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SOM 307 – NERVOUS SYSTEM AND SPECIAL SENSES > WEEK 2: CNS infections > Flashcards

WEEK 2: CNS infections Flashcards

1
Q

Outline the different bacterial Infections of the central nervous system.

A

Meningitis
Suppurative encephalitis
Brain abscess
Paravertebral (epidural) abscess
Tuberculosis
Neurosyphilis
Leprosy (peripheral nerves)
Tetanus (motor cells)

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2
Q

Outline the different viral infections of the central nervous system.

A

Viral infections
1. Aseptic Meningitis
2. Encephalitis

  1. Transverse myelitis: Viral infection causing inflammation of the spinal cord
  2. Progressive multifocal leukoencephalopathy (PML): Caused by the (John Cunningham) JC virus infecting oligodendrocytes in the brain, leading to demyelination.
  3. Subacute sclerosing panencephalitis (late sequel)(SSPE): Late complication of measles virus infection.
    Progressive neurological decline, including cognitive decline, seizures, and movement disorders.
  4. Poliomyelitis: Caused by the poliovirus, leading to inflammation of the spinal cord and brainstem.
  5. Rabies: Caused by the rabies virus transmitted through animal bites.
  6. HIV infection: Caused by the human immunodeficiency virus, which attacks the immune system, including the brain.
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3
Q

Outline protozoal Infections of the central nervous system.

A

Protozoal infections
Malaria
Toxoplasmosis (in immunosuppressed)
Trypanosomiasis
**Naegleria
**Acanthamoeba
Amoebic abscess
**Helminthic infections: There are three types of helminths: flukes (trematodes), tapeworms (cestodes), and roundworms (nematodes). When these worms get into the human body, they can cause parasitic infection,
Cysticercosis
Hydatid disease
Strongyloidiasis
Schistosomiasis (spinal cord)

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4
Q

Outline fungal Infections of the central nervous system.

A

Fungal infections
Candida meningitis
**Cryptococcal meningitis
Histoplasma
Blastomyces
Coccidioides
**Prion diseases
**Creutzfeldt-Jakob disease
**Kuru

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5
Q

What is meningitis?

A

Inflammation of meninges - is a medical emergency.

Meningitis is an infection of the meninges-dura, arachnoid, and pia and the CSF surrounding the brain.

-Caused usually by infection with virus, bacteria or fungi/parasites.

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6
Q

Meningitis is classified on the basis of the characteristics of inflammatory exudate on CSF examination and the clinical evolution of the illness into:

State the courses of the following types of meningitis.
1. Acute Meningitis
2. Chronic Meningitis:
3. Aseptic Meningitis

A

*Acute:
Pyogenic type → Bacteria
*Chronic:
Granulomatous type → Bacteria/fungi/ parasite

*Aseptic - This subtype is characterized by acute viral meningitis.
- It is called “aseptic” because no bacteria can be cultured from the cerebrospinal fluid (CSF) of affected individuals.
-Viruses such as herpes simplex virus, enteroviruses, and arboviruses are common causes of aseptic encephalitis [[3]].

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7
Q

Define the following and state their main causative pathogens.
1. Encephalitis.
2. Meningoencephalitis
3. Brain abscess

A

Encephalitis: inflammation of brain tissue →Viruses

Meningoencephalitis → Viruses
It refers to inflammation of both the brain and the meninges, which are the membranes that surround the brain and spinal cord. Like encephalitis, viruses are a common cause of meningoencephalitis.

Brain abscess: pus in the brain → Complication of bacterial meningitis

-While it is not directly related to encephalitis, it can be a complication of bacterial meningitis
-Brain abscesses can pose harm by placing pressure on the functional tissues of the brain.
-Treatment for brain abscesses may involve surgical drainage of the pus.
.

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8
Q

A 22 year old military recruit presents with altered mental status following a bout of high grade fever.
Three days ago he had reported that he had felt ill and complained of sore throat, chills, a severe cough, and muscle aches followed by headache & stiff neck.

O/E: T- 39.6 °C, RR28/min, BP 82/40 mmHg, HR 133/min.

Purpuric lesions noted over axillae, flanks, wrists and ankles. No papilledema.

FBC –decreased WBC, platelet count and circulating clotting factors.

