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Clinical Pathology > Lecture 52 - Part 1 Clinical Infections - Vascular and CNS > Flashcards

Lecture 52 - Part 1 Clinical Infections - Vascular and CNS Flashcards

1
Q

Bacteraemia

A

not a diagnosis - bacteria have been detected in the blood

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2
Q

what indicates a blood stream infection

A

bacteraemia + symptoms/signs of infection

eg. intravascular catheter-related bloodstream infection

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3
Q

Types of bacteraemia

A

Transient
Intermittent
Continuous

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4
Q

Types of intermittent bacteraemia

A

pneumonia, pyelonephritis, abcess, meningitis, CRBSI

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5
Q

Types of continuous bacteraemia

A

endocarditis, mycotic aneurysm, pacing lead infection, infected DVT

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6
Q

Infective endocarditis

A

infection of the endocardium or devices within the heart

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7
Q

Presentation of Infective endocarditis

A
  • non-specific illness (lethargy, malaise, night sweats, anorexia, weight loss)
  • Heart failure (SOB, orthopnea, PND)
  • Results of extra-cardiac foci of infection (back pain from HVO, stroke, abdominal pain from splenic infarct

Particularly if known heart valve disease, pacemaker, prosthetic valve, congenital heart disease

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8
Q

Clinical examination of infective endocarditis

A 
fevers more than 38
splinter haemorrhages
oslers nodes
janeway lesions
roth spots
conjunctival haemorrhages
splenomegaly
new murmur
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9
Q

Aetiology of infective endocarditis

A

Staphylococci and Streptococci, enterococci, pseudomonads, enterobacteriaceae

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10
Q

Diagnosis of infective endocarditis

A

ECG (transthoracic and transoesophageal) and blood cultures ( 3 sets taken at different times) - 2 in severe sepsis

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11
Q

Non-antimicrobial management of infective endocarditis

A

IE requires antimicrobial therapy - ideally directed towards pathogens identified by blood cultures

in addition, surgery may be required to:

Replace or repair damaged valves
Remove infection when antimicrobials don’t work
Remove infected devices e.g. pacemaker
Prevent complications like stroke
Drain purulent collections e.g. in spleen or spine

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12
Q

Mycotic aneurysm

A

Definition: aneurysm resulting from, or secondarily infected by microorganisms

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13
Q

Pathogenesis of mycotic aneurysm

A

Haematogenous seeding (e.g. secondary to IE)
trauma to arterial wall + direct contamination (e.g. IVDU)
extension from a contiguous infected focus
secondary to septic microemboli (e.g. secondary to IE)

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14
Q

Presentation of mycotic aneurysm

A

usually systemic symptoms of infection and variable symptoms from aneurysm depending on location

  • no localising symptoms
  • painless swelling
  • painful swelling
  • symptoms caused by rupture (e.g. intracerebral haemorrhage, collapse.
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15
Q

Aetiology of mycotic aneurysm

A

Salmonella spp., Staphylococcus aureus, Streptococcus spp., Pseudomonas aeruginosa, Escherichia coli.

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16
Q

Diagnosis of mycotic aneurysm

A

Imaging (e.g. USS) and detection of bacteria within tissue.

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17
Q

Management of myctoic aneurysm

A

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

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18
Q

infected DVT

A

DVTs can be seeded with bacteria during bacteraemia or directly e.g. IVDU injecting into femoral vein, seeds femoral DVT

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19
Q

presentation of INFECTED DVT

A

symptoms/signs of DVT and systemic infection and/or respiratory symptoms (when infected thrombus breaks from DVT travels via the venous system to the lungs – infected pulmonary emboli)

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20
Q

Aetiology of infected DVT

A

Depends on mechanism but commonly S. aureus, streptococci and anaerobes in IVDU

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21
Q

diagnosis of Infected dvt

A

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

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22
Q

Management of infected DVT

A

Antibiotics plus anticoagulation

23
Q

What are the different types of primary infection of the central nervous system (CNS)

A

Meningitis
Encephalitis
Brain Abscess
Subdural Empyema

24
Q

How infectious agents can enter CNS

A

Haematogenous spread:

  • most common
  • usually via arterial route
  • can be retrograde (veins)

Direct implantation

  • most often is traumatic
  • iatrogenic (rare)
  • congenital (meningomyelocele)

Local extension (secondary to establish infections): most often from mastoid, frontal sinuses, infected tooth, etc.

