Meningitis

Question 1

What’s meningitis?
The key symptoms and the severe symptoms

Answer 1

Meningitis is a condition marked by the inflammation of the meninges, the protective membranes covering the brain and spinal cord. The key symptoms include fever, headache, neck stiffness, vomiting, and photophobia (sensitivity to light). In more severe cases, it can cause cerebral dysfunction, such as confusion or coma

Question 2

How do you diagnose Meningitis

Answer 2

Meningitis is diagnosed through cerebrospinal fluid (CSF) analysis, where an abnormal increase in white blood cells (pleocytosis) indicates inflammation. The condition can manifest either acutely (within hours to days) or as a chronic/subacute condition

Question 3

Meningitis is called chronic when it persists over

Answer 3

(symptoms persisting for over 4 weeks).

Question 4

Meningitis can be classified into?

Answer 4

Classification:

• Bacterial Meningitis: Caused by bacterial pathogens, this type is typically more severe and can lead to life-threatening complications.
• Aseptic Meningitis: Refers to meningitis caused by viruses or conditions where no bacterial infection is found.
• Non-Infectious Meningitis: Can be caused by drugs, autoimmune diseases, or infiltrative diseases (e.g., cancer).

Question 5

Meningitis affects all age groups, but certain populations are at higher risk depending on the pathogen which are? :

Answer 5

Newborns: Primarily affected by Group B Streptococcus (GBS), which is transmitted during birth.

• Children: Often affected by meningococcus (Neisseria meningitidis), Pneumococcus (Streptococcus pneumoniae), and Haemophilus influenzae type B (HiB).
• Young adults: Particularly vulnerable to meningococcal infections.
• Elderly: Predominantly affected by pneumococcal disease.

The highest burden of meningitis occurs in Sub-Saharan Africa, especially in the “African Meningitis Belt.” This region frequently experiences epidemics of meningococcal and pneumococcal meningitis.

Question 6

What are the risk factors of meningitis?

Answer 6

Risk Factors:

Overcrowding (increases the spread of infectious agents)

Immunodeficiency or immunosuppression

Smoking and alcohol consumption

Question 7

Route of Transmission of meningitis

Answer 7

The transmission of meningitis-causing pathogens varies by organism:

• Neisseria meningitidis (Nm) and Streptococcus pneumoniae (Pn) are typically transmitted via droplet infection (e.g., coughing, sneezing).

People can carry these bacteria harmlessly in their nasal passages (carriage) and sometimes build immunity, contributing to herd immunity. However, on occasion, the bacteria may invade tissues, causing disease.

• Group B Streptococcus (GBS) is transmitted from mother to child during birth (mother-to-child transmission).

The incubation period for meningitis depends on the organism, typically ranging from 2 to 10 days.

Question 8

What are the Types of Meningitis:

Answer 8

Acute Epidemic Meningitis: Sudden outbreaks, often seen in at-risk regions such as the African Meningitis Belt.

Acute Sporadic Meningitis: Isolated cases not linked to a widespread outbreak.

Subacute Meningitis: Slowly progressive, often with symptoms persisting over a month.

Question 9

What’s the pathophysiology of meningitis

Answer 9

Pathophysiology:

Infectious agents that cause meningitis often begin by colonizing the nasopharynx (back of the throat) and the respiratory tract. These pathogens can invade the central nervous system (CNS) through various routes:

• Bloodstream invasion: The most common route, where bacteria enter the bloodstream and seed into the CNS.
• Retrograde transport along nerves: Some pathogens travel along nerves, such as the olfactory nerve or peripheral nerves, to reach the brain.
• Contiguous spread: The infection spreads directly from adjacent infected areas such as the sinuses (sinusitis), middle ear (otitis media), or following surgery or trauma to the head.

Once the pathogen reaches the CNS, it triggers an inflammatory response in the meninges, which leads to the classic symptoms of meningitis and, if not treated promptly, can result in complications like brain damage or death.

Question 10

What are the classifications of meningitis it’s cause and maybe diagnosis

Answer 10

Let’s break down the classification of meningitis into understandable parts, and I’ll address grammar as we go.

• Description: This type of meningitis usually has an acute onset, meaning symptoms appear suddenly and escalate quickly.
• Cause: The causative organism varies based on the age of the patient. This means that different bacteria are responsible for meningitis in different age groups (e.g., newborns vs. adults).
• Diagnosis: It’s diagnosed using a Gram stain or culture of cerebrospinal fluid (CSF). This involves examining the CSF for bacteria using a microscope (Gram stain) or growing them in a lab (culture).

• Description: The symptoms develop more slowly, over weeks or months, compared to the acute nature of purulent meningitis.
• Common Pathogens: The main culprits are M. tuberculosis (the bacteria that cause tuberculosis), atypical mycobacteria, fungi such as Cryptococcus, Coccidioides, and Histoplasma, and spirochetes (spiral-shaped bacteria) like Treponema pallidum (syphilis) and Borrelia burgdorferi (Lyme disease).
• Diagnosis: This type of meningitis is diagnosed through cultures or, in some cases, serologic tests (blood tests that look for antibodies). For example, in diseases like cryptococcosis and syphilis, blood tests can help confirm the diagnosis.

