Denise - Streptococcus Flashcards

1
Q

How is streptococcus classified
(5)

A

Based on the haemolytic propertied of the organism e.g. Alpha haemolytic strep

Based on the presence of surface antigens determined by immunological assays

Based on biochemical reactions

Based on protein analysis

Based on genetic analysis

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2
Q

Classify step based on haemolysis

A

Alpha haemolytic strep
Beta haemolytic strep
Gamma/no haemolytic strep

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3
Q

How do we classify strep based on their serological groups, how is this done

A

Based on the Lancefield groups of streps

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4
Q

How do we group streps based on Lancefield groups?
(6)

A

C-substance polysaccharide in their cell walls

Antigenic differences

Easily extractable

Classified primarily Beta Haemolytic strep

GAS (Group A strep) and GBS (Group B strep) are the most clinically significant

S. pneumoniae and S. viridans (the alpha haemolytic streps) have no group specific antigen i.e. cannot be grouped based on lancefield groups

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5
Q

Which streps cannot be identified using lancefield groupings and why

A

S. pneumoniae and S. viridans (the alpha haemolytic streps) have no group specific antigen i.e. cannot be grouped based on lancefield groups

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6
Q

Write about S. pneumoniae

A

One of the 12 priority pathogens according to WHO

High burden of disease and rising rates of penicillin resistance

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7
Q

What type of resistance is seen in S. pneumoniae

A

Penicillin resistance

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8
Q

Why is S. pneumoniae listed as one of the 12 priority pathogens

A

High carriage rates
Genetic adaptability
Ability to shift from commensal to pathogenic interaction in its host

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9
Q

Write about the pathogenesis of S. Pneumonia
(3)

A

Colonisation is the prerequisite for both transmission to other individuals and invasive disease in the carrier

Carriers can shed S. pneumoniae in nasal secretions and thereby transmit the bacterium

Dissemination beyond its niche along the nasal epithelium, either by aspiration, bacteraemia or local spread

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10
Q

How does S. pneumonia spread from a carrier to another individual

A

Nasal secretions

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11
Q

How does S. pneumonia spread from the nasal epithelium to cause infection

A

Aspiration (bacteria into respiratory system)

Bacteraemia (bacteria in circulation)

Local spread (spread into tissues)

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12
Q

What infection is caused if there is aspiration of S. pneumonia

A

This will cause pneumonia in the lung

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13
Q

What infection is caused if there if S. pneumonia colonisation leads to bacteraemia

A

This will cause meningitis

This can occur directly from colonisation or can lead on from pneumonia

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14
Q

What does local spread of S. pneumonia from nasal epithelium lead to

A

Otitis media

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15
Q

What factors affect S. pneumonia shedding from nasal epithelium of carriers
(5)

A

Pneumolysin increases shedding

Capsule type and amount increases shedding

Viral co-infection increases shedding

Anticapsule IgG decreases shedding

Anticapsule IgA1 has no effect

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16
Q

How does pneumolysin increase shedding of S. pneumoniae?
(3)

A

Inflammation promotes secretion production by nasal epithelium

Bacteria present in mucus lining epithelium

Runny nose -> sneezing -> facilitates spread

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17
Q

How does capsule type and amount increase shedding?
(2)

A

Capsulated strains of S. pneumonia inhibit entrapment by mucin

S. pneumonia can escape the mucous produced by the S. pneumoniae

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18
Q

How can anticapsule IgG decrease Shedding?

A

IgG binds to bacteria

Agglutination blocks release

Bacteria can’t escape in mucous

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19
Q

Why does anticapsule IgA1 have no effect on S. pneumoniae

A

Bacterial protease relieves agglutination

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20
Q

Why does viral co-infection increase shedding of S. pneumoniae

A

Increases bacterial load and increases mucous production

Nasal epithelium infected with virus -> increases production of mucous

More bacteria present in mucous

Spread by runny nose etc

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21
Q

What are the two types of infections caused by S. pnuemonia

A

Non invasive
Invasive soft tissue infections

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22
Q

List the most common S. pneumonia non invasive infections

A

Acute bacterial pneumoniae
Otitis media

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23
Q

Write about acute bacterial pneumoniae caused by S. pneumoniae
(5)

