k.16b inf. sistem syaraf 2011

7/27/2019 k.16b Inf. Sistem Syaraf 2011

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Dr. Edhie Djohan Utama, SpMK

Departemen Mikrobiologi

FK USU Medan


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Meningitis : Characterized by high fever,

headache, stiff neck (Infeksi Selaput Otak)

Encephalitis : Characterized by changes inmental state, consciousness (kesadaran),

behavior (tabiat) (Infeksi Jaringan Otak)

Brain Abscess : Headache, focal signs andseizures indicate a brain abscess. There are also

characteristic computed tomography (CT) andmagnetic resonance image (MRI) findings .

(Focal Purulent Infection of Brain Tissue)


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General Concepts

The anatomy of the brain and meningens determines the special

character of central nervous system (CNS) infections. Epidural abscesses remain localized, whereas

Subdural abscesses spread over a hemisphere.

Subarachnoid space infections spread widely over the brain and

spinal cord. The blood-brain barrier formed by the tight junctions between

cells of the cerebral capillaries, choroid plexus, and arachnoidlargely prevents macromolecules from entering the brain

parenchyma. As a result, immunoglobulins and immune-

competent cells are scarce in the brain except at foci ofinflammation. The space between cells in the brain parenchymais too small to permit passage even of a virus.

However, tetanus toxin and some viruses travel through theCNS by axoplasmic flow.


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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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1. Meningitis can be caused by viruses, bacteria,

fungi, and protozoa.

2. The three majorcauses of bacterial meningitis

are Haemophilusinfluenzae,Streptococcus

pneumoniae, and Neisseriameningitidis.

These three etiological agents cause more than

70% of the meningitis cases and 70% of the

related deaths.

3. Nearly 50 species ofopportunistic bacteriacan cause meningitis.


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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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TANDA TANDA KLINIS MENINGITIS

SAKIT KEPALA / HEADACHE

DEMAM / FEVER

GANGGUAN SENSORIS KAKU DAN SAKIT KUDUK

TERDAPAT KELAINAN CSF

(Cerebro spinal fluid) : exudat keruh / jernih.


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I. MENINGITIS PURULENTA

MENINGOCOCCUS (40%)

NEISSERIA MENINGITIDIS, menyebabkan meningitis danmeningococcemia. (WATERHOUSE FREDERICHSENSYNDROME = high fever, shock, purpura yg luas, intravascularcoagulation 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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Neisser ia meningitidis

1.N.meningitidis(meningococcus) causesmeningococcal meningitis.

2. This bacterium is found in the throats of

healthy carriers (reservoir).3. The bacteria probably gain access to the

meningen through

the bloodstream.

4. The bacteria may be found in leukocytes in theCSF. (Gram negatives intracellulair diplococci)


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5. Symptoms are due to hyperproduction of

endotoxin.

6. The disease occurs most often in young children, but

can also cause outbreaks among persons living in close

contact (military, college dormitorities, institutional

settings).

7. Military recruits are vaccinated with purified capsular

polysaccharide to prevent epidemics in training camps.

Unfortunately, like other polysaccharide vaccines, it isnot 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 materw/ 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 inf luenzae

1. H.influenzae is part ofthe normal throat

microorganism

2. H.influenzaerequires blood factors (X and Vfactors) for growth;

There are six types ofH.influenzae based onpolysaccharide capsule differences.

H.influenzaetype b (HIB) is the most commoncause of meningitis in children under 4 years old.

3. A conjugated vaccine directed against the capsularpolysaccharide antigen is available. Use of the HIBvaccine has decreased the incidence of meningitis inchildren under five years of age by 99% in the U.S.


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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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Streptococcus pneumoniae(Pneumococcal Meningitis)

1. S. pneumoniae (pneumococcus) is commonly

found in the nasopharynx.

2. Hospitalized patients and young children aremost susceptible to S. pneumoniaemeningitis.

It is rare (3000 cases annually in U.S.) but has

a high mortality rate.