• Description: This form is generally more benign and self-limiting, meaning it often resolves on its own without causing severe complications.
• Cause: It is mostly caused by viruses, especially herpes simplex and enteroviruses. Other causes can include infections like infectious mononucleosis (IM), Leptospirosis (L. spirosis), syphilis (T. pallidum), and Lyme disease.
• Drug-Induced: Aseptic meningitis can also be triggered by certain medications, such as NSAIDs, sulfonamides, and some monoclonal antibodies.

• Description: This refers to cases where meningitis is not treated adequately or is resistant to treatment. The infection may persist or recur because it wasn’t fully eradicated.

• Description: This type is not caused by an infection but by other conditions such as cancer (carcinomatous meningitis), sarcoidosis, systemic lupus erythematosus (SLE), or exposure to chemicals.
• Cause: It can also be triggered by medications like NSAIDs, OKT3 (a type of immunosuppressive drug), and TMP-SMX (an antibiotic combination of trimethoprim and sulfamethoxazole).

• Description: This type arises due to medical procedures like neurosurgery (e.g., craniotomy), the use of internal or external ventricular catheters (devices placed in the brain to drain excess fluid), or head trauma.
• Cause: It can also result from hospital-acquired infections, such as bloodstream infections that spread to the meninges (the protective layers around the brain).

• Description: This is a major health issue, particularly in the African “meningitis belt” (a region in sub-Saharan Africa prone to meningitis outbreaks).
• Cause: The leading cause is Neisseria meningitidis, responsible for 80-90% of cases. Other causes include Streptococcus pneumoniae and Haemophilus influenzae.
• Serogroups: Neisseria meningitidis has 12 identified serogroups (variations of the bacteria): A, B, C, D, X, Y, Z, W135, 29E, H, I, L. These serogroups help in identifying which strain of the bacteria is causing the outbreak.

1. Classification based on causative agents: Make sure you distinguish between bacterial, viral, and non-infectious causes.
2. Diagnosis methods: Focus on how each type of meningitis is diagnosed (e.g., Gram stain for bacterial, culture for chronic, and serologic tests for fungal or spirochete-related cases).
3. Regional impact: Epidemic meningitis in the African meningitis belt is a significant public health issue and should be emphasized, especially the role of Neisseria meningitidis.
4. Preventive measures: For healthcare-associated meningitis, knowing about surgical precautions and infection control could be relevant to include.

Let me know if you need more specific explanations or clarifications!

Question 11

What’s the pathogenesis of Meningococcal Meningitis

Answer 11

• Caused by Neisseria meningitidis (Nm):
  This bacterium is a Gram-negative diplococcus (a type of bacterium with two round cells together) that has a polysaccharide capsule. This capsule makes it hard for the immune system to attack the bacteria, though the organism is described as very fragile in terms of its survival outside the human body.
• Commensal in the human nasopharynx:
  Neisseria meningitidis naturally lives in the nasopharynx (the upper part of the throat behind the nose) in a commensal relationship, meaning it doesn’t cause harm in most people. Around 10-30% of adolescents and young adults carry the bacteria without showing any symptoms. This is what is meant by asymptomatic carriers.

Question 12

What’s the Geographical distribution of Meningococcal Meningitis

Answer 12

• Geographical distribution:
  Neisseria meningitidis has a worldwide distribution, and it can cause sporadic (isolated) cases, clusters (groups of cases), or even large epidemics. Epidemics, especially in certain areas like the “meningitis belt” of Africa, are more common. There are 12 serogroups (types of the bacteria):
  
  • Europe and Americas: Serogroups B, C are more common.
  • Asia: Serogroup A is prevalent.
  • Africa: Serogroups A, C, W135, Y, X are found.

Question 13

How’s Meningococcal Meningitis transmitted?

Answer 13

• Strictly a human disease: The infection spreads only among humans. There is no animal reservoir (it doesn’t infect animals).
• Direct person-to-person transmission: It spreads through respiratory droplets, like when people cough or sneeze. Close contact (within 2 meters) and prolonged exposure increase the likelihood of transmission.
• Incubation period: On average, symptoms appear 4 days after infection, but it can range from 2 to 10 days.
• Carriage in the pharynx: The bacteria are often carried in the pharynx. While some people remain asymptomatic carriers, in others, the bacteria can overwhelm the body’s defenses, leading to infection spreading into the bloodstream (bacteremia) and eventually to the meninges (the protective membranes covering the brain and spinal cord).
• Asymptomatic carriers: In general, about 1-10% of the population may carry the bacteria without symptoms, but during an epidemic, this can increase to 10-25%.

