Division Tropical Medicine and Infectious Diseases Department of Internal Medicine Medical Faculty Veteran National Development University Gatot Soebroto Central Army Hospital Permission and Adapted from Umar Zein, Tropical and Infectious Diseases Division Internal Medicine Department AdamMalik Hospital Medan
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Division Tropical Medicine and Infectious Diseases
Department of Internal Medicine
Medical Faculty Veteran National Development University
Gatot Soebroto Central Army Hospital
Permission and Adapted from Umar Zein, Tropical and Infectious Diseases Division Internal Medicine Department
AdamMalik Hospital Medan
BIO DATA
Nama : Dr. Soroy Lardo, SpPD FINASIMPangkat/Nrp : Letkol CKM/1920013110563Kesatuan : Departemen Penyakit Dalam RSPADStatus : K-3Riwayat Penugasan :Dokter Yonif 132/BS Kodam I/BB Pasiwatkes Rumkit Putri Hijau Kodam I/BBKa Rumkitban Binjai Kodam I/BBKa Bangsal Paviliun Rumkit Putri Hijau Kodam I/BBKasidiklitbang Departemen Paru RSPAD Gatot SoebrotoKabagyanmed Departemen Penyakit Dalam RSPAD Gatot
SoebrotoKasub SMF Penyakit Tropik dan Infeksi DepartemenPenyakit
DalamRiwayat Pendidikan :Fakultas Kedokteran UNPAD 1991Spesialis Penyakit Dalam Fakultas Kedokteran USU 2005
which three serotypes :1. S. typhi 2. S. typhimurium (S. paratyphi A
and B), now called : S. schottmulleri
3. S. choleraesuisCHAMBERS. Infectious Diseases. In: Lawrence, et al. Current MD&T,34th Edition. A Lange medicalbook Int’l Ed. 1995;1173-9.
(Infections caused by Gram-negative bacteria)
Clinical Patterns of Infection
1. Enteric fever (typhoid fever), due to serotype typhi.
2. Acute enterocolitis, caused by serotype typhimurium.
3. Septicemic type, due to serotype choleraesuis, characterized by :
- bacteremia- focal lesions
This is responsible for 75% of reported cases of food poisoning in UKHow in INDONESIA ?
Microbiology :
Most commonly caused by Salmonella typhiSalmonella paratyphi A, B, CThe other serotypes : S.choleraesuis
S.enteretidis S.arizonae
Salmonellosis : Enteric fever Gastroenteritis
Sepsis
Facultative anaerobic/aerobic
Gram (-) bacteria
Rods shape
Family Enterobacteriaceae
Motile
Somatic
Flagelar
Viantigen
Susceptibility to Disinfectants :
1. 1 % Sodioum hypochlorite
2. 2 % Glutaraldehyde
3. Iodine
4. Phenolics
5. Formaldehyde
Physical Inactivation :
1. Sensitive to moist heat (1210C) for at least 15 min
2. Dry heat (160 – 1700C) for at least 1 hour
Survival outside Host :
Ashes – 130 days
Rabbit carcass – 17 days
Dust – up to 30 days
Feces – up to 62 days
Linoleum floor – 10 hours
Ice – 240 days
Epidemiology :Worldwide, except in industrialized regions such us the United State, Canada, western Europe, Australia, and Japan
In the developing world, it affects about 12.5 million persons each year
Over the past 10 years, travelers from the United States to Asia, Africa, and Latin America have been especially at risk
Typhoid fever can be prevented and can usually be treated with antibiotics
Multi-drug resistant strains have appeared in several areas of word
Indonesia 760 – 810 cases / 100.000 / year with death rate 3.1-10.4 %
Infectious Dose : 100,000 organism – ingestion
variable with gastric acidity
and size inoculum
Mode of Transmission :
1. Person-to-person
2. By contaminated food or water
3. By food contaminated by hand of carriers
4. Food contaminated by materials
5. Flies can infect food mechanical vector
Chronic carrierPatient
Healthysubject
StoolVomitUrine
Typhoid fever
IndirectInfection> 90 %
Direct Infection< 10 %
InfectedWaterFood
Route of Transmission of Typhoid Fever
Faktor Penentu Virulensi Salmonella thypi
Somatik (O) ada 2 determinanAntigen (endotoksin – LPS, aceltylated glucosamine dissaccharide lipid A
Capsular Vi (Polysaccharide (Vi) ada 2 determinan antigen (O)- acetyl – N acetyl carboxyl)
Flagella protein (H) antigen (fase 1 dan II)
Outer Membran Proteins (OMPS)
Porin (Omp B,C,D dan OmpR)
Non Porin
PatofisiologiMakanan yg
tercemar
Menembus
mukosa usus
Kelenjar limfe usus
(replikasi)
Duktus Torasiku
s
Masuk PD ke RES (hati, limpa, SST)
Ke Pembul
uh darah
Kapsul Vigagal
fagositosis Replikasi pesat
(7-10hari)
BAKTEREMIA 1
(24-72jam)
BAKTEREMIA2
Bakteremia ke-2
Endotoksin (LPS)
C3a, C5a
pirogen
Hipotalamus demam
IL-1
T-helperIL 2Limfosit BSel Plasma
& Agglutinin O
Limfosit T
Sel Plasma & Agglutinin H & Agglutinin Vi
Limfosit B
agglutinin O terbentuk lebih dahulu daripada agglutinin H dan agglutinin Vi. Aglutinin O cepat menghilang dalam beberapa tahun. Sedangkan agglutinin Vi menghilang setelah penderita sembuh tetapi cenderung menetap pada karrier.
