcus pyogenes cause meningitis?

A

No.

The most common syndromes that Streptococcus pyogenes causes are pyogenic infections, Toxic Shock, Scarlet fever, Rheumatic fever, and necrotizing fasciitis.

53
Q

Which streptococci is associated with subacute endocarditis and colorectal cancer?

A

Streptococcus bovis

Streptococcus bovis/equinus complex (SBSEC) → reclassified to Streptococcus gallolyticus

54
Q

What is the classification of Streptococcus gallolyticus?

A

It belongs to the Group D streptococci.

55
Q

What type of bacteria is Streptococcus gallolyticus?

A

A gram-positive coccus that occurs in chains or pairs.

It is part of the normal GI tract flora in some animals and humans.

56
Q

Is Streptococcus gallolyticus encapsulated or non-encapsulated?

A

It is encapsulated.

57
Q

What type of hemolysis does Streptococcus gallolyticus exhibit?

A

Gamma-hemolysis (no hemolysis on blood agar).

58
Q

In what medium can Streptococcus gallolyticus grow?

A

Bile salt media.

Streptococcus gallolyticus is capable of hydrolyzing bile esculin, a feature that allows it to grow on bile esculin agar. Bile esculin agar is a selective and differential medium used to identify and differentiate enterococci and some other group D streptococci, including Streptococcus gallolyticus, based on their ability to hydrolyze esculin in the presence of bile salts.

59
Q

What special property helps Streptococcus gallolyticus thrive on certain surfaces?

A

It forms biofilms on collagen-rich surfaces, such as heart valves.

60
Q

Where is Streptococcus gallolyticus commonly found in the body?

A

It is part of the normal GI tract flora in some animals and humans.

61
Q

What are the major infections caused by Streptococcus gallolyticus?

A

Bacteremia.
Endocarditis.
Other associated infections include osteomyelitis, UTIs, meningitis, and mastitis.

62
Q

What is the association between Streptococcus gallolyticus and colorectal cancer?

A

There is a strong link between Streptococcus gallolyticus infections and colorectal neoplasia.

63
Q

What antibiotics are effective against Streptococcus gallolyticus?

A

3rd generation cephalosporins
(ceftriaxone, ceftazidime, cefotaxime, cedinir, or cefixime).

Vancomycin.

Penicillin (PCN).

64
Q

What type of bacteria are Enterococcus faecalis and Enterococcus faecium?

A

Gram-positive cocci in the GI tract.

Catalase ⊝, PYR ⊕, typically nonhemolytic.

Colloquially called Group D Streptococcus.

65
Q

What unique environmental condition can Enterococcus species tolerate?

A

Growth in 6.5% hypertonic saline and bile.

66
Q

What test distinguishes Enterococcus species from other gram-positive cocci?

A

Their ability to hydrolyze esculin in the presence of bile.

They are resistant to Penicillin G, causing UTIS biliary tract infections, and infective endocarditis following GI/GU procedures.

67
Q

Which Enterococcus species accounts for the majority of enterococcal infections?

A

Enterococcus faecalis.

Enterococcus faecalis: Common, accounts for the majority of infections.
Enterococcus faecium: Less common, highly resistant, and more dangerous.

68
Q

What are the three main infections caused by Enterococcus species?

A

Urinary tract infections (UTIs): Includes cystitis and pyelonephritis.

Subacute Endocarditis.

Biliary tree infections and diverticulitis.

69
Q

What is the significance of vancomycin-resistant Enterococcus (VRE)?

A

VRE refers to strains of E. faecalis and E. faecium that have developed resistance to vancomycin and other antibiotics. VRE (vancomycin-resistant enterococci) are an important cause of healthcare-associated infection.

Normally Enterococcus spp. can be treated with:
Ampicillin, Vancomycin and carbapenems.

VRE is treated with Linezolid and Tigecycline.

70
Q

What are the treatment options for VRE infections?

A

Linezolid.
Linezolid is an oxazolidinone antibiotic and works by inhibiting bacterial protein synthesis.

Tigecycline.
Tigecycline is a glycylcycline antibiotic and is part of the tetracycline class.