Lumbar Puncture: CSF
Increased Opening pressure
Increased Neutrophils
Low glucose
High protein

-Gram Stain: Gram negative diplococci

What is the possible diagnosis?

A

The combination of symptoms, signs, and laboratory findings suggests a possible diagnosis of meningococcal meningitis. Meningococcal meningitis is caused by the bacterium Neisseria meningitidis and is characterized by inflammation of the meninges (the protective membranes surrounding the brain and spinal cord). It is a severe and potentially life-threatening condition that requires immediate medical attention and treatment with antibiotics.

The presence of purpuric lesions over the axillae, flanks, wrists, and ankles is concerning for meningococcal septicemia, which is a bloodstream infection caused by the same bacterium. Meningococcal septicemia can lead to disseminated intravascular coagulation (DIC), which can explain the decreased platelet count and circulating clotting factors observed in the laboratory findings.

The abnormal CSF findings on lumbar puncture, including increased opening pressure, increased neutrophils, low glucose, and high protein, are consistent with bacterial meningitis. Bacterial meningitis is characterized by an inflammatory response in the CSF, with increased white blood cells (predominantly neutrophils), elevated protein levels, and decreased glucose levels.

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9
Q

Outline the bacterial causes of meningitis- Infective

A

Group B Streptococcus
Listeria Monocytogenes
E. coli
Strep pneumoniae
Neisseria meningitidis
Hemophilus influenzae
Staphylococcus aureus
Mycobacterium tuberculosis
Brucella
Syphilis
Lyme disease (Borelliosis)

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10
Q

Outline the viral causes of meningitis- Infective

A

Enteroviruses (ECHO, Coxsackie, polio)
Mumps
Influenza
Herpes simplex
Varicella zoster
Epstein-Barr
HIV
Lymphocytic choriomeningitis
Mollaret’s meningitis (herpes simplex virus type 2)

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11
Q

Outline the fungi causes of meningitis- Infective

A

Cryptococcus neoformans
Candida
Histoplasma
Blastomyces
Coccidiosis, Sporothrix

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12
Q

Outline the protozoal and parasitic causes of meningitis- Infective.

A

Toxoplasma
Free living amoeba
Cysticercus
Malaria

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13
Q

Outline the viral causes of meningitis- Infective.

A

Viruses (aseptic meningitis)
Enteroviruses (ECHO, Coxsackie, polio)
Mumps
Influenza
Herpes simplex
Varicella zoster
Epstein-Barr
HIV
Lymphocytic choriomeningitis
Mollaret’s meningitis (herpes simplex virus type 2)

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14
Q

Outline the causes of Non-infective (‘sterile’) meningitis.

A

Non-infective (‘sterile’)
*Malignant disease

-Breast cancer
-Bronchial cancer
-Leukemia
-Lymphoma

Inflammatory disease (may be recurrent)

  1. Sarcoidosis
    -Sarcoidosis is an inflammatory disease characterized by the formation of granulomas in various organs of the body, including the lungs, lymph nodes, skin, eyes, heart, and nervous system. Granulomas are clusters of immune cells that develop in response to inflammation.
  2. SLE
    - Systemic Lupus Erythematosus (SLE) is an autoimmune disease in which the immune system mistakenly attacks healthy tissues in various parts of the body. It can affect the skin, joints, kidneys, brain, lungs, and other organs
  3. Behçet’s disease
    -Behçet’s disease is a rare disorder characterized by blood vessel inflammation throughout the body.
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15
Q

State the normal ICP for adults, children and term infants.

A

ADULTS: <10-15 mmHg
CHILDREN: 3-7 mmHg
TERM INFANTS: 1.5-6 mmHg

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16
Q

Compare CSF characteristics for the different pathogens.

Study table on slides.

A
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17
Q

Outline the Bacteria (septic meningitis) causes according to the following age groups.

  1. Age less than 3 months
  2. 3 Months to 18 years
  3. Age 18 to 50 years
  4. Over age 50 years
A
  1. Age less than 3 months

Group B strep (usually present surrounding the vagina at birth
L. Monocytogenes
E. coli
Klebsiella species

  1. 3 Months to 18 years
    N. meningitidis
    S. pneumoniae
    H. influenzae
  2. Age 18 to 50 years
    S. pneumoniae
    N. meningitidis
    H. influenzae
  3. Over age 50 years
    S. pneumoniae
    L. monocytogenes
    Gram (-) bacilli
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18
Q

Outline the Bacteria (septic meningitis) causes according to the following routes of infection.