Imunopatogenesis
Terdapat 4 komponen antigenic penting pada S typhi: 1. Kapsular Vi2. Lapisan luar (antigen O)3. Flagella protein (antigen H)4. Outer Membrane Protein (OMP) 3
2
14
S typhi
Resists the low pH of stomach
Reach SMALL INTESTINE
Membrane bound vacuoles enterocytes, SpiC
Bac must survive the antimiCrobial environment of macrophage, which includes the production of antimicrobial peptides and hydrolytic enzyme
Salmonella next penetrate the mucous layer of the gut
Bacterial proteins mediate in the ACTIN, a-actinin, trombomyosin, talin
Microfold cell (M cell)
Peyers patches, multiply in mononuclear phagocyte
Spread to the phagocyte of the liver, gallbladder & spleen
Small intestine :Plaque Peyeri Necrosis separation of slough Perforation
or healing ( ulceration, hemorrhages up to perforation ) or healed
Relaps orCarrier
(Stepwise fashion fever)
Pathogenesis :
Ingestion of S.typhi
Infection carried in theLymphoid follicle
Draining mesentericLymph node
Entering thoracic ductsPassed through the heart
Primary bacteremia
Liver, GB, Spleen,BMMultiply within MNPC
Secondary bacteremia
Enter the small intestine
Excreted in stool and Urine
Inflammation, necrosis,Ulceration Payer’s patches
MULTIPLICATION
End incubation period
Pathology :
Payer’s patches :
Hyperplasia during the first week Necrosis in second week Ulceration during third week Healing takes place without scarring during forth week The ulcer are oval shaped, in the long axis of lower ileum Separation of the sloughs hemorrhage and perforation
1.Isolation of Organism :
- Blood cultures : positive in 40 – 80 % patients
during the first 7 – 10 days
- Culturing stool
- urine
- rose spots
- duodenal contents via string capsule : positive in
30 – 40 % patients
- bile
- faeces
2. Detection of antigen in body fluid :
- Coagglutination
- Latex agglutination
- ELISA
- CIEP
Urine test Typhidot
3. Detection of antibodies :
- Widal tube test
- Widal slide test
- IHA
- CIEP
- RIA
- ELISA
Anemia
Leucopenia or leucocytosis
Thrombocytopenia
Abnormal liver function
1.Clinical Signs and Symptoms
2.Laboratory findings
3. Isolation of the organism
4.Detection of microbial antigen
5.Titration of antibody against causative agent
Skor Nelwan (Demam Tifoid) Dari hasil pemeriksaan klinis pada saat penderita masuk RS diambil data-data
sesuai dengan yang diajukan oleh Nelwan (1991). Ketepatan diagnosis demam tifoid dihitung dengan skor:
No Gejala Klinis Skor
1 Demam < 1minggu 1
2 Sefalgia (pusing) 1
3 Rasa lemah 1
4 Mual 1
5 Gangguan motilitas saluran cerna 1
6 Nyeri perut 1
7 Anoreksia 1
8 Susah tidur 1
9 Splenomegali 1
Skor Nelwan (2)
No Gejala Klinis Skor
10 Hepatomegali 1
11 Muntah 1
12 Demam > 1minggu 2
13 Apatis 2
14 Lidah tifoid 2
15 Bradikardi relatif 2
16 Feses hitam 2
Skor Maksimal 20
Nilai ramal demam tifoid = skor/20 x 100% menunjukkan persentase kemungkinan terjangkitnya pasien dengan salmonella typhi atau paratyphi. Dari studi yang dilakukan skor 13 ke atas sudah mengarah ke diagnosis demam tifoid, sedangkan skor di bawah 7 kecil kemungkinan penderita terjangkit demam tifoid.
