Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Bacteriology > Streptococcus (Pt. 2) > Flashcards

Streptococcus (Pt. 2) Flashcards

1
Q

What are the alpha hemolytic streptococci?

A

S. pneumoniae and Viridans Group

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How is S. pneumoniae arranged?

A

Diplococci pairs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

List the characteristics of S. pneumoniae (gram __ …)

A
  • Gram +ve diplococci
  • Facultative anaerobic
  • Capsulated
  • Non-motile and non-sporulating
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Which enzyme released by S. pneumonia gives it its alpha hemolytic capability?

A

Pneumolysin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How does pneumolysin partially destroy RBCs?

A

Pneumolysin breaks down hemoglobin (Therefore, hydrogen peroxide produced by the bacterium, oxidize erythrocyte hemoglobin leading to methemoglobin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the main virulence factor of Streptococcus pneumoniae?

A

The capsule is the main virulence factor of Streptococcus pneumoniae. There are more than 90 serotypes of capsules, and they interfere with phagocytosis by host immune cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How does PsaA contribute to virulence?

A

PsaA binds to choline-binding receptors, which are present on various human cells, including epithelial cells. This binding allows Streptococcus pneumoniae to adhere to host cells and establish colonization.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does phosphocholine contribute to virulence of S. pneumoniae?

A

Phosphocholine adheres to respiratory cells and blocks the binding of complements.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the role of choline in Streptococcus pneumoniae’s invasion of host cells?

A

Choline-binding proteins, such as choline-binding protein A, interact with immunoglobulin receptors on the surface of epithelial and mucosal cells, leading to endocytosis of the bacteria.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How can Streptococcus pneumoniae invade the central nervous system (CNS)?

A

Streptococcus pneumoniae can be released into the bloodstream after invading epithelial and mucosal cells. From there, it can potentially reach the CNS, causing invasive infections.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the different ways the S. pneumoniae capsule interferes with phagocytosis?

A
  • The presence of unrecognizable capsular polysaccharides —> Host cell unable to recognize bacterium.
  • The presence of electrochemical forces that repel phagocytic cells.
  • PspA inhibits the deposition of complement factor C3bp —> inhibitor of opsonization.
  • PspC inactivates the complement factor C3bp.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How does Pneumolysin exert its cytotoxic effect on respiratory epithelial cells?

A

1) Pneumolysin interacts with cholesterol present on host cell membrane and enters the lipid membrane
2) Pneumolysin creates pores in cell membrane
3) Cell lysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does Pneumolysin elicit an immune response?

A

The release of Pneumolysin activates complements and triggers the release of cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What does autolysin released by S. pneumoniae do?

A

Autolysin kills the bacterium. It works by destroying the bacteria’s cell wall leading to autolysis. As a result, the peptidoglycan components release will activate the complementary antibodies. Pneumolysin is also released in the process.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What does neuraminidase aid S. pneumoniae in?

A

Neuraminidase aids in adherence and invasion. Neuraminidase cleaves the scialic acid present on host cells, exposing the area to which the bacteria can adhere

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How does S. pneumoniae spread to the site of infection?

A

S. pneumoniae endogenously colonizes the nasopharynx or oropharynx and spreads to the distal sites of the body (Lungs, middle ear, sinuses, blood, meninges)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

When is colonization the highest and in whom?

A

Colonization is highest in the winter and in children (and elderly)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are factors that increase the risk of pneumococcal infection?

A
  • People having antecedent viral respiratory infections.
  • Children and elderly are at higher risk of pneumococcal meningitis
  • People with hematological disorders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Which immunoglobulin prevents S. pneumoniae adherence during colonization and prevents disease from occurring?

A

Secretory IgA (sIgA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Which immunoglobulin is responsible for controlling the multiplication of the S. pneumoniae bacteria after adherence?

A

IgG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are common symptoms of pneumonia?

A

Fever, wet cough, productive (bloody) cough (hemoptysis), shortness of breath, pleuritic chest pain, low mortality rate (5%) (type 3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Where can S. pneumoniae locally spread to and cause infection?

A

S. pneumoniae can spread locally from the lungs and cause bronchitis, otitis, sinusitis, meningitis (from sinuses)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What can happen when S. pneumoniae directly invades the bloodstream?