Question 14

What’s are the risk factors of Meningococcal Meningitis

Answer 14

• Hematogenous spread: After the bacteria invade the mucosal surfaces (like the lining of the nose or throat), they can enter the bloodstream, causing bacteremia. Conditions like infectious endocarditis (infection of the heart lining) can increase the risk of spread.
• Parameningeal focus: This refers to infections near the meninges, such as otitis media (middle ear infection), odontogenic infection (from teeth), or sinusitis (sinus infection), which can increase the risk of meningitis.
• Head trauma or anatomical defects: People who have had penetrating head injuries, anatomical defects in the meninges (e.g., due to trauma), or neurosurgical procedures (like brain surgery or the use of shunts to drain excess fluid) are at higher risk.
• Immunodeficiency: Conditions like asplenia (absence of a spleen), use of corticosteroids, HIV infection, and complement deficiency (a part of the immune system) increase susceptibility.
• Immunosuppression: Medications or diseases that suppress the immune system can raise the risk of infection.
• Contact with others with meningitis: Exposure to someone who has meningitis is a clear risk factor.
• Recent travel: Traveling to areas where meningitis is common (endemic areas) increases risk.
• Overcrowding: Living in crowded conditions (e.g., dormitories, military camps) increases the likelihood of transmission.

Question 15

What’s the pathogenesis of bacterial meningitis

Answer 15

Here’s how bacterial meningitis develops in the body:
1. Infection of the upper respiratory tract: The bacteria first infect the upper respiratory system, often the nasopharynx.
2. Invasion of the bloodstream (bacteremia): From the respiratory system, the bacteria break through into the bloodstream.
3. Seeding and inflammation of the meninges: Once in the bloodstream, the bacteria can reach and infect the meninges, causing meningitis. The infection leads to inflammation, which causes many of the symptoms of meningitis, like headache, stiff neck, fever, and confusion.

Question 16

1. Transmission dynamics: Understanding the close-contact nature of transmission and the importance of respiratory droplets will be crucial in discussing prevention and control measures, especially in settings like schools or during epidemics.
2. Carriage and asymptomatic carriers: You might want to emphasize how asymptomatic carriers play a key role in the spread of meningococcal meningitis.
3. Risk factors: Be ready to explain how underlying conditions like immunodeficiency and previous head trauma or surgery can make certain people more susceptible to the infection.
4. Pathogenesis details: Make sure you can explain the stepwise process from initial infection to the inflammation of the meninges. This pathophysiology is central to understanding how the disease progresses.

Question 17

0

Answer 17

Table1| Typical cerebrospinalfuid (CSĄ findings ininfectious meningits
Cause of White blood cell count
meningtis
Viral
Bacteial
Tuberc ulous
(yptococcal
(cels /mm»/10% cels /) celtype
50-1000
100-500
50- 300
Predominant
20-500
Mononuclear(nay be
neutrophiic eary in
cOuIse)
Neutrophilic
(mononuclear ater
antibiotics)
Mononuclear
Mononuclear
CSE serum glucose
(pomal 20.$)
0.5
0.5
0.3
1314
0.5
Protein (g/)
(nomal 0.2-0.4)
0.40.8
0.5-2.0
0.53.0
0.53.0

Question 18

What are the presenting symptoms in meningitis?

Answer 18

These are the symptoms that a patient will report or experience when they have meningitis or a related condition.

• Patients without meningitis:
  
  • Headache (81%): A common complaint in the majority of patients without meningitis.
  • Fever (67%): Many patients without meningitis still present with fever.
  • Nausea and vomiting (n&v, 53%): Over half of the patients report nausea and vomiting.
  • Photophobia (51%): Sensitivity to light.
  • Stiff neck (45%): Nearly half of the patients experience a stiff neck.
  • Focal symptoms/seizure (21%): Some patients may have neurological symptoms like focal deficits (e.g., weakness in a limb) or seizures.
• Patients with meningitis:
  
  • Headache (92%): Almost all patients with meningitis experience headaches.
  • Fever (71%): The majority of meningitis patients have a fever.
  • Nausea and vomiting (n&v, 70%): Most patients report nausea and vomiting.
  • Photophobia (57%): Light sensitivity remains common.
  • Stiff neck (48%): A stiff neck is a hallmark symptom of meningitis, though it’s not present in all cases.
  • Focal symptoms/seizure (18%): A smaller percentage of patients with meningitis have focal neurological symptoms or seizures.

Question 19

What are the presenting signs in meningitis?

Answer 19

These are the physical signs that a clinician can observe during an examination.

• Patients without meningitis:
  
  • Temperature >38°C (52%): Half of these patients have a fever above 38°C.
  • Neck stiffness (32%): About one-third of patients show neck stiffness.
  • Kernig’s sign (5%) and Brudzinski’s sign (5%): These signs are present in a small proportion of cases.
  • GCS <13 (7%): The Glasgow Coma Scale (GCS) score below 13 indicates altered consciousness in some patients.
• Patients with meningitis:
  
  • Temperature >38°C (43%): Fewer patients with meningitis have fever compared to those without.
  • Neck stiffness (30%): This is also slightly less common among patients with meningitis compared to those without.
  • Kernig’s sign (5%) and Brudzinski’s sign (5%): These two specific signs appear in a minority of meningitis patients.
  • GCS <13 (10%): More patients with meningitis have altered consciousness (GCS < 13).

