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CNS INFECTIONS IN
PEDIATRICS
DR. Ayman Kilany, MD.
Ass. Professor of Neurology
National Research Centre
A 1 year old boy admitted with 4 days history of fever and vomiting.
Couple of days prior to admission, he was seen in the clinic and treated for
otitis media with Amoxicilline.
Examination revealed irritable child with a temp. of 40, and BP 130/90. He
has no focal neurological deficit but his DTR were exaggerated.
A previously healthy 5-month-old girl presents to the ER for evaluation
of fever and lethargy. The patient was in her usual state of health until 7
days ago when she began having fevers up to 38.5°C. She was seen by the
pediatrician 2 days after her fever began and was diagnosed with a viral
syndrome. Over the last 2 days she has become less energetic and playful.
Her oral intake has also decreased. Over the last day her parents have
noticed episodes of unresponsiveness, body stiffening, and left-sided jerking
lasting up to 1 minute.
A 16 year old boy presented with 2 days history of
fever and headache. On examination he has neck
rigidity and positive kernig’s sing.
What is your initial impression?
What is the main factor that alter the clinical picture of
presentation?
This is caused by inflammation of the meninges, particularly the arachnoid
and pia mater. Bacterial infection is usually associated with a
polymorphonuclear response in the subarachnoid space; while…….
viral, tuberculous and fungal infection causes a lymphocytic
response.
Meningitis is divided into acute (develops over hours to days) and chronic
(days to weeks) forms.
What are the common causes of
bacterial meningitis?
Incidence and etiology
N. meningitidis (meningococcus). Gram-negative diplococcus; most
common form of bacterial meningitis in the UK. Characterized by
purpuric rash, septicaemia (mortality 5–20 % ).
S. pneumoniae (pneumococcus). Mortality 20 %.
Group B streptococcus , E.coli , Listeria , Klebsiella in neonates.
H. influenzae type b.
Rarely Streptococcus pyogenes and Staphylococcus aureus.
Pathophysiology of Meningitis
• Route of infection is usually hematogenous
• Other routes include:
• Direct inoculation
• Contiguous spread
• Via nerves
PATHOGENESIS OF MENINGITIS
What are the symptoms and signs of meningitis?
Symptoms:
Triad of fever, headache and neck stiffness;
• may be associated photophobia and myalgia.
Signs:
• meningism (Brudzinski , Kernig, and Tripod signs)
• decreased consciousness
• petechial/purpuric rash in meningococcus;
• seizures (30 % ), cranial nerve signs (15 % ), other focal neurology (10 % );
• Septicaemic shock (particularly with meningococcus).
• In the very young and in the immunocompromised???????
Radiology:
If consciousness is reduced and/or there are focal
neurological signs, CT/MRI to exclude abscess.
Contrast studies may show meningeal
enhancement in any meningitis.
Sequelae of Bacterial Meningitis
Depends on:
Age of the patient
Duration of illness
Type of microorganism
No. of organisms in CSF
Sequelae includes:
Death 5-20% depending in the causative organism, highest with
S.pneumoniae and least with meningococcus
Hearing deficits = 5-10%
Neurologic abnormalities = 14-30%
Tuberculous meningitis
• Caused by M. tuberculosis
• TBM is often the most common form of bacterial
meningitis.
• Extrapulmonary tuberculaosis (TB) is more
common in children.
Clinical features
Non-specific prodromal features develop over days to
weeks.
Staging is useful in predicting prognosis:
• Grade 1: non-specific fever, malaise, loss of weight,
headaches.
• Grade 2: confusion, focal neurological signs, e.g. cranial
nerve palsies, seizures.
• Grade 3: coma, hemiplegia or paraplegia.
Investigations
Sputum
Sensitivity of PCR for acid-fast bacilli (AFB) is low: 20–40% in adults and
(<10%) in children
• Radiology: CXR— 50–90 % has a primary focus on CXR.
