L19: Streptococci Flashcards
How do microorganisms cause disease?
Virulence factors
- Exotoxins
- Endotoxins
Cause host cellular damage
- Direct
- Consequent to host immune response
What is streptococci?
Gram positive cocci
Bacteria forms chains
Stains purple
How can streptococci be classified?
Haemolysis–> how good they are at breaking down RBC
Lancefield antigen–> based on cell wall antigens
Sherman group–> pyogenic, viridans, lactic or enterococcal
How does the haemolysis system of classification work?
alpha haemolysis–> partial haemolysis of RBC–> goes green like a bruise
beta haemolysis–> full haemolysis (complete breakdown), translucent area forms around
non haemolytic haemolysis (gamma)–> no haemolysis
Why would you use a blood agar plate?
Blood contain nutrients
Iron
Required for some bacteria to cultivate
How does the Lancefield classification system work?
Further groups beta haemolytic streptococci
Groups A-G
Based on presence or absence of antigenic carbohydrate on cell wall
Uses antibodies to recognise different bacteria, some will react and others wont
How does the Sherman group classification system work?
Separated into four groups - Pyogenic - Viridans - Lactic - Enterococcal Based on different factors* Only the pyogenic and viridans group still exists
*Based on ability to grow at 10 and 45 degrees, to survive at 60 degrees for 30 minutes, grow at pH 9.6 in 0.1% methylene blue and at different concentrations of sodium chloride
What is the classification of Streptococcus pyogenes?
Lancefield group A beta-haemolytic streptococcus
What are the virulence factors for Streptococcus pyogenes?
Lots of different types of bacteria within the Streptococcus pyogenes species so lots of different virulence factors
1) Hyaluronic acid capsule
2) M protein
3) Adhesins, including lipoteichoic acid, M protein, fibronectin binding proteins
4) Streptolysins O and S
5) Dnase A, B, C and D
6) Hyaluronidase
7) Streptokinase
8) Streptococcal pyrogenic exotoxins
How does the hyaluronic acid capsule act as a virulence factor?
Inhibits phagocytosis by neutrophils and macrophages
Similar to host connective tissue so protects it from defence systems
How does M protein work?
Different variants
Resistant to phagocytosis–> inhibits activation of alternative complement pathway on bacterial cell surface
>150 antigenically different serotypes
How does the adhesins work?
Includes lipoteichoic acid, M protein, fibronectin binding proteins
Adherence is the first step toward colonisation
How does streptolysins O and S work?
Cause lysis of erythrocytes, neutrophils and platelets
How does the DNAses A, B, C and D act as virulence factors?
Degradation of DNA
In response to NETs (neutrophil extracellular traps)–> DNAse break them down releasing the bacteria
How does hyaluronidase work as a virulence factor?
Degradation of hyaluroinc acid in connective tissue allowing the bacteria to spread more easily
What does the virulence factor streptokinase do?
Dissolution of blood clots through conversion of plasminogen to plasmin
Prevents clots stopping the spread of bacteria
What does the virulence factor streptococcal pyrogenic exotoxins do?
Cleave IgG bound to Group A strep
Member of superantigenic Spe family –> cause excess T cell proliferation
What does Streptococcal pyrogenes cause?
Streptococcal pharyngitis
Infection at back of the throat including tonsils
What are the clinical features of Streptococcal pharyngitis? How is it transmitted?
Sore throat Enlarged tonsils Lymphoid hyperplasia Malaise, fever, headache Tonsillopharyngeal exudates Droplet spread
How is streptococcal pharyngitis treated?
Will resolve without treatment
Develop M proteins specific antibody–> protection
Treatment given to prevent late immune complications of Streptococcal pharyngitis
What are some of the potential complications that can arise from streptococcal pharangitis?
Scarlet fever–> Red rash caused by pyrogenic exotoxin, local or haematogenous spread, associated with high fever, sepsis, arthritis and jaundice
Suppurative complications–> complications of pus
- Retroperitoneal abscess–> bacteria collects in retroperitoneal space behind tonsil and spreads down to mediasinum–> infection and clotting
- Peritonsillar cellulitis/abscess
- Mastoiditis, sinusistis, otitis media
- Meningitis, brain abscess
What are the immune complications of streptococcal pharyngitis?
Immune complications means late complication occurs after the infection has been clears due to immune system
Antigens cross react with own antigens–> causes autoimmune condition
- Acute Rheumatic fever
- Acute post-streptococcal glomerulonephritis
What is acute rheumatic fever?
Cause inflammation of the heart (pericarditis or myocarditis), joints and CNS
Rheumatogenic M types –> certain M type caused by a specific type of Streptococcal pyrogene–> rheumatic fever
Possible mechanism
-Autoimmune provoked by previous pharyngitis
-Serum sickness
-Binding of M protein to collagen
- ASO, ASS induced injury
If streptococcal pharyngitis is treated early–> don’t get this
What is acute post-streptococcal glomerulonephritis?
Inflammation of renal glomerulus
Caused again by specific M types (different to ones causing acute rheumatic fever)
What skin infections can be caused by streptococcus pyogenes?
Impetigo
Erysipelas
Cellulitis
Necrotising fasciitis
What is Impetigo?
Crusty lesions form on the skin
Childhood infections 2-5 years
Initial skin colonisation, followed by intradermal innoculation
No ARF but impetigo is most common cause of glomeruonephritis
What is erysipelas?
Invasive skin infection of the deep layers of the skin
Involvement of lymphatic system
Face and lower limbs
Lower limb infections usually secondary to invasion of skin via trauma, skin disease or local fungal infection
What is cellulitis?
Skin and subcutaneous tissue infection
Impaired lymphatic drainage and illict injecting drug use important risk factors
Flucoxacillin treated
What is necrotising fasciitis?
Infection of deeper subcutaneous tissue and fascia
Causes rapid extensive necrosis
Usually result of break in skin
Severe pain, even before gross clinical changes
High fever, fulminant (severe sudden onset) course, high mortality (20-70%)
Loose limbs and lots of tissue
Tissue turns to mush
What is streptococcal toxic shock syndrome?
- Deep tissue infection with strept pyrogenes
- With bacteraemia (bacteria in blood), vascular collapse, organ failure–> sudden death
- Streptococcal pyrogenic exotoxins stimulate T cells inducing monocyte cytokines and lymphokines
- M protein fibrinogen complex formation–> binds to integrins on surface of polymorphonuclear leukocytes activating the cells
- Cells adhere to endothelium and degranulate–> release large amount of hydrolytic enzymes and respiratory burst (ROS) causing damage to endothelium
- Causes hypotension, DIC and organ damage
