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MBBS I CPRS > L51 – Streptococcal Infection and Rheumatic Fever > Flashcards

L51 – Streptococcal Infection and Rheumatic Fever Flashcards

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1
Q

3 main ways of classifying bacteria?

A

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

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2
Q

What test is used to distinguish Aerobic gram positive cocci?

A

Catalase test

+ve = Staphylococcus (in clusters)

-ve = Streptococcus (in chains)

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3
Q

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

A

Grow on blood agar

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

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4
Q

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

A

Lancefield grouping

Bacitracin susceptibility

Biochemical reactions

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5
Q

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

A 
Groups; 
A = Strep. pyogenes 
B = Strep. agalactiae
C/G = Strep. dysgalactiae
Strep. anginosis/ milleri
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6
Q

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

A

Bile solubility

Optochin susceptibility

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7
Q

Name all the properties of Strep. pneumoniae.

A 
Alpha/ Gamma haemolytic
Catalase negative 
Aerobic 
Gram positive 
Optochin susceptible 
Bile soluble 
Cocci
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8
Q

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

A

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

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9
Q

What lancefield group is Strep. pyogenes?

A

Group A Streptococci

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10
Q

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

A 
Bacitracin susceptible 
PYR +ve (pink)
VP -ve 
B-haemolytic 
Gram positive cocci
Aerobic 
Catalase negative
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11
Q

Explain how Lancefield grouping works?

A

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

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12
Q

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

A

Direct damage due to Strep. pyogenes

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

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13
Q

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

A

Local infection or systemic

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14
Q

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

A
  • Pharyngitis
  • Skin infection: Pyoderma, Erysipelas, Cellulitis
  • soft tissue infection: Necrotizing fasciitis, myonecrosis, myositis
  • Pneumonia, (lymphadenitis, puerperal sepsis)
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15
Q

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

A
  • Scarlet fever
  • Streptococcal toxic shock syndrome (STSS)
  • Bacteremia
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16
Q

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

A
  • Rheumatic fever

- Glomerulonephritis

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17
Q

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

A

M protein

Capsule

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18
Q

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

A

Adhere to epithelial cells/ mucosa + antiphagocytic

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19
Q

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

A

Streptokinase

Hyaluronidase

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20
Q

What toxin from Strep. pyogenes cause systemic toxicity?

A

Streptolysin O

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21
Q

Describe the rash of Scarlet fever?

A

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

Piastia’s lines

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22
Q

Describe the flushing in Sclarlet fever?

A

Facial flushing with peri-oral pallor

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23
Q

Describe the tongue in sclarlet fever?

A

Strawberry tongue (white then red as coating diappears)

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24
Q

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

A

Eosinophilia

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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

MBBS I CPRS (78 decks)

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