3. The vaccine for pneumococcal pneumonia

may provide some protection against

pneumococcal meningitis.


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Streptococcus pneumoniae

(Pneumococcus)

spreads from sinuses or middle ear brain

OR

pneumonia in lungs bloodstream

brain


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Listeriosis

1. L ister ia monocytogenescauses 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 and Treatment of the Most

Common Types of Bacterial Meningitis

1. Cephalosporins may be administered initially

before identification of the pathogen.

2. Diagnosis is based on gram stain and

serological tests of the bacteria in CSF.

3. Cultures are usually made on blood agar andincubated in an atmosphere containing

reduced oxygen levels. (Microaerophilic)

II MENINGITIS


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II. MENINGITIS

GRANULOMATOUS

MYCOBACTERIUM TUBERCULOSIS(Tuberculosis meningitis)

COCCIDIODES IMMITIS (meningitis)

CRYPTOCOCCUS NEOFORMAN (meningitis) HISTOPLASMA CAPSULATUM

TREPONEMA PALLIDUM (Syphilis stadium

ke-3, timbul tabes dorsalis dan meningo-vascularsyphilis)

JAMUR-JAMUR LAIN


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MENINGITIS TUBERCULOSA

Infection begins in the lungs and may spread to themeninges by a variety of routes.

Blood-borne spread certainly occurs and 25% ofpatients with miliary TB have TB meningitis,

presumably by crossing theblood-brain barrierbut aproportion of patients may get TB meningitis fromrupture of a cortical focus in the brain (a so-called Richfocus); an even smaller proportion get it from rupture

of a bony focus in the spine. It is rare and unusual forTB of the spine to cause TB of the central nervoussystem, but isolated cases have been described.
http://en.wikipedia.org/wiki/Rich_focushttp://en.wikipedia.org/wiki/Rich_focushttp://en.wikipedia.org/wiki/Central_nervous_systemhttp://en.wikipedia.org/wiki/Central_nervous_systemhttp://en.wikipedia.org/wiki/Central_nervous_systemhttp://en.wikipedia.org/wiki/Central_nervous_systemhttp://en.wikipedia.org/wiki/Rich_focushttp://en.wikipedia.org/wiki/Rich_focus


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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 ofTB 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 ofclinical 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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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


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
http://www.wrongdiagnosis.com/sym/headache.htmhttp://www.wrongdiagnosis.com/sym/blurred_vision.htmhttp://www.wrongdiagnosis.com/sym/confusion.htmhttp://www.wrongdiagnosis.com/sym/tiredness.htmhttp://www.wrongdiagnosis.com/sym/stiff_neck.htmhttp://www.wrongdiagnosis.com/sym/stiff_neck.htmhttp://www.wrongdiagnosis.com/sym/tiredness.htmhttp://www.wrongdiagnosis.com/sym/confusion.htmhttp://www.wrongdiagnosis.com/sym/blurred_vision.htmhttp://www.wrongdiagnosis.com/sym/headache.htm


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Suatu jamur tanah, bersifat endemik dan dapat menyebabkankoksidioidomikosis.

Biasanya dapat sembuh sendiri tetapi juga dapat mematikan.

Dikenal sebagai jamur dimorfik karena jamur ini mempunyai dayaadaptasi morfologik yang unik terhadap pertumbuhan dalamjaringan atau pertumbuhan pada 37C.

Bentuknya seperti bola (=sferul) yang garis tengahnya 15 - 60m,dengan dinding tebal berbias ganda.

Hifa dari jamur ini juga mudah pecah dan mengeluarkan spora.

Infeksi oleh jamur ini biasanya meliputi influenza, demam, lesu,batuk, dan adanya rasa sakit di seluruh tubuh.

Gejalagejala inilah yang biasanya disebut Valley fever danbiasanya gejala ini dapat sembuh sendiri yang dikenal denganinfeksi primer dan hanya dibutuhkan pengobatan suportif atau dapatjuga kronik.

