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Clinical Pathology > Theme 9: Clinical cardio infections: Vascular and CNS > Flashcards

Theme 9: Clinical cardio infections: Vascular and CNS Flashcards

1
Q

What are the two requirements to diagnose bacteraemia?

A

bacteraemia (bacteria detected in the blood) + symptoms/signs of infection

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2
Q

What are the 3 types of bacteraemia?

A
  1. Transient (comes and goes)
  2. Intermittent: pneunomia, pyelonephritis, abscess, meningitis
  3. Continuous: endocarditis, mycotic aneurysm, pacing lead infection, infected DVT
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3
Q

What is CRBSI and what are the 4 possible routes of colonisation and infection?

A

CRBSI - Intravascular catheter-related bloodstream infection

  1. Exit site –> can become contaminated during time of insertion or whilst handling this part
  2. Via hub contamination –> if aseptic technique isn’t used
  3. Haematogenous –> the intravascular portion can be seeded if someone has bacteraemia
  4. Via infusion –> rarely, but contaminated fusion fluid can result in colonisation of the line
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4
Q

Which micro-organisms can cause CRBSI?

A
  • coagulase negative staphylocci (30%)
  • S.aureus
  • candida (1-%)
  • enterococci (10%)
  • coliforms
  • pseudomonas aeruginosa
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5
Q

When should a CRBSI diagnosis be considered?

A

in any patient with an intravascular catheter and,

  1. Systemic signs of infection, or
  2. Bacteraemia or fungaemia
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6
Q

How do we diagnose CRBSI?

A
  • Indirect diagnosis - clinical signs resolve on catheter removal
  • same organism from at least 1 peripheral blood culture or catheter tip or
  • differential time to positivity (DTP)
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7
Q

What is differential time to positivity? (DTP)

A
  • Paired peripheral and through line blood cultures (same volume, same time) should be sent from all lumens when CRBSI is suspected
  • a DTP > 2 hours is highly specific for CRBSI
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8
Q

What is IE?

A

Infective endocarditis is infection of the endocardium or devices within the heart

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9
Q

How does a patient with IE present?

A
  1. Non specific illness (lethargy, malaise, night sweats, anorexia, weight loss)
  2. Heart failure (SOB, orthopnea, PND)
  3. Results of extra-cardiac foci of infection (back pain from HVI, stroke, abdominal pain from splenic infarct)
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10
Q

What are the signs of IE?

A
  • fevers > 38
  • spinter haemorrhages
  • oslers nodes
  • janeway lesions
  • roth spots
  • congunctival haemorrhages
  • splenomegaly
  • new murmur
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11
Q

What are the 3 biggest causes of IE?

A

Staphylococci
Streptococci
Enterococci

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12
Q

How do we diagnose IE?

A

Echocardiography (transthoracic or transoesphageal US of the heart) + blood cultures (3 sets taken at different times)

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13
Q

Why might surgery be required as a non-antimicrobial management, as well as antimicrobial methods, to cure IE?

A
  1. To replace or repair damage valves
  2. Remove infection when antimicrobials don’t work e.g abscess
  3. Remove infected devices e.g pacemaker
  4. Prevent complications like stroke
  5. Drain purulent extra-cardiac abscesses e.g in spleen or spine
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14
Q

What is a mycotic aneurysm?

A

aneurysms resulting from, or secondarily infected by, microorganisms

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15
Q

Explain the pathogenesis of a mycotic aneurysm

A
  1. Haematogenous seeding e.g secondary to IE
  2. Trauma to arterial wall + direct contamination (e.g IVDU)
  3. Extension from a contiguous infected focus
  4. Secondary to septic microemboli
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16
Q

What are the possible causes of a mycotic aneurysm?

A
  • Salmonella spp
  • S.aureus
  • Streptococcus spp
  • Pseudomonas aeruginosa
  • E.coli
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17
Q

How do we diagnose a mycotic aneurysm?

A

imaging e.g USS and detection of bacteria within tissue

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18
Q

How do we manage a mycotic aneurysm?

A

surgical removal, stenting or coiling (depending on location) with antibiotics)

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19
Q

What is an infected DVT?