Question 20

What are the clinical bed side tests you can do to check for meningitis?

Answer 20

• White blood cells (WBCs) in cerebrospinal fluid (CSF):
  
  • Mean WBC in patients without meningitis: 1.
  • Mean WBC in patients with meningitis: 359. This increase in WBCs reflects an immune response to infection in the CSF.

• How to elicit Kernig’s sign: The patient lies on their back with the hip and knee flexed at 90 degrees. The examiner then tries to straighten the leg. Kernig’s sign is positive when this causes resistance and pain in the lower back or hamstrings.
• When it’s positive: This sign is typically positive in cases of meningitis because stretching the inflamed meninges causes pain.

• How to elicit Brudzinski’s sign: The patient lies flat on their back, and the examiner gently lifts the patient’s head (flexing the neck). Brudzinski’s sign is positive when this causes the patient’s knees and hips to involuntarily bend.
• When it’s positive: A positive sign suggests meningitis due to the irritation of the meninges.

Question 21

What are the lab tests you can do for a patient suspected to have meningitis?

Answer 21

Lab Diagnosis
- Investigations:
1. Blood count: This helps detect infection or inflammation.
2. Blood culture: Helps identify the bacteria present in the bloodstream.
3. Lumbar puncture (LP): Essential for collecting CSF to analyze and confirm the diagnosis. The CSF is examined for glucose, protein, WBCs, and any bacteria.
4. Chest X-ray (CXR) + Mantoux test: Used if tuberculosis (TB) is suspected as the cause.

• Other ancillary investigations: Additional tests can be ordered depending on the patient’s clinical picture.

Question 22

CSF (Cerebrospinal Fluid) Examination of bacterial and viral meningitis shows?

Answer 22

• Diagnosis using LP and CSF factors:
  
  • The appearance of the CSF, levels of glucose, protein, and WBC count help differentiate bacterial vs. viral causes.
  • In bacterial meningitis, CSF analysis often shows:
    Appearance: Normal or cloudy
    
    • Low glucose (as the bacteria consume it).
    • High protein (due to the inflammation).
    • CSF leukocytosis (high WBCs in the CSF).
    • Positive Gram stain and culture help identify the bacteria.
      Predominant WBC : Neutrophil
      WBC number:500 - 10,000
    • Polymerase chain reaction (PCR): Can detect bacterial or viral DNA for accurate identification.

Viral infections
Appearance: Normal or cloudy
Glucose: normal
Protein increased
WBC : 10 - 500
Predominant WBC Lymphocyte

Question 23

A lumbar puncture is essential to:

Answer 23

• Confirm the diagnosis of meningitis.
  
  • Identify the pathogen causing the infection.
  • Perform susceptibility testing to determine the best treatment.

Question 24

Not everyone needs a CT scan before a lumbar puncture, but it’s important for certain cases such as?

Answer 24

• Clinical characteristics that predict abnormalities on a CT scan:
  
  • Focal neurological deficits: Indicate areas of the brain are affected.
  • Glasgow Coma Scale (GCS) <10: Indicates a low level of consciousness.
  • Severe immune compromise: Conditions like HIV can increase risk.
  • Seizures on presentation: If a patient has had seizures, a CT may be warranted.

Question 25

• Understand the difference in symptoms and signs between patients with and without meningitis.
• Know how to elicit Kernig’s and Brudzinski’s signs, which are used to diagnose meningitis.
• CSF analysis is crucial in determining the cause of meningitis (bacterial vs. viral) and how to treat it.
• Recognize when a CT scan is necessary before a lumbar puncture to avoid complications like cerebral herniation.

These points cover the essentials for understanding meningitis and the diagnostic process, which will be important for your exam. Let me know if you need further clarification on any points!

Question 26

In CSF test for viral, bacterial, tuberculosis and cryptococcal meningitis
How does the follow look

WBC count
Predominant cell type
CSF glucose ratio
Protein level

Answer 26

1. Viral Meningitis:
   
   • WBC Count: 50-1000 cells/mm³
   • Predominant Cell Type: Mononuclear (may be neutrophilic early in the course)
   • CSF:Serum Glucose Ratio: ≥0.5
   • Protein Level: 0.4-0.8 g/L
2. Bacterial Meningitis:
   
   • WBC Count: 100-500 cells/mm³
   • Predominant Cell Type: Neutrophilic (may become mononuclear after antibiotics)
   • CSF:Serum Glucose Ratio: ≤0.5
   • Protein Level: 0.5-2.0 g/L
3. Tuberculous Meningitis:
   
