Cns infections
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CNS Infections. Path. Four principal routes via which infections may enter the nervous system. Hematogenous spread – arterial circulation, retrograde venous circulation Direct implantation – traumatic, possibly iatrogenic

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CNS Infections

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Cns infections

CNS Infections

Cns infections


Four principal routes via which infections may enter the nervous system

Four principal routes via which infections may enter the nervous system

  • Hematogenous spread – arterial circulation, retrograde venous circulation

  • Direct implantation – traumatic, possibly iatrogenic

  • Local extension – secondary to an established infection in an air sinus – mastoid or frontal, infected tooth, surgical site

  • Peripheral nervous system – certain viruses – rabies, herpes zoster

Meningitis definition and classification

Meningitis – definition and classification

  • Inflammatory process of the leptomeninges and CSF within the subarachnoid space

  • Classified into

    • Acute pyogenic

    • Aspetic (usually acute viral)

    • Chronic (TB, spirochetal, cryptococcal)

Acute pyogenic meningitis causative agents clinical

Acute pyogenic meningitis – causative agents, clinical

  • Causative agent vary with age of patient

    • Neonates – E coli, group B streptococci

    • Adolescents/young adults – neisseriameningitidis

    • Elderly – strep pneumonia, listeriamonocytogenes

    • Immunisation has drastically reduced haemophilusinfluenza

    • Immunosuppressed patient – klebsiella, anaerobic organisms

  • Clinical – systemic signs, headache, photophobia, irritability, clouding of consciousness, neck stiffness

Acute pyogenic meningitis lp associated syndromes

Acute pyogenic meningitis – LP, associated syndromes

  • Lumbar puncture – frankly purulent CSF, under increased pressure, many as 90,000 neutrophils/mm^3, raised protein level, markedly reduced glucose content

  • Waterhouse-Friderichsensyndrome – results from meningitis associated septicaemia with hemorrhagic infarction of the adrenal glands and cutaneouspetechiae

Acute pyogenic meningitis morphology

Acute pyogenic meningitis – morphology

  • Acute – exudates evident within the leptopmeninges over the surface of the brain

  • Vessels are engorged and stand out prominently

  • Location of exudates varies

    • H.influenazae – basal

    • Pneumococcal meningitis – densest over cerebral convexities near the sagittal sinus

    • Fulminant meningitis – inflammation may extend to the ventricles – ventriculitis

  • Micro

    • Neutrophils fill the subarachnoid space in severely affected areas, predominantly around leptomeningeal blood vessels in less severe cases

    • Focal cerebritis – infiltration of inflammatory cells into the substance of the brain (go through the leptomeningeal veins)

  • Leptomeningeal fibrosis and hydrocephalus follow pyogenic meningitis

  • Chronic adhesive arachnoiditis – large quantities of capsular polysaccharide of the organism produce a particularly gelatinous exudates that encourages arachnoid fibrosis

Acute aseptic meningitis clinical lp causative agents

Acute aseptic meningitis – clinical, LP, causative agents

  • Clinical - meingealirritation, fever, alterations of consciousness of relatively acute onset

  • Usually viral

  • Clinical course less fulminant, usually self limiting, treated symptomatically

  • CSF – lymphocytic pleocytosis, protein elevation is only moderate, sugar content is nearly always normal

  • 70% pathogen can be identified – commonly enterovirus

    • Echovirus, coxsackievirus, nonparalytic poliomyelitis – up to 80% of cases

Brain abscesses path predisposing conditions organisms

Brain abscesses – path, predisposing conditions, organisms

  • Arise from

    • Direct implantation of organisms

    • Local extension from adjacent foci – mastoiditis, paranasal sinusitis

    • Hematogenous spread – primary site in heart, lungs, distal bones or after tooth extraction

  • Predisposing conditions

    • Acute bacterial endocarditis (multiple abscesses), cyanotic congenital heart disease (R to F shunt), chronic pulmonary sepsis (bronchiectasis)

  • Streptococci, staphylococci most common organisms in non-immunosuppressed

Brain abscesses morphology

Brain abscesses – morphology

  • Macro – discrete lesions with central liquefactive necrosis, surrounding fibrous capsule, oedema