A

Meningitis, septic arthritis, peritonitis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the different ways one can acquire pneumococcal meningitis?

A

1) Direct invasion into bloodstream (bacteremia)
2) Spread from sinuses to brain in case of thin sinus lining
3) Spread from ears to meninges
3) Direct invasion into brain via head trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Gram Stain +
Sputum Culture +
Blood Culture +

A

Generally regarded as conclusive diagnosis of invasive pneumococcal disease (pneumonia) + bacteremia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Gram Stain +
Sputum Culture +
Blood Culture -

A

Good evdience of nonbacteremic pneumococal pneumonia if a clinical syndrome sugesting pneumonia is present, microscopic examination of Gram-stained sputum is characteristic (diplococci), and culture shows strongly predominant growth of pneumococi with no other likely pathogenic bacteria.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Gram Stain + or -
Sputum Culture -
Blood Culture +

A

With symptoms and signs of pneumonia and an infiltrate on the chest radiograph, these findings are generally taken to indicate invasive pneumococcal pneumonia, even if organisms are not found in sputum.
Sputum culture may be saliva.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Gram Stain +
Sputum Culture -
Blood Culture -

A

In the presence of the appropriate clinical syndrome, still remains suggestive of pneumococcal pneumonia (especially if gram stain shows diplococci) because organisms can be missed on culture as a result of sampling error and overgrowth of streptococci from saliva. Need to correlate w/ symptoms.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Gram Stain -
Sputum Culture +
Blood Culture -

A

Less suggestive of pneumococcal disease. Pneumococci can be isolated by culture of sputum from persons who are colonized (normal subclinical disease).
However, especially in patients already treated with antibiotics, the positive culture may be the only supporting evidence for diagnosis of nonbacteremic pneumococcal pneumonia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Gram Stain -
Sputum Culture -
Blood Culture -

A

Does not support adiagnosis of pneumococcal pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What specimen should be obtained to identify S. pneumoniae?

A

Sputum, nasopharynx, sinus fluid, middle ear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What should sputum specimen contain for it to be sputum not saliva?

A

A lot of PMNs (polymorphonuclear neutrophils), few epithelial cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How does S. pneumoniae look under microscopic view after gram staining?

A

Purple, lancet-shaped diplococci with a hollow unstained capsule (not well seen)

34
Q

Why is it that S. pneumoniae might be hard to grow on some agars?

A

S. pneumoniae is a fastidious organism, meaning it needs more enrichment to grow. Chocolate agar ensures its growth on agar.

35
Q

Which agar is best for growing S. pneumoniae?

A

For growth, chocolate agar is the safest option. However for identification, blood agar shows the characteristic alpha hemolytic ability of S. pneumoniae

36
Q

What is the key test for the laboratory identification of S. pneumoniae?

A

Optochin (ethylhydrocuprein dihydrochloride) test. S. pneumoniae is the only bacteria sensitive to Optochin.

37
Q

What are the different laboratory tests carried out for the identification of S. pneumoniae?

A

1) Catalase test (differentiates between Staph. and Strep. species)
2) Bile solubility test (Sodium deoxycholate)
3) Optochin test

38
Q

What depicts a positive result of S. pneumoniae in a bile solubility test? Explain.

A

The lack of growth (no turbidity) in a bile salt tube depicts a positive result. Bile salts activate autolysin activity, and autolysins released by S. pneumoniae destroy the bacteria and inhibit its growth.

39
Q

Why isn’t the latex agglutination test used to identify S. pneumoniae?

A

S. pneumoniae does not have any Lancefield antigens (No capsular type)

40
Q

What is a common antibiotic used for the treatment of S. pneumoniae?

A

Penicillin

41
Q

What antibiotic is given for individuals with an S. pneumoniae infection that have penicillin allergies?

A

Tetracycline or Macrolide

42
Q

Which antibiotics are given to treat S. pneumoniae strains that are resistant to most common antibiotics?

A

Vancomycin or Fluoroquinolone

43
Q

What prevention technique is most suitable for S. pneumoniae?