Head trauma:

  1. Basilar skull fracture
  2. Penetrating trauma
  3. Post neurosurgery
  4. CSF shunt
A

Head trauma:

  1. Basilar skull fracture
    S. pneumoniae, H. influenzae, group A β-hemolytic streptococci
  2. Penetrating trauma
    Staphylococcus aureus, coagulase-negative staphylococci (especially Staphylococcus epidermidis), aerobic gram-negative bacilli (including Pseudomonas aeruginosa)
  3. Post neurosurgery
    Aerobic gram-negative bacilli (including P. aeruginosa), S. aureus, coagulase-negative staphylococci (especially S. epidermidis)
  4. CSF shunt
    Coagulase-negative staphylococci (especially S. epidermidis), S. aureus, aerobic gram-negative bacilli (including P. aeruginosa), Propionibacterium acnes.
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19
Q

State the 4 main causative agents common on CSF for the study done in PMH across all age groups.

A

Cryptococcus spec
Streptococcus pneumoniae
Hemophilus infections
Mycobacterium tuberculosis

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20
Q

NOTE:

Listeriosis is much more common among patients with human immunodeficiency virus infection or acquired immunodeficiency syndrome compared with the general population. (Listeriosis).

Negri bodies, round eosinophilic cytoplasmic inclusions measuring 1-7 ƒÊm, are pathognomonic of rabies (HE, high power). Hippocampal neurons are the preferential site of Negri body formation.

A
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21
Q

Describe the modes of transmission of meningitis.
I. Hematogenous route: commonest route -from infected site e.g.

II. Direct spread from adjacent infected focus

III. Trauma /defects of the CNS:

V. Intraneural route via peripheral nerves

A

I. Hematogenous route: commonest route -from infected site e.g.
*Pharyngitis
*Pneumonia
*Endocarditis
*Wound infections
*Septic arthritis
*Osteomyelitis
*Poliomyelitis

II. Direct spread from adjacent infected focus
*Otitis media
*Mastoiditis *Sinusitis
*Pyogenic infection of the skin or skull bone

III. Trauma /defects of the CNS:
Creates communication between CNS & other environment
*Fracture of the base of the skull - Sinuses
*Nasal passage defects- URT
*Neurosurgery - external environment
*Congenital defects of e.g. Spinal bifida- meningomyelocele

IV. Intraneural route via peripheral nerves eg:
*Rabies virus
*Herpes simplex virus-1 and 2:Trigeminal/sacral nerve root ganglion
Herpes zoster

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22
Q

Describe the treatment of meningitis according to age group.

CHECK TABLE ON THE SLIDES

A
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23
Q

Why is it advisable to give empirical treatment to meningitis patients immediately before spinal tap?

A

Meningitis is a medical emergency.

The likely hood of finding gram or culture positive CSF may decrease to 5-40% if antibiotics were administered before LP, however, antibiotics given 1-2 hrs before spinal tap do not decrease diagnostic sensitivity of CSF cultures done in conjunction with blood cultures and latex particles agglutination, and because antibiotics therapy takes longer than 12 hrs to sterilize the CSF and often cultures are positive for the first few hrs after antibiotics administration.

24
Q

Outline the complications of meningococcal meningitis.

A

Meningococcal meningitis is a serious bacterial infection that causes inflammation of the membranes (meninges) surrounding the brain and spinal cord. It is caused by the bacterium Neisseria meningitidis, also known as meningococcus.