A

•DVTs can be seeded with bacteria during bacteraemia or inoculated directly e.g PWID injecting into femoral vein seeds femoral DVT, infected PICC seeds axillary vein DVT

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20
Q

How do we diagnose and manage an infected DVT?

A

Diagnosis: multiple (3) blood cultures, confirmation of DVT plus exclusion of other causes e.g IE

Management: antibiotics + anticoagulation

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21
Q

What are the 3 different types of primary infections of the CNS?

A
  • meningitis
  • encephalitis
  • brain abscess
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22
Q

What is meningitis?

A

an inflammatory process of leptomeninges (inner two meninges - arachnoid and pia) and CSF

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23
Q

What is meningoencephalitis?

A

inflammation to meninges AND brain parenchyma

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24
Q

Which 3 ways can we classify meningitis?

A
  1. Acute pyogenic: usually bacterial meningitis
  2. Aseptic: usually viral meningitis, lymphocytic pleocytosis
  3. Chronic: mycobacterium tuberculosis, spirochetes (neurosyphilis)
25
Q

What are the 4 ways infectious agents can enter the CNS?

A
  1. Haematogenous spread: most common
    • Usually via arterial route
    • Can be retrograde (veins)
  2. Direct implantation
    • Most often is traumatic
    • Iatrogenic (rare)
    • Congenital (meningomyelocele)
  3. Local extension (secondary to established infections): most often from mastoid, frontal sinuses, infected tooth etc
  4. Along peripheral nerves
    • Usually viruses
26
Q

Explain the aetiology of acute bacterial meningitis according to age

A
  1. < 1 month = streptococcus agalactiae, E.coli, Listeria monocytogenes
  2. 1-23 months = streptococcus pneumoniae, neisseria meningitidis, E.coli
  3. 2-50 years = streptococcus pneumoniae, N. meningitidis
  4. > 50 years = streptococcus pneumoniae, N.meningitidis, listeria monocytogenes, aerobic gram -ve bacilli
27
Q

What are the clinical features of meningitis?

A
  • Headache
  • Irritable
  • Neck stiffness
  • Photophobia
  • Fever
  • Vomiting
  • Varying levels of consciousness
  • Rash
28
Q

How do we diagnose meningitis?

A
  • blood cultures
  • lumbar puncture: CSF for microscopy, gram stain, culture and biochemistry
  • EDTA blood for PCR for viruses and bacteria
29
Q

What is the difference in CSF in normal condition and in bacterial meningitis?

A

Normal: clear, colourless, 0-5 lymphocytes

Bacterial: cloudy, turbid, 10-2000 lymphocytes, high protein and low glucose

30
Q

What is viral meningitis?

A
  • primarily affects children and young adults
  • milder signs and symptoms
  • may start as respiratory or intestinal infection then viraemia
  • CSF shows raised lymphocyte count- protein and glucose usually normal
31
Q

What are the possible causes of viral meningitis?

A
  • Enteroviruses: Echo, coxsackie A, B
  • Paramyxovirus: mumps
  • Herpes simplex, varicella zoster virus
  • Adenoviruses
  • Other: arboviruses, lymphocytic choriomeningitis, HIV
32
Q

Explain the key features of tuberculosis meningitis

A
  • higher incidence in immigrant populations who come from countries with a higher incidence of TB
  • insidious onset
  • high frequency of complications, cranial nerve palsy
  • CSF has high lymphocyte, high protein and normal glucose
33
Q

What is encephalitis?

A

an acute inflammatory process affecting the brain parenchyma

34
Q

What is the most common cause of encephalitis?

A

Viral infection

90% is caused by herpes virus - HSV-1/2, varicella zooster, cytomegalovirus, EBV

35
Q

What are the symptoms of encephalitis?

A
  • Fever
  • Headache
  • Behavioural changes
  • Altered level of consciousness
  • Focal neurologic deficits
  • Seizures
36
Q

What is the most common cause of sporadic encephalitis in previously healthy people?

A

herpes encephalitis

37
Q

What are some features of herpes encephalitis?

A
  • might be evidence of herpes infection on skin, mucosea
  • causes severe haemorrhagic encephalitis affecting temporal bone
  • focal signs and epilepsy features
  • acute infection or commonly reactivation of latent infection (trigeminal nerve ganglion)
38
Q

How do we treat herpes encephalitis?