   • WBC Count: 50-300 cells/mm³
   • Predominant Cell Type: Mononuclear
   • CSF:Serum Glucose Ratio: ≤0.3
   • Protein Level: 0.5-3.0 g/L
4. Cryptococcal Meningitis:
   
   • WBC Count: 20-500 cells/mm³
   • Predominant Cell Type: Mononuclear
   • CSF:Serum Glucose Ratio: ≤0.5
   • Protein Level: 0.5-3.0 g/L

Question 27

How do you manage bacterial meningitis

Answer 27

Bacterial meningitis is considered a medical emergency, and the goal is to diagnose and treat it as early as possible to avoid complications. Here’s how the management is structured:

1. Early diagnosis: Prompt identification of bacterial meningitis is essential because delay in treatment increases the risk of severe complications or death.
2. Immediate optimum treatment: Once bacterial meningitis is suspected, the patient must receive immediate, appropriate therapy, which includes antibiotics and supportive care.
3. Intensive supportive therapy: Patients may need intensive care for monitoring and managing vital functions, such as breathing, heart function, and blood pressure.
4. Rehabilitation: Some patients may experience neurological damage or other complications that require rehabilitation to recover normal function.
5. Prophylaxis to family: Close contacts of the patient (such as family members) should receive prophylactic antibiotics to prevent the spread of the infection, especially for certain types of meningitis like meningococcal meningitis.
6. Notification to General Practitioner (GP) and Public Health: Meningitis is a notifiable disease, meaning it needs to be reported to public health authorities to manage outbreaks and protect the community.

In any medical emergency, the ABC approach stands for:
- Airway: Ensuring the patient’s airway is clear and open.
- Breathing: Ensuring the patient is breathing adequately. If needed, supplemental oxygen or ventilation may be provided.
- Circulation: Managing the patient’s blood pressure and perfusion.

• Aggressive resuscitation with IV fluids is critical, especially if the patient is in shock or has low blood pressure due to infection.

• This steroid is used mainly in pneumococcal and Haemophilus influenzae type B (HiB) meningitis to reduce inflammation and prevent long-term neurological damage.
• It must be given before or with the first dose of antibiotics. Once bacterial meningitis is confirmed, dexamethasone is continued for 4 days.

• Inotropes are medications used to increase blood pressure (especially diastolic pressure) and improve heart function in patients with severe infection (septic shock).

This phrase emphasizes the need for empiric antibiotic treatment—starting broad-spectrum antibiotics based on the most likely organisms before the exact pathogen is identified.

• Empiric antibiotic treatment is based on:
  
  • Epidemiology: Common causes of bacterial meningitis in the patient’s location.
  • Risk factors: Specific conditions that make a patient more susceptible (e.g., age, immunosuppression).
  • Local resistance patterns: The presence of antibiotic-resistant bacteria in the area, which will guide antibiotic choice.

Question 28

What are the types of Empiric Antibiotic Treatment that cab be administered?

Answer 28

1. IV ceftriaxone 2g twice daily (BD) or cefotaxime 2g four times daily (QDS): These are broad-spectrum antibiotics effective against the most common causes of bacterial meningitis.
2. Dexamethasone 0.15mg/kg four times daily (QDS) for 4 days: It’s started with the first dose of antibiotics (especially for suspected pneumococcal meningitis) and stopped if it turns out to be a non-bacterial cause.
3. IV ampicillin 2g every 4 hours: This is added if Listeria monocytogenes is suspected, particularly in:
   
   • Patients aged over 55 years.
   • Immunosuppressed patients (due to medications or conditions like HIV).
4. Consult with Microbiology:
   
   • This is necessary if the patient is a returning traveler from an area with potential antibiotic resistance, or if they are immunocompromised.

Question 29

Should Dexamethasone be used for Everyone?

Answer 29

The use of dexamethasone for all patients with suspected bacterial meningitis is still debated. However, it is commonly used, especially for pneumococcal meningitis, as it reduces the risk of hearing loss and other neurological complications. But if the infection is found to be non-bacterial, the dexamethasone treatment is usually discontinued.

Question 30

What are the complications of meningitis

Answer 30

1. Septic shock: This is a severe drop in blood pressure due to overwhelming infection, which can lead to disseminated intravascular coagulation (DIC). In DIC, the body’s blood clotting mechanisms are disrupted, leading to both excessive clotting and bleeding, which can cause organ damage.
2. Cerebral edema: Swelling of the brain due to inflammation. This is dangerous as it increases intracranial pressure and can lead to brain damage.
3. Seizures: Meningitis can cause seizures, which are sudden, uncontrolled electrical disturbances in the brain. Seizures may result from direct infection or secondary to swelling and inflammation.
4. Arteritis/Venous thrombosis: Inflammation of the arteries (arteritis) or the formation of blood clots in the veins (venous thrombosis) can impair blood flow to the brain, potentially leading to strokes.
5. Subdural effusions: Fluid may collect between the layers of tissue surrounding the brain, creating pressure and potentially worsening brain inflammation.
6. Hydrocephalus: An abnormal accumulation of cerebrospinal fluid (CSF) in the brain, leading to increased intracranial pressure and brain swelling.
7. Brain abscess: Pockets of pus can form within the brain tissue, which can be life-threatening and may require surgical drainage.
8. Deafness: Hearing loss, especially affecting cranial nerve VIII, is a common long-term complication of meningitis, particularly in bacterial cases.
9. Partially treated meningitis: This refers to cases where antibiotics have been administered before a formal diagnosis, altering typical findings in bacterial meningitis:
   • CSF may appear mainly lymphocytic rather than neutrophil-dominated.
   • Normal glucose levels may still be present.
   • Positive culture results are reduced by 30%.
   • Gram stain sensitivity is also reduced by 20%.