  1. Rash: The rash associated with meningococcal meningitis can manifest in different forms, including morbilliform (measles-like), petechial (small red or purple spots), or purpuric (larger areas of bleeding under the skin)
    .
  2. Disseminated Intravascular Coagulation (DIC): Meningococcal meningitis can lead to DIC, a condition characterized by abnormal blood clotting and bleeding. DIC can result in the formation of more petechiae or purpura, extensive tissue destruction, and organ dysfunction
    .
  3. Shock: Septic shock can occur as a complication of meningococcal meningitis. It is characterized by a severe drop in blood pressure, leading to inadequate blood flow to organs and tissues.
  4. Bilateral Adrenal Hemorrhage (Waterhouse-Friderichsen Syndrome): In rare cases, meningococcal meningitis can cause bleeding into the adrenal glands, resulting in a condition known as Waterhouse-Friderichsen syndrome. This syndrome is associated with adrenal gland failure and can be life-threatening
    .
  5. Addisonian Crisis:
    Another potential complication of Waterhouse-Friderichsen syndrome is an Addisonian crisis. This crisis occurs when the adrenal glands fail to produce sufficient cortisol and other hormones, leading to symptoms such as sudden lower back, abdominal or leg pain, vomiting, diarrhea, and low blood pressure
    .
  6. Renal Failure: Meningococcal meningitis can sometimes lead to kidney damage and renal failure.
  7. Peripheral Gangrene: In rare cases, severe meningococcal disease can cause symmetrical peripheral gangrene, leading to tissue necrosis and the potential need for amputation.
  8. Arthritis: Meningococcal meningitis can result in septic or reactive arthritis, causing joint inflammation and pain.
  9. Pericarditis: Pericarditis, inflammation of the membrane surrounding the heart, can occur as a septic or reactive response to meningococcal meningitis.

Serotypes B, C and Y tend to predominate in more resource-rich countries, whereas serotypes A and W-135 are more common in less developed regions.
Available vaccines target serotypes A, C, Y and W-135 but not B

25
Q

Outline the bacterial, fungal and parasitic Chronic meningitis- Granulomatous type.

A

Bacteria
Mycobacterium tuberculosis
Leptospira species
Treponema pallidum
Borrelia burgdorferi

Fungi
Cryptococcus neoformans
Coccidioides immitis
Histoplasma capsulatum

Parasites
Toxoplasma gondii
Toxocara
Taenia solium (cysticercosis)
Echinococcus granulosus (Hydatid disease)

26
Q

Discuss Clinical and pathological features of neurosyphilis according to YEARS OF INFECTION.

OUTLINE THE PATHOLOGIES AND THE CLINICAL FEATURES

  1. 5 years
A
  1. Meningovascular (5 years)
    PATHOLOGY
    Endarteritis obliterans
    -Endarteritis obliterans is a condition characterized by severe inflammation of the inner lining of an artery, leading to the occlusion or narrowing of the artery’s lumen.

Meningeal exudate
-Meningeal exudate refers to the accumulation of fluid, cells, and debris in the meninges, which are the membranes surrounding the brain and spinal cord.

Granuloma (gumma)
A gumma is a soft, tumor-like growth that can develop in various tissues as a result of the tertiary stage of syphilis.

Gummas are characterized by a central necrotic area surrounded by inflamed tissue, forming a granuloma.

They can occur in organs such as the liver, brain, heart, skin, bone, and testis.

Gummas can lead to a variety of potential problems, including neurological disorders or heart valve disease.
.
CLINICAL FEATURES
Stroke
Cranial nerve palsies
Seizures/mass lesion

27
Q

Discuss Clinical and pathological features of neurosyphilis according to YEARS OF INFECTION.

OUTLINE THE PATHOLOGIES AND THE CLINICAL FEATURES

  1. (5-15 years)
A

General paralysis of the insane (5-15 years)

PATHOLOGY
Degeneration in cerebral cortex/cerebral atrophy
Thickened meninges

CLINICAL FEATURES
Dementia
Tremor
Bilateral upper motor signs

28
Q

Discuss Clinical and pathological features of neurosyphilis according to YEARS OF INFECTION.

OUTLINE THE PATHOLOGIES AND THE CLINICAL FEATURES

  1. 5-20 YEATS
A

Tabes dorsalis (5-20 years)

Degeneration of sensory neurons
Wasting of dorsal columns
Optic atrophy

Lightning pains
Sensory ataxia
-Loss of coordination and proprioception.
Visual failure
Abdominal crises
Incontinence
Trophic changes
-Tabes dorsalis can cause trophic changes, which are changes in the skin, muscles, and bones due to impaired nerve function. These changes can include ulcers, muscle wasting, and joint degeneration.

