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Lecture Outline: infections of the central nervous system ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],CT: Neurocysticercosis
 
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BACTERIAL MENINGITIS
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• Beyond the neonatal period, the 3 most common organisms that cause acute bacterial meningitis are  Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae type b  (Hib).  • Neonates - Group B or D streptococci, nongroup B streptococci, Escherichia coli, and L monocytogenes • Infants and children -H influenzae (48%), S pneumoniae (13%), and N meningitidis • Adults -S pneumoniae, (30-50%), H influenzae (1-3%), N meningitidis (10-35%), gram-negative bacilli (1-10%), staphylococci (5-15%), streptococci (5%), and Listeria species (5%)
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The classic presentation of meningitis includes the triad fever, sever neck stiffness/rigidity, called meningismus, and change in mental status (eg, lethargy, confusion,  irritability, delirium, and coma) Signs of meningeal irritation are observed in only approximately 50% of patients with bacterial meningitis, and their absence certainly does not rule out meningitis.
Brudzinski Sign of Meningitis: • Brudzinski sign:  is positive if the patients hips and knees flex automatically when the examiner flexes the patients neck while the patient is supine.
Kernig’s Sign of Meningitis: Kernig sign:  flex patients hip to a 90° angle and then attempting passively straighten the leg at the knee produces pain in the hamstrings and resistance to further extension. Should present bilaterally to support the meningitis diagnosis.
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Systemic findings upon physical examination may provide clues to the etiology. Skin findings range from a nonspecific blanching, erythematous, maculopapular rash to a petechial or purpuric rash, most characteristic of meningococcal meningitis. Commonly affects the trunk and extremities. Symptoms in infants Cardinal signs of meningitis (eg, fever, vomiting, stiff neck) are rarely present.  For neonatal meningitis, these signs are the exception, rather than the rule. • Lethargy and/or change in level of alertness • Poor feeding and/or vomiting • Respiratory distress • Bulging fontanelle  • Paradoxic irritability (ie, quiet when stationary, cries when held) • High-pitched cry • Hypotonia • Approximately 6% of affected infants and children show signs of disseminated intravascular coagulopathy and endotoxic shock. These signs are indicative of a poor prognosis.
General guidelines  The cornerstone in the diagnosis of meningitis is examination of the CSF. Measure the opening pressure and send the fluid for cell count (and differential count), chemistry (ie, CSF glucose and protein), and microbiology (ie, Gram stain and cultures).The opening pressure of CSF should be measured in older children. Similarly, the color of the CSF (eg, turbid, clear, bloody) should be recorded.
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Meningitis:  CSF findings ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
CSF Characteristics Bacterial Viral Fungal TB Opening Pressure Elevated Slightly elevated Normal or High Ususally high Glucose Low Normal  Low Low Protein Very high Normal  High High Rbcs Few None None None Wbcs (c/mm3) >200 <200 <50 20-30 Diff PMNs Mono Mono  Mono Appearance Turbid Clear Turbid Cob-web
LP ,[object Object],[object Object],[object Object],[object Object]
Neonatal Initiate treatment as soon as bacterial meningitis is suspected. Ideally, blood and cerebrospinal fluid (CSF) cultures should be obtained before antibiotics are administered.  Fluid and electrolyte management Ampicillin and an aminoglycoside combination (ampicillin and cefotaxime Resistant bugs- Vancomycin and either ceftriaxone or cefotaxime Dexamethasone-Decreased inflammation, reduction in cerebral edema
 
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],Meningovascular syphilis.  Imaging findings include meningeal enhancement and small infarcts or  foci of ischaemia with a predilection for the basal ganglia and the middle cerebral artery regions , revealed in the subacute phase by areas of contrast enhancement. Cerebral atrophy is a frequent accompaniment.
[object Object],[object Object],[object Object],Argyll Robertson pupil
[object Object],[object Object]
[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object]
 
 
Viral Meningitis ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Viral Meningitis-Clinical  Manifestations ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Viral Meningitis-Treatment ,[object Object],[object Object]
 
Herpes Simplex Encephalitis ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Herpes Simplex Encephalitis-Pathophysiology ,[object Object]
Axial FLAIR MRI in herpes simplex encephalitis shows extensive signal change in the right temporal lobe (arrow). Destruction of inferior frontal and anterior temporal lobes – necrotizing inflammation
Herpes Simplex Encephalitis ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
 