A

Lower respiratory tract infection

Preceeded by viral infection

Community acquired infection Pneumonia CAP

Older adults

Seasonality - increased in winter months

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24
Q

Write about otitis media caused by S. pneumonia

A

Most common cause of middle ear infection in children

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25
What indicates an S. pneumonia invasive infection
Isolation of S. pneumoniae from a normally sterile site e.g. blood or CSF
26
What are the main invasive infections caused by S. pneumoniae
Blood stream infection (SEPSIS) Meningitis
27
What percentage of S. pneumoniae pneumonia infections will lead to BSIs i.e. SEPSIS
15-30% of people with pneumoniae will lead to invasive disease
28
Write about S. pneumonia caused meningitis (2)
Majority of invasive pneumococcal disease (IPD) infections are caused by a subset of predominant streptococcus pneumoniae serotypes Approximately 8-10 of 90 different serotypes cause meningitis
29
Write about S. pneumoniae epidemiology
Young children Older adults Immunocompromised Mortality rate is now much greater in adults >65 years of age than in children <2
30
Comment on the recent trends in invasive S. pneumonia
IPD is a notifiable disease in Ireland Ever increasing number
31
What does IPD include
Meningitis BSI Sterile site infection
32
Comment on incidence rate of IPD versus age of patients (3)
Less common in children under 2 Increasingly common in those over 65 Very low amounts in teenagers (near zero infections)
33
What are the virulence factors of S. pneumoniae? (5)
Surface structure (capsule) Pili Choline Binding protein A Autolysins LytA Pneumolysin
34
How does a capsule affect virulence of S. pneumoniae? (6)
Capsule is antiphagocytic Capsule is antigenic Polysaccharide Essential for colonisation -> non capsulated strains are usually avirulent Target for Pneumococcal Conjugate Vaccines >90 strains recognised based on capsular carbohydrates
35
How do pili affect virulence of S. pneumoniae
Not all pneumococci express pili Attachment to the epithelial cells in the nasopharynx and upper respiratory tract
36
How does choline binding protein A affect? (6)
Polypeptides Number varies from 13 to 16 Anchors the protein to the choline residues present in the cell wall Responsible for remodelling the cell wall Responsible for adhesion Promotes invasion
37
What are the two main enzymes responsible for virulence of S. pneumonia
Autolysins LytA Pneumolysin
38
What does autolysins LytA do in S. pneumoniae
Cell wall degrading protease Responsible for the release of virulence factors
39
What does pneumolysin do? (6)
Cytolytic protein Released by autolysin Attacks cell membranes Proinflammatory Inhibits PMN Activates complement
40
Describe the process behind autolysins LytA and pneumolysin in S. pneumoniae. (5)
S. pneumoniae infection Autolysin is responsible for lysis of S. pneumoniae Lysis releases the virulence factors out of S. pneumoniae Pneumolysin released Pneumolysin damages mammalian cell membranes
41
What is done with S. pneumoniae on day 1 of laboratory investigation? (2)
Direct gram stain Inoculation on blood agar
42
What specimens are seen in S. pneumoniae infections (6)
Sputum Pleural fluid or lung aspirate Pus Aspirates CSF Blood
43
What investigation is done on CSF and blood for S. pneumoniae
Direct Molecular detection Film array ME
44
What investigation is done on CSF? (4)
White cells increased Bacteria Glucose decreased protein increased
45
What investigation is carried out on day 1 for S. pneumoniae? (2)
Direct microscopy gram stain Only done on blood cultures which have flagged positive
46
How does S. pneumoniae appear on gram stain
Gram positive diplococci lancet shaped
47
Write about the growth requirements for S. pneumonia (6)
Fastidious Blood agar 37 degrees celsius 5% CO2 O2 Anaerobically
48
Write about the colonial morphology of S. pneumoniae
Alpha haemolysis Draughtsman colonies or mucoid colonies
49
What are the basic characteristic results of S. pneumonia
Gram positive diplococci KOH negative Catalase negative Oxidase negative Lanceolate shaped
50
What confirmatory identification tests are done for S. pneumonia on day 2 (3)
Optochin susceptibility Bile susceptible Vitek or Maldi TOF identification
51
Why might the Vitek be used instead of Maldi for S. pneumoniae ID
Maldi lack of discrimination between s. pneumoniae and other closely related alpha-haemolytic streptococci
