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LECTURE MENINGITIS
Prof. Abbas Hayat
Acute, Chronic,
Bacterial, Viral,
Fungal, Parasitic,
Diagnosis and
Treatment.
NAME OF DISEASE:
Purulent meningitis Bacterial meningitis
• OVERVIEW:
The disease usually begins as an infection by normal body flora, of:
• The ear (otitis media) - Haemophilus influenzae
• The lung (lobar pneumonia) - Streptococcus pneumoniae
• The upper respiratory tract (rhinopharyngitis) - Neisseria meningitidis,
Haemophilus, influenzae, Streptococcus, Group B
• The skin and subcutaneous tissue (furunculosis) S. aureus
• The bone (osteomyelitis) - S. aureus
• The intestine - E. coli
This localized infection
develops into a Bacteremia
with a metastatic infection in
the leptomeninges.
This is exceedingly rapid in
acute bacterial meningitis
and death may occur in
hours.
Males are affected twice as often
as females.
All ages Diabetics, alcoholics,
elderly, debilitated, diseased
(untreated):
• Listeria monocytogenes
• Streptococcus pneumoniae
• Treponema pallidum
ETIOLOGICAL AGENT:
Neonates
(0-2 weeks)
Infants (2
weeks to 3
months)
Children (3
months -
6years)
Normal
adults (6
years to
21)
E.coli
Strept. Group B
Staph. aureus
Listeria
monocytogene
Strept, Group A
Strept, Group
B
Listeria
monocytogen
es
Escherichia
coli
H. influenzae
N. meningitidis
Strept.
Pneumoniae
Staph. aureus
M.
tuberculosis
N.meningitidi
s
Strept.
pneumoniae
PATHOLOGY:
The mechanism of pathology
may be either:
•1. Endotoxemic shock
•2. Disseminated
intravascular coagulation
CLINICAL SYMPTOMS:
1- Infectious manifestations:
- Chills - Headache - Fever - Myalgia -
Malaise
2- Increased intracranial pressure, manifested as
- Headache - lethargy - Vomiting --
Papilledema
- Unilateral or bilateral 6th nerve palsy,
3- Meningeal irritation
(noted by elicitation of Brudzinski's and/or
Kernig's sign) .
- Stiff neck- Spasms of the Gracilis, Sartorius
and/or Biceps
Femoris muscle - Nuchal rigidity.
4. Hemorrhage:
- Petechia - Purpura
- Ecchymosis.
5. Eye affects:
- Photophobia
- Venous congestion of ocular fundi
- Unequal pupils, Pupil dilation
- Sluggish reaction to light.
6. Mental state:
- Drowsiness - Coma
- Delirium - Stupor
– The infant with meningitis has signs of
infection but commonly is `simply fretful
and refuses food’.
• Vomiting occurs early in the disease
and is often repeated,……….
dehydration that may prevent the full
fontanelle as associated with
increased intracranial pressure.
• Fever may be absent and there may
be hypothermia.
• As the disease progresses, apnea
episodes, twitching, seizures (up to
30% of cases), opisthotonos, and
coma and death result.
• Skin rashes occur with meningococcemia,
with or without meningitis.
• From the 1st to the 3rd day, at least one-
third of patients with meningococcal meningitis
develop petechiae, most prominently in areas
subjected to pressure; for example, Axillary
folds and the belt line.
• Purplish ecchymoses and maculopapular
nodules up to 2 cm in diameter may also be
present, tending to appear first on the trunk
and later on the extensor surfaces of the thighs
and forearms.
The CSF should be examined in every
patient in whom the clinical findings are
consistent with even the possibility of
meningitis, no matter how minimal the
manifestations are.
Examine the CSF for:
1. Pressure
2. Appearance: clear or turbid
3. Wet Mount
4. Gram Stain for bacteria.
5. Geimsa stain for Presence of
neutrophils or lymphocytes or R.B.C.s.
Examination of the cerebrospinal fluid
(CSF)
6- Cell count:
Normal 0-5 cells /mm3 Markedly increased in
bacterial tuberculous and viral accordingly
7- Glucose measurement:
Normal 60 % of blood glucose, decreases in bacterial
meningitis.
8- Concentration of protein
Normal 40-60 mg/dl ++++ in bacterial +++in
tuberculous ++ in viral.
9- Look for Bacterial antigens in C.S.F
by specific Antibodies.
10- Culture.
LAB. FINDINGS IN CSF
Casual
Org.