  • Most common brain regions in descending order – frontal lobe, parietal lobe, cerebellum

  • Micro – exuberant granulation tissue, neovascularisation around the necoriss that is responsible for marked vasogenic oedema

  • Collagen produced by fibroblasts from walls of vessels, outside fibrous capsule zone of reactive gliosis with numerous gemistocyticastrocytes

Brain abscesses clinical csf prognosis

Brain abscesses – clinical, CSF, prognosis

  • Destructive lesions – patients present progressive focal deficits, signs of raised intracrnail pressure

  • CSF – under increased pressure, white cell count raised, protein raised, sugar content is normal

  • Source of infection may be apparent

  • Increased intracranial pressure and herniation may be fatal

  • Abscess rupture lead to ventriculitis, meiningitis, venous sinus thrombosis

  • Surgery, antibiotics, otherwise high mortality reduced to 10%

Subdural empyema path clinical symptoms csf treatment

Subdural empyema – Path, clinical, symptoms, CSF, treatment

  • Bacterial/fungal infection of skull bones or air sinuses can spread to subdural space – empyema

  • Arachnoid, subarachnoid is unaffected, subdural empyema can produce a mass effect

  • Thrombophlebitis may develop in the bridging veins that cross the subdural space

    • Venous occlusions and infarction

  • Symptoms – source of infection related, febrile, headache, neck stiffness, focal neurologic signs, lethargy, coma

  • CSF similar to abscess

  • Treatment – surgical drainage, resolution occurs from the dural side, if complete -> thickened dura may be the only residual finding

Chronic bacterial meningoencepahlitis tb csf symptoms complications related infecitons

Chronic bacterial meningoencepahlitis – TB – CSF, symptoms, complications, related infecitons

  • CSF – moderate pleocytosis (mononuclear cells), protein level is elevated strikingly so, glucose moderately reduced or normal

  • Symptoms – headache, malaise, mental confusion, vomiting

    • Most serious complication – arachnoid fibrosis – hydrocephalus

      • Obliterative endarteritis – arterial occlusion, infarction of underlying brain

      • Spinal roots may also be affected

  • AIDS patients also at risk of infection with M. avium-intracellulare – setting of disseminated infection

    • Lesion – confluent sheets of macrophages filled with organisms, minimal granulomatous reaction

Chronic bacterial meningoencepahlitis tb morphology

Chronic bacterial meningoencepahlitis – TB – morphology

  • Morphology

    • Macro

      • Subarachnoid space contains a gelatinous or fibrinous exudates, most often at the base of the brain -> oliterateing the cisterns and encasing cranial nerves

    • Meningoencephalitis – most common pattern of involvement

    • Micro – mixture of lymphocytes, plasma cells, macrophages

      • Florid cases – well formed granulomas, caseous necrosis, giant cells

      • Arteries in subarachnoid space

        • Obliterative endarteritis

        • Inflammatory infiltrates in their walls, marked intimal thickening

    • Organisms often seen with acid-fast stains

    • Infection can spread to the choroid plexus and ependymal surface- through CSF

    • Long standing duration – dense, fibrous adhesive arachnoiditis

    • Tuberculoma – single or multiple well circumscribed intraparenchymal mass

      • May be several cm in diameter – mass effect

      • Micro – central core caseous necrosis surrounded by typical tuberculousgranulomatous reaction, calcification may occur in inactive lesions

Neurosyphillis major forms path morphology

Neurosyphillis – major forms –path/morphology

  • Meningovascularneurosyphilis

    • Chronic meningitis involving the base of the brain, cerebral convexities, spinal leptomeninges

    • Obliterative endarteritis (Huebner arteritis)

    • Perivascular inflammation, plasma cells, lypmhocytes

  • Paretic neurosyphilis

    • Insidious but progressive loss of mental and physical functions with mood laterations terminating in severe dementia

    • Micro – lesions associated with parenchymal damage in the cerebral cortex

      • Loss of neurons, proliferations of microglia, gliosis, riondepositsi -> Prussian blue stain