52
How is S. pneumonia treated
B lactams -> penicillin (if not resistant) Macrolide -> Erythromycin Cephalosporin -> Cefotaxime
53
Write about S. pneumoniae resistance (3)
PNSP -> penicillin non-susceptible pneumococci increased gradually with age 11% isolate in younger patients but 29% in older patients over 75 Reduced susceptibility to cefotaxime and erythromycin is also observed in older patients
54
What is done with S. pneumonia which is confirmed (3)
CSF sent to IMSRL (Irish Meningitis and sepsis Reference Laboratory) on Temple street Real time PCR directly on specimen Serogroup Capsule-PCR
55
What Pneumococcal vaccines are there currently (3)
PCV7 - infants PCV13 - infants PPV23 - for adults over 65 and immunocompromised
56
What is the PPV23 vaccine (5)
Pneumococcal polysaccharide vaccine Purified capsular polysaccharide from 23 capsular types of S. pneumoniae Accounts for up to 90% of IPD Only for those >2 years old Uptake is poor - only 30%
57
Why is the PPV23 vaccine only suitable for those over 2?
An adequate antibody response does not develop in those under 2 years of age
58
What are the PCV vaccines (6)
Pneumococcal Conjugated Vaccines PCV7 and PCV13 Conjugated to a protein for enhanced immunogenicity Immunogenic from 6 weeks of age Active against 75-90% of IPD serotypes Uptake great with >90%
59
Comment on the outcome of S. pneumoniae vaccination (4)
Clear evidence that the vaccines have reduced the burden of IPD in children However, number of non vaccine type infections has increased Evidence of herd protection seen Vaccine uptake for PPV23 needs to be improved
60
Write about S. viridans (6)
Commensals in the GIT, Respiratory and female genital tracts and are most prevalent in the oral cavity Considered to be of low pathogenicity Many species but not usually differentiated May gain access to bloodstream through minor trauma to gums Propensity to adhere to cardiac valves In those with damaged heart valves can cause sub acute bacterial endocarditis
61
How can S. viridans gain access to blood stream?
Through minor trauma to gums
62
What can S. viridans cause to those with damaged heart valves
Sub acute bacterial endocarditis
63
What is Streptococcal endocarditis (4)
Patients with abnormal or damaged heart valves Bacteria infects valves during a bacteraemia Prophylactic penicillin may be given prior to dental treatment Caused by oral streptococci e.g. S. mitis or S. oralis
64
What species might cause streptococcal endocarditis
Oral streptococci e.g. S. mitis, S. oralis
65
Where is S. mutans often found
Found in mouth/on teeth Produces biofilm which can be involved in plaque formation and tooth decay
66
What infections can S. mutans cause
Tooth decay
67
What are the basic characteristics of S. viridans
Gram positive cocci in chains Catalase negative Oxidase negative Fastidious Facultative anaerobes Alpha haemolysis
68
What is done to S. viridans on day 1
Isolation on blood agar
69
What is done to S. viridans on day 2
Gram stain Investigate haemolysis Biochemical speciation Identification on Vitek or MALDI
70
What is done on day 3 for S. viridans
Optochin susceptibility testing
71
How does S. viridans react to optochin
S. viridans is resistant to optochin
72
What is meant by Lancefield grouping? (3)
Lancefield Groups based on differences in cell wall polysaccharides 13 Lancefield Groups Groups A, B, C, D, F and G most commonly implicated in human infections
73
What is Lancefield group A
Streptococcus pyogenes
74
What is Lancefield group B
Streptococcus agalactiae
75
What is Lancefield group C
Found in pharynx: can cause pharyngitis, sinusitis, impetigo, endocarditis
76
What is Lancefield group D
Enterococci Can cause wound lesions, urinary tract infections and some cases of SBE
77
What is Lancefield group F
Streptococcus anginosus; grow better anaerobically
78
What is Lancefield group G
Resemble group A strains
79
What are the three types of infections caused by S. pyogenes
Non invasive Invasive soft tissue Non-suppurative sequelae
80
List the main non invasive infections caused by S. pyogenes
Pharyngitis Scarlet fever Skin infections
81
What is pharyngitis (5)
Common infection Abrupt onset Difficult to differentiate from viral infection 5-30% of cases in children 5-10% of cases in adults
82
What are the four symptoms of pharyngitis
Headache Fever Reddening Pus
83
Write about scarlet fever caused by S. pyogenes (5)