Obat yang dipakai antara lain berupa Amphotericin B, Ketokonazol,Mikonazol.

Penyakit ini tidak dapat ditularkan dari orang ke orang.


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Patogenesis dan Gambaran Klinik Infeksi dari jamur ini didapat melalui inhalasi artrospora yang terdapat di udara.

Infeksi pernafasan yang nantinya timbul dapat bersifat asimptomatis dan mungkinhanya terbukti dengan pembentukan antibody presipitasi dan tes kulit positif dalam2-3 minggu.

Disamping itu penyakit yang menyerupai influenza, yang disertai demam, lesu,batuk, dan rasa sakit di seluruh tubuh juga dapat terjadi.

Kurang dari 1% orang yang terinfeksi C. immitis, penyakitnya berkembang menjadibentuk yang menyebar dan sangat fatal. Hal ini dapat sangat menyolok terlihat pada

wanita yang sedang hamil. Ini disebabkan karena kadar estradiol dan progesterone

yang meningkat pada wanita hamil dapat menambah pertumbuhan C. immitis.

Sebagian besar orang dapat dianggap kebal terhadap reinfeksi, setelah testes

kulitnya menjadi positif.

Akan tetapi, bila individu seperti ini kekebalannya ditekan dengan obat ataupenyakit, penyebarannya dapat terjadi beberapa tahun setelah infeksi primernya.

Koksidioidomikosis yang menyebar dapat disamakan juga dengan tuberkolosis,

dengan lesi pada banyak organ tubuh, tulang dan susunan saraf pusat.


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Diagnosis Diagnosis koksidioidomikosis didasarkan atas:

1. Pemeriksaan langsung : kerokan kelainan kulit, dahak ataubilasan bronkus. Pewarnaan khusus oleh jamur pada jaringan(terlihat bulatanbulatan kecil berisi endospora: tidak terlihatselsel ragi bertunas)

2. Biakandari dahak, bilasan bronkus, biopsy atau kerokan kulit(bahan-bahan ini sangat menular)

3. Serologi diagnostic yaitu:

- Tes presipitin tabung untuk mengukur titer IgM

- Reaksi peningkatan komplemen untuk mengukur titer IgG- Aglutinasi lateks dan uji imunodifusi sebagai alat penyaring

pada daerah endemic ternyata dapat mendeteksi 93% kasus

4. Tes kulit pada stadium awal infeksi


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2. Cryptococcal meningitis

Cryptococcal meningitis is a life-threatening infection that can

occur if there has been exposure to a fungus called Cryptococcusneoformans. This fungus is found in the environmentworldwide, particularly in soil contaminated with birddroppings. This fungus enters the body most commonly throughthe lungs. Infection does not usually appear until a person's CD4counts have dropped below 100.

Cryptococcal meningitis can not be passed from one person toanother. This fungus most commonly affects the brain, causingthe condition called meningitis. Meningitis is an infection andswelling of the lining of the brain and spinal cord. Cryptococcus

can also cause infections of the lungs, skin and prostate gland.

Cryptococcal meningitis may be very slow in developing, so atfirst, very vague symptoms may appear: mild headache, fever,nausea.


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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 toHistoplasma capsulatum

Meningitis due toHistoplasma capsulatum andMycobacteriumtuberculosis in a returned traveler with acquired immunodeficiency

syndrome The spores of the fungus are released into the air when contaminated

soil is disturbed (for example, by plowing fields, sweeping chickencoops, or digging holes) and the airborne spores can then be inhaledinto 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). Inaddition,H capsulatum can be isolated from respiratory secretions,lymph nodes, localized lesions, and cerebrospinal fluid (CSF).

Although culture is the gold standard for diagnosis, isolation can

take up to 4 weeks, and therefore is impractical as a criterion fortreatment initiation.