• CT/MRI with contrast: triad of meningeal enhancement (particularly in
basal cisterns), hydrocephalus, and infarction (secondary to vasculitis).
INDEX of SUSPICION
Management
What are the other causes of meningitis?
Aseptic Meningitis
• An inflammatory process of the meninges which is
characterized by CSF pleocytoins, increased protein and
absence of microorganisms on Gram’s stain and on
routine culture
• Common causes are:
• Enteroviruses 90%
• Arbovirus 5%
• Mumps 2%
Non-Viral
Partially treated meningitis
Mycoplasma pneumonia
Tuberculosis
Leptospirosis
Toxoplasmosis
Kawasakie
Malignancy
A 4 year old boy was brought to ER after having an
episode of seizure. Upon presentation to ER he continued
to have seizure and was unconscious.
What other questions in history you want to ask?
What are the possible diagnoses?
Clinical features include fever, headache,
encephalopathy, focal neurological signs, and
seizures.
Insidious onset occurs with abnormal behavior and
memory problems that can be mistaken for psychiatric
illness.
A viral cause attributed in 50% cases, with unknown
aetiology most common, but HSV, enterovirus and
varicella the most frequently diagnosed.
Possible Causes of Acute Encephalitis
Viral – Commonly Arboviruses Eastern equine  high mortality
or Enteroviruses California  severe disease
or Herpes virus
Others include:
Mumps
Measles
Rubella
Herpes viruses
Pox virus
Parvovirus
Influenza A & B
Rabies
Herpes virus
Lymphocytic choriomeningitis
II. Non-viral:
Ricketsial
Mycoplasma
Tuberculosis
Syphilis
Leptospirosis
Cat-scratch disease
Fungal
Toxoplasma
Trichinosis
Cysticanosis
Schistosanicosis
Echinococcosis
III. Para-infections
With specific
diseases: Measles
Ricketsia
Rubella
Influenza
Varicella
Mycoplasma
Mumps
With
vaccine: Measles
Influenza
Yellow fever
Rabies
Typhoid
Presentation of Herpes simplex
• Insidious or acute onset
• Fever
• Behavioral changes
• Disturbance of consciousness
• Seizure
• Neurological changes localized to temporal or frontal
lobe
(The most frequent cause of sporadic, fatal encephalitis)
Diagnosis
CSF analysis
LP prior to treatment important as HSV PCR can revert to
negative after 48–72 h, resulting in unnecessary prolonged
treatment with aciclovir.
PCR for herpes simplex in CSF
EEG and MRI
Herpes zoster encephalitis
• Can occur during acute infection or due to later
reactivation.
• The presence of a rash is unreliable: prognosis is poorer
in those without a rash.
• After chicken pox, virus lies dormant in ganglia along
entire neuraxis.
Encephalitis is due to large or small vessel vasculitis.
Management Antibiotics until a bacterial
etiology is excluded
Proven HSV-1 and -2: IV aciclovir for 21 days. Monitor
renal function.
If relapse occurs, re-treat and consider prophylaxis with oral
acyclovir or valaciclovir for 90 days.
CMV: ganciclovir and foscarnet combination therapy.
No harm from using 3–5-day pulse of methylprednisolone or
dexamethasone.
Prognosis
Depends on the cause and severity of the illness at
presentation. Mortality is improved by 40% in HSV-
1 and -2 encephalitis if acyclovir is given promptly.
Acute post-infectious cerebellitis
Most commonly described after varicella infection: also enterovirus, EBV,
mumps and measles.
More common in younger children (2–7 yrs of age).
Abrupt onset ataxia and behavioural disturbance within 5–14 days of the
chicken-pox rash (occasionally can be pre-eruptive).
Symptoms are worst at onset or within 1–2 weeks then improve over 4–8
weeks, with full recovery for the majority.
Management is supportive. Antivirals are not
routinely given.
Neuroimaging is only recommended in an atypical
presentation or course (progressive deterioration,
waxing and waning, altered sensorium, diminished
reflexes).
