L51 – Streptococcal Infection and Rheumatic Fever Flashcards Preview

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Flashcards in L51 – Streptococcal Infection and Rheumatic Fever Deck (76):
1

3 main ways of classifying bacteria?

 Aerobic vs. anaerobic
 Gram positive vs. Gram negative
 Cocci vs. bacilli / rod

2

What test is used to distinguish Aerobic gram positive cocci?

Catalase test

+ve = Staphylococcus (in clusters)

-ve = Streptococcus (in chains)

3

In catalase negative Aerobic gram positive cocci, what test is done to distinguish the two main subgroups?

Grow on blood agar

2 groups:
either Beta-haemolytic
or Alpha/ Gamma hemolytic

4

In Beta-haemolysis, catalase negative, aerobic, gram positive cocci, What 3 tests are done to further distinguish the bacteria?

Lancefield grouping

Bacitracin susceptibility

Biochemical reactions

5

In the biochemical reactions done to beta-haemolytic, catalase negative, aerobic, gram positive cocci, what are the subgroups of bacteria?

Groups;
A = Strep. pyogenes
B = Strep. agalactiae
C/G = Strep. dysgalactiae
Strep. anginosis/ milleri

6

What tests are done to distinguish ALPHA/ GAMMA haemolytic, catalase negative, aerobic, gram positive cocci?

Bile solubility

Optochin susceptibility

7

Name all the properties of Strep. pneumoniae.

Alpha/ Gamma haemolytic
Catalase negative
Aerobic
Gram positive
Optochin susceptible
Bile soluble
Cocci

8

Name 3 bacteria that are alpha/gamma haemolytic, optochin resistant, bile INsoluble, catalase negative aerobic gram positive cocci.

Viridans streptococci
Strep. bovis
Enterococci (a type of strep)

9

What lancefield group is Strep. pyogenes?

Group A Streptococci

10

What are all the properties of Strep. pyogenes in microbiological testing? (include PYR, VP, Bacitracin, blood agar, Gram, O2, Catalse)

Bacitracin susceptible
PYR +ve (pink)
VP -ve
B-haemolytic
Gram positive cocci
Aerobic
Catalase negative

11

Explain how Lancefield grouping works?

Particles coated with antibody against specific carbohydrate (streptococcal
antigen) on bacteria cell surface > look for
agglutination

12

What are the 2 main routes of damage Strep. pyogenes can cause?

Direct damage due to Strep. pyogenes

Indirect damage due to immune-mediated response (non-supprative complications = inflammation without pus)

13

What are 2 extents of direct damage due to strep. pyogenes?

Local infection or systemic

14

Name some local infections caused by direct damage by strep. pyogenes?

- Pharyngitis

- Skin infection: Pyoderma, Erysipelas, Cellulitis

- soft tissue infection: Necrotizing fasciitis, myonecrosis, myositis

- Pneumonia, (lymphadenitis, puerperal sepsis)

15

Name some systemic infections caused by direct damage by strep. pyogenes?

-Scarlet fever
-Streptococcal toxic shock syndrome (STSS)
-Bacteremia

16

Name some immune-mediated response/ indirect damage caused by strep. pyogenes?

-Rheumatic fever
-Glomerulonephritis

17

What are some antiphagocytic factors on Strep. pyogenes (Group A strep)?

M protein
Capsule

18

What is the function of M protein and Capsule on group A strep?

Adhere to epithelial cells/ mucosa + antiphagocytic

19

What are some proteases allowing Strep pyogenes to invade and spread through tissue?

Streptokinase
Hyaluronidase

20

What toxin from Strep. pyogenes cause systemic toxicity?

Streptolysin O

21

Describe the rash of Scarlet fever?

Day 2 rash- diffuse red rash over upper chest, spread peripherally, blanches on pressure, sand-paper like skin

Piastia's lines

22

Describe the flushing in Sclarlet fever?

Facial flushing with peri-oral pallor

23

Describe the tongue in sclarlet fever?

Strawberry tongue (white then red as coating diappears)

24

What is the blood test staining by H&E like in sclarlet fever?

Eosinophilia

25

Which layer of skin is affected by which infections by group A strep?

Epidermins = impetigo (pustules> crusts)

Dermis = Erysipelas + Cellulitis

Subdermis = Necrotizing fasciitis + myonecrosis

26

What is the laboratory criteria of STSS?

isolation of Group A Strep.

27

How does Strep. pyrogenic exotoxins inflict a huge inflammatory response?

Toxin: SpeA,B,C
Superantigen binds to NON-SPECIFIC domain of MHC II and T-cell bridge > inflict large response

28

What are some widespread effects of STSS?

