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MBBS 3: Pediatrics > CNS Infections > Flashcards

CNS Infections Flashcards

1
Q

Pathogenesis of bacterial infection?

A
  1. bacterial invasion
  2. Production of cytokines ( e.g TNF, IL-1
  3. Increased Blood Brain Barrier Permeability (BBBP)
  4. Hypercoagulability
  5. Raised intracranial pressure (vasogenic, cytotoxic and interstitial oedema)
  6. Reduced Cerebral Blood Flow
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2
Q

Clinical features of acute bacterial infection in neonates?

A
  1. Irritability
  2. Poor feeding
  3. A bulging fontanelle
  4. Hypo/hyperthermia
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3
Q

Clinical features of ABI in older children?

A
  1. Fever
  2. Signs of raised intracranial pressure (headache, nausea and vomiting)
  3. signs of meningeal irritation (neck stiffness, Kernig’s sign and Brudzinski’s sign)
  4. Signs of cortical involvement (encephalopathy, coma)
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4
Q

Risk factors of ABI in neonates?

A
  1. Premature rupture of membranes
  2. Low birth weight
  3. Male babies
  4. Difficulty delivery with extensive manipulations
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5
Q

Causative organisms for ABI in neonates?

A
  1. E. Coli
  2. Group B Streptococcus
  3. L. monocytogenes
  4. Klebsiella
  5. Enterobacter
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6
Q

Causative organisms in infants (1 month - 2 years)?

A
  1. Group B Streptococcus
  2. S. Pneumoniae
  3. H. Influenzae
  4. N. meningitidis
  5. Salmonella species
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7
Q

Causative organisms in childhood and adolescence?

A
  1. S. Pneumoniae
  2. N. Meningitidis
  3. H. Influenzae type B
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8
Q

What is strep. pneumoniae?

A

Gram-positive diplococcus

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9
Q

When should you suspect strep. pneumoniae?

A

Should be suspected in meningitis associated with:
1. Skull fracture
2. Paranasal sinuses
3. Frontal bone CSF leak
4. Otorrhoea

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10
Q

Medical conditions to suspect strep. pneumoniae?

A
  1. Sickle cell patients (functional asplenia)
  2. Immunodeficiency e.g HIV infection
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11
Q

What is neisseria meninigitidis?

A
  • Gram negative intracellular organism
  • Epidemic forms are A and C
  • Other groups are A. B, C, D, X, Y, Z and W135
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12
Q

Clinical features of N. meningitides?

A
  1. Very rapid onset (a few hours)
  2. Petechial and purpuric rash can rapidly progress to purpura fulminans
  3. Petechial rash contains organisms
  4. Endotoxin can induce shock, bilateral adrenal haemorrhage and DIC
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13
Q

What is hemophilus influenzae?

A

Gram-negative pleomorphic bacillus
Onset of meningitis is moderately slow

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14
Q

Epidemiology of H. influenzae?

A

Found in situations of overcrowding and splenoctemized patients
Common in infants and pre-school children less than 2 years old

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15
Q

Sequelae associated with H. influenzae?

A
  1. Subdural effusions
  2. Hearing loss
  3. Epileptic fits
  4. Mental retardation
  5. Cerebral infarctions
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16
Q

CSF analysis of bacterial meningitis?

A

white cells - 100 – 50,000
Neutrophil predominant
glucose - 1.1 – 1.6
<0.5 = severe infection
protein - Mild to moderately increased

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17
Q

CSF analysis for viral meningitis?

A

white cells - 25 – 500
Lymphocytes predominant
glucose - normal
protein - mildly increased

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18
Q

CSF analysis of TBM?

A

white cells - 25 – 100 (can go up to 500)
Lymphocyte predominant but neutrophils predominate early
glucose - Less than 2.2 – 2.7
Usually less than 0.5
protein - moderately increased

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19
Q

Complications of acute bacterial meningitis?

