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PHARM 213 Infectious Diseases > 2. Epidemiology, Presentation & Diagnosis > Flashcards

2. Epidemiology, Presentation & Diagnosis Flashcards

1
Q

ID: Environment

A
  • Climate
  • Geography
  • Healthcare systems
  • Exposure
  • Social
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2
Q

ID: Host

A
  • Symptoms
  • Immunity/Susceptibility
  • Risk behaviour
  • Lifestyle
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3
Q

ID: Pathogen

A
  • Virulence
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4
Q

Infections could be:

A
  • Endogenous - arise from within the body e.g. bacteria
  • Exogenous - superficial layers of the skin
  • Subclinical - asymptomatic
  • Clinical - disease
  • Caused by flora, colonising organisms, or exogenous organisms
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5
Q

Types of skin infections:

A
  • Cellulitis - affects dermis & subcutaneous tissues (deeper layers)
  • Erysipelas - superficial layers of the skin
  • Impetigo - school sores
  • Shingles / Chicken pox - caused by the same virus
  • Necrotising faciiitis
  • Carbuncles (boils) - caused by S. aureus
  • Lymphangitis (associated with cellulitis)
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6
Q

Cellulitis: How does bacteria cause illness?

A
  • Bacteria colonise skin
  • Bacterial toxins (cytolysins) damage epithelial cells
  • Damaged epithelial cells release cytokines (e.g. IL-1, TNF-a, IL-8 which contributes to neutrophil chemotaxis)
    + Cytokines are produced by injured & healthy cells (via stimulation of TLRs)
    + IL-1 & TNF-a instruct capillary endothelial cells to express cellular adhesion molecules (e.g. selectins, CAMs)
  • Skin macrophages & dendritic cells follow chemical gradient to the site of infection - also release cytokines
  • Selectins interact with carbohydrates on neutrophils causing them to slow, roll & tether to epithelium - diapedesis
  • Tethered neutrophils are pulled between the epithelium (vie PECAM interactions) & migrate to the site of infection - chemotaxis
  • PAMPs (e.g. peptidoglycan lipotechoic acid) bind to PRRs (e.g. toll-like receptors) which activate innate immunity
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7
Q

Complement immune response

A
  1. Lectin pathway: Bacterial carbohydrates binds to proteins
  2. Alternative pathways: Complement spontaneously starts to form on cell surfaces
  3. Classical pathways: Antibody, immunoglobin binds to bacterial antigen
  • Once triggered a number of proteins combine to for C3 convertase which cleaves C3 into C3a & C3b
    + C3b is an opsonin - binds to bacteria & enhances recognition & phagocytosis
  • Some C3b binds back to the C3 convertase to form C5 convertase which cleaves C4 in C5a & C5b
    + C5b binds with C6 to C9 to form the membrane attach complex (MAC) which lyses bacteria (gram negative)
  • C3a & C5a are anaphylatoxins - increase vascular permeability
    + C5a is also a chemotactic protein
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8
Q

End result of bacterial infections (Cellulitis)

A
  • Increased vascular permeability in the skin leads to erytherma
  • Changes to larger vessels & lymphatic vessels leads to swelling
  • Purulent materials contain neutrophils & other phagocytes, dead cells, viable bacteria, dead bacteria, cell debris & extracellular protein
  • Cytokines, cellular debris & bacterial degradation products stimulate nerves to cause pain
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9
Q

Causes of cellulitis

A
  • Streptococcus pyrogenes
  • Staphylococcus aureus
  • Other bacteria
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10
Q

Causes of boils/furuncles:

A
  • S. aureus
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11
Q

Causes of other skin infections:

A
  • Fungi

- Viruses

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12
Q

Streptococcus pyrogenes:

A
  • Gram positive cocci
  • Colonises 10-15% of oropharynx
  • Also causes: Pharyngitis, Skin & soft tissue infections
  • Bone & joint infections
  • Rheumatic fever
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13
Q

How does S. pyrogenes avoid the immune system & cause disease”

A
  • Various toxins (streptolysins) damage cells such as neutrophils & platelets
  • DNAses digest DNA to avoid being trapped in neutrophil extracellular traps
  • Streptokinase activates plasminogen into plasmin which digests fibrin
  • Adhesins which bind to host tissues (MSCRAMMs = microbial surface components recognising adhesive matrix molecules)
  • Hyaluronic acid capsule prevents opsonisation & phagocytosis
  • C5a peptidase degrades C5a reducing chemotaxis
  • M proteins (another MSCRAMM) binds factor H, which degrades complement
    + M proteins also interfere with C3 binding to C3b receptor on phagocyte cell
    + There are different types of M proteins & often a particular M protein is associated with a particular disease
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14
Q

