Session 6 Flashcards
(27 cards)
What is a surface?
Interface between a solid and either a liquid or gas.
At what point is in the infection model are surfaces important?
On the patient
What surfaces are present on the patient?
Skin:
Epithelium
Hair
Nails
Mucosal surfaces Conjunctival Gastrointestinal Respiratory Genitourinary
What organisms live on the skin that we should be aware of?
Viruses
• Papilloma
• Herpes simplex
Bacteria Gram positive: • Staph aureus (coagulase positive) • Coagulase negative staphylococci • Corynebacterium Gram negative: • Enterobacteriaceae
Fungi
• Yeasts
• Dermatophytes
Parasites
• mites
What are opportunistic pathogens?
Normally don’t cause infection in fit healthy patients but given the right opportunity can cause disease e.g. when patient is immunosuppressed or when a biologic barrier is bypassed e.g. skin.
Give examples of normal flora living on different parts of the body
Eye - viridans group streptococci
Nares - Staph aureus
Nasopharynx - Neisseria meningitidis, Streptococcus pneumoniae, Haemophilus influenzae
Mouth - Viridans Streptococci
Somach - Helicobacter, streptococci, staphylococci, lactobacilli
Intestine - aerobic and anaerobic streptococci, Clostridium, yeasts
Urethra - Enterobacteriaceae, lactobacilli
Vagina - Lactobacilli, yeasts
How do surfaces affect how people get infections?
- micro-organisms carried on skin and mucosal surfaces
- normally harmless or even beneficial
- transfer to other sites can be harmful
What is dysbiosis?
Unnatural balance of normal flora which can lead to infection e.g. as a result of antibiotic treatment.
How do people get infections?
•Invasion e.g. Strep pyogenes pharyngitis •Migration e.g. Escherichia coli urinary tract infection •Inoculation e.g. Coagulase negative staphylococcus prosthetic joint infection •Haematogenous e.g. viridans Strep endocarditis
Why is it important in knowing there’s bacteria living on people’s urethra?
When taking a urine sample some bacteria will come off the urethra and be present in sample.
Give some examples of natural surface infections
External •Cellulitis •Pharyngitis •Conjunctivitis •Gastroenteritis •Urinary tract infection •Pneumonia
Internal •Endovascular -Endocarditis -Vasculitis •Septic arthritis •Osteomyelitis •Empyema
Give examples of where prosthetic surface infections can take place
- Intravascular lines
- Peritoneal dialysis catheters
- Prosthetic joints
- Cardiac valves
- Pacing wires
- Endovascular grafts
- Ventriculo-peritoneal shunts
What pathogens can cause prosthetic valve endocarditis?
Native valve endocarditis and prosthetic valve endocarditis >1 year post-operation - Viridans Streptococci, Enterococcus faecalis, Staph aureus, HACEK group Candida
prosthetic valve endocarditis <1 year post-operation - Coagulase negative staphylococci
What are the causative organisms for prosthetic joint infections?
coagulase negative staphylococci and Staphylococcus aureus
What are the causative organisms of cardiac pacing wire endocarditis?
coagulase negative staphylococci Staphylococcus aureus
What processes are involved in the pathogenesis of infection at surfaces?
•Adherence to host cells or prosthetic surface using pili or fimbriae.
•Biofilm formation
•Invasion and multiplication
•Host response
Pyogenic (neutrophils -> pus)
Granulomatous (fibroblasts, lymphocytes, macrophages -> nodular inflammatory lesions)
What are biofilms?
Matrix of mucopolysaccharide, proteins, DNA and other molecules made and excreted by bacteria working together to surround themselves making a better environment for them to live in, attach to surfaces and protect themselves against host response and antibiotics.
What is quorum sensing?
Method of communication between bacteria. Controls: •Sporulation •Biofilm formation •Virulence factor secretion….
- Three principles
- Signalling molecules –autoinducers(AI)
- Cell surface or cytoplasmic receptors
- Gene expression ->co-operative behaviours and more AI production.