Complications: Headache, seizures, cerebral edema, hydrocephalus, syndrome of inappropriate antidiuretic hormone secretion (SIADH), residual neurological deficits (especially affecting cranial nerve VIII), and deafness are common. Some patients may also experience permanent brain damage or death.

Question 31

What are the Prognosis of Meningitis

Answer 31

Mortality rates:

• Streptococcus pneumoniae: ~25%
• Neisseria meningitidis: 5-10%
• Haemophilus influenzae: ~5%

Certain factors increase the likelihood of a worse prognosis:

• Extremes of age: Both very young children and the elderly are more vulnerable.
• Delays in diagnosis and treatment.
• Severe symptoms such as stupor, coma, seizures, or focal neurological signs.

Septic shock.

Question 32

How do you Prevent Meningitis

Answer 32

Prevention of Meningitis

Immunization: Vaccination is the most effective method of preventing bacterial meningitis. Safe and affordable vaccines for organisms like Neisseria meningitidis, Haemophilus influenzae, and Streptococcus pneumoniae provide long-lasting protection.

Management of sick patients and their contacts: Once a case is identified, close contacts should receive chemoprophylaxis (preventive antibiotics) to reduce the risk of spread.

Environmental control: Reducing airborne infections, particularly in hospital settings, is crucial. This may involve isolation procedures or improved ventilation.

Surveillance: Regular monitoring for meningitis outbreaks, particularly in areas like sub-Saharan Africa, is important for early detection and containment of epidemics.

Question 33

Summary of Key Facts for Your Essay

Meningitis is a severe infection with a high mortality rate and potential for long-term complications (such as brain damage and deafness).

Bacterial meningitis is particularly dangerous, causing death in about 10% of cases and leaving 20% of survivors with lasting complications.

Epidemics of bacterial meningitis are common in areas like sub-Saharan Africa, especially in the “meningitis belt.”

Vaccines are highly effective in preventing bacterial meningitis, making them the cornerstone of public health interventions.

Prompt recognition and treatment are essential to prevent severe outcomes.

Question 34

Question 1: Explain the pathophysiology of bacterial meningitis, and how it leads to neurological complications.

Answer 34

Answer: Bacterial meningitis begins with infection of the upper respiratory tract or mucosal surfaces, such as the nasopharynx, followed by invasion into the bloodstream (bacteremia). Bacteria, like Neisseria meningitidis, then penetrate the blood-brain barrier, seeding the meninges and causing inflammation. This inflammatory response triggers the release of cytokines and other immune mediators, leading to:

Cerebral edema: Swelling of the brain due to increased permeability of the blood-brain barrier, which raises intracranial pressure.
Increased intracranial pressure (ICP): This results from both cerebral edema and increased CSF production or blocked absorption, contributing to symptoms like headaches, seizures, and vomiting.
Vascular inflammation (arteritis or venous thrombosis): Inflammation can lead to strokes or venous clots, reducing blood supply to brain tissue.
Subdural effusions: Fluid can accumulate between the meninges, causing pressure on the brain.
Hydrocephalus: CSF flow is disrupted, leading to excessive accumulation and further increasing ICP.
Seizures: Direct irritation of the brain by the infection or secondary to raised ICP.
Neurological complications arise due to the increased pressure, reduced blood supply, and the direct inflammatory effects on brain tissue, which can lead to permanent brain damage, hearing loss, and cognitive deficits.

Question 35

Discuss the clinical presentation of bacterial meningitis and how you differentiate it from viral meningitis.

Answer 35

Answer: The clinical presentation of bacterial meningitis often includes:

Question 36

Question 1: Describe the pathogenesis of bacterial meningitis and the key steps involved in its progression.

