INTRODUCTION
Due to the application of integrated curriculum at the Faculty of Medicine Udayana University, the discipline-based subjects of the previous curriculum such as Biology, Anatomy, Physiology, Internal Medicine, etc have been integrated and incorporated into several blocks. One of these blocks is Infections and Infectious Diseases. In this block will be explained in general about pathogenesis, pathophysiology, sign, symptoms, clinical features, diagnosis, and management of certain infectious diseases commonly occur in community.
This guide book aims to give general information for medical students about infections and infectious diseases and important for facilitators and resource person while facilitate or guiding the students in learning process. This study guide consists of general information on learning time table, block team members, facilitators, and the core curriculum including learning outcomes, learning situations, learning tasks and self-evaluation items.
The block Infection and Infectious Diseases has the equivalent of (six) credits. As a block of six credits, the learning processes will be carried out for 30 days starts from 27th of November 2013 as shown in the Time Table. The final examination will be conducted on 13th of Junuari 2014. During the 30 days of learning activities, the students will discuss several topics in varied forms of learning situations such as independent learning, small group discussion, lecture, and skill lab.
More than half of the learning material must be learned independently and in small group discussions. A lecture is given only to emphasize crucial things or objectives of material and to prepare the students before discussion. For small group discussion, the students will be given learning tasks to solve and discuss. After discussion, students also have to evaluate their learning progress independently (self evaluation).
From this block, we hope every medical student have knowledge and skill to diagnose and manage infections and certain infectious diseases commonly occur in community, as a frontline in community health.
Since the integrated curriculum of the Faculty of Medicine Udayana University is still in progress, this Study Guide will also, naturally, have some revisions in the future. Therefore, we kindly invite readers to give any comments or suggestions for its improvement and development.
Planners
CURRICULUM OF THE BLOCK
AIMS
* To comprehend the biology of the infectious diseases
* To apply and interpret common laboratory diagnosis of infectious diseases
* To diagnose and manage common infectious diseases
* To carry out basic immunization in children and adults
LEARNING OUTCOMES
* Comprehend the practical and clinical implications of the biology of infection
* Apply the general principles of approach to patients with infectious diseases
* Apply and interpret common laboratory diagnosis of common infectious diseases
* Apply the basic principles of immunization in children and adults
* Diagnose and manage common bacterial infections (common Gram positive and negative, spirochetal)
* Diagnose and manage common parasitic infections (common nematode, trematode, cestode, and protozoal infections)
* Diagnose and manage common fungal infections
* Clinically diagnose and manage common viral infections (caused by common respiratory virus, herpesvirus, arbovirus)
* Clinically diagnose and manage puerperial Infection
CURRICULUM CONTENT
1. The biology of infection: bacterial, viral, fungal and parasitic.
a. Principles of bacterial infections such as Staphylococci, Streptococci, Neisseria, Salmonella, Vibrio, anaerobic bacteria¸ Leptospira, Mycobacteria, Gram positive bacilli)
b. Principles of viral infections such as respiratory virus (influenza virus, mumps, measles), retrovirus (HIV), herpesvirus (HSV 1, HSV 2, VZV, arbovirus (dengue virus, Japanese B encephalitis virus).
c. Principles of fungal infections such as Candida, Pneumocytis jiroveci, Histoplasma, Cryptococcus
d. Principles of parasitic infections such as Plasmodium, Toxoplasma gondii, Entamoeba histolytica and soil transmitted helminthes.
2. General approach to the patients with infection such as:
a. Clinical manifestations (local and systemic infections)
b. Laboratory examination to support diagnosis of infections i.e. Microbiological examination, Parasites examination, Clinical pathology examination, Pathology examination and Imaging examination
3. Management patients with infection such as:
a. Common bacterial infections such as bacterial meningitis, typhoid fever,
diarrhea, endocarditis, diphtheria, tetanus, food poisoning, genital
gonorrhoeae, non gonococcal urethritis, etc.
b. Common parasitic infections such as malaria, amoebiasis, toxoplasmosis.
c. Common fungal infection such as dermatophytosis, systemic candidiasis,
histoplasmosis, cryptococcosis, pneumocytis jiroveci pneumonia.
d. Common viral infections such as mumps, measles, influenza (especially
H5N1), SARS, varicella, herpes labialis, herpes genitalis, dengue fever,
Japanese B encephalitis, and HIV.
