11. Strep And Sars Covid Flashcards
How do microorganism cause disease
Steps:
- Exposure
- Adherence
- Invasion
- Multiplication
- Dissemination
Virulence factors (disease- causing factors
factors in the microorganism that help them establish infection.
• Cell wall components
• Capsule
• Antigens on surface
Enzymes - causing diseases
- Catalase
* Coagulase
Toxins
– diarhoea or destroy cells to give themselves a suitable environment
• Exotoxins
• Endotoxins
• Enterotoxins
Host cellular damage
• Direct or indirect
• Consequent to host immune response
e.g. coronavirus, Tb, sepsis
Examples of bacteria which produce exotoxins:
- Clostridium tetani
- Clostridium botulinum
- Corynebacterium diphtheriae
- Staphylococcus aureus
- Streptococcus pyogenes
Exotoxins
Extotoxins –> proteins produced into the environemnt that come out of bacteria
Endotoxins
Endotoxins – constituents of gram negative bacteria cell wall, lipid portion of LPs in cell wall
Enterotoxins
—> Toxins which affect intestine and are produced by a number of bacterial species including:
- Escherichia coli (E.coli) - cause diarrhoea
- Staphylococcus aureus (S.aureus) - diarrhoea food poisoning
- Vibrio cholera (V.cholera)- affect gut = diarrhoea
•Staphylococci - visual
•Staphylococci grow in all directions and are normally seen as bunches of Gram positive cocci under the microscope – grow in all directions
Streptococci - visual
•Streptococci normally appear in chains as they grow along one apex – grow in one diraction
Staphylococci - catalase test
• Staphylococci are catalase positive – produce catalase
Streptococci - catalase test
• Streptococci are catalase negative – do not produce catalase
Staphylococci - coagulase test
- Staphylococcus epidermidis (S.epidermidis) among other Staphylococci is Coagulase-negative
- Staphylococcus aureus (S.aureus) is Coagulase-positive
Coagulase
• Coagulase is an enzyme which produces clotting of the plasma by converting fibrinogen to fibrin in the immediate vicinity of the bacteria. - virulence factor of staphy
○ The resulting fibrin meshwork surrounds the bacterial cells or infected tissues, protecting the organism from innate immune mechanisms such as phagocytosis and the anti-staphylococcal activity of normal serum.
Streptococci - features
- Gram positive cocci
- Catalase negative
- Facultative anaerobes - (capable of growth both aerobically and anaerobically) presence and absence of oxygen
- Erythrogenic toxins (pyrogenic exotoxins) - affect small capillaries = red rash
- Cytolytic toxins (streptolysins S and O) - affect the cells
Streptococci
• Commensals – found in:
– Nasopharangeal carriage
– GI tract
– Female genital tract
Streptococci – classification by haemolysis
α (alpha) haemolysis
β (beta) haemolysis
Non-haemolytic γ (gamma)
α (alpha) haemolysis - streptococci
- ‘viridans’ streptococci
* Streptococcus pneumoniae
β (beta) haemolysis - strep
• Streptococcus pyogenes
Non-haemolytic γ (gamma) - strep
• Enterococcus faecalis
What you see when you grow streptocci on blood agar plates
- Alpha hemolysis = green area, incomplete lysis of rbc
- Beta heamolysis = complete clearing of the area e.g. strep pyogenes
- Non harmolytic gamma – enteroccoci
Classification of Streptococci – Lancefield Grouping
• Lancefield, 1933 –beta-haemolytic streptococci are classified based on carbohydrate antigen (substance C) in the cell wall referred to as Lancefield group A to V (excluding I and J)
Most of the grouping refers to beta hamolytic strep
• Most important are beta haemolytic Lancefield group A and B
Virulence factors of Streptococci – M protein
—> long structure very important in strep, helps microoragnism to evade phagocytosis
• Major virulence factor for the Group A streptococci
• Inhibits complement and protects organisms from phagocytosis