A
  1. Subdural effusions
    – mainly HiB (to a lesser extent - N. meningitidis and S. Pneumoniae)
  2. Epileptic fits
    – focal or generalized.
  3. Cerebral oedema
    – vasogenic and cytotoxic
  4. Hydrocephalus
    – esp in neonatal meningitis - TBM, S. pneumonia (Arachnoditis and occlusion of CSF flow)
  5. Syndrome of inappropriate ADH secretion (SIADH)
    – 15 – 20%; (water intoxication: irritability and convulsions)
  6. Cranial palsies
    – most commonly sensorineural hearing loss;
  7. Hemiplegias – vasculitis and infarction
  8. Brain abscess
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20
Q

Treatment for acute bacterial meningitis?

A
  1. Antibiotics
  2. Prevent/treat complications
  3. General care of unconscious child
  4. Steroids (Dexamethasone 10-15 minutes before initiation of antibiotics in children more than 2 months)
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21
Q

What is the Herson-Todd scoring?

A

prediction of morbidity in acute bacterial meningitis

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22
Q

Scoring of Herson-Todd?

A

Factor on admission - 3
Severe coma - 2
Hypothermia - 2
Seizures - 2
Shock (BP<60 mmHg) - 1
Age <12 months - 1
CSF WBC < 1000/cu mm - 1
Haemoglobin <11g/100ml - 1
CSF glucose <1mmol/L - 0.5
Symptoms for more than 3 days - 0.5
- score of 5.5 or greater is associated with a poor prognosis

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23
Q

Prevention of N.meningitidis?

A
  1. Rifampicin 10mg/kg twice a day for 2 days
  2. Ceftriaxone 250mg imi sta (adults); 125mg imi stat children
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24
Q

Prevention of H. influenzae?

A

Rifampicin 20mg/kg twice a day for 4 days; < 1month 10mg/kg twice a day for 4 days.

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25
Q

Prophylaxis of acute bacteria meningitis for close contacts?

A
  1. H. Influenza conjugated vaccine
  2. pneumococcal vaccine.
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26
Q

What is a brain abscess?

A

Localized suppuration within the brain tissue

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27
Q

How brain abscesses develop?

A

Organisms
– via blood steam or extension from nearby focus (paranasal sinuses, middle ear)

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28
Q

Most common organisms that cause brain abscesses?

A
  1. Streptococci, staphylococci, pneumococci, H. influenzae, Bacteroides
  2. Anaerobes in 25% of cases
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29
Q

Predisposing factors that cause brain abscesses?

A
  1. Congenital cyanotic heart disease with R to Left shunt
  2. Purulent otitis media, mastoiditis, sinusitis
30
Q

Clinical features of brain abscesses?

A
  1. Raised intracranial pressure with headache, vomiting papillodema
  2. Sepsis and fever
  3. Focal neurological signs with seizures
  4. May manifest as meningitis if abscess breaks into ventricles
31
Q

Brain abscess management?

A
  1. Appropriate antibiotics with repeat CT monitoring
  2. Surgical drainage if no response to antibiotics
32
Q

Features of subdural empyema?

A
  1. Raised intracranial pressure with headache, vomiting papillodema
  2. Sepsis and fever
  3. Focal neurological signs with seizures
  4. May manifest as meningitis if abscess breaks into ventricles
33
Q

Common causes of subdural empyema?

A

sepsis from:
1. Meningitis
2. subdural haematomas
3. Mastoiditis
4. Sinusitis
5. brain abscess

34
Q

Diagnosis of subdural empyema?

35
Q

Management of subdural empyema?

A

Antibiotics and Surgical drainage

36
Q

Viruses that affect the CNS and what area of the brain is affected?

A
  1. polio - anterior horn cells
  2. varicella - cerebellar
  3. herpes - temporal lobes
  4. rabies - cortex
37
Q

Indirect relationship of HIV on the brain?

A
  1. opportunistic infections
  2. neoplasms
  3. cerebrovascular disease
38
Q

Opportunistic infections that have an indirect relationship with HIV?