4. Immunization in children and adults, and general advice to international traveler
5. Puerperial Infection
STANDAR KOMPETENSI DOKTER
PLANNERS TEAM
No Name Departement Phone 1 Prof. Dr. dr. Tuti Parwati Merati, SpPD, KPTI (Coordinator) Internal Medicine 08123806626 2 Dr. dr. Bagus Komang Satriyasa, M.Repro (Secretary) Pharmacology 087777790064
0361-7893599 3 Dr. dr. Dewa Made Sukrama, M.Si, SpMK Microbiology 081338291965 4 Prof. Dr. dr. Raka Sudewi, Sp.S (K) Neurology 0816710244 5 dr. IGK Darmada, SpKK Dermatology and Venereology 081338044921 6 dr. I.B. Ngurah, M.For Pharmacology 08123687288 7 dr. Agus Somia, Sp.PD Internal Medicine 08123989353 8 dr. Made Sudarmaja, M.Kes Parasitology 08123953945
LECTURER
NO NAME DEPT PHONE 1. Prof. Dr. dr. Tuti Parwati Merati, SpPD, KPTI Internal Medicine 08123806626 2. Prof.Dr. dr. Raka Sudewi, Sp.S (K) Neurology 0816710244 3. Prof.Dr.dr. I.B. Rai, SpP (K) Pulmonology 08123804579 4. dr. Agus Somia, SpPD Internal Medicine 08123989353 5. dr. A.A.G.P. Wiraguna, SpKK Dermatology & Venereology 081338645288 6. Prof.dr. M. Swastika Adiguna, SpKK (K) Dermatology & Venereology 08123828548 7. dr. IGA. Sumedha Pindha, SpKK (K) Dermatology & Venereology 08155735977 8. dr. Dwi Lingga, SpA (K)/dr W. Gustawan,M.Sc., Sp.A Child Health 08125684656/
08123848241 9. dr. IGK. Darmada, SpKK/ dr. Darmaputra, Sp.KK Dermatology & Venereology 081338044921 10. dr. Ni Made Aditarini Sp. MK Microbiology 081338675344 11. dr. Luh Ariwati Parasitology 08123662311 12. dr. Nyoman Mahartini, SpPK Clinical Pathology 081337165577 13. dr. I.B. Ngurah, M. For Pharmacology 08123687288 14. Dr. dr. Bagus Komang Satriyasa, M.Repro Pharmacology 087777790064 15. dr. Kadek Swastika, M.Kes Parasitology 08124649002 16. Prof. dr.Dewa Putu Widjana, DAP&E, Sp.ParK. Parasitology 08113804500 17. Prof. dr. IGM. Aman, SpFK Pharmacology 081338770650 18. dr. Sri Budayanti, Sp.MK Microbiology 08583711398 19. dr.Dewa Ayu A. Sri Laksmi,M.Sc Parasitology 081392017107 20. dr. Made Susila Utama, Sp.PD Internal Medicine 08123815025 21. dr.Made Agus Hendrayana, M.Ked Microbiology 08123921590 22. dr.Lely Rahayu, Sp.THT-KL ENT 08113809882 23. dr. A. Wiwiek Indrayani, M.Kes Pharmacology 08886855027 24. dr. K. Januartha, M.Kes Microbiology 08123831710 25. dr. Made Jawi, M.Kes Pharmacology 08179787972 26. dr. I Nyoman Bayu Mahendra,Sp.OG Obstetrics & Gynecology 081339550423 27. I.B. Nyoman Putra Dwija, S.Si, M.Biotech Microbiology 08179747502 28. dr.Putu Ayu Asri Damayanti,M.Kes Parasitology 085338565783 29. dr.Made Sudarmaja,M.Kes Parasitology 08123953945
FACILITATORS
(REGULAR CLASS)
NO NAME GROUP DEPT PHONE VENUE
1 dr. I Gusti Nyoman Sri Wiryawan, M.Repro 1 Histology 08123925104 2nd floor: R.2.01 2 dr. I Gede Budhi Setiawan, Sp.B(K)Onk 2 Surgery 08123923956 2nd floor: R.2.02 3 dr. I Made Bagiada, Sp.PD 3 Interna 08123607874 2nd floor: R.2.03 4 dr. I Made Muliarta, M.Kes. 4 Fisiology 03618087592 2nd floor: R.2.04 5 dr. I Made Oka Negara, S.Ked 5 Andrology 08123979397 2nd floor: R.2.05 6 dr. Ketut Agus Somia, Sp.PD-KPTI 6 Interna 08123989353 2nd floor: R.2.06 7 dr. I Made Sudarmaja, M.Kes 7 Parasitology 08123953945 2nd floor: R.2.07 8 dr. I Made Sudipta, Sp.THT-KL 8 ENT 08123837063 2nd floor: R.2.08 9 dr. I Made Suka Adnyana, Sp, BP 9 Surgery 081236288975 2nd floor: R.2.21 10 dr. I Gusti Ayu Sri Darmayani, Sp. OG 10 DME 081338644411 2nd floor: R.2.22