Answer 36

Answer:
The pathogenesis of bacterial meningitis typically follows three key steps:

1. Infection of the Upper Respiratory Tract: Bacteria like Neisseria meningitidis, Streptococcus pneumoniae, or Haemophilus influenzae often colonize the nasopharynx, the back of the throat, without causing immediate illness. These pathogens are commensals in the nasopharynx of healthy individuals but can become pathogenic under certain conditions.
2. Invasion of the Bloodstream (Bacteremia): Under certain conditions, the bacteria invade the bloodstream, bypassing the body’s immune defenses. This can happen due to immune suppression, anatomical defects in the meningeal structures, or breaches like sinusitis or head trauma. Once in the bloodstream, the bacteria multiply and evade immune clearance due to virulence factors such as polysaccharide capsules.
3. Seeding and Inflammation of the Meninges: Once the bacteria cross the blood-brain barrier (BBB), they invade the cerebrospinal fluid (CSF) and seed the meninges, leading to inflammation. The immune system responds by sending white blood cells, especially neutrophils, into the CSF, which releases inflammatory cytokines and enzymes. This inflammatory response increases the permeability of the BBB, leading to cerebral edema, increased intracranial pressure, and damage to the brain and spinal cord.

Question 37

Question 2: Explain how you would differentiate between bacterial, viral, and fungal causes of meningitis based on cerebrospinal fluid (CSF) analysis.

Answer 37

Answer:
Differentiating bacterial, viral, and fungal meningitis is largely based on the findings in the cerebrospinal fluid (CSF) analysis:

1. Bacterial Meningitis:
   
   • Appearance: Turbid or cloudy CSF.
   • Glucose: Significantly low (<40 mg/dL), as bacteria consume glucose.
   • Protein: Elevated levels (>100 mg/dL) due to increased permeability of the blood-brain barrier.
   • WBC Count: Elevated with neutrophilic predominance (>1000 cells/µL).
   • Culture/Gram Stain: Positive for bacteria in most cases.
2. Viral (Aseptic) Meningitis:
   
   • Appearance: Clear to slightly turbid CSF.
   • Glucose: Normal, as viruses do not consume glucose in the same way.
   • Protein: Mildly elevated or normal (50-100 mg/dL).
   • WBC Count: Elevated with lymphocytic predominance (10-500 cells/µL).
   • Culture/Gram Stain: Negative for bacteria; PCR may be positive for viruses.
3. Fungal Meningitis:
   
   • Appearance: Clear to slightly cloudy CSF.
   • Glucose: Decreased but less dramatically than in bacterial meningitis.
   • Protein: Elevated but less than in bacterial meningitis (50-150 mg/dL).
   • WBC Count: Elevated with lymphocytic predominance.
   • Culture/Smear: Positive for fungi; India ink stain may show Cryptococcus.

Question 38

Question 4: What are the key clinical signs you would expect to see in a patient with meningitis, and how would you elicit Kernig’s and Brudzinski’s signs?

Answer 38

Answer:
Key clinical signs of meningitis include:

• Headache (severe, typically frontal).
• Fever (>38°C).
• Neck stiffness (nuchal rigidity).
• Nausea and vomiting.
• Photophobia (sensitivity to light).
• Seizures (focal or generalized).
• Altered mental status (ranging from confusion to coma).

Kernig’s Sign:
- To elicit Kernig’s sign, the patient is placed in a supine position with their hips and knees flexed to 90°. The examiner then attempts to extend the patient’s knee. A positive Kernig’s sign is when the patient experiences pain or resistance to knee extension, indicating meningeal irritation.

Brudzinski’s Sign:
- To elicit Brudzinski’s sign, the patient is again in a supine position. The examiner gently flexes the patient’s neck towards the chest. A positive Brudzinski’s sign is when this movement causes involuntary flexion of the hips and knees, which also suggests meningeal irritation.

Question 39

Question 3: Discuss the management of bacterial meningitis, including empiric antibiotic treatment, and justify the use of corticosteroids.

Answer 39

Answer:
The management of bacterial meningitis involves early diagnosis and immediate initiation of treatment, as the condition is a medical emergency. The key aspects of management include:

1. Empiric Antibiotic Treatment:
   
   • IV Ceftriaxone (2g twice daily) or Cefotaxime (2g four times daily) is the first-line treatment for most cases of bacterial meningitis.
   • IV Ampicillin (2g every 4 hours) is added if Listeria monocytogenes is suspected, particularly in patients >55 years of age, those with immunosuppression, or those with a history of consumption of unpasteurized dairy.
   • For patients with recent travel to endemic areas or a history of immunocompromised status, consultation with microbiology is essential for considering potential penicillin-resistant pathogens or unusual organisms.
2. Corticosteroids (Dexamethasone):
   
   • Dexamethasone (0.15 mg/kg every 6 hours) is given for 4 days in suspected cases of pneumococcal meningitis. It is administered before or with the first dose of antibiotics.
   • The rationale is that corticosteroids reduce inflammation, particularly in pneumococcal and Haemophilus influenzae meningitis, which helps reduce complications like cerebral edema and hearing loss.
   • Dexamethasone should be discontinued if a non-bacterial cause of meningitis is identified.
3. Supportive Care:
   
   • Aggressive fluid resuscitation to maintain adequate perfusion.
   • Inotropes to increase aortic diastolic pressure and improve myocardial contractility if septic shock is present.
   • Prophylaxis for close contacts, usually with rifampicin or ciprofloxacin, to prevent spread of the infection.

