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Dr. Edhie Djohan Utama, SpMK
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INFEKSI PADA SISITIM SYARAF PUSAT
BISA DISEBABKAN OLEH SEMUA AGENT YANGINFECTIOUS :
= BAKTERI -
PYOGENIK
= MYCOBACTERIA
= FUNGI
= SPIROCHAETA
= VIRUS
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INFEKSI SELAPUT OTAK (Meningitis)
I. MENINGITIS PURULENTA MENINGOCOCCUS (40%)
PNEUMOCOCCUS HAEMOPHILUS INFLUENZAE
STAPHYLOCOCCUS AUREUS
LISTERIA MONOCYTOGENES
II. MENIGITIS GRANULOMATOUS MYCOBACTERIUM TUBERCULOSIS
COCCIDIODES IMMITIS (meningitis) CRYPTOCOCCUS NEOFORMAN (meningitis)
HISTOPLASMA CAPSULATUM
TREPONEMA PALLIDUM
JAMUR JAMUR LAIN
III. ASEPTIC MENINGITIS ENTEROVIRUS
POLIOMYELITIS
COXSACKIEVIRUS
ECHOVIRUS (Enteric Cytopathic Human Orphan)
RABIES
HERPES SIMPLEX
PARAMYXOVIRUS (Mumps virus)
LEPTOSPIRA
CLOSTRIDIUM TETANI
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I. MENINGITIS PURULENTA
MENINGOCOCCUS (40%)
NEISSERIA MENINGITIDIS, menyebabkan meningitis danmeningococcemia. (WATERHOUSE FREDERICHSENSYNDROME = high fever, shock, purpura yg luas, intravascular coagulation dan adrenal insuffiency)
PNEUMOCOCCUS
DIPLOCOCCUS PNEUMONIAE / STREPTOCOCCUSPNEUMONIAE (bacterial menigitis)
HAEMOPHILUS INFLUENZAE
STAPHYLOCOCCUS AUREUS
(Toksin mediated menimbulkan shock syndrome) LISTERIA MONOCYTOGENES (Acute meningitis pada
newborn)
80% meningitis disebabkan oleh Meningococcus
dan Pneumococcus ( Levinson & Jawetz )
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a. Neisseria Meningitidis
1. N. meningitidis (meningococcus) causes meningococcal meningitis.
2. This bacterium is found in the throats of
healthy carriers (reservoir). The bacteria
probably gain access to the meninges through
the bloodstream.3. The bacteria may be found in leukocytes in the
CSF. (Gram negatives intracellulair diplococci)
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4. Symptoms are due to hyperproduction of
endotoxin.5. The disease occurs most often in young children, but
can also cause outbreaks among persons living in close
contact (military, college dormitorities, institutionalsettings).
6. Military recruits are vaccinated with purified capsular
polysaccharide to prevent epidemics in training camps.
Unfortunately, like other polysaccharide vaccines, it is
not effective in very young children.
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Neisseria meningitidis ( Meningococcus )
Spread in respiratory droplets
Inactivate IgA using IgA protease Colonize the nasopharynx using fimbriae sore throat
Endocytized bloodstream (capsule to avoid phagocytosis)
Endotoxin:
1. affects blood vessel permeability cross BBB (attach to dura mater w/ fimbriae)
2. drop in blood pressure shock
3. clotting of blood hemorrhage (rash) and DIC
Mortality in untreated - 85%
Optimal - 1%
Crowding - military, dorms, day-care
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Haemophilus influenzae type B
Inactivate IgA using IgA protease
Colonize the nasopharynx
Penetrate submucosa (invasive) bloodstream(capsule to avoid phagocytosis)
Endotoxin
Inflammation, DIC
Mortality 6%
Mental retardation
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d. Listeriosis
1. Listeria monocytogenes causes meningitis in :
newborns, the immunosuppressed, pregnant
women, and cancer patients.
2. Acquired by ingestion of contaminated food, itmay be asymptomatic in healthy adults.
3. The organisms are capable of growing at
refrigerator temperatures.
4. L. monocytogenes can cross the placenta and
cause spontaneous abortion and stillbirth.