      • Granular ependymitis – proliferation of subependymalglia

  • Tabesdoraslis

    • Result of damage by the spirochete to the sensory nerves in the dorsal roots

      • Impaired joint position sense and resultant ataxia, loss of pain sensation, skin and joint damage (Charcot joints), lightning pains – sensory disturbances

    • Micro – loss of both axons and myelin in the dorsal roots, pallor and atrophy in the dorsal columns of the spinal cord

  • Neuroborreliosis symptoms

    Neuroborreliosis– symptoms

    • Lyme disease

    • Caused by spirochete Boreeliaburgdorferi – transmitted by ticks (Ixodes)

    • Symptoms highly variable – aseptic meningitis, facial nerve palsies, mild encephalopathy, polyneuropathies

    Viral meningoencephalitis defn characteristic histo complications

    Viral meningoencephalitis – defn, characteristic histo, complications

    • Viral encephalitis – parenchymal infection of the brain – associated with meningeal inflammation, sometimes involvement of the spinal cord

    • Characteristic histo: perivascularcuffs and parenchymal mononuclear cell infiltrates, glial cell reactions (microglial nodules), neuronophagia

    • Complications – congential malformations (intrauterine – rubella), postenecepahlitic parkinsonism, immune mediated disease – perivenousdemyelination

    Anthropod borne viral encephalitis epi clinical csf morphology

    Anthropod-borne viral encephalitis – epi, clinical, CSF, morphology

    • Arboviruses – epidemic – tropical regions

    • In Australia – Murray Valley, in US – west nile virus

    • All animal hosts, mosquito vectors

    • Clinically – generalised neuro deficits – seizures, confusion, delirium, stupor, coma, focal signs, reflex asymmetry, ocular palsies

    • CSF – colourless, slightly elevated pressure, initially neutrophilpleocytosis converts to lymphocytes, protein level elevated, glucose normal

    • Morphology

      • Lymphocytic meiningoencephalitis – tendency for inflammatory cells perivascularly

      • Multiple foci of necrosis of gray and white matter

      • Neuronophagia – single cell neuronal necrosis with phagocytosis of the debris

      • Some cases prominent cortical involvement, others basal ganglia bear the brunt

    Hsv 1 epi symptoms morphology

    HSV-1- epi, symptoms, morphology

    • Encephalitis – most common in children and young adults – 10% of patients had a history of prior herpes

    • Symptom – alterations in mood, memory, behaviour

    • Diagnosed with PCR

    • Morphology

      • Inferior and medial regions of the temporal lobes, orbital gyri of the frontal lobes

      • Necrotising, often hemorrhagic

      • Perivascular inflammatory infiltrate present

      • Cowdry type A intranuclear viral inclusion bodies – neurons and glia

    • Antiviral agents provide effective treatment

    • Some times – subacute course – weakness, lethargy, ataxia, seizures

    Other viral encephalitis hsv 2 herpes zoster cmv

    Other viral encephalitis – HSV-2, herpes zoster, CMV

    • HSV-2 - Encephalitis – 50% of neonates delievered by vaginal birth to women with active primary HSV genital infection

      • AIDS – acute- hemorrhagic, necrotizing encephalitis

    • Herpes zoster (varicella) - Reactivation in adults – painful vesicular eruption – limited dermatomaldistribution, usually self-limited

      • Granulomatousarteritis

      • Immunosuppressed – acute necephalities – demyelination followed by necrosis

    • CMV

      • Foetuses and immunosuppressed

      • Utero – periventricular necrosis – serfver brain destruction – microcepahly – calcification

      • Most common pathogen in AIDS affecting CNS – 15-20%

      • Morphology

        • CMV inclusion bearing cells

        • Tendency for subependymal regions of the brain

        • Severe hemorrhagic necrotizing ventriculoencepahlitis and a choroid plexitis

    Poliomyelitis morphology clinical

    Poliomyelitis – morphology, clinical

    • Still regions where it remains a problem

    • Causes subclinical or mild-gastritis – in a small fraction it invades the CNS

    • Morphology

      • Mononuclear cell perivascular cuffs and neuronophagia of the anterior horn motor neurons of the spinal cord

      • Cranial motor nuclei sometimes involved

    • Clinical

      • Initially meningeal irritation, may progress to involve the spinal cord

        • Flaccid paralysis – muscle wasting, hyporeflexia

      • Death can occur from paralysis

      • Myocarditis may also occur

      • Post-polio syndrome – may develop 25-35 years after resolution – progressive weakness associated with decreased muscle mass and pain, unclear pathogenesis.