Appear
ance
Cells/
mm3
Microbi
ology
Protein Glucose
Normal Clear
colorle
ss
0-5 lympho Sterile 20-40
mg/dl
40-60
mg/dl
Bacterial
meningit
is
Turbid 500-
20,000
mainly
polymorph
s,few
lymphos
Bacteria Markedly
increased
++++
Reduced
or
absent
Viral
(aseptic
meningitis)
Slightly
turbid
10-500
mainly
lympho
Rarely
Isolated
Serology
Normal
or
Slightly
raised
+
Normal
or
slightly
raised
+
Tuberculous
meningitis
Slightly
Turbid
Spider
Web
coagul
am
10-500
mainly
lympho,
polys in
early
stages
AFB.
medium.
Moderat
ely
Raised
++
Usually
reduced
DIFFERENTIAL DIAGNOSIS:
• Bacterial Meningitis:
Polymorphonuclear cells outnumber monocytes
Papilledema occurs late in disease when it occurs,
acute onset.
High lactate, Low glucose of CSF.
• Tubercular Meningitis:
Insidious onset
Slight changes in CSF chemistry
Positive tuberculin test
low chloride.
• Fungal Meningitis:
Insidious onset, history of lung infection, yeast
cells in CSF, slight changes in CSF chemistry.
• Syphilitic Meningitis:
Insidious onset, slight change in CSF chemistry,
positive RPR test.
• Parasitic Meningitis
Acute onset, slight change in CSF chemistry,
presence of IgM in CSF .(Trypanosoma cruzi
infection = Chagas' disease, sleeping
sickness).
(Acanthamoeba or Naegalaria species) Entry via
contaminated water or in children swimming in
contaminated water. 90% mortality, presense of
vegetative forms of amoeba on direct
examination of C.S.F.
• Viral Meningitis:
Acute onset, slight change in CSF chemistry.
Monocytes outnumber PMN's.
• Subarachnoid hemorrhage:
Red blood cells in CSF.
• Meningioma
X-ray for tumor presence.
• Meningismus
History of non-CNS viral disease ( a non-infective
state resembling meningitis).
• Brain Abscess
PMN's may outnumber monocytes, papilledema
occurs early in disease, acute or insidious onset.
Sterile CSF.
• Tetanus
Trismus, clean mentation.
THERAPY:
• General:
The risk of death during early phases of acute bacterial
meningitis relates to problems other than the
infection.
• A combination of fever, dehydration secondary to
vomiting, and decreased food and fluid intake &
subsequent alkalosis predisposes patients, especially
children, to seizures.
• Respiratory arrest or airway obstruction follows;
if significant CNS or myocardial hypoxia occurs, fatal
cardiac arrhythmias or brainstem damage may result.
• Procedures commonly employed include:
1. Correction of fluid and electrolyte
deficits.
2. Provision for adequate oxygenation.
3. Monitoring of cardiovascular function
(Give a cardiac-active glycoside if
necessary).
4. Monitoring intracranial pressure -
administer urea or mannitol to reduce
cerebral edema.
Administration of antibiotics –
Empiric regimen
• Neonate (up to 1 month old) -
Ampicillin + Cefotoxime or
Ampicillin + Gentamycin
• Neonate (1-3 months old)-
Ampicillin + Dexamethazone or
Ampicillin + Dexamethazone +
Cefotoxime
• Other (3 months - 50 years old)
Cefotoxime + Vancomycin
• (Over 50 years old or alcoholic)-
Ampicillin + Cefotoxime
CHRONIC MENINGITIS
•Tubercular meningitis
•Cryptococcosis
•Fungal meningitis
•Syphilitic meningitis
•Amoebic meningitis
TREATMENT: of Fungal
Meningitis.
1. Amphotericin B injected I.V. and into
the subarachnoid space.
2. Fluconazole
3. Ketoconazole
4. Itraconazole
5. Flucytosine (5-fluorocytosine)-
penetrates into all body fluids, including
CSF. Less toxic but higher doses required.
• Thanks for concealing your mobile
phones

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Meningitis ppt

  • 1. LECTURE MENINGITIS Prof. Abbas Hayat Acute, Chronic, Bacterial, Viral, Fungal, Parasitic, Diagnosis and Treatment.
  • 2. NAME OF DISEASE: Purulent meningitis Bacterial meningitis • OVERVIEW: The disease usually begins as an infection by normal body flora, of: • The ear (otitis media) - Haemophilus influenzae • The lung (lobar pneumonia) - Streptococcus pneumoniae • The upper respiratory tract (rhinopharyngitis) - Neisseria meningitidis, Haemophilus, influenzae, Streptococcus, Group B • The skin and subcutaneous tissue (furunculosis) S. aureus • The bone (osteomyelitis) - S. aureus • The intestine - E. coli
  • 3. This localized infection develops into a Bacteremia with a metastatic infection in the leptomeninges. This is exceedingly rapid in acute bacterial meningitis and death may occur in hours. Males are affected twice as often as females.
  • 4.