Poliomyelitis ,[object Object],[object Object],[object Object]
Poliomyelitis-clinical manifestations ,[object Object],[object Object],[object Object],[object Object]
Poliomyelitis-clinical manifestations ,[object Object],[object Object],[object Object],[object Object]
 
Rabies Virus (Rhabdovirus) ,[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Rabies Virus (Rhabdovirus)
[object Object],[object Object],[object Object],Rabies Virus (Rhabdovirus) Patient with rabies, 1959
Rabies Virus (Rhabdovirus)-Treatment Post-exposure prophylaxis (PEP) ,  One dose of human rabies immunoglobulin (HRIG)  and  four doses of rabies vaccine over a fourteen day period . As much as possible of this dose should be infiltrated around the bites, with the remainder being given by deep intramuscular injection at a site distant from the vaccination site.
 
 
Brain and spine Tuberculosis ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Brain and spine Tuberculosis-Pathophysiology ,[object Object],[object Object],[object Object],[object Object]
Brain and spine Tuberculosis-Treatment ,[object Object],[object Object]
TUBERCULOMA T1 w  MRI IMAGE Tuberculoma is the round gray mass in the left corpus callosum. The red meninges on the right are consistent with irritation and probable meningeal reaction to tuberculosis. Tuberculomas are conglomerate caseous foci within the substance of the brain. Under conditions of poor host resistance, this process may result in focal areas of cerebritis or frank abscess formation, but the usual course is coalescence of caseous foci and fibrous encapsulation (ie, tuberculoma).
 
Progressive multifocal leukoencephalopathy  ,[object Object],[object Object],[object Object],[object Object]
Progressive multifocal leukoencephalopathy  ,[object Object],[object Object],This sliced fixed brain shows multiple isolated or confluent gray demyelinative foci. Atrophy may be present.
Progressive multifocal leukoencephalopathy  ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
 
Neuro-Cyptococcosis ,[object Object],[object Object],Cryptococcus neoformans
Neuro-Cyptococcosis-Clinical manifestations ,[object Object]
Neuro-Cyptococcosis-Pathophysiology Multicystic form of cerebral cryptococcosis: lesions in  basal ganglia and cerebellum  The fungus enters the human body through inhalation into the lungs. The cerebrospinal fluid is an ideal site for infection as it lacks complements and immunoglobulins.
Opaque thick fibrotic CSF obstruction - hydrocephalus. Gelatinous material within the subarachnoid space and small cysts within the parenchyma (&quot;soap bubbles“) Specially in the basal ganglia. Neuro-Cyptococcosis-Pathology
Neuro-Cyptococcosis-Treatment Amphotericin B  0.7-1.0 mg/kg/day +  5-flucytosine  100 mg/kg/day for 6-10 weeks. +  fluconozole  consolidation   6-12 months . Prognosis The majority of the patients improve with adequate therapy. Mortality is seen in about 10% and more common in HIV-positive individuals.
 
 
[object Object],[object Object],Neurocysticercosis
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Neurocysticercosis
[object Object],Neurocysticercosis-Pathophysiology
Neurocysticercosis Viable cysticercus cellulosae  LIVING ( viable ) Stage :  CT - appears as hypodense  lesion that doesn’t show ring enhancement  or perilesional oedema “ HOLE with DOT appearance ” Similar findings in T1w Images.
Neurocysticercosis Multiple parenchymal calcifications CALCIFIED Stage : Not visualised in MRI CT- hyperdense nodules with no edema or enhancement. Old nonviable cysts eventually calcify simplifying detection.
[object Object],Neurocysticercosis-Management and Therapy
 
Toxoplasmosis ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],Toxoplasmosis T1-MRI multiple contrast enhancing  necrotic focal lesions with predispostion to the basal ganglia and subcortical region.
Toxoplasmosis Diagnosis The indirect fluorescent Ab test measuring  IgG Ab  is the most widely used diagnostic tool. Detection of  T. gondii  in human blood samples may be also achieved by using the  PCR . Treatment Acute • Pyrimethamine (antimalarial)  4-6 weeks • Sulfadiazine -in combination with pyrimethamine. • Clindamycin  • Cotrimoxazole or spiramycin-used for pregnant women to prevent the infection of their child. Latent • In people with latent toxoplasmosis, the cysts are immune to these treatments, as the antibiotics do not reach the bradyzoites in sufficient concentration. • Atovaquone+Clindamycin Pyrimethamine spiramycin Atovaquone Clindamycin
 