Scarletina Erythematous rash of skin and mucous membranes Rash looks like sunburn and feels like sandpaper Strawberry tongue Erythrogenic toxin
84
What non invasive skin infections does S. pyogenes cause
Impetigo Erysipelsia
85
What is impetigo
Honey crust lesions Pus filled blisters
86
What is erysipelsia? (5)
Acute skin infection Cellulitis Diffuse redness Pain Potential spread to the bloodstream
87
What invasive soft tissue infections does S. pyogenes cause
Necrotising facitis Streptococcal Toxic Shock Syndrome
88
Write about necrotising facitis (7)
Rare infection Tissues under the skin and muscles Pain Redness Swelling Fluid filled blisters/swollen tissues Associated with wounds/breaks in the skin Predisposition includes: cancer, diabetes, dialysis and steroids Infected tissue has to be cut off
89
What predisposes someone to necrotising facitis? (4)
Cancer Diabetes Dialysis Steroids
90
What is streptococcal Toxic Shock Syndrome
Caused by superantigen 1-2 weeks after the onset of acute illness
91
What are the main symptoms of toxic shock syndrome (5)
High fever Rash Hypotension Multiorgan failure Desquamation typically of the palms and soles
92
What are the two non suppurative sequelae infections caused by S. pyogenes
Rheumatic fever Glomerular nephritis
93
What is a non suppurative sequelae
Immune reactions 1-5 weeks after infection
94
What causes rheumatic fever
Its seen post pharyngitis
95
What causes glomerular nephritis
Its seen post skin infection
96
What are cutaneous infections
Infections of upper respiratory tract and of skin and soft tissue
97
What are the three main cutaneous infections caused by S. pyogenes
Pharyngitis Cellulitis Impetigo
98
What is the main destructive soft tissue infection caused by S. pyogenes?
Necrotising faciitis
99
What are the two toxin mediated infections caused by S. pyogenes
Scarlet fever Toxic Shock Syndrome
100
What are the non-suppurative sequelae caused by S. pyogenes?
Acute glomerulonephritis Rheumatic fever
101
Write about S. pyogenes epidemiology
Only invasive infections are notifiable iGAS (invasive group A streptococci) Streptococcal Toxic Shock/ Necrotising Faciitis/ BSI Increase in notified iGAS infections since october 2022
102
Write about S. pyogenes virulence (4)
Wide range of virulence factors Enable bacteria to attach to host cells Spread by penetrating host tissues Evade the immune response
103
What are the S. pyogenes virulence factors (8)
Capsule M protein Streptolysins Anti C5a peptidase Streptokinase Hyaluronidase Exotoxins SPE A and C DNase
104
Write about M protein (8)
Surface adhesin Inhibits phagocytosis Binds Fc portion of IgG M types 1, 3, 12 and 28 are the most common isolates found in patients with shock and multiorgan failure Strains lacking M protein are less virulent Rheumatic heart disease T-protein surface antigen R-protein on some strains
105
List the S. pyogenes Toxins and ExoEnzymes (6)
Pyrogenic exotoxins Streptolysin O and S Streptokinase C5a peptidase Streptodornases Hyaluronidase
106
What does pyrogenic exotoxins do
Cause various effects, including the rashes seen in scarlet fever and streptococcal toxic shock disease
107
What does Streptolysin O and S do
Damages mammalian cells, resulting in cell lysis and release of lysosomal enzymes Lysis of RBCs, PMNs and platelets
108
What does streptokinase do
Catalyses conversion of plasminogen to plasmin, causing lysis of clots, facilitating the rapid spread of organisms
109
What does C5a peptidase do (2)
Inactivates complement component C5a Cleaves the chemoattractant C5a
110
What does streptodornases do
DNAses degrade the viscous DNA in necrotising tissue or exudates, aiding the spread of infection
111
What does hyaluronidase do
Disrupts the organisation of ground substance, facilitating the spread of infection Breaks down tissue hyaluronic acid
112
What does streptolysin S do
Oxygen stable Not antigenic Leucocidal action
113
What does Streptolysin O do (3)
Oxygen labile Cytotoxic for red blood cells, neutrophils, platelets, cardiac tissue Responsible for haemolysis that we see on blood agar
114
What are the streptococcal exotoxins (3)
SPE-A SPE-B SPE-C
115
What does SPE stand for
Streptococcal pyrogenic exotoxins
116
What are SPE-A and SPE-C (3)
Erythrogenic toxins Similar to staph enterotoxins Associated with invasive infections and toxic shock syndrome
117
What is SpeB
Cysteine protease Associated with tissue destruction
118