Kesimpulan Penelitian : SENSITIFITAS DAN SPESIFISITAS DIAGNOSIS KLINIS DALAM
MENDIAGNOSIS DEMAM TIFOID PENDERITA RAWAT INAP DI BANGSALPENYAKIT DALAM RSUP SARDJITO (TAHUN 1998-2000)
Sri Wahyuni, Soebagjo Loehoeri, Nurfaita Mislihar
Subbagian Penyakit Tropik dan Infeksi, Bagian Ilmu Penyakit DalamFK-UGM/RSUP Dr. Sardjito Yogyakarta
Konas Petri Malang 2005
1. Gejala yang dominan pada kasus demam tifoid adalah demam, nausea, lidah tifoid dan bradikardi relatif.
2. Hasil perbandingan diagnosis klinis terhadap diagnosis laboratoris memiliki sensitifitas sangat rendah (18,18%), spesifisitas tinggi (87,5%), nilai ramal positif rendah (25%) dan nilai ramal negatif tinggi (84%). Berdasarkan indikator-indikator tersebut dapat dinyatakan kurang efektif untuk digunakan sebagai pegangan diagnosis. Perlu pendukung yang lain
yaitu dengan pemeriksaan laboratoris.
Suspect Typhoid cases
General Nursing care and Diet
Specific antibiotic therapy
Treatment of Chronic carriers
Management of complications
Antibiotic Therapy :
Chlaramphenicol 4 X 500 mg 11-14 days Ampicillin 50 -100 mg /kg BW/ day Trimetropin – sulfametoksazole 2 x 2 tab Ceftriaxone 50 – 100 mg/ kg BW / day Cefoperazone 100 mg/kg BW/ day Cefotaxim 2 – 3 x 1 gr Ciprofloxacin 2 x 500 mg Fleroksasin 1 x 400 mg Ofloxacin 1 x 600 mgPerfloxacin 1 x 400 mg Levofloxacin 1 x 500 mg
DISKUSI
• Tabel 1. Perbandingan Reda Demam (Defervescence) Demam Tifoid Non-Komplikata FluorokuinolonNama Obat Disis Lama
PemberianPenurunan Demam
Siprofloksasin (5) 500 BID 6 hari 3,60 hari
Ofloksasin (6) 600 mg OD 7 hari 3,40 hari
Pefloksasin (7) 400 mg OD 7 hari 3,10 hari
Fleroksasin (8) 400 mg OD 5 hari 3,40 hari
Levofloxacine (9) 500 mg OD 7 hari 2,43 hari
DISKUSI
• Tabel 2. Betalaktam untuk pengobatan demam tifoid
Beta Laktam Dosis Lama Pemberian
Ampisilin 4x1 gram IV atau Oral
Dua minggu
Amoksisilin 50-150mg/kgBB/hari
Dua minggu
Sefiksim 10-15mg/kgBB/hari Sepuluh hari
Seftriakson 4 gram/hari Tiga hari
3 gram/hari Empat hari
2 gram/hari Enam hari
DISKUSI
• Tabel 3. Berbagai jenis antimikroba untuk demam tifoid
Antimikroba Dosis Lama Pemberian
Kloramfenikol Hari ke 1 4x250 IV/oral
Hari ke 2 4x500 IV/oral
2 minggu
Kotrimoksazol 2 x 2 tab oral 2 minggu
Azitromisin 2 x 500 mg IV/oral 1 minggu
Aztreonam 3 x 1 gram IV 1 minggu
Multi drugs Resistance Salmonella typhi (MDRST)
Resistance to :
• Chloramphenicol
• Amoxycillin
• Cotrimoxazole
Komplikasi ( Dikutip dari Butler dan Scheld, 2004)
Abdomen Perforasi usus terutama ilium , terjadi pada 1- 3 %Pendarahan saluran cerna, terjadi pada 10 % pasienHepatitisKholesistitis
Kardiovaskuler Perubahan elektrokardiografi asimptomatisMiokarditisSyok
Lain lain Abses LokalFaringitisRelapsKarier khronis
Penelitian Kompilasi Tifoid dari RS Sanglah Denpasar:
Pada 49 penderita dengan komplikasi tersebut 43 (87,7) orang datang dengan keluhan utama demam, 38 (77,5) orang datang ke rumah sakit pada akhir minggu pertama hingga minggu kedua setelah demam. Sebanyak 7 (14,2) datang pada minggu ketiga setelah demam. Keluhan utama penderita lainnya : kesadaran menurun 1 (2,0) , nyeri ulu hati 1 (2,0), mual muntah 1 (2,0) dan 3 (6,1) dengan berak darah. Komplikasi yang terjadi pada penderita baik intestinal (24,4) maupun ekstra intestinal (75,5), adapun jenis komplikasi yang terjadi pada penderita dapat dilihat pada grafik 1.
