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inf & imm > Week 3 TB, Bacteraemia, Line Infx and Endocarditis > Flashcards

Week 3 TB, Bacteraemia, Line Infx and Endocarditis Flashcards

1
Q

What is the difference between bacteraemia, systemic inflammatory response syndrome (SIRS), septicaemia and sepsis/ septic shock?

A

1) Bacteraemia
- Presence of bacteria in the bloodstream
- Px can still be well

2) Septicaemia
- Presence of bacteria
- Px is unwell and displaying symptoms

3) Sepsis / septic shock
- Often interchangeable with septicaemia
- Most serious infection
- May have manifestations such as SIRS
- Septic shock usually has signs of end organ damage

4) SIRS
- Systemic inflammatory response to a variety of severe clinical insults
- HR >90/min
- RR > 20/min
- >38degC or <36degC
- WBC <4000 or >12,000

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2
Q

What are the components of the MEWS (Modified Early Warning System)?

A
  • HR
  • RR
  • SpO2
  • Temperature
  • BP
  • Conscious level
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3
Q

How to detect central-line associated bacteraemia or septicaemia? (IMPT)

A
  • Same as non-line associated
  • Blood taken from line and peripheral vein (same bacteria to be detected in both to be considered CL-associated as CL may just be colonised by skin flora)
  • Positive growth from the line culture >2 hrs BEFORE growth from PV culture
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4
Q

How to detect bacteraemia or septicaemia, if not associated with lines? (IMPT)

A
  • Blood taken from peripheral vein
  • Take 2 sets of blood cultures (1 for aerobic culture, 1 for anaerobic)
  • 10 mL in each bottle (maximise yield and insufficient volume may lead to false positives)
  • Trigger for blood culture may be pyrexia
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5
Q

Endocarditis brief and risk factors?

A
  • Infection of the endocardium of the chambers and heart valves

Risk factors:
- Men, elderly
- Congenital heart disease
- Valvular heart disease
- Prosthetic heart valve

  • Left (aortic and mitral valve) more affected
  • Right (tricuspid) endocarditis is more common in IV drug users
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6
Q

Endocarditis causes?

A
  • Usually due to bacteraemia from line-associated infx
  • Staphylococci
  • Streptococci (esp Strep viridans and Strep bovis)
  • Candida
  • Enterobacteriacea, Pseudomonas aeruginosa and Mycobacteria are more uncommon
  • IV drug use
  • Invasive medical procedures
  • Colonic cancer (by Strep)
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7
Q

Complications of endocarditis?

A
  • Congestive heart failure (due to damaged heart valve)
  • Stroke (septic emboli in brain)
  • Brain / lung / kidney abscess (from septic emboli)
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8
Q

What samples to send when testing for endocarditis?

A
  • 3 sets of blood cultures of 10 mL each (all samples must show the same bacteria growth)
  • Blood taken before antibiotics are given
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9
Q

What are the treatment options for endocarditis?

A
  • Weeks of IV antibiotics
  • Valve surgery (but only if)
    ~ Heart failure
    ~ Persistent sepsis
    ~ Septic emboli in major organs
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10
Q

What are coagulase-negative staphylococci?

A
  • Gram-positive aerobes
  • Bacteria which cannot form coagulase (an enzyme that promotes thrombus formation by converting fibrinogen to fibrin)
  • Usually part of commensal bacteria flora
  • Able to form biolfims (helps to avoid host defenses)
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11
Q

Which group of people are more likely to develop infections from coagulase-negative Staphylococcus?

A
  • Medical implants (eg prosthetic heart, pacemakers)
  • Allows the bacteria to colonise, proliferate and gain access to the systemic circulation
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12
Q

What are the main mycobacterial groups?

A
  • Mycobacterium tuberculosis complex
  • Mycobacterium avium complex (MAC) / Non-tuberculosis mycobacteria (NTM)
  • Mycobacterium leprae
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13
Q

What are the bacteria that falls under Mycobacterium tuberculosis complex (MTBC)?

A
  • Mycobacterium tuberculosis (MTB)
  • M bovis (cattle, unpasteurised milk)
  • M caprae (cattle)
  • M microti (rodents)
  • M pinnipedii (seals)
  • M africanum
  • M cannetti
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14
Q

What is the microbiology of MTB?

A
  • Acid-fast aerobic bacilli
  • Waxy, lipid outer wall prevents effective staining using Gram staining
  • Lipid wall protects MTB from disinfectants
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15
Q

Mode of transmission of MTB?

A
  • Inhalation of droplets which were aerosolised by coughing, sneezing or talking
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16
Q

What is the infectivity level of patient bases? (IMPT)

A
  • Positive sputum AFB smear: Highly infectuous
  • Negative sputum AFB smear, positive culture: less infectious
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17
Q

What is the pathogenesis of primary MTB?