How do we manage surface infections?
Diagnosis
•Aim is to identify infecting organism and its antimicrobial susceptibilities.
•Challenges:
-Adherent organisms
-Low metabolic state/small colony variants
•Blood cultures
•Tissue/prosthetic material sonication and culture
Treatment •Aim: -Sterilise tissue -Reduce bioburden •Antibacterials •Remove prosthetic material •Surgery –resect infected material •Challenges: -Poor antibacterial penetration into biofilm -Low metabolic activity of biofilm micro-organisms -Dangers/difficulties of surgery
Prevention: Natural surface •Maintain surface integrity •Prevent bacterial surface colonisation •Remove colonising bacteria Prosthetic surfaces •Prevent contamination •Inhibit surface colonisation •Remove colonising bacteria
Describe Streptococci and its classification
• Gram positive cocci in chains.
Classification by haemolysis:
α (alpha) haemolysis (partial breakdown and looks green on an agar plate) e.g. ‘viridans’ streptococci
β (beta) haemolysis (complete haemolysis and looks yellow on agar) - Streptococcus pyogenes
Non-haemolytic γ (gamma) (no haemolysis)- Enterococcus faecalis
Can also be classified according to Lancefield antigen and Sherman group
Species - Lancefield antigen - Sherman group S pyogenes - A(β) -pyogenic
S pneumoniae - NA(α) viridans(but can be pyogenic)
S anginosusspp (S millerigroup) - A,C,F,G, or not detectable (α, β, ɣ) - viridans(but important cause of abscesses)
S mutans spp group - NA (α, ɣ) viridans
How is Streptococcus pyogenes classified?
Lancefield group A beta-haemolytic streptococcus
What are the Streptococcus pyogenes virulence factors and what does each one do?
Hyaluronic acid capsule - Inhibits phagocytosis by neutrophils and macrophages. Poor immunogen because of similarity to human connective tissue hyaluronate
M protein - Resistance to phagocytosis by inhibiting activation of alternative complement pathway on bacterial cell surface. > 150 antigenically different serotypes as a consequence of nucleotide variants of emm gene.
Adhesins, including lipoteichoic acid, M protein, fibronectin binding proteins - Adherence is first step in colonisation/infection
Streptolysins O and S - Lysis of erythrocytes, neutrophils, platelets DNAsesA, B, C and D - Degradation of DNA
Hyaluronidase - Degradation of hyaluronic acid in connective tissue
Streptokinase - Dissolution of clots through conversion of plasminogen to plasmin
Streptococcal pyrogenic exotoxins - Cleaves Ig G bound to Group A strep. Member of superantigenic Spe family (clonal T-cell proliferation)
What is Streptococcal pharyngitis?
In layman's terms - Tonsillitis • Streptococcus pyogenes • Peak incidence 5-15 years • Droplet spread • Association with overcrowding • Untreated patients develop M protein specific antibody
Clinical features: Abrupt onset sore throat Malaise, fever, headache Lymphoid hyperplasia Tonsillopharyngeal exudates Throat swab -> Group A strep
What are the possible complications of Streptococcal pharyngitis?
Scarlet fever
• Due to infection with streptococcal pyrogenic exotoxin strain of S.pyogenes
• Local or haematogenous spread
• High fever, sepsis, arthritis, jaundice, rash
Suppurative complications • Peritonsillar cellulitis/abscess • Retropharyngeal abscess • Mastoiditis, sinusitis, otitis media • Meningitis, brain abscess
Acute rheumatic fever • Inflammation of heart, joints, CNS • Follows on from pharyngitis • Rheumatogenic M types • Possible mechanisms: – Auto-immune – Serum sickness – Binding of M protein to collagen – ASO, ASS induced tissue injury
Acute post-streptococcal glomerulonephritis
• Acute inflammation of renal glomerulus
• M type specific but NOT same as ARF M types
• Antigen-antibody complexes in glomerulus