24.4
24.436.7
16.710.2 2.1 Hepatitis tifosa
Perdarahan usus
Tifoid toksik
Pneumonia
Meningitis
Artritis
Tabel 1. Komplikasi demam tifoid di beberapa RS di Indonesia.5-10
Komplikasi Demam Tifoid Pada Penderita Dewasa di Bangsal Menular RS Sanglah Denpasari.a.ratih wulansari manuaba*, tuti parwati merati**, sjaiful I biran**
**Divisi Tropik dan Infeksi *Lab/SMF. Penyakit Dalam, FK UNUD/RS Sanglah, Denpasar Konas Petri Malang 2004
10.2
57.1
22.4
4
6.1
0 10 20 30 40 50 60
> 20 hari
16 - 20 hari
11 - 15 hari
6 - 10 hari
1 - 5 hari
Lama perawatan penderita dengan komplikasi.
Biliary carriers
Urinary carriers
Intestinal carriers (faecal)
1- 5 % thypoid patient
Problem : cholelitiasis dan nephrolitiasis
Tifoid carrier treatmentAntibiotic treatment of tifoid carrier fever
With cholelithiasis complicationCholesistektomi + regimen above for 28 days, 80 %
curable or cholesistektomi with one of the regimen below:
1. Ciprofloxacin 750mg/ twice perday 2. Norfloxacon 400 mg/ twice /dayCefixime 400 mg bid for 6 days for MDR or non MDR
Prevention
Decontamination : HospitalizationLouse control: Bathing and laundering of clothes
in hot water with detergent Reduction of exposure Identification and eradication Prevention of transmission Protection of the risk infection
Typhoid Vaccines :
1. Parenteral killed whole cell vaccines
* Heat and phenol killed
* Acetone killed and dried
2. Live attenuated Ty21a vaccine (TYPHORAL@ )
3. Polysaccharide subunit vaccine (TYPHIM V@)
Vaksinasi Tifoid Tsunami NAD 3-4 Januari 2005
Vaskinasi Tifoid di Tsunami NAD 2-4 Januari 2005
Tsunami NAD 3-4 Januari 2005
TERIMA KASIH
References :
1. Hohmann, L.E : Approach to the patient with typhoid fever, @2000 UpToDate.www.uptodate.com.(800)998-6374.(781)273-4788
2. Salmonella typhi, From : http://www.medinfo.ufl.edu/year2/mmid/bms5300/bugs/saltyphi.html
3. Material Safety Data Sheet – Infections Substances, Section I : Infectious Agent, From : http://www.hc-sc.gc.ca/pphb-dgspsp/msds-ftss/msds134e.html
4. Typhoid Fever, From : http://www.cdc.gov/ncidod/dbmd/diseaseinfo/typhoidfever_g.htm
5. Ichhpujani, R.L , Bhatia, R : Typhoid Fever, Top Publications, 4093, Nai Sarak, Delhi 110 006, India, 1997.
6. Zulkarnaen,I : Pola Kepekaan Salmonella typhi terhadap beberapa antibiotika,Demam Tifoid, Peran Mediator, Diagnosis dan Terapi, Subbgian Penyakit Tropik dan Infeksi FK UI, Jakarta, 2000
7. Suhendro, Inada,K , Hendarwanto, Zulkarnain,I : Patterns of Cytokine and Nitric Oxide in Typhoid Fever, Demam Tifoid, Peran Mediator, Diagnosis dan Terapi, Subbgian Penyakit Tropik dan Infeksi FK UI, Jakarta, 2000
8. Nasronudin. Demam Tifoid. Dalam Penyakit Infeksi di Indonesia dan Solusi Kini dan Mendatang. Edisi ke 2. Airlangga University Press. 2011 , Surabaya. h: 187 -190
9. Nasronudin. Imunopatogenesis, Diagnosis dan Tata Laksana Demam Tifoid Masa Kini. Dalam Penyakit Infeksi di Indonesia dan Solusi Kini dan Mendatang. Edisi ke 2. Airlangga University Press. 2011 , Surabaya. h: 191-208