    Rabies morphology clinical

    Rabies – morphology, clinical

    • Severe encephalitis transmitted to humans by the bite of a rabid animal – dogs, bats etc

    • Morphology

      • Brain – oedema, vascular congestion

      • Micro – widespread neuronal degeneration, inflammatory reaction – most severe in the brainstem

      • Negri bodies – cytoplasmic, round to oval, eosinophilic inclusions that can be found in pyramidal neurons of the the hippocampus and Purkinje cells of the cerebellum – areas devoid of inflammation

    • Clinical

      • Virus enters CNS by ascending along peripheral nerves from wound site -> incubation period depends on distance between wound and brain -> typically 1-3 months

      • Early symptoms – malaise, headache, fever, local parathesias around the wound

      • As infection advances – extraordinary CNS excitability – slightest touch is painful, violent motor responses progressing to convulsions

      • Foaming – contracture of the pharyngel musculature on swallowing -> aversion to swallowing -> hydrophobia

      • Periods of alternating mania and stupor progress to coma and death

    Hiv morphology

    HIV - morphology

    • Neuropathologic changes demonstrated at post-mortem in 80-90% of AIDs

    • HIV aspetic meningitis occurs within 1-2 weeks of seroconversion in 10% of patients

    • Morphology

      • Chronic inflammatory reaction

      • Microglial nodules – multinucleated giant cell

      • Especially in the subcortical white matter, diencephalon, brainstem

      • Disorder of white matter – multifocal or diffuse areas of myelin pallor, axonal swelling, gliosis

    • HIV related dementia – related to the extent of activated microglia in the brain

    Progressive multifocal leukoencephalopathy clinical morphology

    Progressive multifocal leukoencephalopathy – clinical, morphology

    • Viral encephalitis – JC polyomarivurs – preferentially infects oligodendrocytes -> demyelination is the main effect

    • Exclusive to immunosuppressed individuals

    • Most people have serological exposure to JC virus by the age of 14 years

    • Clinically – focal, relentlessly progressive neurologic symptoms and signs

    • Imaging – extensive, often multifocal, lesions in the hemisphere or cerebellar white matter

    • Morphology

      • Patches of irregular, ill-defined destruction of the white matter – mm to entire lobes

      • Micro

        • Centre – lipid laiden macrophages, loss of axons

        • Edge – greatly enlarged oligodendrocytes nuclei – glassy amphophilic viral inclusions – viral antigen

        • May be bizarre giant astrocytes – one to several irregular, hyperchromatic nuclei

    Subacute scleroing panencephalitis

    Subacute scleroingpanencephalitis

    • Rare progressive clinical syndrome – cognitive decline, spasticity of limbs, seizures

    • Occurs in children or young adults - after early-age acute infection of measles

    • Disease – altered measles virus in the CNS

    • Morph

      • Micro – widespread gliosis, myelin degeneration, viral inclusions -> nuclei of oligodendrocytes, neurons, also get neurofibrillary tangles

    Fungal meningoencaphlitis common agents patterns of infection

    Fungal meningoencaphlitis – common agents, patterns of infection

    • Brain usually involved with widespread hematogenous dissemination

    • Most often – candidaalbicans, mucor species, aspergillus fumigates, Cryptococcus neoformans

    • Endemic areas – histoplasmacapsulatum, coccidiodiesimmitis, blastomycesdermatitidis

    • Three main patterns of fungal infection

      • Vasculitis – seen with mucromycosis and aspergillosis – direct fungal invasion of blood vessel walls, also seen in candidiasis

        • Vascular thrombosis produces infarction – usually hemorrhagic

      • Parenchymal invasion – granulomas or abscesses – often coexists with meningitis

        • Commonly – candida, Cryptococcus

        • Candida – multiple microabscesses

        • Mucormycosis – direct extension – common in DKA (?)