29
Q

Discuss Argyll Robertson pupils - a clinical feature of syphilis common in any stage.

A

Argyll Robertson pupils -the pupils are small and irregular and react to convergence but not directly to light.

30
Q

Discuss the diagnosis of Neurosyphilis infection.

Describe the different serological tests.

A

Serological tests are commonly used for the diagnosis of syphilis and can help detect the presence of antibodies against Treponema pallidum, the bacteria that causes syphilis. Here are some of the serological tests that are used:

*Rapid Plasma Reagin (RPR): RPR is a nontreponemal screening test that measures the host’s antibody response to nontreponemal antigens. A positive result on the RPR test requires confirmation by a treponemal-specific test.

*Venereal Disease Research Laboratory (VDRL): VDRL is another nontreponemal screening test that detects anticardiolipin antibodies. Similar to the RPR test, a positive VDRL result requires confirmation by a treponemal-specific test.

*Enzyme Immunoassay (EIA): EIA is an enzyme-based immunoassay that detects treponemal antibodies. It is one of the treponemal-specific tests used for confirmation of positive nontreponemal screening tests.

*Treponema Pallidum Hemagglutination Assay (TPHA): TPHA is an indirect hemagglutination assay used for the detection and titration of antibodies against Treponema pallidum. It is a specific treponemal test for syphilis.

*Treponema Pallidum Particle Agglutination Assay (TPPA): TPPA is an indirect agglutination assay that detects antibodies against Treponema pallidum. It is another specific treponemal test used for the diagnosis of syphilis.

*Fluorescent Treponemal Antibody-Absorbed Test (FTA-ABS): FTA-ABS is a fluorescent antibody test that detects antibodies against Treponema pallidum. It is a highly specific treponemal test used for confirmation of positive nontreponemal screening tests.

31
Q

Describe the diagnostic properties for an active disease in syphilis.

A

Active disease is suggested by an

-Elevated cell count, usually lymphocytic
-Protein content may be elevated to 0.5-1.0 g/L with an increased gamma globulin fraction.
-Serological tests in the CSF are usually positive, but progressive disease can occur with negative CSF serology.

32
Q

Discuss the treatment of syphilis and neurosyphilis.

A

Treatment- Benzathine penicillin 2.4 million units

Neuro syphilis -Procaine Penicillin with probenecid X 2 weeks

33
Q

Thick mucoid exudate within the subarachnoid space (▴), ventricles (♦), and brain parenchyma (▾) in an immunocompromised patient with Cryptococcus neoformans meningitis. Perivascular collections of the organisms can cause small cystic spaces within the brain. The CSF may have a mild to moderate leukocytosis, an elevated protein, but decreased glucose.

Name the possible diagnosis.

A

Cryptococcal meningitis

34
Q

Focal areas of hemorrhage with prominent brain swelling and a midline shift. This resulted from a disseminated Aspergillus infection in an immunocompromised patient who was markedly neutropenic. The branching, septate hyphae of Aspergillus are prone to cause vascular invasion with thrombosis and subsequent infarction.

Name the possible diagnosis.

A

Aspergillosis

35
Q

Discuss the pathogenic causes of Protozoal meningitis: Amoebic Meningoencephalitis.

Granulomatous amoebic encephalitis.

A

Acanthamoeba spp. and Balamuthia mandrillaris are widespread in the environment.

Affect the immunocompromised.

Enter via the skin or the respiratory tract.
Causes a chronic condition -granulomatous amoebic encephalitis.

36
Q

Discuss the pathogenic causes of Protozoal meningitis: Amoebic Meningoencephalitis.

Primary amoebic meningoencephalitis

A

Naegleria -The free-living amoeba can multiply in stagnant fresh water, lakes and swimming pools.

If inhaled, they can reach the meninges via the olfactory tract and cribriform plate.

Causes Primary amoebic meningoencephalitis.

Affects healthy individuals with no obvious defect in immunity.

The disease shows a rapid onset, and the mortality rate is high.

37
Q

Discuss the diagnosis of Amoebic Meningoencephalitis.

A

Diagnosis: PCR on brain tissue or CSF.

38
Q

Discuss the treatment of Amoebic Meningoencephalitis.