- However, once the body starts to produce antibodies to M proteins, these act as opsonins and bind to the M proteins – coat microorganisms that have M protein facilitating phagocytosis of the bacteria
- Involved in adherence
Virulence factors of Streptococci – Streptolysin (Cytotoxic)
—> Streptolysin O (oxygen labile – inactivated by oxygen
• Destroys red and white blood cells
• Responsible for beta haemolysis of Group A streptococci
• This enzyme is antigenic and following infection gives rise to antibodies (ASO)
• ASO antibodies confirm recent infection – to streptolysin O oxygen labile toxin produced by streptococci
–> responsible for clearing that you see on the plate
Streptolysin S (oxygen stable) • Responsible for beta haemolysis but is not antigenic
Virulence factors of Streptococci - Pyrogenic exotoxin
– also called erythrogenic toxin
—> produced by steptococi
• Found in a few strains of beta haemolytic Group A streptococci(step pyogennes) which can cause scarlet fever
○ Damaging small capillaries to give red rash
Hyaluronic acid capsule
Virulence factors of Streptococci
• Inhibits phagocytosis by neutrophils and macrophages Poor immunogen because of similarity to human connective tissue hyaluronate
Hyaluronidase
Virulence factors of Streptococci
• Degradation of hyaluronic acid in connective tissue
Streptokinase
Virulence factors of Streptococci
• Dissolution of clots through conversion of plasminogen to plasmin
Species of streptococci
Streptococcus pneumoniae Viridans streptococci Streptococcus bovis Streptococcus pyogenes Streptococcus agalactiae
Streptococcus pneumoniae
- Alpha haemolytic
- No lancefield group
- Pneumonia Otitis media Sinusitis Meningitis Peritonitis
Viridans streptococci
- Alpha haemolytic
- No lancefield
- Dental infections (S.mutans) Endocarditis – subacute bacterial endocarditisBacteraemia Abscesses (S.milleri)
Streptococcus bovis
• Alpha and gamma haemolytic
• Group D
UTI Endocarditis, Sepsis, Colorectal cancer
Streptococcus pyogenes
- Beta haemolytic
- Group A
- Pharyngitis Skin infections Scarlet fever Toxic shock syndrome Necrotising fasciitis Pneumonia Bacteraemia
Streptococcus agalactiae
- Beta or gamma haemolytic
- Group B
- Most common cause of meningitis in 1-3 months old
How infections cause disease
Strep and staph
- Strep pyogenes toxins can form a super antigen
• Superantigen don’t react in same way as normal antigens- Superantigen bind to MHCII and start the process of cytokine release and atrtacting cells into the area
- As so much of the superantigen attaches to MHCII – cell overreacts to give toxic shock syndrome
Enzyme release
• Local inflammation, invasion of tissue
• Skin infection, pharyngitis, otittis media
Nacteramia
• Metastatic spread
• Menigntisis, arthritsi, osteomyelitis
Antigen • Immunce complex formation • Post streptoccoal glomerulonerphritis • Antibody formation --> antibodies can react with body tissue to form disease • = acute rheumatic fever
Streptococcal pharyngitis
Clinical features
- Abrupt onset sore throat
- Malaise, fever, headache
- Lymphoid hyperplasia
- Tonsillopharyngeal exudates
- Throat swab -> Group A strep
—> Streptococcus pyogenes = quite frequently isolated in strep pharyngitis
• Peak incidence 5-15 years
• Droplet spread
• Association with over-crowding
• Untreated patients develop M protein specific antibody- act as opsonins to remove pathogen
Normally gets better by itself without antibiotics
Complications of Streptococcal pharyngitis
Toxins produced can cause Scarlet fever –> interfere with small capillaries = bleeding
• Due to infection with streptococcal pyrogenic exotoxin strain of S.pyogenes
• Local or haematogenous spread
• High fever, sepsis, arthritis, jaundice
Complications of Streptococcal pharyngitis Rheumatic fever
- Rheumatic fever is a rare complication of streptococcal throat infection that can affect many connective tissues, especially in the heart, joints, skin, or brain