(ENGLISH CLASS)
NO NAME GROUP DEPT PHONE VENUE
1 dr. I Gede Ngurah Harry Wijaya Surya, Sp OG 1 Obgyn 0811386935 2nd floor: R.2.01 2 dr. I Gst.Ngr.Ketut Budiarsa , Sp.S 2 Neurology 0811399673 2nd floor: R.2.02 3 dr. I Gusti Ayu Agung Elis Indira , Sp.KK 3 Dermatology 081338718384 2nd floor: R.2.03 4 dr. Agus Roy Rusly Hariantana Hamid, Sp.BP 4 Surgery 08123511673 2nd floor: R.2.04 5 dr. I Gusti Ayu Putu Eka Pratiwi, M.Kes.,Sp.A 5 Pediatric 08123920750 2nd floor: R.2.05 6 dr. I Nyoman Arcana , Sp.Biok 6 Biochemistry 0811397960 2nd floor: R.2.06 7 dr. I Gusti Ayu Sri Mahendra Dewi, Sp.PA(K) 7 Clinical Anatomy 081338736481 2nd floor: R.2.07 8 dr. I Gusti Ketut Darmada, Sp.KK(K) 8 Dermatology 081338044921 2nd floor: R.2.08 9 dr. I Gusti Made Gde Surya Chandra Trapika, M.Sc 9 Pharmacology 08123622361 2nd floor: R.2.21 10 dr. I Gusti Ngurah Mahaalit Aribawa, Sp.An. 10 Anesthesi 0812396811 2nd floor: R.2.22
TIME-TABLE (Block Infection and infectious Diss.)
DAY/ DATE
Time Topic Learning situation Place PIC Regular Class English Class 21
Wednesday
Nov. 27th 13 08.00-08.30 09.00-09.30 Lecture 1
Introduction to the block (Agent ,Host Environment, and infection manifestation)
Introduction to the Block
Class room
Prof. Dr. dr. Tuti Parwati Merati, SpPD, KPTI 08.30-09.00 09.30-10.00 Lecture 2
bacterial classification dr. K. Januarta, M.Kes 09.00-10.30 12.00-13.30 Individual learning – – 10.30-12.00 13.30-15.00 Small group discussion Disc. Room Facilitator 12.30-14.00 10.00-11.30 Student Project Prof. Dr. dr. Tuti Parwati Merati, SpPD, KPTI dr. K. Januarta, M.Kes 14.00-15.00 15.00-16.00 Plenary Session Class room Prof. Dr. dr. Tuti Parwati Merati, SpPD, KPTI dr. K. Januarta, M.Kes 2
Thursday
Nov. 28th 13 08.00-09.00 09.00-10.00 Lecture 3
Mechanism of bacterial Pathogenesis Lecture Class room dr. Agus Hendrayana, M.Ked 09.00-10.30 12.00-13.30 Individual learning 10.30-12.00 13.30-15.00 Small Group Discussion 12.30-14.00 10.00-11.30 Student Project Class Room dr. Agus Hendrayana, M.Ked 14.00-15.00 15.00-16.00 Plenary Class Room dr. Agus Hendrayana, M.Ked 3
Friday
Nov. 29th13
08.00-08.30
09.00-093.0
Lecture 4
Viral classification Lecture Class Room Dr. dr. Sri Budayanti, Sp.MK 08.30-09.00 09.30-10.00 Lecture 5
Mechanism of Viral Pathogenesis Lecture Class room Dr.dr. Sri Budayanti, Sp.MK 09.00-10.30 12.00-13.30 Individual Learning 10.30-12.00 13.30-15.00 Small group discussion Disc. Room 12.30-14.00 10.00-11.30 Student Project Dr. dr. Sri Budayanti, Sp.MK 14.00-15.00 15.00-16.00 Plenary Class room Dr. dr. Sri Budayanti, Sp.MK 4
Monday
Des. 2th13 08.00-08.30
09.00-093.0
Lecture 6 Manifestation of virus and bacterial infection Lecture Class Room dr.Agus somia, Sp.PD
08.30-09.00 09.30-10.00 Lecture 7