A

Treatment: Amphotericin B, with miconazole and rifampin, has been used for Naegleria; a variety of drugs have been used for Acanthamoeba

39
Q

State the distinguishing feature between encephalitis and meningitis.

A

ENCEPHALITIS: Absence of normal brain function-
MENINGITIS: Presence of normal brain function

40
Q

Discuss general infections of the CNS.

A

**Altered Mental Status:

-Infections of the nervous system can cause changes in mental status, including confusion, disorientation, and altered consciousness.

**Motor or Sensory Deficits: Focal dysfunction can result in

  1. Motor deficits such as.

*Hemiparesis (weakness on one side of the body) or *Flaccid paralysis (loss of muscle tone and strength).

  1. Sensory deficits, such as
    *Paresthesia (abnormal sensations) or numbness, can also occur.

**Altered Behavior and Personality Changes: Infections affecting the nervous system can lead to changes in behavior and personality. This can manifest as mood swings, irritability, inappropriate behavior, or a decline in cognitive function.

**Speech or Movement Disorders:
In some cases, infections of the nervous system can cause speech disorders, such as difficulty speaking or slurred speech. Movement disorders, including tremors or involuntary movements, may also be present.

41
Q

Discuss viral encephalitis.

A

Viral encephalitis can be either primary or postinfectious .

Primary infection is characterized by viral invasion of the CNS.

-Neuronal involvement shown by inclusion bodies on light microscopy or viral particles on electron microscopy. The virus can often be cultured from brain tissue.

In postinfectious encephalitis (also called acute disseminated encephalomyelitis or ADEM), a virus cannot be detected or recovered, and the neurons are spared.

-Perivascular inflammation and demyelination are prominent.

-Immune-mediated disease

-The inability to recover a virus and the type of histologic abnormalities observed suggest that postinfectious encephalitis

42
Q

Discuss the diagnosis of viral encephalitis.

A
  1. LP- Cell count, Glucose, protein-consistent with aseptic meningitis
  2. CSF Culture — Viral cultures
  3. Imaging — Results of imaging in patients with encephalitis may or may not demonstrate abnormal radiographic findings on CT or MRI modalities.

-CT scanning is useful to rule space-occupying lesions or brain abscess.

-MRI is sensitive for detecting demyelination, which may be seen in other clinical states presenting with mental status changes (eg. progressive multifocal leukoencephalopathy).

The location of abnormal signal can sometimes be suggestive of specific etiologies:

-Temporal lobe involvement -HSV encephalitis, VZV, EBV, human herpes virus .

-Thalamus or basal ganglia - Creutzfeldt-Jacob disease, arbovirus, and tuberculosis West Nile -infection, thalami, temporal structures, brainstem and cerebellum.

-Hydrocephalus – non viral etiologies, such as bacteria, fungal, or parasitic agents.

  1. Electroencephalography is often abnormal in acute encephalitis. Focality in the temporal lobe region is suggestive of HSV encephalitis
  2. Polymerase chain reaction
  3. Serology
  4. Brain biopsy
43
Q

Discuss HSV encephalitis (HSE)

A

HSV encephalitis (HSE) is a type of infectious encephalitis that occurs when the herpes simplex virus (HSV) enters the brain. HSV can be of two types: HSV-1 and HSV-2. HSV-1 is commonly associated with infections of the mouth and throat, including cold sores, while HSV-2 is typically associated with genital herpes.

The most common form of severe sporadic acute focal encephalitis

*Neonates acquire a primary and disseminated infection with a diffuse encephalitis after vaginal delivery from a mother shedding HSV-2 in the genital tract.

*HSE in older children and adults is due to HSV-1, due to virus reactivation in the trigeminal ganglia, the infection passing back to the temporal lobe of the brain,

Minority due to primary infection.

Herpetic skin or mucosal lesions may be present.

-The diagnosis is indicated by finding temporal lobe enhancement using CT and MRI scans
-HSV DNA detection using PCR.
-An electroencephalogram (EEG).

Early and prolonged treatment -intravenous acyclovir.
The 21-day treatment course is important, as relapse can occur.

44
Q

Outline the treatment of HSE.