- Develops 2-4 weeks after streptococcal throat infection
- Caused by cross- reactive antibodies produced as a result of cross reacting antigens on the joint tissue, heart, brain and the streptococcal antigens (specially M protein)
- Characterised by fever, rash, carditis (inflammation of the heart) and arthritis
Rheumatic heart disease
- heart valves can be inflamed and become scarred over time resulting in narrowing or leaking of the heart valve making it harder for the heart to function normally. Can take years and may result in heart failure
- Can cause permanent damage
Complications of Streptococcal pharyngitis —> Acute post-streptococcal glomerulonephritis
1 week after impetigo or pharyngitis
• Acute inflammation of renal glomerulus
• Antigen-antibody complexes on the basement membrane of the glomerulus cause disease
Impacts the kidney
Infective endocarditis
Infection of inner surface of the heart usually the valves (mitral valve). (positive blood culture)
Symptoms include: • Fever • Heart murmur • Feeling tired • Heart failure • Petechia - are tiny purple, red, or brown spots on the skin caused by bleeding under the skin.
Skin infections with Streptococcus pyogenes
Skin layer and infections specific to the layer
- The superficial keratin layer= (impetigo)
- the superficial epidermis = (erysipelas)
- the subcutaneous tissue =(cellulitis)
- the fascia = (necrotizing fasciitis)
• Impetigo
– Childhood infection, 2-5 years
– Initial skin colonisation, followed by intradermal innoculation
– Impetigo is most common cause of glomeruonephritis
Common in crowded places
Strep pyogennes in superficial keratin layer
• Erysipelas
– Dermis infection
– Face, lower limbs
– Facial lesions
– Lower limb infection usually secondary to invasion of skin via trauma
Strep pyogennes infection of epidermis
• Cellulitis
– Skin and subcutaneous tissue infection
– Impaired lymphatic drainage and illicit injecting drug use important risk factors
Strep pyogennes infection of subcutaneous tissue
• Necrotising fasciitis
– Infection of deeper subcutaneous tissues and fascia.
– Rapid, extensive necrosis
– Usually secondary to skin break
– Severe pain, even before gross clinical changes – High fever, fulminant course, high mortality (20-70%)
Strep pyogenes infection of fascia
Toxic shock syndrome
- TSS is mainly caused by Streptococcus pyogenes or Staphylococcus aureus
- Due to production of exotoxins (superantigens) by the infecting bacteria which enter deep tissues and bloodstream
Signs and symptoms:
• Fever
• Nausea
• Diarrhoea
• Hypotension • Organ failure
Superantigens
---> Superantigens bypass the normal immune response by binding directly to MHC class II antigen on the antigen presenting cell and the outer portion of the T cell receptor on the T helper cells. • Stimulated T helper cells produce vast amounts of cytokines resulting in toxic shock
Treatment of TSS Treatments includes:
- IV fluids
- Antibiotics
- Incision and drainage of abscess (if present)
- Intravenous immunoglobulin
Complications of Streptococcal pharyngitis
- Peritonsillar abscess(quinsy) – pus behind the tonsils
- Retropharyngeal abscess - collection of pus in the back of the throat
- Cellulitis- infection involving inner layer of the skin affecting dermis and subcutaneous fat
- Mastoiditis, sinusitis, otitis media
- Meningitis, brain abscess
Treatment of Streptococcal infections
• Phenoxymethylpenicillin (most streptococci are still sensitive to penicillin) = so can give penicillin as a treatment to strep infections
- In necrotising fasciitis and toxic shock syndrome (TSS) Clindamycin is added to Phenoxymethylpenicillin because Clindamycin inhibits protein synthesis in the bacteria. This results in reduction of toxin production.
- Combinations of antibiotics