Differential includes Miller–Fisher syndrome.
Ayman Kilany, Paediatric CNS infection

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Ayman Kilany, Paediatric CNS infection

  • 1. CNS INFECTIONS IN PEDIATRICS DR. Ayman Kilany, MD. Ass. Professor of Neurology National Research Centre
  • 2. A 1 year old boy admitted with 4 days history of fever and vomiting. Couple of days prior to admission, he was seen in the clinic and treated for otitis media with Amoxicilline. Examination revealed irritable child with a temp. of 40, and BP 130/90. He has no focal neurological deficit but his DTR were exaggerated.
  • 3. A previously healthy 5-month-old girl presents to the ER for evaluation of fever and lethargy. The patient was in her usual state of health until 7 days ago when she began having fevers up to 38.5°C. She was seen by the pediatrician 2 days after her fever began and was diagnosed with a viral syndrome. Over the last 2 days she has become less energetic and playful. Her oral intake has also decreased. Over the last day her parents have noticed episodes of unresponsiveness, body stiffening, and left-sided jerking lasting up to 1 minute.
  • 4. A 16 year old boy presented with 2 days history of fever and headache. On examination he has neck rigidity and positive kernig’s sing.
  • 5. What is your initial impression? What is the main factor that alter the clinical picture of presentation?
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  • 7. This is caused by inflammation of the meninges, particularly the arachnoid and pia mater. Bacterial infection is usually associated with a polymorphonuclear response in the subarachnoid space; while……. viral, tuberculous and fungal infection causes a lymphocytic response. Meningitis is divided into acute (develops over hours to days) and chronic (days to weeks) forms.
  • 8. What are the common causes of bacterial meningitis?
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  • 10. Incidence and etiology N. meningitidis (meningococcus). Gram-negative diplococcus; most common form of bacterial meningitis in the UK. Characterized by purpuric rash, septicaemia (mortality 5–20 % ). S. pneumoniae (pneumococcus). Mortality 20 %. Group B streptococcus , E.coli , Listeria , Klebsiella in neonates. H. influenzae type b. Rarely Streptococcus pyogenes and Staphylococcus aureus.
  • 11. Pathophysiology of Meningitis • Route of infection is usually hematogenous • Other routes include: • Direct inoculation • Contiguous spread • Via nerves
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  • 14. What are the symptoms and signs of meningitis?
  • 15. Symptoms: Triad of fever, headache and neck stiffness; • may be associated photophobia and myalgia. Signs: • meningism (Brudzinski , Kernig, and Tripod signs) • decreased consciousness • petechial/purpuric rash in meningococcus; • seizures (30 % ), cranial nerve signs (15 % ), other focal neurology (10 % ); • Septicaemic shock (particularly with meningococcus). • In the very young and in the immunocompromised???????
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  • 22. Radiology: If consciousness is reduced and/or there are focal neurological signs, CT/MRI to exclude abscess. Contrast studies may show meningeal enhancement in any meningitis.
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  • 24. Sequelae of Bacterial Meningitis Depends on: Age of the patient Duration of illness Type of microorganism No. of organisms in CSF
  • 25. Sequelae includes: Death 5-20% depending in the causative organism, highest with S.pneumoniae and least with meningococcus Hearing deficits = 5-10% Neurologic abnormalities = 14-30%
  • 26. Tuberculous meningitis • Caused by M. tuberculosis • TBM is often the most common form of bacterial meningitis. • Extrapulmonary tuberculaosis (TB) is more common in children.
  • 27. Clinical features Non-specific prodromal features develop over days to weeks. Staging is useful in predicting prognosis: • Grade 1: non-specific fever, malaise, loss of weight, headaches. • Grade 2: confusion, focal neurological signs, e.g. cranial nerve palsies, seizures. • Grade 3: coma, hemiplegia or paraplegia.