Question 40

Question 5: What are the most common complications associated with meningitis, and how do they affect prognosis?

Answer 40

Answer:
Common complications of meningitis include:

1. Septic Shock: This can lead to multi-organ failure and DIC, significantly increasing mortality risk.
2. Cerebral Edema: Swelling in the brain can lead to increased intracranial pressure, brain herniation, and brain damage.
3. Seizures: Common in meningitis, particularly in bacterial forms, and can cause long-term neurological damage.
4. Hydrocephalus: Accumulation of CSF in the brain, leading to increased pressure and potential for brain damage.
5. Hearing Loss: Damage to the auditory nerves, especially cranial nerve VIII, is a common long-term complication.
6. Neurological Deficits: Patients may suffer from residual motor or cognitive deficits after recovery, particularly in cases with delayed treatment or complications like cerebral infarctions.
7. Mortality: Mortality varies by pathogen:
   • Streptococcus pneumoniae: ~25%.
   • Neisseria meningitidis: 5-10%.
   • Haemophilus influenzae: ~5%.

The prognosis is worse in patients with extremes of age (very young or elderly), those who experience delays in treatment, and those presenting with coma, seizures, or septic shock.

Question 41

What are the Mechanisms that lead to Increased ICP in Meningitis

Answer 41

.
Mechanisms Leading to Increased ICP in Meningitis
1. Interstitial Edema:
- This occurs when the normal flow of cerebrospinal fluid (CSF) is obstructed, often due to hydrocephalus (an accumulation of CSF in the ventricles of the brain). In meningitis, inflammation can block CSF drainage, leading to an abnormal buildup of fluid.
- The fluid accumulation increases pressure inside the skull, which compresses brain tissue.

2. Cytotoxic Edema:
   
   • In cytotoxic edema, there is swelling of the brain cells themselves. This swelling is triggered by toxic factors released by bacteria and the immune system’s response to the infection, primarily via neutrophils (a type of white blood cell that fights infection).
   • The infected cells lose their ability to regulate water and sodium, leading to excess water retention in the cells, contributing to brain swelling.
3. Vasogenic Edema:
   
   • This type of edema arises from damage to the blood-brain barrier (BBB), which normally prevents harmful substances from crossing into the brain. In meningitis, inflammation increases the permeability of the BBB, allowing fluids and plasma proteins to leak into the brain tissue, leading to swelling.

Question 42

What’s the Pathophysiology of Increased ICP

Answer 42

The combined effect of interstitial, cytotoxic, and vasogenic edema leads to a vicious cycle:
- Obstructed CSF flow and swelling cause increased intracranial pressure (ICP).
- Worsening cerebral edema further compromises the cerebral blood flow (CBF).
- As ICP rises, it compresses the brain tissue and blood vessels, reducing the brain’s access to oxygen and nutrients.
- This can lead to ischemia (insufficient blood supply) and cell death if left untreated.

If medical intervention is delayed or inadequate, the rising ICP will continue unchecked. Eventually, this will result in endothelial injury, vasospasm (sudden narrowing of blood vessels), and thrombosis (blood clots), worsening the situation by blocking both blood flow and CSF flow further.

Question 43

What are the Systemic Effects and Outcomes of ICP

Answer 43

In addition to the effects in the brain, systemic hypotension (low blood pressure) from septic shock can reduce cerebral perfusion, depriving the brain of the oxygen it needs, thus worsening the brain’s condition. This systemic and cerebral damage can lead to diffuse central nervous system (CNS) ischemia—a reduction of blood flow throughout the brain—eventually causing death due to brain herniation or other systemic complications.

Question 44

Cerebral Edema and Its Role in ICP
Edema (swelling) in meningitis arises from various pathways:

Answer 44

• Increased CSF viscosity: Due to plasma components entering the subarachnoid space (the space where CSF flows), the CSF becomes thicker. This reduces venous outflow, contributing to interstitial edema.
• Accumulation of bacterial debris and immune cells like neutrophils leads to cytotoxic edema, as mentioned earlier.
• These forms of edema increase intracranial hypertension, which reduces cerebral blood flow. Without proper blood flow, brain cells switch to anaerobic metabolism, producing lactate (a byproduct of oxygen-deprived metabolism) and causing lactic acidosis.

Hypoglycorrhachia refers to low glucose levels in the CSF. In meningitis:
- Anaerobic metabolism increases lactate levels in the brain.
- At the same time, glucose transport into the CSF is impaired due to inflammation and damage to the blood-brain barrier.
- This depletion of glucose in the brain leads to neuronal dysfunction, as brain cells rely on glucose for energy.

If left untreated:
- Neuronal injury begins as a result of poor oxygenation, reduced glucose availability, and lactate accumulation.
- This injury can range from transient dysfunction (temporary and reversible) to permanent neuronal damage and death of brain cells, resulting in cognitive and neurological deficits.