A

Vaccination

44
Q

What are the two types of vaccinations for the prevention of S. pneumoniae?

A

1) Pneumovax (PPVSV23)
- Non-conjugated
- 23- valent polysaccharide vaccine
- For elderly, children younger than 2 years, adults with asthma/ smoking habits

2) Prevnar (PCV7)
- Conjugated
- 7-valent pneumococcal vaccine
- For children over 5 years
- Replaced by higher-valent version (PCV13) for protection against additional serotypes —> For children over 5 years and adults with risk factors

45
Q

What are the different Enterococcal species?

A

• E. Faecalis
• E. Faecium
• E. Gallinarum
• E. casseliflavus

46
Q

Is Enterococcus the only bacteria belonging to group D?

A

No. Other non-enterococcal bacteria like S. bovis and S. equinis also belong to group D.

47
Q

What are the characteristics of Enterococci?

A

• Gram-positivecocci
• arranged in pairs and short chains
• Cell wall with group-specific antigen (group D glycerol teichoic
acid)
• Facultativeanaerobic
• Fastidious: require blood for growth
• Nonhemolyticorα-hemolytic
• The bacteria can grow in the presence of high concentrations of NaCl and bile salts

48
Q

How does Enterococcus adhere to host surfaces?

A

Enterococcus adheres to host surfaces, such as intestinal and vaginal tissues, through collagen binding adhesins and carbohydrate adhesins.

49
Q

What are some virulence factors produced by Enterococcus?

A

Enterococcus secretes cytolysins and proteases that cause localized tissue damage. These factors contribute to the pathogenicity of Enterococcus and can resist antibiotic treatment.

50
Q

What poses a challenge in the treatment of Enterococcus infections?

A

Enterococcus can be inherently resistant to many commonly used antibiotics.

51
Q

Where are Enterococcus commonly found in the human body?

A

Enterococcus, specifically Enterococcus faecalis, is commonly found in high concentrations in the large intestine (e.g., 107 organisms per gram of feces). It is also present in the genitourinary tract. Enterococcus faecium is less frequent.

52
Q

Which species of enterococcus has the highest number of cases?

A

Enterococcus faecalis. Enterococcus faecium is less common.

53
Q

In what situations can Enterococcus be isolated from the respiratory tract or skin surface?

A

Enterococcus may be isolated from the respiratory tract or on the skin surface of hospitalized patients who have been treated with broad-spectrum antibiotics. This can contribute to the emergence of vancomycin-resistant enterococci.

54
Q

What is the most common hospital-acquired infection caused by Enterococcus?

A

The most common hospital-acquired infection associated with Enterococcus is urinary tract infection (UTI).

55
Q

What are the common symptoms of Enterococcus UTI?

A

Enterococcus UTI is characterized by dysuria (pain during urination) and pyuria (presence of pus in the urine). It is commonly seen in hospitalized patients with indwelling urinary catheters and those receiving broad-spectrum antibiotics.

56
Q

What clinical manifestation is associated with Enterococcus peritonitis?

A

Enterococcus peritonitis is characterized by abdominal swelling and tenderness. It typically occurs after abdominal trauma or surgery. Patients with Enterococcus peritonitis are usually acutely ill, febrile, and may have positive blood cultures.

57
Q

What is the clinical presentation of Enterococcus endocarditis?

A

It is associated with persistent bacteremia. Enterococcus endocarditis can present acutely or chronically, depending on the course of the infection.

58
Q

Explain how the REGIIIy enzyme produced by the intestines can lead to an overgrowth of enterococcus bacteria in the intestinal lining

A

REGIIIy is triggered by the presence of gram negative bacteria.
When antibiotics are taken, and gram negative bacteria levels decrease, REGIIy is consequently triggered less and . As a result, the balance is disrupted and gram positive bacteria like enterococcus can overgrow.

59
Q

What are the growth characteristics of Enterococcus in the laboratory?

A

Enterococcus can grow in a CO2-rich environment on various media, including blood agar and chocolate agar.

60
Q

Is Enterococcus catalase positive or negative?

A

Enterococcus is catalase negative

61
Q

How can Enterococcus be differentiated from Streptococcus pneumoniae?