  • 5. All ages Diabetics, alcoholics, elderly, debilitated, diseased (untreated): • Listeria monocytogenes • Streptococcus pneumoniae • Treponema pallidum
  • 6. ETIOLOGICAL AGENT: Neonates (0-2 weeks) Infants (2 weeks to 3 months) Children (3 months - 6years) Normal adults (6 years to 21) E.coli Strept. Group B Staph. aureus Listeria monocytogene Strept, Group A Strept, Group B Listeria monocytogen es Escherichia coli H. influenzae N. meningitidis Strept. Pneumoniae Staph. aureus M. tuberculosis N.meningitidi s Strept. pneumoniae
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  • 8. PATHOLOGY: The mechanism of pathology may be either: •1. Endotoxemic shock •2. Disseminated intravascular coagulation
  • 9. CLINICAL SYMPTOMS: 1- Infectious manifestations: - Chills - Headache - Fever - Myalgia - Malaise 2- Increased intracranial pressure, manifested as - Headache - lethargy - Vomiting -- Papilledema - Unilateral or bilateral 6th nerve palsy, 3- Meningeal irritation (noted by elicitation of Brudzinski's and/or Kernig's sign) . - Stiff neck- Spasms of the Gracilis, Sartorius and/or Biceps Femoris muscle - Nuchal rigidity.
  • 10. 4. Hemorrhage: - Petechia - Purpura - Ecchymosis. 5. Eye affects: - Photophobia - Venous congestion of ocular fundi - Unequal pupils, Pupil dilation - Sluggish reaction to light. 6. Mental state: - Drowsiness - Coma - Delirium - Stupor
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  • 14. – The infant with meningitis has signs of infection but commonly is `simply fretful and refuses food’. • Vomiting occurs early in the disease and is often repeated,………. dehydration that may prevent the full fontanelle as associated with increased intracranial pressure. • Fever may be absent and there may be hypothermia. • As the disease progresses, apnea episodes, twitching, seizures (up to 30% of cases), opisthotonos, and coma and death result.
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  • 17. • Skin rashes occur with meningococcemia, with or without meningitis. • From the 1st to the 3rd day, at least one- third of patients with meningococcal meningitis develop petechiae, most prominently in areas subjected to pressure; for example, Axillary folds and the belt line. • Purplish ecchymoses and maculopapular nodules up to 2 cm in diameter may also be present, tending to appear first on the trunk and later on the extensor surfaces of the thighs and forearms.
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  • 20. The CSF should be examined in every patient in whom the clinical findings are consistent with even the possibility of meningitis, no matter how minimal the manifestations are. Examine the CSF for: 1. Pressure 2. Appearance: clear or turbid 3. Wet Mount 4. Gram Stain for bacteria. 5. Geimsa stain for Presence of neutrophils or lymphocytes or R.B.C.s. Examination of the cerebrospinal fluid (CSF)
  • 21. 6- Cell count: Normal 0-5 cells /mm3 Markedly increased in bacterial tuberculous and viral accordingly 7- Glucose measurement: Normal 60 % of blood glucose, decreases in bacterial meningitis. 8- Concentration of protein Normal 40-60 mg/dl ++++ in bacterial +++in tuberculous ++ in viral. 9- Look for Bacterial antigens in C.S.F by specific Antibodies. 10- Culture.
  • 22. LAB. FINDINGS IN CSF Casual Org. Appear ance Cells/ mm3 Microbi ology Protein Glucose Normal Clear colorle ss 0-5 lympho Sterile 20-40 mg/dl 40-60 mg/dl Bacterial meningit is Turbid 500- 20,000 mainly polymorph s,few lymphos Bacteria Markedly increased ++++ Reduced or absent
  • 24. DIFFERENTIAL DIAGNOSIS: • Bacterial Meningitis: Polymorphonuclear cells outnumber monocytes Papilledema occurs late in disease when it occurs, acute onset. High lactate, Low glucose of CSF. • Tubercular Meningitis: Insidious onset Slight changes in CSF chemistry Positive tuberculin test low chloride.
  • 25. • Fungal Meningitis: Insidious onset, history of lung infection, yeast cells in CSF, slight changes in CSF chemistry. • Syphilitic Meningitis: Insidious onset, slight change in CSF chemistry, positive RPR test. • Parasitic Meningitis Acute onset, slight change in CSF chemistry, presence of IgM in CSF .(Trypanosoma cruzi infection = Chagas' disease, sleeping sickness).
  • 26. (Acanthamoeba or Naegalaria species) Entry via contaminated water or in children swimming in contaminated water. 90% mortality, presense of vegetative forms of amoeba on direct examination of C.S.F. • Viral Meningitis: Acute onset, slight change in CSF chemistry. Monocytes outnumber PMN's. • Subarachnoid hemorrhage: Red blood cells in CSF.