Serologic Tests : In patients with intact immune systems, antibodiesdevelop at high levels within 4-6 weeks in most symptomatic

Histoplasma infections and are useful for diagnosis in thosepatients. Detection ofH capsulatum antigen in body fluids permitsrapid diagnosis of DH.

P t i f H l


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Patogenesis ofH.capsulatum Inhalation ofH capsulatum microconidia into the lungs.

Convert to the yeast phase within the lung parenchyma. It is thought

that the yeast are phagocytized by macrophages within the lung in anattempt to clear the infection.

The macrophages then carry the organism to regional lymph nodes,and then throughout the reticuloendothelial system within 14-21 daysof the initial exposure.

Macrophages from HIV-infected individuals, particularly those withlower CD4 counts, manifest defective activity in their interaction with

H capsulatum.

In those with intact immune function, an inflammatory response

occurs at the site of infection, with either caseating or noncaseatinggranuloma formation.

Yeast may remain viable in the granuloma for extended periods oftime.

Neurologic complications have been reported in up to 20% of patients


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Spirochaeta

Syphilis can cause varied neurologic diseases over the lifetime ofthe untreated patient.

During secondary syphilis, 6 weeks to 3 months after primaryinfection, a benign mild meningitis may accompany the primaryCNS invasion that occurs in approximately 25 percent of untreated

patients.

Later complications include acute meningovascular inflammatorydisease leading to stroke (meningovascular syphilis) 3 to 5 yearsafter the primary infection, progressive dementia (general paresis) 8to 10 years later, or a chronic arachnoiditis involving primarily the

posterior roots of the spinal cord (tabes dorsalis) 10 to 20 years after

infection. This development of vasculitis, parenchymal involvementand chronic arachnoiditis parallel the complications that occur overweeks during untreated bacterial meningitis.


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III. ASEPTIC MENINGITIS

ENTEROVIRUS

POLIOMYELITIS

COXSACKIEVIRUS

ECHOVIRUS (Enteric Cytopathic Human Orphan)

RABIES

HERPES SIMPLEX

PARAMYXOVIRUS (Mumps virus) LEPTOSPIRA

CLOSTRIDIUM TETANI


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Poliomyelitis

1. The symptoms of poliomyelitis are usually headache,

sore throat, fever, stiffness of the back and neck, and

occasionally paralysis (less than 1% of cases).

2. Poliovirus is found only in humans and is

transmitted by the ingestion of water contaminatedwith feces.

3. Poliovirus first invades lymph nodes of the neck and

small intestine. Viremia (free viruses in the blood) and

spinal cord involvement may follow.

4. Diagnosis is based on isolation of the virus from feces

and throat secretions.

I f ti f N l Ti


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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, intestinelymphatics 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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KLINIS POLIOMYELITIS

ABORTIVE

NONPARALYTIC POLIOMYELITIS

(ASEPTIC MENINGITIS)

PARALYTIC POLIOMYELITIS

PROGRESSIVE POST POLIOMYELITIS

MUSCLE ATROPHY


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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-SUMTULANG 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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Poliovaccine

5. The Salk vaccine (an inactivated polio

vaccine, IPV) involves injection of formalin-

inactivated viruses and boosters every few

years.

6. The Sabin vaccine (oral polio vaccine, OPV)

contains three attenuated live strains of

poliovirus and is administered orally.

Polio wil l be eliminatedthrough vaccination.

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 Ne ral Tiss e


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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, is usually acquired through the bite of

a rabid warm-blooded animal.

This virus spreads by axonal transport from theinoculated skin or muscle to the corresponding

dorsal root ganglion or anterior horn cells and

then to populations of neurons throughout theCNS.

The early involvement of neurons of the limbic

system cause the typical behavioral changes ofclinical rabies.

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, orinvasionthrough minute skin abrasions. The virus multiplies

in skeletal muscle and connective tissue.