      • Chronic meningitis

    Cryptococcal meningitis csf morphology

    Cryptococcal meningitis – CSF, morphology

    • Opportunistic infection – HIV/AIDs – may be fulminant and fatal

    • CSF – few cells, high protein – using India ink stain – yeasts can be visualised – in tissue use PAS or silver stains

    • Morphology

      • Chronic meningitis – basal leptomeninges – opaque, thickened by reactive tissue -> may obstruct outflow of CSF from the foramina of luschka and megendie -> hydrocephalus

      • Gelatinous material within subarachnoid space

      • Soap bubbles – small cysts in the parenchyma – prominent in basal ganglia

      • Parenchymal lesions – aggregates of organisms within perivascular (Virchow-Robin) spaces

    Cerebral toxicoplasmosis clinical morphology

    Cerebral toxicoplasmosis – clinical, morphology

    • Opportunistic infection – HIV immunosuppression

    • Clinical symptoms – subacute –evolve over 1-2 wk period, focal or diffuse

    • Ring-enhancing lesion – not pathognomonic – also seen in lymphoma, TB, fungal

    • Non-immunosuppressed – pregnancy – cerebritis in the fetus -> multifocal cerebral necrotising lesions that may calcify -> severe damage to the developing brain

    • Morphology

      • Brain abscesses – gray-white junction, and deep gray nuclei

      • Acute lesions – central foci of necrosis, petechieal haemorrhages – chornic inflammation

      • Organisms seen on H&E, Giemsa stains

      • Blood vessels – fibrinoid necrosis, thrombosis

      • Treatment – coagulation necrosis surrounded by lipid-laiden macrophages

      • Chronic lesions – small cystic spaces, containing scattered lipid and hemosiderinlaiden macrophages

    Cerebral amebiasis

    Cerebral amebiasis

    • Rapidly fatal necrotising encephalitis – naegleria species

    • Chronic granulomatousmeningoencepahlitis – acanthamoeba

    • Methenamine silver or PAS stains – visualise organisms

    Transmissible spongiform encephalopathies pathogenesis

    Transmissible spongiform encephalopathies - pathogenesis

    • Prions – abnormal forms of cellular protein that cause transmissible neurodegenerative disorders

    • Path/molecular genetics

      • PrP 30-kD cellular protein in neurons

      • Disease – PrP undergoes conformational change from PrPc to PrPsc (alpha helix to beta pleated sheet)

      • With this change – resistant to digestion with proteases

      • Acumulation of PrPsc in neural tissue -> unsure how this causes a problem _. Cytoplasmic vacuoles -> neuronal death

      • PrPsc may be created normally at a very low rate

      • PrPsc facilitates the conversion of PrPc to PrPsc – infectious nature

      • PRNP – encodes PrP

        • Variety of mutations – familial forms

    Ckd and vckd

    CKD and vCKD

    • Creutzfedlt-Jakob disease

      • Most common prion disease

      • Clinically – rapidly progressing dementia, startle myoclonus

        • Onset – subtle memory and behaviour changes

      • Incidence 1/million

      • Peak incidence in the 7th decade

      • Familial forms due to mutation in PRNP (codon 129 met or val)

      • Average survival 7 months from onset of symptoms

    • Variant creutzfedlt-Jakob disease

      • Affects young adults

      • Behavioural disorders appeared at early stages, neuro symptoms progress slower

      • Characterised – extensive cortical plaques with surrounding halo of spongiform change

      • Linked with bovine spongiform encephalopathy

    Morphology of ckd

    Morphology of CKD

    • Progression to dementia so rapid – little cortical atrophy

    • Spongiform transformation of the cerebral cortex - uneven formation of small, apparently empty, microscopic vacuoles of varying size

    • Advanced stage – severe neuronal loss, reactive gliosis, expansion of vascuolated areas into cystlike spaces – status spongiosus

    • Kuru plaques – extracellular deposits of aggregates of abnormal protein – Congo-red or PAS positive