A

HSV: acyclovir 10mg/kg IV
CMV: ganciclovir

45
Q

Discuss the pathogenesis of HIV meningitis and encephalitis.

A

-Infects macrophages and microglia in the CNS

-HIV invades the CNS shortly after initial infection, resulting in an increase in cells in the CSF and a mild meningitis illness.

At a later stage, a subacute encephalitis may develop, often with dementia.

-It can eventually give rise to progressive multifocal leukoencephalopathy (PML)

**Headaches, memory loss, changes in mental status, speech and vision difficulties, loss of strength, limb weakness, seizures, partial paralysis and loss of coordination.

In HIV-related dementia, the brain is shrunken, with enlarged ventricles and vacuolation of myelin tracts.

HIV-associated neurocognitive disorders (HAND)-
is correlated with long-term central nervous system inflammation.

46
Q

Discuss the clinical presentations of brain abscess.

A

Presents with gradual onset of severe headache , sharp and constant, interfering with sleep, develop seizures and confusion.

Headache: Headache is a common symptom of brain abscess. It may be persistent or intermittent and can vary in intensity.

  1. Fever: Fever is often present in cases of brain abscess, as it is a sign of infection.

Focal Neurological Deficits: Brain abscess can cause focal neurological deficits, which are symptoms related to specific areas of the brain that are affected. These deficits can include weakness or paralysis on one side of the body (hemiparesis), speech difficulties (aphasia), sensory abnormalities, or vision changes.

Altered Mental Status: Brain abscess can lead to altered mental status, including confusion, disorientation, and changes in consciousness.

Seizures: Seizures can occur in some cases of brain abscess, particularly if the lesion is located in the temporal lobe.

Nausea and Vomiting: Nausea and vomiting can be present due to increased intracranial pressure.

Progressive Symptoms: The symptoms of brain abscess can progress rapidly, leading to a worsening clinical presentation over time

47
Q

Outline the main causative agents of brain abscess according to the route of infection.

A

Streptococcus viridians, Staphylococcus aureus most common.

Paranasal sinuses – Streptococcus spp (especially S. milleri), Haemophilus spp, Bacteroides spp, Fusobacterium spp

Odontogenic sources – Streptococcus spp, Bacteroides spp, Prevotella spp, Fusobacterium spp, Haemophilus spp

Otogenic sources – Enterobacteriaceae, Streptococcus spp, Pseudomonas aeruginosa, Bacteroides spp

Lungs – Streptococcus spp, Fusobacterium spp, Actinomyces spp

Urinary tract – Pseudomonas aeruginosa, Enterobacter spp

Penetrating head trauma – Staphylococcus aureus, Enterobacter spp, Clostridium spp

Neurosurgical procedures – Staphylococcus spp, Streptococcus spp, Pseudomonas aeruginosa, Enterobacter spp

Endocarditis –Streptococci Viridians, S. aureus

Congenital cardiac malformations (especially right-to-left shunts) – Streptococcus spp

48
Q

Discuss Congenital Central Nervous system Infection.

  1. Intra uterine infection
  2. Maternal genitourinary tract during birth
A

Intra uterine infection
CMV – mental deficiency
Rubella -8th cranial nerve damage,
- cerebral palsy
Herpes simplex-encephalitis
Toxoplasma gondii - intracerebral calcification,
ventriculitis, microcephaly, hydrocephalous,
mental deficiency
Treponema pallidum- congenital syphilis

Maternal genitourinary tract during birth
Group B hemolytic streptococcus
Listeria monocytogenes
HIV

49
Q

Discuss the classic trad of rubella.

A

Cataract
Cardiac abnormalities
Deafness

50
Q

Discuss the classic triad of congenital toxoplasmosis.

A

Chorioretinitis (inflammation of the retina),

Hydrocephalus (excessive accumulation of cerebrospinal fluid in the brain), and

Intracranial calcifications (calcium deposits in the brain).

However, other clinical manifestations can also occur, such as:
-Hepatosplenomegaly (enlargement of the liver and spleen), jaundice, rash, fever, neurologic disorders, and psychomotor retardation

51
Q

Guillain Barre syndrome-Infectious polyneuritis

A

Guillain-Barré syndrome (GBS), also known as infectious polyneuritis, is a rare autoimmune disorder that affects the peripheral nervous system.

