k.16 Inf. Sis. Syaraf Pst ( Jan 2009)(1)

7/27/2019 k.16 Inf. Sis. Syaraf Pst ( Jan 2009)(1)

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Dr. Edhie Djohan Utama, SpMK



INFEKSI PADA SISITIM SYARAF PUSAT

BISA DISEBABKAN OLEH SEMUA AGENT YANGINFECTIOUS :

= BAKTERI -

PYOGENIK

= MYCOBACTERIA

= FUNGI

= SPIROCHAETA

= VIRUS



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



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 )



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)



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.



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



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



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.



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.

http://en.wikipedia.org/w/index.php?title=Ventricular_shunt&action=edit&redlink=1



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.

http://en.wikipedia.org/wiki/Isoniazid

http://en.wikipedia.org/wiki/Rifampicin

http://en.wikipedia.org/wiki/Pyrazinamide

http://en.wikipedia.org/wiki/Ethambutol

http://en.wikipedia.org/wiki/Hydrocephalus

http://en.wikipedia.org/w/index.php?title=Ventricular_shunt&action=edit&redlink=1



http://en.wikipedia.org/wiki/Ethambutol

http://en.wikipedia.org/wiki/Pyrazinamide

http://en.wikipedia.org/wiki/Rifampicin

http://en.wikipedia.org/wiki/Isoniazid



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



Fungal meningitis

Chronic presentation

1. Coccidioides immitis

2. Cryptococcus neoformans - AIDS



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.htm

http://www.wrongdiagnosis.com/sym/blurred_vision.htm

http://www.wrongdiagnosis.com/sym/confusion.htm

http://www.wrongdiagnosis.com/sym/tiredness.htm

http://www.wrongdiagnosis.com/sym/stiff_neck.htm

http://www.wrongdiagnosis.com/sym/stiff_neck.htm

http://www.wrongdiagnosis.com/sym/tiredness.htm

http://www.wrongdiagnosis.com/sym/confusion.htm

http://www.wrongdiagnosis.com/sym/blurred_vision.htm

http://www.wrongdiagnosis.com/sym/headache.htm



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.



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.



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.



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



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



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



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



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



PENGOBATAN DAN PENCEGAHAN



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





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



Rabies



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



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.



ENCEPHALITIS

INFECTIONS OF THE NEURAL TISSUE



A b i l E h liti



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.



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.




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



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



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.



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 ! ! !



DAFTAR PUSTAKA



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

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

6. Pelczar,M.J.Jr., Chan,E.C.S. and Krieg,N.R. : MicrobiologyConcepts and Applications. International Ed. McGraw-Hill, Inc, 1993

Internet

k.16 Inf. Sis. Syaraf Pst ( Jan 2009)(1)

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