A

1) Airborne droplet nuclei of MTB reach terminal airspaces in the lungs, where multiplication begins
2) In the lungs, there is usually an initial primary focus
3) Macrophages in the lungs ingest the bacteria but are destroyed when they multiply
4) Macrophageal destruction attracts lymphocytes and more macrophages to the site
- Infected macrophages at the site of infx may lead to Pneumonitis
- Infected macrophages may also travel through the lymphatic circulation (hilar @GI, mediastinal, supraclavicular, retroperitoneal @GIT)
- Finally, infected macrophages may be spread by blood to lymph, kidneys, vertebral body, meninges and apical-posterior areas of the lungs (most common)

5) For the first few weeks after primary infection, there is unrestrained MTB replication in both primary and lymphohaematogenous metastatic foci
6) 3-9 weeks after primary infection, cell-mediated immunity and hypersensitivity occurs
7) In most cases, infection is controlled by the immune system
8) In some cases, the bacterial load in the initial primary focus (Ghon focus) reaches sufficient size for hypersensitivity to lead to necrosis and radiologically visible calcification (on X-ray)

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18
Q

What does a tuberculin skin test (TBT) and Gamma Interferon Release Assay (IGRA) show?

A
  • Positive result shows previous exposure to MTB
  • Does not indicate whether infx is active or not (but can tell when TB is active because patient would have symptoms)
  • Both tests depend on cell-mediated immunity (T-cell)
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19
Q

What is the clinical significance of granuloma formation in TB?

A

Pathologic features of tuberculosis are the result of the degree of hypersensitivity and local concentration of antigen

19
Q

What does small antigen load + high tissue hypersensitivity indicate?

A
  • Good organisation of cells and capillaries results in a well-formed granuloma
  • Constitutes a successful tissue reaction with a contained infection
  • Will heal with eventual fibrosis, encapsulation and scar formation
20
Q

What does high antigen load + low tissue hypersensitivity indicate?

A
  • Poor organisation of immune cells lead to incomplete necrosis
  • Forms caseating/cheesy granuloma
  • Tends to liquefy and discharge through the bronchial tree to produce a tuberculous cavity with high numbers of MTB
  • Infectious material sloughed from a cavity creates new exudative foci in other parts of the lung
21
Q

What are the possibilities of progression following primary infection?

A

1) Latent TB infection (due to encapsulation)
2) Formation of large hilar or mediastinal lymph nodes
3) Extrapulmonary TB
4) Re-activation of TB
5) Pleural effusion
6) Miliary/disseminated tuberculosis

22
Q

What happens when there is formation of large hilar/mediastinal lymph nodes?

A
  • Infection erodes into a bronchus and spreads infection distally
  • Infection cavitates and spread via the bronchi
  • Bronchial collapse
  • Occurs mostly in children
23
Q

What happens when there is formation of extrapulmonary TB?

A
  • TB that affects organs and tissues outside the lungs
  • May present as:
    ~ Meningitis
    ~ Lymphadenitis
    ~ Pericarditis
    ~ Peritonitis
    ~ Hepatitis etc
24
Q

What happens during re-activation of MTB?

A
  • Deposition of MTB in the apical-posterior area of the lung where disease progressed w.o interruption of became latent
  • After a period of latency, when immune system becomes too weak, reactivation occurs
25
Q

How does pleural effusion occur because of TB?

A
  • Subpleural primary focus ruptures
  • Common in adolescents and young adults
26
Q

What happens during miliary TB?

A
  • Worst-case scenario
  • Caseous material directly reaching the bloodstream
  • In very young people, miliary TB is often followed by tuberculous meningitis
  • Also seen in the very old, HIV and immunocompromised
27
Q

What are some risk factors for latent Tb to re-activate?

A
  • Recent infection due to close contact to a person with TB
  • Infancy, 15-25 y/o, old age
  • Inability to contain latent infection due to immunosuppression
28
Q

Is latent TB infectious? (IMTP)

A
  • Asymptomatic and non-infectious
29
Q

What is the management for latent TB?

A
  • With drugs that are similar to those used for active TB
  • 6/9 mth isoniazid daily
  • 3 mth rifapentine + isoniazid weekly
  • 3/4 mth rifampicin + isoniazid daily
  • 3/4 mth rifampicin daily
30
Q

What are the s/s of active MTB?