A

acyclovir

39
Q

What is the criteria for recurrent meningitis?

A
  • > 2 episodes of meningitis
  • symptom-free intervals
  • normal CSF between episodes
  • must be differentiated from chronic meningitis
40
Q

What is mollaret meningitis?

A

meningitis due to a viral infection (aseptic meningitis) that occurs multiple times

41
Q

What is rabies?

A
  • acute, progressive viral encephalitis
  • highest case fatality of any infectious agent
  • one of the most ancient diseases described
  • model zoonosis
42
Q

How does rabies cause infection?

A
  • Rabies virus enter through bite, grows at trauma site for a week and multiplies, then enters nerve endings and advances toward the ganglia, spinal cord and brain
  • Infection cycle completed when virus replicates in the salivary glands
43
Q

explain the 4 clinical phases of rabies

A
  1. Prodromal phase - fever, nausea, vomiting, headache, fatigue, burning, tingling sensation at site of wound
  2. Furious phase - agitation, disorientation, seizures, twitching, hydrophobia
  3. Dumb phase - paralysed, disorientated, stuporous
  4. Progress to coma phase, resulting in death
44
Q

What is neurosyphillis?

A

-syphillis infection leading to CNS invasion occurs early in infection in 35% of patients

45
Q

What are the symptoms of neurosyphilis?

A

Early form:

  • acute meningitis
  • meningovascular stroke

Late symptomatic forms (>2 years)

  • general paresis
  • tabes dorsalis
46
Q

What is tabes dorsalis?

A

slow degeneration of the nerve cells and nerve fibres that carry sensory information to the brain

47
Q

How do we diagnose neurosyphillis?

A

by blood and CSF serology

48
Q

What is a brain abscess?

A

a focal suppurative process within the brain parenchyma (pus in the substance of the brain)

49
Q

How can a brain abscess occur?

A
  • direct spread from “contiguous” suppurative focus e.g from ear 40%
  • haematogenous spread from a distant focus e.g endocarditis
  • trauma e.g open cranial fracture
  • cryptogenic
50
Q

Brain abscesses are often polymicrobial (mixed). What pathogens can they be made up of?

A
  • streptococci (70%)
  • S.aureus (10%- but most common after trauma/surgery)
  • anaerobes
  • gram -ve enteric bacteria
    other: fungi, mycobacterium tuberculosis, toxoplasma gondii
51
Q

What is the clinical presentation of brain abscesses?

A
  • Headache (most)
  • Focal neurological deficit (30-50%)
  • Fever (<50%)
  • Nausea, vomiting
  • Seizures
  • Neck stiffness
  • Papilloedema
52
Q

Why is drainage of a brain abscess the treatment of choice?

A
  • to urgently reduce ICP
  • to confirm diagnosis
  • to obtain pus for microbiological investigation
  • to enhance efficacy of antibiotics
  • to avoid spread of infection into the ventricles
53
Q

How can small brain abscesses be printed?

A

with antibiotics alone

54
Q

what do you have to consider when choosing antibiotics for treatment of CNS infections?

A

penetrations of drugs through BBB and into CSF/ brain tissue is variable

55
Q

What is the non-antimicrobial drug of choice for meningitis?

A

dexamethasone

56
Q

How does coarctation of the aorta lead to hypertension?

A
  • Narrowing of aorta increases pressure at that site
  • These are the arteries that branch off to supply the arms, and we take BP from the arms
  • But we have low pressure distal to the narrowing
  • One of the organs experiencing hypotension will be the kidneys
  • Kidneys have a big role at maintaining BP through RAAS - if the kidney senses the BP has fallen, they compensate through the chain of events below
  • So the BP increases further
57
Q

What are the effects of hypertension superior to the coarctation of the aorta?

A
  • headache
  • saccular aneurysms
  • stroke
  • coronary diseases
58
Q

What are the effects of hypotension distal to the coarctation of the aorta?

A
  • decreased perfusion of the renal
  • claudication in the legs
  • decreased pulses in the inferior limbs
59
Q

How can an abdominal aneurysm present?

A
  • ruptured
  • pulsatile abdominal mass
  • limb ischaemia
  • PR bleeding

Clinical Pathology (57 decks)

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