SCARE

Soft tissue necorsis (necrotizing fasciitis, myositis, gangrene)

Coagulopathy

ARDS

Renal , Liver impairment

Erythematous macular rash

29

What are the 2 main ways to diagnose ACUTE Group A strep by microbiological testing? What method is used for non-acute diagnosis

1) Culture: swab at site of infection> blood culture
2) Rapid antigen detection test


Non-acute= serology of Anti-streptolysin I (ASO) titer

30

What is the treatment of Group A strep? What antibiotic is added in STSS?

1) Penicillin (or similar) x 10days
2) Anti-inflammatory: Aspirin, Corticosteroid
3) Surgery for uncontrolled HF due to acute mitral regurgitation (valvular damage in rheumatic fever)





STSS = clindamycin or linezolid

31

What is Group A strep highly resistant against?

Clindamycin and erythromycin

32

What is the definition of acute rheumatic fever?

result of valvular damage caused by abnormal immune response to Group A Strepococcal infection

33

Why do strep. pyogennes infection seem like a cold at the beginning?

Group A strep has latency of ~ 3 weeks (1-5 weeks)

Accompanying GAS pharyngitis with/without skin infection

34

Why does acute rheumatic fever cause auto-immune damage to heart valves?

Molecular mimicry: similar structure between Streptococcal M protein
and cardiac proteins in host tissues > exaggerated T-cell mediated immune response (immunity targeting
against the M protein) also react with cardiac proteins

35

What is the consequence of REPEATED GAS infection on the heart?

Repeated / ongoing infections may drive valvular inflammatory response
> episodes of recurrent ARF > rheumatic heart disease

36

What is the leading cause of heart failure in children and young adults in developing countries?

Acute rheumatic fever

37

What are 5 major criterias for Jones criteria for acute rheumatic fever? CASSE

Major:
1) Carditis: valvulitis, myocarditis, pericardits

2) Arthritis (usually migratory: from one ankle to another)

3) Sydenham’s chorea: involuntary movements, muscle weakness,
emotional instability

4) Subcutaneous nodules: surfaces of joints / spine

5) Erythema marginatum (skin rash)

38

What are 5 minor criterias for Jones criteria for acute rheumatic fever? FARP

1) Fever
2) Arthralgia (joint pain)
3) Raised erythrocyte sedimentation rate (ESR) / C-reactive protein (CRP)
4) Prolonged PR interval

39

What are 2 Supportive laboratory evidence of streptococcal infection?

 Elevated ASO (anti-streptolysin O) titer
 Positive throat culture for GAS

40

According to Jones criteria, what combo of cirteria constitutes acute rheumatic fever?

2 major symptoms
or
1 major + 2 minor symptoms

41

How to Eliminate risk factors for GAS infection within community?

Hygiene
Access to medical care
Living condition

42

What is the difference in intention between primary and secondary prophylaxis with antibiotics in GAS?

Primary = prevent 1st attack/ rheumatic fever or treat pharyngitis

Secondary = prevent recurrences/ repeated attacks due to new strain

43

What is the difference in the drug admin. frequency between primary and secondary prophylaxis?

Primary = within 9 days after onset

Secondary = Intramuscular penicillin once 4 weeks or longer (e.g. lifelong if moderate/ severe rheumatic heart disease)

44

List some sudden onset symptoms of Post-Strep. GN?

Hypertension
Edema
Haemturia
Hypocomplementemia
Fever

Adult > chronic GN > renal failure
Chilren > reversible

45

What is the latency of GN after Throat or skin infection?

Throat > 1-2 weeks > GN with high ASO titre

Skin > 4-6 weeks > GN with low ASO titre

46

Explain the pathogenesis of Post-Strep. GN? Starting from circulating immune complexes deposition

Circulating immune complexes deposition

Molecular mimicry (M12)

> Deposition of certain streptococcal antigen into glomerulus

47

Name all the properties of Strep. agalactiae?

Lancefield group B
Bacitracin resistant
CAMP test +ve
Hippurate hydrolysis +ve
Narrow zone B-haemolysis
Gram positive cocci
Catalse negative
Aerobic

48

What early onset infant diseases are caused by Group B Strep.?

Pneumonia
Meningitis
Bacteremia without focus

49

What Late onset infant diseases are caused by Group B Strep.?

Meningitis
Other local infections: Osteomyelitis, septic arrthritis
Bacteremia without focus

50

What diseases beyond early infancy are caused by Group B Strep.?

Bacteremia without focus

51

How to prevent GBS infection in pregnant women?

Screen and give antibiotics before birth to reduce early-onset GBS diseases

52

What are GBS diseases in pregnant women?

1)UTI
2)Infection of genital tract, placenta, amniotic sac
3)Post-partum bacteremia (fever)

53

What are GBS diseases in Non-pregnant women?

Skin/soft tissue infection
Septic arthritis, osteomyelitis
Pnuemonia
Endocarditis
Meningitis
Bacteremia without focus

54

Name some predisposition to adult GBS disease?