  • 27. • Meningioma X-ray for tumor presence. • Meningismus History of non-CNS viral disease ( a non-infective state resembling meningitis). • Brain Abscess PMN's may outnumber monocytes, papilledema occurs early in disease, acute or insidious onset. Sterile CSF. • Tetanus Trismus, clean mentation.
  • 28. THERAPY: • General: The risk of death during early phases of acute bacterial meningitis relates to problems other than the infection. • A combination of fever, dehydration secondary to vomiting, and decreased food and fluid intake & subsequent alkalosis predisposes patients, especially children, to seizures. • Respiratory arrest or airway obstruction follows; if significant CNS or myocardial hypoxia occurs, fatal cardiac arrhythmias or brainstem damage may result.
  • 29. • Procedures commonly employed include: 1. Correction of fluid and electrolyte deficits. 2. Provision for adequate oxygenation. 3. Monitoring of cardiovascular function (Give a cardiac-active glycoside if necessary). 4. Monitoring intracranial pressure - administer urea or mannitol to reduce cerebral edema.
  • 30. Administration of antibiotics – Empiric regimen • Neonate (up to 1 month old) - Ampicillin + Cefotoxime or Ampicillin + Gentamycin • Neonate (1-3 months old)- Ampicillin + Dexamethazone or Ampicillin + Dexamethazone + Cefotoxime • Other (3 months - 50 years old) Cefotoxime + Vancomycin • (Over 50 years old or alcoholic)- Ampicillin + Cefotoxime
  • 31. CHRONIC MENINGITIS •Tubercular meningitis •Cryptococcosis •Fungal meningitis •Syphilitic meningitis •Amoebic meningitis
  • 32. TREATMENT: of Fungal Meningitis. 1. Amphotericin B injected I.V. and into the subarachnoid space. 2. Fluconazole 3. Ketoconazole 4. Itraconazole 5. Flucytosine (5-fluorocytosine)- penetrates into all body fluids, including CSF. Less toxic but higher doses required.
  • 33. • Thanks for concealing your mobile phones

Editor's Notes

  1. In Adults
  2. Brudziński's neck sign: With the patient lying on his back and the neck is bent forward, reflective flexion of the knees take place. Brudziński's neck sign: With the patient lying on his back and the neck is bent forward, reflective flexion of the knees take place. Brudziński's neck sign: With the patient lying on his back and the neck is bent forward, reflective flexion of the knees take place.
  3. K(1840–1917), a Baltic German neurologist, is positive when the thigh is bent at the hip and knee at 90 degree angles, and subsequent extension in the knee is painful (leading to resistance).[3] This may indicate subarachnoid hemorrhage or meningitis.[4] Patients may also show opisthotonus—spasm of the whole body that leads to legs and head being bback and body bowed backwards. Kernig's signKernig's sign (after Waldemar Kernig (1840–1917), a Baltic German neurologist, is positive when the thigh is bent at the hip and knee at 90 degree angles, and subsequent extension in the knee is painful (leading to resistance).[3] This may indicate subarachnoid hemorrhage or meningitis.[4] Patients may also show opisthotonus—spasm of the whole body that leads to legs and head being bent back and body bowed backwards
  4. The glass testSome doctors and Foundations refer to the ‘drinking glass’ or ‘pressure' test – pressing a clear tumbler firmly against the rash, to see if it fades under pressure (like a harmless rash does), or stays red, indicating a septicemic rash. The concern with this test is that it is not 100% reliable, especially in the early stages, and can give you a false sense of security. You need to keep testing at regular intervals. However if a rash appears, along with other symptoms, it's wise not to wait around trying to diagnose it yourself, but go straight to a doctor or hospital. The glass testSome doctors and Foundations refer to the ‘drinking glass’ or ‘pressure' test – pressing a clear tumbler firmly against the rash, to see if it fades under pressure (like a harmless rash does), or stays red, indicating a septicemic rash. The concern with this test is that it is not 100% reliable, especially in the early stages, and can give you a false sense of security. You need to keep testing at regular intervals. However if a rash appears, along with other symptoms, it's wise not to wait around trying to diagnose it yourself, but go straight to a doctor or hospital. The glass testSome doctors and Foundations refer to the ‘drinking glass’ or ‘pressure' test – pressing a clear tumbler firmly against the rash, to see if it fades under pressure (like a harmless rash does), or stays red, indicating a septicemic rash. The concern with this test is that it is not 100% reliable, especially in the early stages, and can give you a false sense of security. You need to keep testing at regular intervals. However if a rash appears, along with other symptoms, it's wise not to wait around trying to diagnose it yourself, but go straight to a doctor or hospital.
  5. xanthochromia [zan′thəkrō′mē·ə] a pale yellow or straw-colored discoloration of cerebrospinal fluid. It is caused by the presence of hemoglobin breakdown products, indicating that the cerebrospinal fluid has contained blood in the recent past.