3. Encephalitis occurs when the virus moves alongperipheral 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 postexposuretreatment includesadministration of human rabies immune globulin(RIGH) along with multiple intramuscular injectionsof vaccine.

8. Preexposure treatment consists of vaccination.

VIRUS PENYEBAB ENCEPHALITIS


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VIRUS PENYEBAB ENCEPHALITIS TOGAVIRIDAE (Genus Alphavirus)

Chikungunya Eastern equine encephalitis (EEE), transmisi nyamuk Culiseta

Western Equine Encephalitis (WEE), transmisi oleh nyamuk Culex

St.Louis Encephalitis (SLE), trasmisi oleh nyamuk Culex

California Encephalitis (CE), transmisi oleh nyamuk Aedestriseriatus

FLAVIVIRUS

Flavivirus berukuran kecil (40 nm), berbeda dalam morfogenesisdan berbeda dalam struktur genomnya dari Togavirus

Yang teriinfeksi sering menyebabkan encephalitis, dasarnya adalahneurotrofik khususnya pd binatang pengerat

VIRUS RABIES

Progressive encephalitis terjadi jika virus mencapai / menyebar ke

CNS, gejala klinis hyrdophobia

A b i l E h liti


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ArboviralEncephalitis

1. Symptoms of encephalitis are chills,

headache, fever, and eventually coma.

2. Many types ofarboviruses 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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ArboviralEncephalitis (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

Botulism


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Botulism

1. Botulism is caused by an exotoxin produced by

Clostridiumbotulinumgrowing in foods.

2. Serological types of botulinum toxin vary invirulence, with type A being the most virulent.

3. The toxin is a neurotoxin that inhibits thetransmission of nerve impulses.

4. Blurred vision occurs in 1-2 days; progressive flaccid

paralysis follows for 1-10 days, resulting inrespiratory and cardiac failure.

5. C. botulinum will not grow in acidic foods or in anaerobic environment.


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6. Endospores are killed by proper canning. Theaddition of nitrites to foods inhibits outgrowth afterendospore germination.

7. The toxin is heat labile and is destroyed by boiling(100C) 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 ofhoney products.

9. Wound botulism occurs when C. botulinum grows inanaerobic wounds.

10. Fordiagnosis, 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 Clostridiumtetani. Endospores allow for long-term survival in

soil.

2.C.tetani produces theneurotoxin 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 ! ! !

B i Ab


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Brain Abscess

An abscess is a focus of purulent infection and is usually due to

bacteria. Brain abscesses develop from either a contiguous focus of infection

(such as the ears, the sinuses, or the teeth) or hematogenous spread

from a distant focus (such as the lungs or heart, particularly with

chronic purulent pulmonary disease, subacute bacterial endocarditis,or cyanotic congenital heart disease).

In many cases the source is undetected.

Many brain abscesses have a mixed flora of aerobic and anaerobic

bacteria. Approximately 60 to 70 percent contain streptococci; and

Staphylococcus aureus, enterobacteria andBacteroidesare

frequently present.

Fungi cause fewer than 10 percent of brain abscesses


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Lyme disease

Lyme disease also may be complicated by early andlate neurologic involvement.

Mild meningitis and facial palsy often accompany the

initial rash and systemic symptoms following the tick

bite.

In 15 percent of untreated patients, subacute or

recurrent meningitis, encephalitis, cranial nerve

palsies, and peripheral neuropathies develop 1 to 9months later, and rarely a chronic meningoencephalitis

has been described years later.

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 MacmillanCo New Jork 1961

4. Lennette,E.H.,Balow,A., Hausler,W. and Truant, J.P. : Manual ofClinical Microbiology, 3 Amer Society for Microbiol, Washington,

D.C., 1980

5. Levin, W and Jaetz E. : Medical Microbiology & Immunology.6 thEd. Lange Medical Books / McGraw-Hill , 2000.

k.16b inf. sistem syaraf 2011

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