Prion Related Diseases • The prion diseases are a large group of related neurodegenerative conditions, which affect both animals and humans.  • Prion diseases are unique in that they can be inherited, they can occur sporadically, or they can be infectious.  • These diseases all have long incubation periods but are typically rapidly progressive once clinical symptoms begin.  Table. Prion-Related Diseases, Hosts, and Mechanism of Transmission Disease Host Mechanism Kuru Human Cannibalism! Sporadic CJD Human Spontaneous PrP C  to PrP Sc  conversion or somatic mutation Iatrogenic CJD Human Infection from prion-containing material Familial CJD Human Mutations in the PrP gene vCJD Human Infection from BSE GSS Human Mutations in the PrP gene FFI Human D178N mutation in the PrP gene, with M129 polymorphism Sporadic fatal insomnia Human Spontaneous PrP C  to PrP Sc  conversion or somatic mutation Scrapie Sheep Infection in susceptible sheep BSE Cattle Infection from contaminated food
Prion Related Diseases ,[object Object],[object Object],[object Object],[object Object],[object Object],Prion-related diseases. Spongiform change in prion disease. This section shows mild parenchymal vacuolation and prominent reactive astrocytosis (abnormal increase in the number of astrocytes due to the destruction of nearby neurons).
Prion Related Diseases-Clinical Manifestations ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Prion Related Diseases -Diagnosis Imaging Studies MRI is an important imaging test. MRI may show  hyperintense signals in the cortical ribbon, basal ganglia, and the thalamus  Two characteristic radiological signs have been described.  The &quot;hockey stick&quot; sign , which refers to increased signal in the putamen and head of the caudate nucleus resembling a hockey stick, and the &quot;pulvinar&quot; sign, which corresponds to a usually bilaterally increased signal in the pulvinar thalamic nuclei.  Shows characteristic signal changes of an MRI taken from a patient with sporadic CJD, using diffusion-weighted imaging (DWI). An abnormal signal is shown in both the basal ganglia (red arrows) and the cortical ribbon (yellow arrow).
 
 
Tetanus Tetanus, -characterized by a prolonged contraction of skeletal muscle. The primary symptoms are caused by tetanospasmin, a neurotoxin produced by the Gram-positive, obligate anaerobic bacterium  Clostridium tetani.  Infection generally occurs through wound contamination and often involves a cut or deep puncture wound.  Risus sardonicus  is a highly characteristic, abnormal, sustained spasm of the facial muscles that appears to produce grinning. The name of the condition derives from the appearance of raised eyebrows and an open &quot;grin&quot; - which can appear malevolent to the lay observer - displayed by those suffering from these muscle spasms. Opisthotonos ( o-pis-to-ton-is )
Tetanus-Pathophysiology ,[object Object],[object Object],[object Object],[object Object]
Tetanus-Treatment ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
 
Botulism ,[object Object],[object Object],[object Object]
Botulism ,[object Object],[object Object],[object Object],[object Object]
That’s all folks!

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Short presentation version cns infections Lecture