Along peripheral nerves: usually viruses: Rabies, Herpes zoster

25
Q

What is meningitis

A

Meningitis refers to an inflammatory process of leptomeninges and CSF (Meningoencephalitis refers to inflammation to meninges and brain parenchyma)

26
Q

classification of meningitis

A

Acute pyogenic: usually bacterial meningitis
Aseptic : usually viral meningitis
Chronic: Mycobacterium tuberculosis (TBM), spirochetes (neurosyphilis), Cryptococcus

27
Q

Clinical features which suggest meningitis

A 
Headache
irritable
neck stiffness
photophobia
fever
vomiting
varying levels of consciousness
rash

groups below may have non-specific presentation

  • neonates
  • elderly
  • immunosuppressed
28
Q

Common bacterial pathogens in 0-4 wks

A

Streptococcus, agalactiae, Escherichia coli, Listeria monocytogenes, Klebsiella pneumoniae, Enterococcus spp, Salmonella spp

29
Q

Common bacterial pathogens in 4-12 wks

A

S, agalactiae, E coli, L. monocytogenes, Haemophilus influenzae, Streptococcus pneumoniae, Neisseria meningitidis

30
Q

Common bacterial pathogens in 3 months to 18 yrs

A

H influenzae, N meningitidis, S pneumoniae

31
Q

Common bacterial pathogens in 18-50 yrs

A

S pneumoniae, N. meningitidis

32
Q

Common bacterial pathogens in over 50 yrs

A

S pneumoniae, N meningitidis, L. monocytogenes, aerobic gram-negative bacilli

33
Q

Laboratory diagnosis for meningitis

A

Blood cultures
Lumbar puncture: CSF for microscopy, Gram stain, culture & Biochemistry
EDTA blood for PCR

34
Q

CSF Abnormalities in Meningitis

A

Normal
- Clear colourless, 0-5 lymphocytes,

Bacterial
- Cloudy turbid, 100-2000 polymorphs, orgs, high protein, low glucose

Viral (aseptic) - clear, slightly cloudy, 10-500 lymphocytes, protein normal, glucose normal

TB (chronic)
- Clear, slighlty cloudy, 10-500 lymphocytes protein high and glucose low

cryptococcal
-clear, 10-200 lymphocytes, protein slightly elevated, glucose slightly reduced

35
Q

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 (50-200/cu/mm); protein and sugar usually normal
full recovery expected

36
Q

Causes of viral meningitis

A

Enteroviruses: Echo, coxsackie A,B, polio
Paramyxovirus: mumps
Herpes simples, VZV
Adenoviruses
Other: arboviruses, lymphocytic choriomeningitis, HIV

37
Q

Tuberculous meningitis

A

Higher incidence in immigrant populations who come from countries with high TB incidence

Insidious onset
High frequency of complications, cranial nerve palsies
Delayed diagnosis makes complications more likely
CSF shows predominantly lymphocytic response but polymorphs also present
High protein, low/absent sugar
-Remember increasing MDR TB

38
Q

Encephalitis

A
  • Acute inflammatory process affecting the brain parenchyma
  • Viral infection is the most common and important cause, with over 100 viruses implicated worldwide

Symptoms

  • fever
  • headache
  • behavioural changes
  • altered level of consciousness
  • focal ner
39
Q