A
  1. CMV
  2. Herpes simplex virus
  3. varicella-zoster)
  4. fungal infection (Candida and Aspergillosis)
  5. cryptococcal meningitis
  6. Listeria monocytogenes
  7. toxoplasmosis
39
Q

Neoplasms that have an indirect relationship of HIV on the brain?

A

CNS lymphoma

40
Q

Cerebrovascular diseases that have an indirect relationship of HIV on the brain?

A
  1. strokes (ischaemia from emboli or infectious vasculitis
  2. secondary to haemorrhage
  3. increased hypercoagulable state
41
Q

Direct relationship of HIV on the brain?

A

progressive encephalopathy

42
Q

Features of progressive encephalopathy?

A
  1. Loss of developmental milestones (motor and language)
  2. Intellectual fall-off
  3. Motor deficits (spasticity, ataxia, weakness)
43
Q

Causes of viral meningitis?

A

Caused by haematogenous spread of the following viruses:
1. HIV
2. Mumps
3. Coxsackie
4. Echovirus
5. Poliovirus
6. Herpes simplex virus (HSV types 1 and 2
7. Adenovirus
8. Varicella-zoster
9. Epstein-Barr
10. Lymphocytic choriomeningitis
11. Undetermined viruses

44
Q

Clinical features of viral meningitis?

A
  1. Fever
  2. Headache – often relieved by an LP
  3. Vomiting
  4. Neck stiffness
  5. May progress to mental depression (confusion, delirium)
  6. Usually no focal neurological findings
  7. Benign course in the majority of cases
45
Q

What is Encephalitis (meningoencephalitis, encephalomyelitis)?

A

Invasion of the CNS by virus
OR
Immune reaction between virus and the host ( post-infectious menigoencephalitis or para-infectious demyelinating encephalomyelitis)
- Often no clinical distinction between the two.

46
Q

Causes of primary encephalitides?

A
  1. HSV
  2. Rabies
  3. Varicella-Zoster
  4. Enterovirus
  5. Arbovirus
47
Q

Causes of para-infectious encephalitis?

A
  1. Measles
  2. Mumps
  3. Chicken-pox
  4. Epstein-Barr
  5. Rubella
  6. Adenovirus
  7. Influenza A
  8. Para-influenza
48
Q

Clinical features of encephalitis?

A

Vary with the infecting virus
1. Seizures and disturbances of consciousness
2. Neurological manifestation common than in viral meningitis

49
Q

How you get infected by herpes simplex virus?

A
  • Viruses may enter the brain via the meningeal nerves, or from the nasal mucosa through the cribriform plate
  • Primary infection is rare except in neonates and young infants in whom most of the infections are caused by HSV type 2 and tend to be more severe than type 1 disease
50
Q

Characteristics of herpes simplex virus infection?

A
  • Characterized by focal haemorrhagic necrotic lesions
  • Predilection for the temporal and orbital areas
  • Most cases are due to reactivation of latent disease
  • Primary infection is rare except in neonates
51
Q

Clinical features of herpes simplex virus infection?

A
  1. Prodrome of fever and malaise
  2. Mucosal lesions - may or may not be present
  3. Focal fits and focal neurological signs (hemiplegias)
  4. Signs of temporal lobe
    - disordered behavior
    - olfactory and memory hallucinations
    - aphasia)
  5. Lethargy, obtundation, coma
52
Q

Diagnosis of herpes simplex virus infection?

A
  1. EEG:
    - Symmetrical foci of spikes over temporal lobes, on an abnormally slow background
  2. CT or MRI:
    - Attenuation in the temporal lobes
    - Large areas of temporal lobe atrophy and cysts (weeks later)
  3. Biopsy – difficult and hazardous
  4. A rise in HSV antibodies esp IgM in CSF – take time to develop
53
Q

Treatment of herpes simplex virus?

A
  1. Acyclovir
    - Started as soon as possible to prevent mortality and morbidity
    - Duration: 10 days
  2. Steroids – not recommended
54
Q

Diagnosis of encephalitis?