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  • 7. • Beyond the neonatal period, the 3 most common organisms that cause acute bacterial meningitis are Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae type b (Hib). • Neonates - Group B or D streptococci, nongroup B streptococci, Escherichia coli, and L monocytogenes • Infants and children -H influenzae (48%), S pneumoniae (13%), and N meningitidis • Adults -S pneumoniae, (30-50%), H influenzae (1-3%), N meningitidis (10-35%), gram-negative bacilli (1-10%), staphylococci (5-15%), streptococci (5%), and Listeria species (5%)
  • 8.
  • 9. The classic presentation of meningitis includes the triad fever, sever neck stiffness/rigidity, called meningismus, and change in mental status (eg, lethargy, confusion, irritability, delirium, and coma) Signs of meningeal irritation are observed in only approximately 50% of patients with bacterial meningitis, and their absence certainly does not rule out meningitis.
  • 10. Brudzinski Sign of Meningitis: • Brudzinski sign: is positive if the patients hips and knees flex automatically when the examiner flexes the patients neck while the patient is supine.
  • 11. Kernig’s Sign of Meningitis: Kernig sign: flex patients hip to a 90° angle and then attempting passively straighten the leg at the knee produces pain in the hamstrings and resistance to further extension. Should present bilaterally to support the meningitis diagnosis.
  • 12.
  • 13. Systemic findings upon physical examination may provide clues to the etiology. Skin findings range from a nonspecific blanching, erythematous, maculopapular rash to a petechial or purpuric rash, most characteristic of meningococcal meningitis. Commonly affects the trunk and extremities. Symptoms in infants Cardinal signs of meningitis (eg, fever, vomiting, stiff neck) are rarely present. For neonatal meningitis, these signs are the exception, rather than the rule. • Lethargy and/or change in level of alertness • Poor feeding and/or vomiting • Respiratory distress • Bulging fontanelle • Paradoxic irritability (ie, quiet when stationary, cries when held) • High-pitched cry • Hypotonia • Approximately 6% of affected infants and children show signs of disseminated intravascular coagulopathy and endotoxic shock. These signs are indicative of a poor prognosis.
  • 14. General guidelines The cornerstone in the diagnosis of meningitis is examination of the CSF. Measure the opening pressure and send the fluid for cell count (and differential count), chemistry (ie, CSF glucose and protein), and microbiology (ie, Gram stain and cultures).The opening pressure of CSF should be measured in older children. Similarly, the color of the CSF (eg, turbid, clear, bloody) should be recorded.
  • 15.
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  • 17. CSF Characteristics Bacterial Viral Fungal TB Opening Pressure Elevated Slightly elevated Normal or High Ususally high Glucose Low Normal Low Low Protein Very high Normal High High Rbcs Few None None None Wbcs (c/mm3) >200 <200 <50 20-30 Diff PMNs Mono Mono Mono Appearance Turbid Clear Turbid Cob-web
  • 18.
  • 19. Neonatal Initiate treatment as soon as bacterial meningitis is suspected. Ideally, blood and cerebrospinal fluid (CSF) cultures should be obtained before antibiotics are administered. Fluid and electrolyte management Ampicillin and an aminoglycoside combination (ampicillin and cefotaxime Resistant bugs- Vancomycin and either ceftriaxone or cefotaxime Dexamethasone-Decreased inflammation, reduction in cerebral edema
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  • 35. Axial FLAIR MRI in herpes simplex encephalitis shows extensive signal change in the right temporal lobe (arrow). Destruction of inferior frontal and anterior temporal lobes – necrotizing inflammation
  • 36.
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  • 43.
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  • 45. Rabies Virus (Rhabdovirus)-Treatment Post-exposure prophylaxis (PEP) , One dose of human rabies immunoglobulin (HRIG) and four doses of rabies vaccine over a fourteen day period . As much as possible of this dose should be infiltrated around the bites, with the remainder being given by deep intramuscular injection at a site distant from the vaccination site.
  • 46.  
  • 47.  
  • 48.
  • 49.
  • 50.
  • 51. TUBERCULOMA T1 w MRI IMAGE Tuberculoma is the round gray mass in the left corpus callosum. The red meninges on the right are consistent with irritation and probable meningeal reaction to tuberculosis. Tuberculomas are conglomerate caseous foci within the substance of the brain. Under conditions of poor host resistance, this process may result in focal areas of cerebritis or frank abscess formation, but the usual course is coalescence of caseous foci and fibrous encapsulation (ie, tuberculoma).