Causes of viral encephalitis

A

Herpes virus - HSV-1, HSV-2, Varicella Zoster virus,
cytomegalovirus, Epstein-barr virus, human herpes virus 6
-adenoviruses
-influenza A
- Enteroviruses, Poliovirus
-Measles, mumps and rubella viruses
-Rabies
-Arboviruses: Japanese encephalitis; St. Louis encephalitis virus, West Nile encephalitis virus

40
Q

Herpes encephalitis

A

Most common cause of sporadic encephalitis in previously healthy
May be evidence of herpes infection of skin, mucosae
Causes severe haemorrhagic encephalitis affecting temporal lobe
Focal signs and epilepsy features
2-4 cases/million people/year
Acute infection or more commonly reactivation of latent infection (trigeminal nerve ganglion)
30% mortality with treatment
70% mortality without treatment

High mortality so treatment urgently needed with

Aciclovir

41
Q

treatment for herpes encephalitis

A

Aciclovir

42
Q

Recurrent meningitis symptoms

A

> 2 episodes meningitis
Symptom-free intervals
Normal CSF between episodes
Must be differentiated from chronic meningitis

43
Q

Rabies

A

Acute, progressive viral encephalitis
Highest case fatality of any infectious disease
One of the most ancient diseases described
Model zoonosis

44
Q

Pathogenesis of rabies

A

Virus enters 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

45
Q

Clinical phases of rabies

A

Prodromal phase – fever, nausea, vomiting, headache, fatigue; some experience pain, burning, tingling sensations at site of wound

Furious phase – agitation, disorientation, seizures, twitching, hydrophobia

Dumb phase – paralyzed, disoriented, stuporous
Progress to coma phase, resulting in death

46
Q

Brain abscess

A

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

47
Q

how do brain abscesses occur

A

Direct spread from “contiguous” suppurative focus (e.g. from ear 40%, sinuses, teeth)

Haematogenous spread from a distant focus e.g. endocarditis, bronchiectasis (often multiple abscesses)

Trauma (e.g., open cranial fracture, post-neurosurgery)

Cryptogenic (no focus is recognised ~15-20 per cent of cases).

48
Q

Causes of brain abscesses

A

bacteria depend on the pathogenic mechanism involved
Brain abscesses are often mixed (polymicrobial)

Streptococci (60-70 %) e.g. Streptococcus “milleri”
Staphylococcus aureus (10-15 percent) most common pathogen in abscesses after trauma/surgery
Anaerobes e.g. Bacteroides spp.
Gram negative enteric bacteria (E.coli, Pseudomonas spp.)
Others e.g. fungi, Mycobacterium tuberculosis, Toxoplasma gondii

49
Q

Clinical presentation of brain abscesses

A 
Headache
Focal neurological deficit (30-50%)
fever (<50%)
Nausea, vomiting
seizures
neck stiffness
papilloedema
50
Q

Management of brain abscesses

A

Drainage is treatment of choice (N.B small abscesses can be treated with antibiotics alone)
to urgently reduce intracranial pressure
to confirm diagnosis
to obtain pus for microbiological investigation
to enhance efficacy of antibiotics
to avoid spread of infection into the ventricles

51
Q

Principles in antibiotic treatment of CNS infections

A

Physiological properties of blood-brain barrier and blood CSF-barrier are distinct

Penetration of drugs into CSF and brain tissue differ

Ampicillin, Penicillin, Cefotaxime, Ceftazidime, and Metronidazole achieve therapeutic concentrations in intracranial pus

52
Q

Steroids used for CNS infections

A

Dexamethasone
10mg IV 15 minutes prior to antibiotics
Shown to decrease morbidity & mortality in S. pneumoniae but NOT N. meningitidis

53
Q

What is neurosyphilis

A

Central nervous system invasion occurs early in infection in 30-40% of patients
Asymptomatic neurosyphilis can occur at any stage of syphilis
Early symptomatic forms (months to a few years)
Acute meningitis
Meningovascular (stuttering stroke)
Late symptomatic forms (> 2 years)
General paresis
Tabes dorsalis
Diagnosis by blood & CSF serology

Clinical Pathology (16 decks)

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