A
  1. CSF analysis – similar to viral meningitis
  2. CT/MRI – normal except in herpes simplex encephalitis: hypodensities in the temporal lobes
55
Q

Parasitic infections?

A
  1. Malaria
  2. Neurocysticercosis
56
Q

Fungal infections?

A
  1. Candida albicans
  2. Cryptococcosis
57
Q

Causes of subacute sclerosing panencephalitis?

A

A result of prior measles infection
- 1 to 3 years or more previously

58
Q

Clinical features of subacute sclerosing panencephalitis?

A
  1. Slow onset of personality changes and intellectual deterioration
  2. Fall-off from school
  3. Apraxic- agnostic predominance
  4. Subsequent involuntary movements – myoclonic jerks
  5. Progress to severe dementia and death
  6. Treatment has been unsuccessful
59
Q

What is apraxia?

A

Apraxia is characterized by an inability to perform purposeful movements, but not accompanied by a loss of sensory function or paralysis

60
Q

What is agnosia?

A

loss of the ability to interpret sensory stimuli, such as sounds or images

61
Q

What is neurocysticercosis?

A

Caused by ingestion of ova of Taenia solium
– pig tape worm – human is an intermediate host. Cysts evoke an inflammatory response and surrounding oedema
- Death of cysts results in intense inflammatory response and produce signs and symptoms.

62
Q

Characteristics of neurocysticercosis?

A
  • Larva lodge in the CNS – particularly in vascular area (grey matter)
  • Inflammatory response and surrounding oedema results
  • Cysts can survive 2-5 years
  • Intense inflammation induced by dead cysts cause symptoms
63
Q

Symptoms of neurocysticercosis?

A
  1. Focal seizures
  2. Headache
  3. Focal neurological signs
  4. Raised intracranial pressure
  5. Psychotic symptoms
  6. Coma
  7. Obstructive hydrocephalus
64
Q

Diagnosis of neuro cysticercosis?

A

CT/MRI scan (usually diagnostic)
1. Solitary or multiple cysts within cerebral hemispheres
2. Patches of hypodensity with ring enhancement
3. Single or multiple calcified lesions
- These different appearances on CT represent the cysts in different stages of their life cycle.

65
Q

Treatment of neurocystisercosis?

A
  1. Albendazole (15mg/kg/d for 8 days)
    OR
    Praziquantel (50mg/kg/d for 14 days)
                          AND
  2. Steroids to prevent Herxheimer reaction
  3. Anticonvulsants if seizures are present
66
Q

What is the Herxheimer reaction?

A

Systemic reaction caused by the release of endotoxin-like substances when large numbers of cysts are killed.

67
Q

What is cryptococcosis?

A
  • The most common fungal infection of the CNS
  • Fungus is found in soil and pigeon droppings
  • Primary infection occurs in respiratory system
  • Hematogenously spread to CNS
  • Occurs specifically in immunocompromised patients (HIV/AIDS, neoplasia, steroid therapy)
68
Q

Clinical manifestations of cryptococcosis?

A
  1. Headache and meningeal irritation
  2. Cranial nerve palsies
  3. Raised intracranial pressure + Papilledema
  4. Impaired level of consciousness
69
Q

Clinical diagnosis of cryptococcosis?

A
  1. CSF
  2. CT scan
70
Q

CSF analysis in cryptococcosis?

A
  1. high pressure
  2. Elevated lymphocytes
  3. Increased proteins
  4. Low sugar
  5. Indian ink: encapsulated organism
  6. Antigen by latex agglutination test
71
Q

CT scan of cryptococcosis?

A
  1. cerebral oedema
  2. hydrocephalus
  3. mass lesions (granulomas)
  4. basilar enhancement
72
Q

Treatment of cryptococcosis?

A
  1. Amphotericin B (1mg/kg/d)
    AND
    Fluorocytosine (15mg/kg/d)
  2. Duration of treatment: 6 weeks
  3. HIV positive patients gets life-long prophylactic treatment with fluconazole

MBBS 3: Pediatrics (43 decks)

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