Mostly post infectious due to some viral infections.

Inflammatory demyelinating condition of peripheral nervous system

Associated with a variety of viral infection, glandular fever and Mycoplasma infection as well as with immunization with non infectious material.

CSF is clear, with normal WBC, and high protein concentration (>1200mg/100ml)

Clinical Features:
Paraesthesia and Acute onset of weakness in limbs
Paraplegia

52
Q

What are prions?

A

*Abnormal folded proteins.
*Found in abnormal configuration which is resistant to proteases

Prions are abnormal, pathogenic agents that are associated with a family of rare progressive neurodegenerative disorders known as prion diseases or transmissible spongiform encephalopathies (TSEs).

These diseases affect both humans and animals and are characterized by long incubation periods, spongiform changes in the brain, neuronal loss, and a lack of inflammatory response.

The normal form of the prion protein is called PrPC (cellular prion protein), while the infectious form is called PrPSc (scrapie prion protein).

PrPSc induces abnormal folding of PrPC, leading to the accumulation of misfolded proteins in the brain, which causes brain damage and the characteristic signs and symptoms of prion diseases.

53
Q

Prions (unconventional agents) cause five fatal CNS infections in mammals.

Discuss them in brief.

A

Kuru: The disease is characterized by progressive cerebellar ataxia, tremors, and other neurological symptoms. Kuru has a long incubation period and is ultimately fatal.

Creutzfeldt-Jakob Disease (CJD): CJD is the most common form of prion disease in humans. It can occur in several different forms, including sporadic, familial, iatrogenic, and variant CJD. Sporadic CJD is the most common form and typically occurs spontaneously without any known cause. Familial CJD is inherited and caused by mutations in the PRNP gene. Iatrogenic CJD is acquired through medical procedures, such as contaminated surgical instruments or tissue grafts. Variant CJD (vCJD) is associated with the consumption of prion-contaminated beef products and has a different clinical and pathological profile compared to other forms of CJD.

Gerstmann-Sträussler-Scheinker Syndrome (GSS): GSS is a rare genetic prion disease characterized by progressive cerebellar ataxia, dementia, and other neurological symptoms. It is associated with mutations in the PRNP gene. GSS has a slower progression compared to other prion diseases, with an average disease duration of several years.

Fatal Insomnia (FI): Fatal insomnia is an extremely rare prion disease characterized by progressive insomnia and autonomic dysfunction. It is caused by a mutation in the PRNP gene. The disease leads to severe sleep disturbances, cognitive decline, and ultimately death.

Variant CJD (vCJD): vCJD is a specific form of CJD that is associated with the consumption of prion-contaminated beef products, particularly in the United Kingdom during the BSE (mad cow disease) epidemic. It has distinct clinical and pathological features compared to other forms of CJD. vCJD has a younger age of onset and is characterized by psychiatric symptoms, sensory abnormalities, and a prolonged disease course.

54
Q

Discuss pathogenesis and clinical features of Prion diseases.

A

Infectious particle is the PrP protein,

Prions do not elicit inflammatory or immune responses in a host.

Pathogenesis of these infections is not well understood but they have similar features.

*Loss of neurons
*Proliferation of astrocytes
*Vacuoles seen in the brain cortex and cerebellum (spongiform changes)
*Plaque formation

55
Q

CJD-like illness characterized by younger age of onset, lack of characteristic EEG findings, longer course of disease, and more extensive spongiform change with plaques (▾) compared with typical cases of CJD.

Name the possible diagnosis.

A

Variant Creutzfeldt-Jakob disease.

56
Q

. The vacuoles in the cerebral cortical gray matter seen here (▴) represent a spongiform encephalopathy.

Name the possible diagnosis.

A

Creutzfeldt-Jakob disease

57
Q

Subacute progressive neurological disease.
Discovered 1957 in the Fore people of New Guinea

Symptoms are failure of muscular coordination, hyperactive reflexes, and muscular spasms.

Causes diffuse neuronal degeneration and spongiform change of the cerebral cortex and basal ganglia.

Leads to progressive dementia and death.

Name the disease.

A

Kuru

SOM 307 – NERVOUS SYSTEM AND SPECIAL SENSES (23 decks)

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