A
  • Fever (due to ^ IL-1)
  • Night sweats
  • Weight loss (due to TNF)
  • Chronic cough
  • Lymphadenopathy
  • Malaise
  • Anorexia
  • Haemoptysis (bloody sputum)
31
Q

How to diagnose active TB? (IMPT)

A
  • s/s
  • Physical examination
    ~ Percussion dullness (pleural effusion possible)
    ~ Crackles upon auscultation
    ~ Whispered pectoriloquy
  • Blood tests
    ~ Normocytic, normochromic anaemia
    ~ Hyponatremia (low sodium)
    ~ ^ LFT
    ~ Pyuria/^ WBC
    ~ CSF contains WBC, protein and glucose
  • Chest X-ray
    ~ Can show hilar lymphadenopathy, apical infiltrate, or bilateral apical cavitations (holes)
    ~ Miliary nodules can also be seen (for active TB)
  • Microbiological tests
    ~ At least 2 sets of early morning sputum (nasogastric aspirate for children)
    ~ Urine or CSF AFB smear
    ~ Specimens for biopsy or fluid test
    ~ Blood tests
  • Histopathology
    ~ To test for caseating granulomas and AFB
32
Q

How to carry out culture for Active MTB?

A
  • 15-20 hrs to replicate and requires 8 weeks incubation in a special culture media (or 4-6 weeks to grow acc to Prof CKL?)
  • Solid media
    ~ 3-8 weeks
    ~ Agar contains glycerol (encourage growth) and malachite green (reduce contaminants)
  • Liquid media
    ~ Grown in Mycobacterial Growth Indicator Tube (MGIT)
    ~ 1-3 weeks
33
Q

How is active TB treated?

A
  • Isolate patient
  • Empirical treatment
    ~ Treatment done w/o results/diagnosis
    ~ Rifampicin, Isoniazid, Ethambutol, Pyrazinamide
    ~ Course of usually 6 months
    ~ TB drugs may interact with HIV drugs
  • Directly observed therapy (DOT)
    ~ To ensure drug compliance and prevent Abx resistance

When px is no longer infectious:
- Around 2 weeks after effective treatment
- 3 consecutive negative AFB smear specimens

34
Q

What drugs are MDR and XDR TB resistant to?

A

MDR-TB
- Rifampicin and Isoniazid

XDR-TB
- Rifampicin, Isoniazid, Fluoroquinolone

35
Q

What is the timeline for MCS and PCR for TB and drug resistance?

A

1) Microscopy
- AFB -> Pos culture (weeks)
- Pos culture -> Sensitivity (weeks)
- Sensitivity (weeks)
- Final results 1-2 months

2) PCR (2 hours)
- Information on presence of TB and Rifampicin resistance

36
Q

How to prevent MTB infection?

A
  • BCG vaccine
    ~ Live-attenuated derived from M bovis
    ~ Does not prevent infection but prevents progression to clinical disease
    ~ Prevents miliary TB in young children
    ~ Not recommended to give to immunocompromised patients as virus may be too strong
37
Q

What are the causes of leprosy?

A
  • Mycobacterium leprae
  • Transmitted mostly through respiratory droplets and nasal secretions
  • Occurs mostly in males >30 y/o
38
Q

What are the clinical manifestations of leprosy?

A
  • Peripheral sensory nerve damage
  • Hypopigmentation
  • Erythematous skin lesions
  • Hypoesthesia (loss of sensation)
  • Weakness
39
Q

What is tuberculoid leprosy?

A
  • Px with strong cell-mediated immune response to M leprae
  • s/s:
    ~ 1-2 hypopigmented skin lesions
    ~ Thickened peripheral nerves
    ~ Biopsy of skin lesions rarely show any bacilli
40
Q

What is lepromatous leprosy?

A
  • Px with absent cell-mediated immune response against M leprae
  • s/s:
    ~ Intense oedema of affected tissue
    ~ Facial lip swelling w/ collapse of nose bridge~ Tissue biopsy w/ undifferentiated macrophages packed with AFB
    ~ Mycobacteremia spreading to nasal and pharyngeal mucosa, eye, muscles, testicles and bone marrow~ Highly infectious due to nasal discharge
41
Q

How to diagnose leprosy?

A
  • Physical examination
  • Histology for skin, nerve and retina (gold standard)
  • Examination of slit skin smears for AFB
  • PCR
42
Q

What is the treatment for leprosy?

A
  • Rifampicin, Dapsone and Clofazimine
  • Correct deformities
  • Prevent further blindness and further damage to anaesthetic limbs
  • Treat reactions to anti-leprosy drugs
43
Q

What is Non-tuberculous Mycobacteria (NTM) and what is an example? (IMPT)

A
  • Bacteria closely related to M tuberculosis but do not cause the disease
  • AFB positive
  • Ubiquitous in the environment (household water, potting soil, vegetable matter, animals and birds)
  • Cases in chronic infections involve patients with underlying disease
  • eg Mycobacterium avium complex (MAC)
44
Q

What is MAC?

A
  • Not spread from person to person
  • Can be caused by:
    ~ Disseminated disease (HIV, CD4 < 50/mm3)
    ~ Lymphadenitis
    ~ Pulmonary diseases
45
Q

What is the treatment for Non-tuberculosis mycobacteria?

A
  • NTMs are resistant to many antibiotics
  • Combination drugs done together
  • Months to years of treatment

inf & imm (19 decks)

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