  • 52.  
  • 53.
  • 54.
  • 55.
  • 56.  
  • 57.
  • 58.
  • 59. Neuro-Cyptococcosis-Pathophysiology Multicystic form of cerebral cryptococcosis: lesions in basal ganglia and cerebellum  The fungus enters the human body through inhalation into the lungs. The cerebrospinal fluid is an ideal site for infection as it lacks complements and immunoglobulins.
  • 60. Opaque thick fibrotic CSF obstruction - hydrocephalus. Gelatinous material within the subarachnoid space and small cysts within the parenchyma (&quot;soap bubbles“) Specially in the basal ganglia. Neuro-Cyptococcosis-Pathology
  • 61. Neuro-Cyptococcosis-Treatment Amphotericin B 0.7-1.0 mg/kg/day + 5-flucytosine 100 mg/kg/day for 6-10 weeks. + fluconozole consolidation 6-12 months . Prognosis The majority of the patients improve with adequate therapy. Mortality is seen in about 10% and more common in HIV-positive individuals.
  • 62.  
  • 63.  
  • 64.
  • 65.
  • 66.
  • 67. Neurocysticercosis Viable cysticercus cellulosae  LIVING ( viable ) Stage : CT - appears as hypodense lesion that doesn’t show ring enhancement or perilesional oedema “ HOLE with DOT appearance ” Similar findings in T1w Images.
  • 68. Neurocysticercosis Multiple parenchymal calcifications CALCIFIED Stage : Not visualised in MRI CT- hyperdense nodules with no edema or enhancement. Old nonviable cysts eventually calcify simplifying detection.
  • 69.
  • 70.  
  • 71.
  • 72.
  • 73. Toxoplasmosis Diagnosis The indirect fluorescent Ab test measuring IgG Ab is the most widely used diagnostic tool. Detection of T. gondii in human blood samples may be also achieved by using the PCR . Treatment Acute • Pyrimethamine (antimalarial) 4-6 weeks • Sulfadiazine -in combination with pyrimethamine. • Clindamycin • Cotrimoxazole or spiramycin-used for pregnant women to prevent the infection of their child. Latent • In people with latent toxoplasmosis, the cysts are immune to these treatments, as the antibiotics do not reach the bradyzoites in sufficient concentration. • Atovaquone+Clindamycin Pyrimethamine spiramycin Atovaquone Clindamycin
  • 74.  
  • 75. Prion Related Diseases • The prion diseases are a large group of related neurodegenerative conditions, which affect both animals and humans. • Prion diseases are unique in that they can be inherited, they can occur sporadically, or they can be infectious. • These diseases all have long incubation periods but are typically rapidly progressive once clinical symptoms begin. Table. Prion-Related Diseases, Hosts, and Mechanism of Transmission Disease Host Mechanism Kuru Human Cannibalism! Sporadic CJD Human Spontaneous PrP C to PrP Sc conversion or somatic mutation Iatrogenic CJD Human Infection from prion-containing material Familial CJD Human Mutations in the PrP gene vCJD Human Infection from BSE GSS Human Mutations in the PrP gene FFI Human D178N mutation in the PrP gene, with M129 polymorphism Sporadic fatal insomnia Human Spontaneous PrP C to PrP Sc conversion or somatic mutation Scrapie Sheep Infection in susceptible sheep BSE Cattle Infection from contaminated food
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  • 77.
  • 78. Prion Related Diseases -Diagnosis Imaging Studies MRI is an important imaging test. MRI may show hyperintense signals in the cortical ribbon, basal ganglia, and the thalamus Two characteristic radiological signs have been described. The &quot;hockey stick&quot; sign , which refers to increased signal in the putamen and head of the caudate nucleus resembling a hockey stick, and the &quot;pulvinar&quot; sign, which corresponds to a usually bilaterally increased signal in the pulvinar thalamic nuclei. Shows characteristic signal changes of an MRI taken from a patient with sporadic CJD, using diffusion-weighted imaging (DWI). An abnormal signal is shown in both the basal ganglia (red arrows) and the cortical ribbon (yellow arrow).
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  • 80.  
  • 81. Tetanus Tetanus, -characterized by a prolonged contraction of skeletal muscle. The primary symptoms are caused by tetanospasmin, a neurotoxin produced by the Gram-positive, obligate anaerobic bacterium Clostridium tetani. Infection generally occurs through wound contamination and often involves a cut or deep puncture wound. Risus sardonicus  is a highly characteristic, abnormal, sustained spasm of the facial muscles that appears to produce grinning. The name of the condition derives from the appearance of raised eyebrows and an open &quot;grin&quot; - which can appear malevolent to the lay observer - displayed by those suffering from these muscle spasms. Opisthotonos ( o-pis-to-ton-is )
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Notes de l'éditeur

  1. Probenecid –blocks kidney excreation of penicillin and increases its blood levels