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Diagnosis
Diagnosis of TB meningitis is made by analysing CSF collected by
lumbar puncture. When collecting CSF for suspected TB meningitis,a minimum of 1ml of fluid should be taken (preferably 5 to 10ml).
The CSF usually has a high protein, low glucose and a raisednumber of lymphocytes. Acid-fast bacilli are sometimes seen on aCSF smear , but more commonly, M. tuberculosis is grown inculture. A spiderweb clot in the collected CSF is characteristic of TB meningitis, but is a rare finding.
More than half of cases of TB meningitis cannot be confirmedmicrobiologically, and these patients are treated on the basis of clinical suspicion only. The culture of TB from CSF takes aminimum of two weeks, and therefore the majority of patients withTB meningitis are started on treatment before the diagnosis isconfirmed.
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Treatment
The treatment of TB meningitis is isoniazid, rifampicin, pyrazinamide and ethambutol for two months, followed by isoniazid and rifampicin alone for a further tenmonths. Steroids are always used in the first six weeks of treatment (and sometimes for longer).
Treatment must be started as soon as there is areasonable suspicion of the diagnosis. Treatment mustnot be delayed while waiting for confirmation of thediagnosis.
Hydrocephalus occurs as a complication in about a thirdof patients with TB meningitis and will require aventricular shunt.
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Fungal meningitis Meningitis caused by a fungal infection. Meningitis is
an inflammation of the lining around the brain andspinal cord. Fungal meningitis is relatively rare andresults when airborne yeast cells are inhaled. Thecondition mostly occurs in people with a compromised
immune systems such as AIDS sufferers.
1. COCCIDIODES IMMITIS (meningitis)
2. CRYPTOCOCCUS NEOFORMAN (meningitis)
3. HISTOPLASMA CAPSULATUM
Chronic presentation
1. Coccidioides immitis
2. Cryptococcus neoformans - AIDS
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Fungal meningitis
Chronic presentation
1. Coccidioides immitis
2. Cryptococcus neoformans - AIDS
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Symptoms of Fungal meningitis
Headache Blur red vision (diplopia and unequal, sluggish
pupils )
Confusion
Tiredness
Stif f neck
Positive Kernig's sign, nuchal rigidity,
irritability or restlessness
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1. Coccidioides Immitis
Coccidioides Immitis adalah suatu jamur. Biasanya terdapat di tanah, sehingga
disebut jamur tanah. Jamur ini bersifat endemik dan dapat menyebabkan
koksidioidomikosis.Infeksi biasanya dapat sembuh sendiri tetapi juga dapat mematikan. Jamur jenis ini juga dikenal sebagai jamur dimorfik karena jamur ini mempunyai daya adaptasimorfologik yang unik terhadap pertumbuhan dalam jaringan atau pertumbuhan pada37°C.
Coccidioides immitis bentuknya seperti bola (=sferul) yang garis tengahnya 15 - 60μm,
dengan dinding tebal berbias ganda. Hifa dari jamur ini juga mudah pecah danmengeluarkan spora.
Infeksi oleh jamur ini biasanya meliputi influenza, demam, lesu, batuk, dan adanya
rasa sakit di seluruh tubuh. Gejala – gejala inilah yang biasanya disebut “Valley
fever” dan biasanya gejala ini dapat sembuh sendiri yang dikenal dengan infeksi primer dan hanya dibutuhkan pengobatan suportif atau dapat juga kronik.
Obat yang dipakai antara lain berupa Amphotericin B, Ketokonazol, Mikonazol.
Penyakit ini tidak dapat ditularkan dari orang ke orang.
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Special tests to confirm Cyptococcal meningitis:
Special tests are needed :
Lumbar puncture (spinal tap): taking fluid
from your spinal column through a needle in
your back. This fluid in then sent for special
tests. Blood tests: to check whether you have
been exposed to the fungus.
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Meningitis due to Histoplasma capsulatum
Meningitis due to Histoplasma capsulatum and Mycobacteriumtuberculosis in a returned traveler with acquired
immunodeficiency syndrome
The spores of the fungus are released into the air whencontaminated soil is disturbed (for example, by plowing fields,sweeping chicken coops, or digging holes) and the airborne sporescan then be inhaled into the lungs, the primary site of infection.