  • 28. Investigations Sputum Sensitivity of PCR for acid-fast bacilli (AFB) is low: 20–40% in adults and (<10%) in children • Radiology: CXR— 50–90 % has a primary focus on CXR. • CT/MRI with contrast: triad of meningeal enhancement (particularly in basal cisterns), hydrocephalus, and infarction (secondary to vasculitis). INDEX of SUSPICION Management
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  • 31. What are the other causes of meningitis?
  • 32. Aseptic Meningitis • An inflammatory process of the meninges which is characterized by CSF pleocytoins, increased protein and absence of microorganisms on Gram’s stain and on routine culture • Common causes are: • Enteroviruses 90% • Arbovirus 5% • Mumps 2%
  • 33. Non-Viral Partially treated meningitis Mycoplasma pneumonia Tuberculosis Leptospirosis Toxoplasmosis Kawasakie Malignancy
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  • 35. A 4 year old boy was brought to ER after having an episode of seizure. Upon presentation to ER he continued to have seizure and was unconscious. What other questions in history you want to ask? What are the possible diagnoses?
  • 36. Clinical features include fever, headache, encephalopathy, focal neurological signs, and seizures. Insidious onset occurs with abnormal behavior and memory problems that can be mistaken for psychiatric illness. A viral cause attributed in 50% cases, with unknown aetiology most common, but HSV, enterovirus and varicella the most frequently diagnosed.
  • 37. Possible Causes of Acute Encephalitis Viral – Commonly Arboviruses Eastern equine  high mortality or Enteroviruses California  severe disease or Herpes virus Others include: Mumps Measles Rubella Herpes viruses Pox virus Parvovirus Influenza A & B Rabies Herpes virus Lymphocytic choriomeningitis
  • 39. III. Para-infections With specific diseases: Measles Ricketsia Rubella Influenza Varicella Mycoplasma Mumps With vaccine: Measles Influenza Yellow fever Rabies Typhoid
  • 40. Presentation of Herpes simplex • Insidious or acute onset • Fever • Behavioral changes • Disturbance of consciousness • Seizure • Neurological changes localized to temporal or frontal lobe (The most frequent cause of sporadic, fatal encephalitis)
  • 41. Diagnosis CSF analysis LP prior to treatment important as HSV PCR can revert to negative after 48–72 h, resulting in unnecessary prolonged treatment with aciclovir. PCR for herpes simplex in CSF EEG and MRI
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  • 43. Herpes zoster encephalitis • Can occur during acute infection or due to later reactivation. • The presence of a rash is unreliable: prognosis is poorer in those without a rash. • After chicken pox, virus lies dormant in ganglia along entire neuraxis. Encephalitis is due to large or small vessel vasculitis.
  • 44. Management Antibiotics until a bacterial etiology is excluded Proven HSV-1 and -2: IV aciclovir for 21 days. Monitor renal function. If relapse occurs, re-treat and consider prophylaxis with oral acyclovir or valaciclovir for 90 days. CMV: ganciclovir and foscarnet combination therapy. No harm from using 3–5-day pulse of methylprednisolone or dexamethasone.
  • 45. Prognosis Depends on the cause and severity of the illness at presentation. Mortality is improved by 40% in HSV- 1 and -2 encephalitis if acyclovir is given promptly.
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  • 51. Acute post-infectious cerebellitis Most commonly described after varicella infection: also enterovirus, EBV, mumps and measles. More common in younger children (2–7 yrs of age). Abrupt onset ataxia and behavioural disturbance within 5–14 days of the chicken-pox rash (occasionally can be pre-eruptive). Symptoms are worst at onset or within 1–2 weeks then improve over 4–8 weeks, with full recovery for the majority.
  • 52. Management is supportive. Antivirals are not routinely given. Neuroimaging is only recommended in an atypical presentation or course (progressive deterioration, waxing and waning, altered sensorium, diminished reflexes). Differential includes Miller–Fisher syndrome.