    Fatal familial insomnia

    Fatal familial insomnia

    • Named after the sleep disturbances it causes

    • Specific mutation in PRNP gene

    • Lasts fewer than 3 years – neuro signs – ataxia, autonomic disturbances, stupor, coma

    • Morphology – no spongiform pathology, but there is neuronal loss andreactivegliosis in anterior ventral and dorsomedial nuclei of the thalamus, also inferior olivary nuclei



    Viral meningitis investigations management

    Viral meningitis – investigations, management

    • Investigations

      • Dx by LP -> glucose normal, protein normal or slightly elevated, excess of lymphocytes -> VERIFY THAT ANITBIOTICS HAVE NOT BEEN GIVEN PRIOR TO LP

    • Management

      • Condition usually benign and self limiting

      • Recovery usually in days

      • Complete recovery without therapy is the rule

    Bacterial meningitis management

    Bacterial meningitis - management

    • Management

      • Take specimens – blood culture, PCR, throat swab

      • Start empirical antibiotics

      • If no clinical signs indicating mass lesion, hydrocephalus, cerebral oedema – then – LP, otherwise CT first

    Bacterial meningitis treatment

    Bacterial meningitis- treatment

    • Benzylpenicillinimmediately if bacterial meningitis suspected

    • Adults 18-50, meningococcal rash

      • Ceftriaxone

  • Suspected penicillin resistant pneumococcal infection

    • Ceftriaxone, vancomycin (or rifampicin)

  • Adults over 50, listeria is suspected

    • Ceftriaxone + ampicillin (or co-trimoxazole)

  • When the bacteria is known

    • N. meningitidis – benzylpenicillin

    • Strep pneumoniae – ceftriaxone

      • If resistant – vancomycin

    • H influenza – ceftriaxone

    • Listeriamonocytogenes – ampicillin plus gentamicin

    • Strep suis – cefriaxone

  • If allergic to penicillins – chloramphenicol, vancomycin

  • Coricosteroids – dexamethasone – limit to 2 days

  • Viral encephalitis investigations management

    Viral encephalitis – investigations, management

    • Investigations

      • CT/MRI – low density lesions in temporal lobe

      • LP – exclude mass lesion

        • Excess lymphocytes – polymorphonuclear cells may dominate in early stages, glucose normal, protein may be elevated

      • EEG usually abnormal in early stages – periodic slow wave activity in temporal lobes

      • PCR – viral DNA

    • Management

      • Anticonvulsant treatment is often necessary

      • Raised ICP -> dexamethasone

      • HSV – acyclovir -> should be given to all patients suspected of viral encephalitis

      • Mortality – 10-30%, surviviros – residual epilepsy, cognitive impairments

    Cerebral abscess investigations management

    Cerebral abscess – investigations, management

    • Investigations

      • CT – single or multiple low density areas with ring enhancement (contrast), surrounding cerebral oedema

      • LP – if CT is ok

      • Elevated WCC and ESR

      • Consider cerebral toxicoplasmosis, or TB secondary to HIV

    • Management

      • Antimicrobial therapy once diagnosis is made

        • Site- source – organisms – treatment

        • Frontal lobe – paranasal sinuses, teeth – streptococci, anaerobes – cefuroxime, metronidazole

        • Temporal lobe – middle ear – streptococci, enterobaceteriaceae – ampicillin, metronidazole, ceftazidime (or gentamicin)

        • Cerebellum – sphenoid sinus, mastoid/middle ear – Pseudomonas, anaerobes - ampicillin, metronidazole, ceftazidime (or gentamicin)

        • Any site – penetrating trauama – staphylococci – flucloxacillin

        • Multiple – metastatic and cryptogenic – streptococci, anaerobes – benzylpencillin if endocarditis or cyanotic heart disease, otherwise cefuroxime plus metronidazole

      • Surgical treatment – burr-hole aspiriation, excision – esp if capsule

      • Anticonvulsants often necessary

      • Mortality 10-20% - may be related to delay in initiation of treatment

    Gullian barre syndrome clinical

    Gullian-barre’ syndrome - clinical

    • Develops in 70% of patients 1-4weeks after RTI or diarrhoea – particaulrly campylobacter