In AIDS patients with DH, H capsulatum can be isolated readilyfrom blood (91% sensitivity) and bone marrow (90% sensitivity). In addition, H capsulatum can be isolated from respiratory secretions, lymphnodes, localized lesions, and cerebrospinal fluid (CSF). Although culture is thegold standard for diagnosis, isolation can take up to 4 weeks, and therefore is
impractical as a criterion for treatment initiation.
Serologic Tests : In patients with intact immune systems, antibodies develop athigh levels within 4-6 weeks in most symptomatic Histoplasma infections andare useful for diagnosis in those patients. Detection of H capsulatum antigen in
body fluids permits rapid diagnosis of DH.
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Infections of Neural Tissue
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Infections of Neural Tissue
Poliovirus ( poliomyelitis )
fecal/oral route of transmission
spread by contaminated water
90% asymptomatic infections
10% flu-like illness
0.01% paralytic poliomyelitis
Replicates inside epithelial cells of nose, throat, intestine lymphatics bloodstream
If enters CNS infected cells die paralytic polio
Historical rate of paralytic polio US - 21,000/yr Peak year US - 1958
Last case wild virus in US - 1979
Western hemisphere declared free - 1994
Discontinuation of oral polio vaccine - 1999
Worldwide eradication
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TRANSMISI VIRUS POLIO
POLIOVIRUS KELUAR BERSAMA
FECES, DISEBARKAN MELALUI
MAKANAN DAN MINUMAN YANG
TERKONTAMINASI.
BISA MELALUI BERSIN DAN BATUK
KARENA DIJUMPAI PADA MUCOSAHIDUNG DAN MULUT
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PATHOGENESIS POLIOVIRUS
MULTIPLIKASI PADA MEMBRAN MUCOSASALURAN MAKANAN DAN JUGA PADA SEL
SEL MUCOSA PHARYNX
KEMUDIAN MENEMBUS DAN MASUK KEKELENJAR LYMPHE TERDEKAT
MASUK KEDALAM DARAH SUSUNAN
SYARAF PUSAT GRAY MATTER SUM-SUM
TULANG BELAKANG MERUSAK MOTOR
NEURON KELUMPUHAN OTOT
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Viral meningitis = aseptic meningitis
Fairly common (40%)
Self-limiting, non-fatal
CSF is clear
Many different viruses
1. Enteroviruses - 40%
2. Mumps virus - 15% 3. Other
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VACCINE POLIOMYELITIS
SALK VACCINE : parenteral
Menghasilkan humoral AB
Diberikan 4kali dalam 1-2 tahun
Efektivitas 70-90%
SABIN VACCINE : per oral Trivalent vaccine
Idealnya diberikan pada usia 6 bulan berturut turut 3kali jarak 6-8 minggu
Efektivitas 100%Menghasilkan IgM, IgG dan secretory IgA dalam
saluran pencernaan
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PENGOBATAN DAN PENCEGAHAN
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PENGOBATAN DAN PENCEGAHAN
INFEKSI POLIOVIRUS
PENGOBATAN :
Diberikan obat penghilang rasa sakit
Obat kejang kejang otot
Mengatur respirasi
Hydrasi
PENCEGAHAN :
Salk vaccine (killed vaccine) Suntikan
Sabin vaccine : Live attenuated strain per oral
Infections of Neural Tissue
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Infections of Neural Tissue
Viral - RABIES
Rabies - Rhabodovirus Bite, Multiplies at site
Travels to local nerves
Peripheral nerves spinal cord brain
Long incubation (tergantung lokasi gigitan) Prodromal phase - flulike symptoms, tingling, burning,
depression
Excitation phase - muscle function, speech, vision, anxiety,hydrophobia
Paralytic phase - muscles weaken, consciousness fades, death
Mortality - 100% with best treatment
Post exposure prophylaxis (PEP) - has never failed in US
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Rabies
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Rabies
1. Rabies virus (rhabdovirus) causes an acute, usually
fatal, encephalitis called rabies.2. Rabies may be contracted through the bite of a rabid
animal, by inhalation of aerosols, or invasionthrough minute skin abrasions. The virus multiplies
in skeletal muscle and connective tissue.