 Diabetes mellitus (= immunocompromising)
 Liver disease
 Neurological impairment
 Malignancy
 Renal failure
 Cardiovascular disease
 Immunosuppression

55

List all properties of Strep. Dysgalactiae?

Lancefield group C/G
Aerobic
Gram positive cocci
Catalase negative
PYR -ve ,VP -ve
Bacitracin resistant

56

List some clinical manifestations of Strep. Dysgalactiae ?

 Pharyngitis: post-streptococcal glomerulonephritis (PSGN), no rheumatic fever
 Skin, soft tissue infection
 Septic arthritis (sterile reactive arthritis)
 Osteomyelitis
 Pneumonia / sinusitis
 Endocarditis
 Meningitis
 Neonatal sepsis
 Bacteremia (common)

57

Which Lancefield group of Strep. Dysgalactiae is more likely to manifest in bacteremia?

Group G >> group C

58

List all the properties of Streptococcus anginosus group (aka Streptococcus milleri).

 Can belong to multiple groups: Lancefield group A/C/F/G/none
 Bacitracin-resistant
 PYR –ve, VP +ve (opposite to GAS)
 May be α/γ hemolysis
 Characteristic ‘caramel’ smell

59

What are 3 major clinical manifestations of Streptococcus anginosus?

1) Abscess formation: Dental, Brain, Liver, Subphrenic, Pelvic, Lung abscess and Lung empyema

2) Endocarditis (common)

3) Bacteremia in neutropenic cancer patients: Acute respiratory distress syndrome (ARDS)
& Toxic shock

60

Viridans Streptococci is a group of different strep. found where in body?

Common Oral flora

61

What are the major manifestations of V.S. infection?

Infective Endocarditis

Meningitis

Pneumonia

Dental Carries > brush teeth > Bacteremia

62

What are the differences in mannitol fermentation between biotype I and Biotype II Strep. bovis?

I = ferment mannitol
II = not ferment mannitol

63

What are the differences in major manifestation between biotype I and Biotype II Strep. bovis?

I = endocarditis
II = Cholangitis (infection of biliary tract)

64

What are the differences in Underlying disease between biotype I and Biotype II Strep. bovis?

I = Colonic lesion (e.g. carcinoma, polyps)
II = Hepatobiliary disease

65

List all properties of Enterococci?

Lancefield group D
Hydrolyze bile esculin
PYR +ve
Optochin resistant
Bile insoluble
Alpha/Gamma hemolyis
Catalase negative
Aerobic
Gram positive cocci

66

What environment does Enterococci grow in?

 6.5% NaCl (high concentration; vs. normal saline = 0.9% NaCl)
 40% bile salt (can survive in gut)
 45 degrees celcius

67

What are some clinical manifestations of Enterococci?

 Urinary tract infection (UTI)
 Bacteremia, endocarditis
 Perforated peritoneum  intra-abdominal infection
 Pelvic infection
 Wound, soft tissue infection in hospitalized patients
 Meningitis

68

List all properties of Strep. pneumoniae.

Non-groupable by Lancefield
Optochin sensitive
Bile soluble (clear)
Mucoid
Heavily encapsulated
Alpha/ Gamma haemolytic
Catalase negative
Aerobic
Gram Positive Cocci

69

List some clinical manifestations of Strep. pneu.

 Respiratory tract: (ENT): otitis media, sinusitis (next to nose, mouth)
 Pneumonia / exacerbation of COPD / asthma
 Meningitis
 Bacteremia
 Conjunctivitis in eye (by unencapsulated strains)

70

What are 3 main categories of predisposition to S. pneu.?

Local defect
Congenital immunodeficiency
Acquired immunodeficiency

71

What local defects predispose S. pneu?

Local defect:
 Cochlear implant in ear
 Chronic pulmonary disease (e.g. COPD, asthma)

72

What congenital immunodeficiency predispose S.pneu?

Congenital immunodeficiency: agammaglobulinemia / hypogammaglobulinemia > low level of antibodies

73

What acquired immunodeficiency predispose S.pneu?


 Splenectomy = decrease osponization of bacteria

 Defective / loss of antibody (e.g. nephrotic syndrome, multiple myeloma, lymphoma,
drug-induced neutropenia)

 HIV

 Chronic disease (e.g. DM, alcoholism, cirrhosis)

74

What are the 2 types of pneumococcal vaccine?

1. Old = pneumococcal polysaccharide vaccine (PPV)

2. New = pneumococcal protein conjugate vaccine (PCV) = Better immunogenicity in children, adults

75

What are the recommended populations of pneumococcal vaccine?

Routine children vaccine
Elderly >65
Age 2-64 with high risk conditions

76

What are high risks conditions for pnuemococcal infections?

Immunocompromised states (HIV, malignancies, transplant, drugs)

History of invasive pnuemococcal disease

Chronic cardiac, pulmonary, liver, renal disease

Diabetes

CSF leakage

Cochlear implants

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