    • Predominantely cell mediated inflammatory response directed at the myelin protein of spinal roots, peripheral and extra-axial cranial nerves -> complemented mediated destruction of myelin sheath and associated axon

    • Clinical – distal paraesthesia and limb pains – precede rapidly ascending muscle weakness

      • Facial and bulbar weaknes commonly develops

      • Ventilar support in 20%

      • Widespread loss of reflexes

      • 80% recover in 4-6 months, 4% die, rest have neuro deficits

    Gullian barre syndrome investigations management

    Gullian-barre’ syndrome – investigations, management

    • Investigations

      • CSF – protein elevated at some stage of the illness, no rise in cell number

      • Electrophysiological studies – conduction blokd and multifocal motor slowing – delayed F waves

      • Identify underlying cause – campylobacter, CMV, mycoplasma

      • Acute porphyria – exclude by urinary porphyrin estimation

    • Management

      • Regularly monitor respiratory function

      • Corticosteroid shown to be ineffective

      • Plasma exchange and IV immunoglobulin shorten duration of ventilation assistance

    Myasthenia gravis clinical

    Myasthenia gravis - clinical

    • 15-50, F > M in younger, reverse in older

    • Cardinal symptom – fatigable weakness of the muscles – movement initially strong, rapid weakening occurs – worsening symptoms towards end of day or after exercise is characteristic

    • No sensory signs or involvement of CNS – but weakness of oculomotor muscles may mimick a central eye movement disorder

    • First symptoms – ptosis, diplopia

      • Also – weakness of chewing, swallowing, speaking or limb movement

      • Limb muscle- commonly shoulder girdle

    • Respiratory failure is not an uncommon cause of death

    • Prognosis variable, remission spontaneously sometimes

      • If confined to eye muslces – prognosis excellent

      • Young F higher remission rates if thymectomy

      • Rapid progression more than 5 years after its onset is uncommon

    Myasthenia gravis investigations

    Myasthenia gravis - investigations

    • Tensilon test

      • Inject – short acting anti-cholinesterase (edroponoium bromide) – test drug with small amount - then bigger amount 8 minutes later – improvement in muscle power occurs within 30 seconds persists for 1-2 minutes

    • Ice pack test

      • Ice on eye to help extra ocular muscles

    • Serological testing

      • AChRA is found in 50% of cases

      • Anti-MuSK (muscle specific kinase) especially in negative AChRA patients

      • 6-12% of patients are seronegative

    • Electrophysiological confirmation

      • Repeptitive nerve sitmulation

      • Single fibre

    Myasthenia gravis treatment

    Myasthenia gravis - treatment

    • Principles of treatment

      • Maximise the activity of AchR in the neuromuscular junction

        • Anticholinesterase

          • Pyridostigmine – 30-120 mg, 6hourly

            • Muscarinic side effects

      • Limit or abolish the immunological attack on motor end plates

        • Thymectomy – antibody + under 25, symptoms not confined to extraocular eye muscles, unless disease established for more than 7 years

        • Plasma exchange – removing antibody blood – marked improvement – brief – crisis management, pre-operative

        • Plasmapheresis – remove offending autoantibodies

        • Intravenous immunoglobulin – alternative to plasma exchange in the short term treatment of severe myasthenia, MOA of action uncertain

        • Corticosteroid treatment – improvement commonly preceded by marked exacerbation of symptoms – should be initiated in hospital

          • Usually to continue for months to years

        • Others – azathioprine – reducing dosage of steroids

    Shigella clinical management

    Shigella – clinical, management

    • Clinical

      • Burning discomfort in affected dermatome – discrete vesicles 3-4 days later

      • Severe disease suggests an underlying immunodeficiency

      • Thoracic dermatomes commonly involved

      • Ophthalmic division of trigeminal nerve is also involved

      • Ramsay Hunt syndrome – facial palsy, ipsilateral loss of taste and buccal ulceration, rush in the external auditory canal – geniculate ganglion involvement

      • Granulomatous cerebral angiitis – cerebrovascularcompliation – stroke-like syndrome

    • Management and prevention

      • Acyclovir – reduce early and late onset pain

      • Analgesia

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