3. Encephalitis occurs when the virus moves along peripheral nerves to the CNS.
4. Symptoms of rabies include spasms of mouth andthroat muscles, followed by extensive brain andspinal cord damage and death.
Rabies
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Rabies
5. Laboratory diagnosis may be made by directimmunofluorescent tests of saliva, serum, and CSF or
brain smears.
6. Reservoirs for rabies in the United States includeskunks, bats, foxes, and raccoons. Domestic cattle,dogs, and cats may get rabies. Rodents and rabbitsseldom get rabies.
7. Current postexposure treatment includesadministration of human rabies immune globulin(RIGH) along with multiple intramuscular injectionsof vaccine.
8. Preexposure treatment consists of vaccination.
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ENCEPHALITIS
INFECTIONS OF THE NEURAL TISSUE
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A b i l E h liti
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Arboviral Encephalitis
1. Symptoms of encephalitis are chills,
headache, fever, and eventually coma.
2. Many types of arboviruses transmitted by
mosquitoes cause encephalitis.
3. The incidence of arboviral encephalitis
increases in the summer months when
mosquitoes are most numerous.
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Arboviral Encephalitis (lanjutan)
4. Diagnosis is based on serological tests.
5. Control of the vector is the most effective
way to control encephalitis.
6. Horses are frequently infected by EEE
(eastern equine encephalitis) and WEE
(western equine encephalitis) viruses.
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Infections of Neural Tissue
Bacterial
Tetanus - Clostridium tetani - tetanospasmin (mimicsstrychnine poisoning)
Botulism - Clostridium botulinum
Genes for toxin are carried on a bacteriophage
Toxin prevents release of acetylcholine
Produces a limp, flaccid, paralysis
Eyes blurry, double vision Throat slurring speech, difficulty swallowing
Difficulty breathing
Cardiac problems
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6. Endospores are killed by proper canning. Theaddition of nitrites to foods inhibits outgrowth after endospore germination.
7. The toxin is heat labile and is destroyed by boiling(100°C) for 5 minutes.
8. Infant botulism results from the growth of Clostri-
dium botulinum in an infant's intestines and has beenassociated with the ingestion of honey products.
9. Wound botulism occurs when C. botulinum grows inanaerobic wounds.
10. For diagnosis, mice protected with antitoxin areinoculated with toxin from the patient or foods.
Tetanus
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Tetanus
1. Tetanus is caused by production of an exotoxin in
a localized infection of a wound by Clostridium tetani . Endospores allow for long-term survival in
soil.
2. C. tetani produces the neurotoxin tetanospasmin,which causes rigid paralysis with the symptoms
of tetanus: spasms, contraction of muscles
controlling the jaw, and death resulting from
spasms of respiratory muscles.
3. C. tetani is an anaerobe that will grow in unclean
wounds and wounds with little bleeding.
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TETANUS INFECTION CONTROL
1. Acquired immunity results from DPT immunization thatincludes tetanus toxoid.
2. Following an injury, an immunized person may receive abooster of tetanus toxoid. (TT)
3. ATS prophylaxis (1500 IU)
4. An unimmunized person may receive (human) tetanusimmune globulin (ATS therapeutis)
5. Debridement (removal of tissue) and antibiotics may beused to control the infection.
Angka kematian 55% - 65% jika tidak imun ! ! !
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DAFTAR PUSTAKA
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DAFTAR PUSTAKA 1. Alcamo, Edward : Fundamentals of Microbiology. 6th ed. Jones
& Bartlett Publshers, Boston, Toronto, London, Singapore., 2001
2. Brook,G.F., Butel,J.S., and Ornston,L.N. : Jawetz, Melnick &Adelberg's Medical Microbiology. 20th Ed. A Lang Medical Book,Prentice Hall Int Inc. 1995.
3. Burdon, K.L. : Textbook of Microbiology. 4 th EdThe Macmillan
Co New Jork 1961
4. Lennette,E.H.,Balow,A., Hausler,W. and Truant, J.P. : Manual of Clinical Microbiology, 3 Amer Society for Microbiol, Washington,D.C., 1980
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