What are the exotoxins SPE A and C also called
Superantigens
119
What does DNase do
Degrades extracellula
120
What specimens is S. pyogenes found in
Throat swabs Pus Skin
121
What are the growth requirements of S. pyogenes
Fastidious Blood agar Haemolysis enhanced anaerobically 37 degrees Celsius 5% CO2, O2, Anaerobically
122
What confirmatory tests are done on S, pyogenes
Rapid latex agglutination on patient samples
123
What is the colonial morphology of S. pyogenes (5)
Beta haemolysis Gram positive cocci in chains KoH negative Catalase negative Oxidase negative
124
What confirmatory test is done on day 2 for S. pyogenes (4)
Lancefield Grouping MacConkey Susceptible to bacitracin PYR
125
How does S. pyogenes grow on MacConkey?
Fails to grow on MacConkey
126
How does S. pyogenes grow with Bacitracin
S. pyogenes is susceptible to bacitracin
127
Is S. pyogenes PYR positive or negative?
Its PYR positive
128
What is PYR
Pyrrolidonyl arylamidase
129
Write about S. agalactiae
Opportunistic pathogen Often colonisation Capsule may contribute to virulence
130
Write about the colonisation of S. agalactiae (5)
Found in the intestines of up to 30% of adults Found in the vagina of up to 25% of women Asymptomatic May be intermittent 90% of adults posses no protective antibodies to Gram B Strep
131
Write about the pathophysiology of group B streptococcus
Prenatal onset GBS Early-onset GBS Late-onset GBS
132
Write about the prenatal-onset of group B strep
Occurs when a baby is infected with GBS during pregnancy
133
Write about the early-onset of group B strep
Occurs when a baby is infected with GBS within the first week of life
134
Write about the late-onset of group B strep
Occurs when a baby is infected with GBS after 1 week to several months of age
135
Write about the epidemiology of Group B strep
Infections in adults: the elderly, pregnant women, others with other disease Most common cause of life-threatening infection in newborn babies
136
Write about early onset infectious GBS
Up to 80% of GBS infection in babies 0-6 days (usually <24 hours) Usually septicaemia, also meningitis and pneumonia 11% mortality
137
Write about late onset infectious group B septicaemia (5)
Up to 20% of GBS infection in babies 7+ days (rare after 3 months) Usually meningitis with septicaemia 5% mortality 50% of GBS meningitis survivors have neurological sequelae
138
What specimens are Group B streps found in
Urine Sample UTI Blood cultures BSI CSF
139
What specimens come in for surveillance in carriage of Group B strep
High vaginal swab Screening for GU carriage Carriage preceeds infection
140
What are the growth requirements for Group B strep
Fastidious Grown on blood agar -> haemolysis enhanced anaerobically 37 degrees celsius 5% CO2
141
What is done on day 1 for Group B streps
Isolation on blood agar Direct detection using geneXpert -> S. agalactiae
142
What are the basic characterisation results for Group B strep, S. agalactiae
Lancefield group B KOH Negative Oxidase Negative CAMP factor Hydrolysis of hippurate Does not hydrolyse aesculin Some grow on MacConkey agar (bile)
143
What is the CAMP test
Detects the production of extracellular protein CAMP factor CAMP factor acts synergistically with the beta lysin produced by S. aureus A zone of enhanced lysis of sheep or bovine blood CAMP positive = Group B strep CAMP negative = Not GBS
144
What is the Hippurate hydrolysis test (4)
Used to differentiate S. agalactiae from other Beta Haemolytic streps Hippurate is hydrolysed by hippuricase into Benzoic acid and glycine Ninhydrin reagent is used as an indicator to detect Glycine Ninhydrin reacts with glycine to form a deep blue or purple colour
145
What do we done when we confirm we have a Group B strep (3)
CSF sent to Irish Meningitis and Sepsis Reference Lab in Temple Street Real Time PCR directly on specimen Serogroup capsule - PCR
146
Write about Group C and G streptococcus (4)
Commensal flora of the human upper airway Asymptomatic colonisers of the skin, gastrointestinal tract and female genital tract S. dysgalactiae subspecies S. equisimilis (SDSE) Resembles S. pyogenes infections
147
Write about the non enterococcal group D (7)
Streptococcus bovis Faecal flora Alpha or non haemolytic Occasionally causes UTI and Endcarditis Bile Aesculin Positive PYR Negative Does not grow in 6.5% salt
148
Write about beta haemolytic strep treatment
Penicillin Clarithromycin (allergy) Necrotizing fasciitis - surgery + clindamycin