A

Enterococcus is resistant to optochin, whereas Streptococcus pneumoniae is susceptible to optochin.

62
Q

What happens when Enterococcus is exposed to bile?

A

Enterococcus does not dissolve when exposed to bile, which is a distinguishing feature from other bacteria.

63
Q

What is the growth requirement for Enterococcus in terms of salt concentration?

A

Enterococcus can grow in broth containing 6.5% NaCl, which is a high salt concentration.

64
Q

How can the hydrolysis of esculin in the presence of bile help in the diagnosis of Enterococcus?

A

Enterococcus is able to hydrolyze esculin in the presence of bile, which can be detected using selective media such as bile esculin agar.

65
Q

What is the significance of the PYR test in the diagnosis of Enterococcus?

A

Enterococcus produces the enzyme l-pyrrolidonyl arylamidase (PYR), which can be detected using a PYR test. A positive PYR test result can help in the identification of Enterococcus species.

66
Q

What are the recommended antibiotics for the treatment of Enterococcus infections?

A

ampicillin and vancomycin.

67
Q

What is the synergistic combination therapy used for Enterococcus infections?

A

In some cases, a synergistic combination of an aminoglycoside (such as gentamicin) and a cell wall-active antibiotic (such as ampicillin or vancomycin) may be used to treat Enterococcus infections. This combination therapy can enhance the effectiveness of treatment.

68
Q

What is the major problem in Enterococcus treatment?

A

The major problem in Enterococcus treatment is the development of antibiotic resistance. Enterococcus species have become resistant to aminoglycosides, ampicillin, penicillin, and even vancomycin, which is often considered a last-line antibiotic for many infections.

69
Q

Which Lancefield group do S. Viridans belong to?

A

They do not contain Lancefield antigens

70
Q

What are the characteristics of Streptococcus viridans?

A

Streptococcus viridans is a heterogeneous collection of streptococci that includes both α-hemolytic and nonhemolytic strains. Many of these bacteria produce a green pigment on blood agar media.

71
Q

Where do Streptococcus viridans commonly colonize in the human body?

A

Streptococcus viridans commonly colonize the oropharynx (back of the throat), gastrointestinal tract, and genitourinary tract.

72
Q

Why are Streptococcus Viridans not found on skin?

A

They are rarely found on the skin surface due to the toxic effect of surface fatty acids on these bacteria.

73
Q

What are the nutritional requirements for the growth of Streptococcus viridans?

A

Streptococcus viridans, like most other streptococci, is nutritionally fastidious. It requires complex media supplemented with blood products and often requires an incubation atmosphere augmented with 5% to 10% carbon dioxide for optimal growth.

74
Q

What is the most common cause of subacute bacterial endocarditis?

A

Streptococcus viridans is the most common cause of subacute bacterial endocarditis, which is an infection of the inner lining of the heart valves or the heart chambers.

75
Q

Is Streptococcus mutans a part of the normal flora?

A

Yes, Streptococcus mutans is a part of the normal flora in the human oral cavity.

76
Q

How does Streptococcus mutans adhere to the surface of the tooth?

A

Streptococcus mutans is equipped with receptors that allow it to adhere to the surface of the tooth, creating a slimy environment.

77
Q

What does Streptococcus mutans synthesize with the enzyme dextransucrase?

A

Streptococcus mutans synthesizes dextran, a sticky polysaccharide, with the enzyme dextransucrase.

78
Q

What is the role of dextran in Streptococcus mutans biofilm formation?

A

Dextran contains a capsule that binds to the enamel surface, forming a biofilm consisting of 300-500 bacterial cells.

79
Q

How does Streptococcus mutans contribute to dental caries (tooth decay)?

A

Streptococcus mutans can depolymerize dextran to glucose and use it as a carbon source. This process produces lactic acid within the biofilm, leading to the decalcification of enamel and the formation of dental caries.

80
Q

What is the causative agent of tooth decay?

A

The combination of acid production by Streptococcus mutans and the presence of plaque results in the causative agent of tooth decay.

81
Q

How is Streptococcus Viridans identified in testing?

A

Alpha hemolysis —> Optochin resistant —-> Bile esculin negative growth

Bacteriology (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions