Neuroinfeksi Flashcards
Belajar tentang infeksi Neurologis
Pasien dengan gejala meningitis Dan tinta India positive. Diagnosis :
Cryptococcus
Terdapat negri bodies pada PA
Diagnosis
Rabies
Tatalaksana Pilihan CMV (Cytomegalovirus)
Fase induksi (3 minggu)
- foscarnet 60 mg/kgBN/8jam
- Ganciclovir 5 mg/kgBB 12 jam
Ganciclovir Merupakan analog 2-deoxyguanosine , yg merupakan obat antivirus yg memiliki efek Klinis pada virus CMV
meningitis Listeria monocytogenes tatalaksana Pilihan adalah
Penicillin 6x2 g selama 3 minggu
Penicillin/ampicillin + gentamicin
Penicillin/ampicillin tidak bisa diberikan tunggal pada infeksi listeria.
Sefalosporin generasi 3 tidak aktif melawan listeria.
Acute HIV aseptic meningitis
seroconversion syndrome (fase awal HIV). Klinis : febrile illness, headache, meningeal irritation. By definition, alertness and cognition are preserved. LCS : lymphocytic pleocytosis (but usually less than 25 cells/μL) peningkatan protein level (less than 100 mg/dL), normal glucose levels.
Lyme disease
Disebabkan Borrelia burgdorferi.
Klinis:
• Stage 1 (infeksi lokal):dalam 4 mg setelah digigit kutu, erythema chronicum migrans ( bull’s eye rash)
• Stage 2 (penyebaran infeksi) (beberapa Hari/minggu setelah merah):
systemic manifestations; fever, chills, migratory
musculoskeletal pain, arthralgias, fatigue,Cardiac involvement.After weeks
or months, lymphocytic meningitis,
neuropathies, including cranial and peripheral
neuropathies.
• Stage 3 (persistent infection) (months after the secondary
stage): Intermittent episodes of oligoarthritis,
encephalomyelitis,encephalopathy, and dementia. An axonal
polyneuropathy may also occur.
mucormycosis
mucormycosis, which is a zygomycosis. This
fungus tends to enter through the respiratory tract, producing nasal
and sinus disease and pulmonary infections. In the presence of
predisposing factors and trauma, it may invade blood vessels and
gain entry into the CNS, where it can produce an acute necrotizing
reaction and vascular thrombosis, including venous sinus
thrombosis, especially affecting the cavernous sinus. Externally,
patients have a destructive inflammatory and necrotizing lesion
affecting the face, especially in the nasal and maxillary areas.
Diabetes mellitus and diabetic ketoacidosis are major and frequent
risk factors for this condition. Other predisposing conditions
include malignancies, high-dose steroids, organ transplantation,
immunosuppression, and iron chelation therapy (with
deferoxamine). The organisms causing this infection are mucor,
rhizopus, and rhizomucor, which are fungi and not acid-fast bacilli.
These fungi are seen as infrequently septated or nonseptated
hyphae on histopathologic specimens.
HIV-associated neurocognitive disorder ( AIDS-dementia
complex)
Umumnya pada HIV stadium lanjut.
Spektrum terdiri atas :
- asymptomatic neurocognitive impairment (ANI)
- minor neurocognitive disorder (MND)
- HIV-associated dementia. (HAD). biasanya pada CD4<200 cells/mm3
The etiology of this
condition is the retrovirus itself rather than an opportunistic
infection. Progressive cognitive decline and prominent
psychomotor dysfunction are the main clinical manifestations.
These patients have significant difficulties with attention and
concentration, along with fine motor dysfunction, gait
incoordination, and tremors. However, focal neurologic deficits are
not common.
Pemeriksaan :
- MRI kepala : atropi difus, umumnya mengenai basal ganglia, white matter, regio cortical.
Nile virus (WNV) encephalitis
West Nile virus (WNV) encephalitis, which is an
arboviral infection that spreads in the summer months, can occur in
epidemics, and is transmitted by mosquitoes of the genus Culex.
Most infected patients are asymptomatic, up to 20% may show
signs of a febrile viral illness, and less than 1% develop a severe
neurologic presentation. Patients with severe neurologic
presentation will have manifestations of encephalitis; however,
WNV can also invade the anterior horn cells leading to flaccid
weakness with arreflexia, similar to poliomyelitis. WNV infection
may also manifest with cranial neuropathies and tremors. Elderly
patients are particularly at risk for neurologic disease, especially
encephalitis, however, meningitis and flaccid paralysis may also
occur in young and middle-aged patients.
WNV encephalitis is diagnosed by serology and detection of
immunoglobulin M (IgM) antibodies in the CSF. CSF PCR is less
sensitive, but is diagnostic when positive. MRI is nondiagnostic.
Treatment is supportive
Cryptococcal meningitis
Disebabkan Cryptococcus neoformans/gatii.
histopathologis : budding yeasts near blood
vessels and surrounded by an inflammatory infiltrat.
Umumnya pada immunocompromise dan opportunistic infeksi HIV
lanjut.
CSF : protein tinggi, pleositosis (pada immunocompromised tdk Ada reaksi inflamasi)
Sitologi : pseudohifa, jamur crypto
Tatalaksana Cryptococcal meningitis
The initial treatment regimen is amphotericin plus flucytosine
for 2 to 3 weeks. These patients should be monitored closely, since
amphotericin is associated with renal failure, hypokalemia, and
hypomagnesemia; and flucytosine may cause hematologic
abnormalities. If the patient is doing well on amphotericin and
flucytosine, or the meningitis is mild, the treatment can be
switched to fluconazole 200 mg twice daily for 8 to 10 weeks.
Afterward, the patient should be kept on long-term maintenance
therapy with fluconazole 200 mg daily to prevent recurrences.
Highly active antiretroviral therapy, by promoting immune
reconstitution, plays a major role in the long-term treatment of
HIV patients with cryptococcal meningitis, after the acute infection
has cleared
Toxoplasmosis
Infeksi oportunistik pd AIDS, terutama tanpa ARV adekuat. Pada immunosuppressive lanjut dgn CD4< 200/μL
Klinis : nyeri kepala, defisit Neurologis
Imaging : CT ; lesi hipodense menyangat kontras. Predileksi basal ganglia, Dan corticomedullary junction , kadang Di fossa posterior.
The organism is
usually acquired earlier in life and remains dormant until the
immune system declines and T. gondii becomes active.
Tatalaksana Toxoplasmosis Encephalitis
Terapi induksi (6 minggu)
Pirimetamin loading 200 mg , dilanjutkan 50 mg (75 mg bila BB>50 kg)
+ Clindamycin 4x600 mg / sulfadiazine 4-8 gr per Hari
Terapi rumatan : setengah dosis terapi induksi, Atau cotrimoxazole 2x1 hingga CD4>200
Terapi perlu penambahan asam folat
Standard therapy is sulfadiazine plus pyrimethamine. Since both
agents affect the folate metabolism pathways, folinic acid should
be provided to avoid hematologic complications. An alternative
therapy is clindamycin, especially in patients who are allergic to
the sulfa components and cannot take sulfadiazine. Long-term
suppressive therapy is needed to prevent relapses. Highly active
antiretroviral therapy promotes immune reconstitution, and
patients whose CD4 counts rise above 200/μL may not need further
suppressive therapy. Trimethoprim-sulfamethoxazole is used for
prophylaxis. Patients with HIV and CD4 counts of less than 100/μL
with positive IgG antibodies to toxoplasma should be given
prophylaxis.
primary CNS lymphoma (PCNSL) pada AIDS.
These patients usually present with focal neurologic
manifestations, which progress slowly over days to weeks. Since
PCNSL in AIDS patients is frequently associated with Epstein–Barr
virus, positive CSF PCR for this virus helps to make the diagnosis.
CSF findings usually demonstrate a lymphocytic pleocytosis,
elevated protein, and low to normal glucose levels. Cytology may
detect atypical cells; however, this test has low sensitivity. Flow
cytometry is helpful in making the diagnosis showing monoclonal
B lymphocytes. CT scan has poor sensitivity, and MRI is a better
tool, showing one or more lesions usually in the periventricular
and deep regions of the brain. These lesions may have contrast
enhancement, surrounding edema, and produce mass effect.
Definitive diagnosis is done with brain biopsy.
Corticosteroids are helpful in the treatment of edema and mass
effect, and the lesion itself tends to shrink with this treatment.
However, the use of steroids may alter the results and the
sensitivity of the brain biopsy. Whenever possible, their use should
be delayed until after the biopsy is obtained. The use of
chemotherapy is controversial in this setting, and may not be
optimal in patients with a baseline poor performance status related
to the underlying disease. Radiation therapy is used as palliative
treatment. The use of highly active antiretroviral therapy has
improved the overall prognosis in patients with AIDS and PCNSL
progressive multifocal leukoencephalopathy
PML
progressive multifocal leukoencephalopathy
(PML), caused by JC virus, which is a polyomavirus. PML occurs in
patients with end-stage AIDS. A large percentage of the general
population has antibodies against this virus, certainly without
clinical manifestations; and therefore, the presence of serum
antibodies is not helpful for the diagnosis. Only those patients with
severe immunosuppression develop clinical manifestations; PML in
immunocompetent individuals is exceedingly rare but can occur.
PML is a demyelinating condition and presents with a gradually
progressive course of multiple focal neurologic manifestations,
with visual field deficits and visual agnosias being common, given
the predominant involvement of parieto-occipital regions.
Hemiparesis, sensory deficits, language disorders and ataxia may
occur.
The diagnosis can be suspected with the history and clinical
manifestations, supported with MRI findings and CSF JC virus DNA
PCR, and confirmed with brain biopsy (though brain biopsy is not
necessary in the setting of typical clinical, imaging, and CSF
findings).
MRI shows multiple white matter nonenhancing lesions that tend
to coalesce and predominate in the parieto-occipital regions. Brain
biopsy is the gold standard diagnostic test; neuropathologic
findings include myelin loss, giant astrocytes, and altered
oligodendrocytes, with enlarged nuclei and viral inclusions. On
electronic microscopy, the viral particles give a “spaghetti and
meatballs” appearance.
HIV neuropathy
HIV neuropathy, which is a distal sensory
neuropathy seen in patients with HIV, more frequently as the CD4
count drops. This condition is a predominantly sensory, axonal
length-dependent symmetric polyneuropathy. It is thought to be
related to direct effects of the virus and cytokine upregulation.
These patients should continue antiretroviral therapy for virus
suppression, and the treatment is symptomatic for the neuropathic
pain.
Bacterial meningitis penyebab:
Penyebab : *1 - 23 bln :Streptococcus pneumoniae, Neisseria meningitidis, Streptococcusagalactiae, Haemophilus influenzae, Escherichia coli.*2 - 50 th: Streptococcus pneumoniae, Neisseria meningitidis. *> 50 th : Listeria monocytogenes,Streptococcus pneumoniae, Neisseria meningitidis.* Riw Neurosurgical
: aerobic gram-negative
bacilli (including Pseudomonas aeruginosa), Staphylococcus aureus,
Staphylococcus coagulase negative (such as epidermidis).
*CNS instrumentation, these same agents and
Propionibacterium acnes should be considered. *Unlike in communityacquired meningitis, Streptococcus pneumoniae is not a common
cause of hospital-acquired meningitis.
Meningitis bakterial pemeriksaan LCS
Pemeriksaan LCS rutin :
Peningkatan protein, penurunan glukosa, peningkatan neutrofil
Pemeriksaan gram :
90 % disebabkan Streptococcus
pneumoniae, 86% of those caused by Haemophilus influenzae, 75%
of those caused by Neisseria meningitidis, 50% of those caused by
gram-negative bacilli, and 33% of cases caused by Listeria
monocytogenes have positive Gram stain results.
Even though the yield of CSF Gram stain can be as low as 20% in
patients who have received antibiotics, this test is easy to do, is
rapid and inexpensive, and is recommended for all patients with
suspected bacterial meningitis.
Tatalaksana meningitis bakterial
Neisseria meningitidis: cephalosporin (gen 3); ceftriaxone /cefotaxime, 7 days.
Streptococcus pneumoniae ;vancomycin and ceftriaxone, 10 - 14 days.
Listeria monocytogenes; ampicillin
+ gentamicin
for more than 21 days.
Haemophilus influenzae ;ampicillin if the organism is β-lactamase negative; however, if it is
β-lactamase positive, cephalosporin gen3. Pseudomonas aeruginosa :usually a hospital-acquired
infection and is typically resistant to ceftriaxone. Ceftazidime and
cefepime have been used to treat this infection, at least 21 days.
Abses brain
brain abscesses. These lesions
originate from invasion of brain parenchyma by bacterial
organisms, commonly polymicrobial, with a combination of
streptococci, staphylococci, enterobacteria, and anaerobes. The
bacterial agents spread via hematogenous routes or from a
contiguous infected site, such as the sinuses, ears, or teeth. They
also can be encountered after open trauma or neurosurgical
interventions.
Patients may present with fever, headaches, neck stiffness, focal
neurologic findings, and altered mental status. The diagnosis is
made on the basis of clinical suspicion and the presence of risk
factors, along with clinical and radiologic findings, with the MRI
showing ring enhancing lesions with surrounding edema.
Lumbar puncture may be contraindicated in the presence of mass
effect, and therefore CSF may not be available. The presence of
atypical lymphocytes and monoclonal B cells in the CSF are seen in
lymphoproliferative disorders and not in brain abscesses.
Brain abscesses evolve through different stages, with initial
cerebritis in the first few days, then the formation of central
necrosis with surrounding vasogenic edema, and the subsequent
formation of a capsule. The abscess eventually matures, with the
development of collagenous tissue in the capsule and regression of
the vasogenic edema. Caseating granulomas are not seen in
cerebral bacterial abscesses.
Optimal treatment requires drainage of the abscess in
combination with intravenous antibiotics. Given that these lesions
are most commonly polymicrobial, the treatment of choice is a
combination of antibiotics, usually a third-generation cephalosporin
(for streptococci and gram-negative bacilli), metronidazole (for
anaerobes), and vancomycin (for staphylococci). The IV antibiotic
regimen is continued for 6 to 8 weeks, and subsequent continuous
oral antibiotics may be required beyond the initial treatment
period
Tatalaksana brain abscesses
- drainage abses
- the treatment of choice is a
combination of antibiotics, usually a third-generation cephalosporin
(for streptococci and gram-negative bacilli), metronidazole (for
anaerobes), and vancomycin (for staphylococci). The IV antibiotic
regimen is continued for 6 to 8 weeks, and subsequent continuous
oral antibiotics may be required beyond the initial treatment
period.
septic cavernous sinus thrombosis
septic cavernous sinus thrombosis, which can be a
complication of bacterial sinus infections, and manifests with
proptosis, compromise of the cranial nerves (CNs) traveling within
the sinus (CNs V1 and V2, III, IV, and VI), retinal vein
engorgement with retinal hemorrhages, and papilledema.
Patients with intracranial infections may also develop thrombosis
of other sinuses such as the superior sagittal or the transverse
sinuses. Diagnosis is based on clinical suspicion and radiologic
studies. Brain MRI, MRV and/or angiography with visualization of
the venous phase may be useful. Treatment involves antibiotic
therapy, covering gram-positive agents, staphylococci, gramnegative organisms, and anaerobes.
Morbus Hansen / lepra
Hansen disease, or leprosy. This disease has a long
incubation period (from years to decades) and is caused by
Mycobacterium leprae, which is thought to spread through the
respiratory tract but does not typically produce a respiratory
illness. This mycobacterium has tropism toward peripheral nerves,
especially in cooler areas of the body.
Leprosy has two major variants, a lepromatous variant and a
tuberculoid variant, in addition to intermediate forms between the
two. The lepromatous variant occurs in patients with impaired cellmediated immunity, making it possible for the organism to spread
to the skin and peripheral nerves, causing a maculopapular rash,
nodules, and poorly demarcated skin lesions. The manifestations
can be systemic, and patients present with sensory loss
predominantly in the coolest regions of the body, such as the pinna
of the ear, tip of the nose, dorsal surfaces of the hands, forearms
and feet, and dorsolateral surface of the legs. The tuberculoid form
occurs in patients with good cellular immunity, in which the
disease is less disseminated, the skin lesions are better localized,
and the patient will also have asymmetric peripheral neuropathies
with thickened nerves. The ulnar nerve is commonly affected, and
the syndrome may resemble mononeuritis multiplex. Other
commonly involved nerves include the greater auricular, radial,
common peroneal, and sural nerves.
The diagnosis is suspected based on clinical and epidemiologic
data. Skin and/or nerve biopsies are often necessary,
demonstrating inflammatory granulomas with epithelioid and
mononuclear infiltrates and acid-fast organisms.
Tatalaksana morbus Hansen
Chronic therapy is usually needed, using rifampin, dapsone, and
clofazimine.