Diagnosis of bacterial illness (cellulitis)

A
  • Clinical (look at skin) + Blood tests looking for antibodies/cytokines
  • Lab swabs of purulent material
  • If admitted to hospital, blood cultures should also be taken
    + Very sick individuals should be tested for sepsis (e.g renal failure)
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15
Q

Treatments for cellulitis

A
  • Antimicrobial drugs that are primarily directed at S. pyrogenes & S. aureus
  • Analgesia
  • Lifestyle changes such as supportive care (maintain “normla” physiology), rest & elevation
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16
Q

Treatment of cellulitis - Penicillin

A
  • Penicillin binds to transpeptidase, preventing cross-linking
  • Inhibition of transpeptidase impairs repair of cell wall & leads to release of autolysis that digest the cell wall
  • Bacterium dies

Penicillins:

  • Peptidoglycan is the main component of bacterial cell wall
    + N-acetylmuramic acid (NAM)
    + N-acetylglucosamine (NAG)
    + Glycans have peptide chains – alanine, glutamine, lysine & alanine
    + Cross-linked terminal peptides (lysine to terminal alanine)
  • Transpeptidase (penicillin binding protein – PBP) forms bonds between tetrapeptide chains
17
Q

Penicillins - B lactam antibiotics

A
  • Structure: B-lactam ring + Thiazolidine ring + Side chain
  • Includes all penicillin derivatives, cephalosporins, carbapenems & the monobactam
  • All S. pyrogens are susceptible to penicillin, but only 10% of S. aureus are
18
Q

Cellulitis - Risk factors

A

~1500 cases at Auckland Hospital

Risk factors for cellulitis include:

  • Prior cellulitis (24%)
  • Diabetes (21%)
  • Morbid obesity (18%)
  • Chronic venous insufficiency (12%)
  • Heart failure (12%)
  • Prior DVT (4%)
  • Peripheral vascular disease (4%)
  • Immunosuppressed (3%)
  • Maori & Pacific people are at increased risk of skin infection in NZ
19
Q

Endocarditis

A
  • Inflammation on heart valves or other cardiac structure (e.g. ventricular septal defect)
  • Almost always caused by bacterial infection
  • Clumps on heart valves will grow a ton of bacteria
20
Q

Endocarditis & heart function

A
  • As myocardium contracts, blood flows through the aortic valve into the aorta
  • As the myocardium relaxes, the aortic valve closes & prevents blood falling back into the left ventricle
  • If the aortic valve is leaking, as the myocardium relaxes, blood can flow back into the ventricle – this blood flow (regurgitation) is turbulent
  • The shearing forces of turbulent blood flow, over long time periods, can damage endothelial cells on the surface of the connective tissue (valve) and can expose the connective tissue matrix
  • A wide range of bacteria (staphylococci & streptococci) have surface molecules that recognise & bind to exposed connective tissue
  • Bacteria in the blood stream that bind to exposed connective tissue due to turbulent blood flow caused by a leaking heart valve can form a mass – a vegetation = ENDOCARDITIS
  • Endocarditis can occur on any heart valve, septal defect, pacemaker wire…
21
Q

Common risk factors for endocarditis

A 
- Valve damage:
\+ Rheumatic fever
\+ Mitral valve prolapse
\+ Bicuspid aortic valve
\+ Congenital heart disease
- Old age
- Prosthetic valve
- Other cardiac device
- IV drug use
- Recent cardiac surgery
- Central venous catheters
22
Q

Clinical features of endocarditis

A

Systemic:

  • Fever (80%)
  • Chills (60%)
  • Aches/pain (20%)
  • Weight loss
  • Sweating
  • Lethargy

Valve:

  • Leaking
  • Cardiac abscess
  • Need for surgery (30%)

Embolic:

  • Infection at another site
  • Stroke
  • Leg/gut artery occlusion

Vasculitis:

  • Glomerulonephritis (20%)
  • Splinter haemorrhages (30%)
  • Other (10%)
23
Q

Diagnosis of endocarditis

A
  • Persistent bacteraemia with usual organism
  • Ultrasound of heart valves to visualise vegetations
  • Presence of other phenomena
24
Q

Treatment of endocarditis

A
  • Sterilise the valve with surgery of antibiotics
  • Usual treatment with bactericidal antibiotic (penicillin)
  • 10 - 30% mortality

PHARM 213 Infectious Diseases (13 decks)

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