Basic concept of Parasitic Infections Lecture Class room Prof. dr. D.P. Widjana, DAP&E, Sp.Par.K 09.00-10.30 12.00-13.30 Individual Learning 10.30-12.00 13.30-15.00 Small group discussion Disc. Room 12.30-14.00 10.00-11.30 Student Project dr.Agus somiaSp.PD
Prof. dr. D.P. Widjana, DAP&E, Sp.Par.K 14.00-15.00 15.00-16.00 Plenary Class room dr.Agus somiaSp.PD
Prof. dr. D.P. Widjana, DAP&E, Sp.Par.K 5
Tuesday
Des.3rd13 08.00-09.00 09.00-10.00 Lecture 8
Treatment of Viral Infection (PK/PD) Lecture
Class room Prof. IGM Aman, Sp.FK 09.00-10.30 12.00-13.30 Individual learning – 10.30-12.00 13.30-15.00 Small group discussion Disc. Room Facilitator 12.30-14.00 10.00-11.30 Student Project Prof. IGM Aman, Sp.FK 14.00-15.00 15.00-16.00 Plenary Session Class room Prof. IGM Aman, Sp.FK 6
Wednesday
Des.4th13 08.00-09.00 09.00-10.00 Lecture 9
Treatment of Microbacterial Infections I (Type of antimicrobacterial) (PK/PD) Lecture
Class room
Dr.dr. B.K. Satriyasa,M.Repro 09.00-10.30 12.00-13.30 Individual learning – 10.30-12.00 13.30-15.00 Small group discussion Disc. Room 12.30-14.00 10.00-11.30 Student Project Class room Dr.dr. B.K. Satriyasa,M.Repro 14.00-15.00 15.00-16.00 Plenary Session Class room Dr.dr. B.K. Satriyasa,M.Repro 7
Thusday
Des.5th13 08.00-08.30
09.00-10.00 Lecture 10
Treatment of Microbacterial Infections II (Resistance, rational treatment, and drug combination) Lecture
dr. Made Jawi, M.Kes 08.30-09.00 12.00-13.30 Lecture 11
Antimicrobial susceptibly Individual learning dr. Ni Made adi Tarini, Sp.MK 09.00-10.30 13.30-15.00 Small group discussion Disc. Room Facilitator 10.30-12.00 10.00-11.30 Student Project Class room dr. Ni Made adi Tarini, Sp.MK dr. Made Jawi, M.Kes 12.30-14.00 15.00-16.00 Plenary Session Class room Dr. Made Jawi, M.Kes 8
Friday
Des.6th13 08.00-08.30
09.00-093.0
Lecture 12:
Respond Host against parasitic and clinical manifestation Lecture Class room dr. I Made Susila Utama,Sp.PD 08.30-09.00 09.30-10.00 Lecture 13
Treatment of parasitic infection (PK/PD) Lecture Class room dr. A. Wiwiek Indrayani, M.Kes 09.00-10.30 12.00-13.30 Individual learning 10.30-12.00 13.30-15.00 Small group discussion Disc. Room Facilitator 12.30-14.00 10.00-11.30 Student Project Class room dr. I Made Susila Utama,Sp.PD
dr. A. Wiwiek Indrayani, M.Kes 14.00-15.00 15.00-16.00 Plenary Session Class room dr. I Made Susila Utama,Sp.PD
dr. A. Wiwiek Indrayani, M.Kes 9
Monday
Des.9th13 08.00-08.30
09.00-093.0
Lecture 14:
The Role of Immunity to infection (Basic) Lecture Class room Dr.dr. Dewa Made Sukrama, M.Si, Sp.MK 08.30-09.00 09.30-10.00 Lecture 15: Infection of Mycobacterium (TBC)
Lecture Class room Prof Dr.dr. IB Rai,Sp.P
09.00-10.30 12.00-13.30 Individual learning 10.30-12.00 13.30-15.00 Small group discussion Disc. Room 12.30-14.00 10.00-11.30 Student Project Class room Dr.dr. Dewa Made Sukrama, M.Si, Sp.MK
Prof Dr.dr. IB Rai,Sp.P
14.00-15.00 15.00-16.00 Plenary Session Class room Dr.dr. Dewa Made Sukrama, M.Si, Sp.MK
Prof Dr.dr. IB Rai,Sp.P
10
Tuesday
Des.10th13 08.00-08.30
09.00-093.0
Lecture 16: Infection of Mycobacterium (Leprosy)
Lecture Class room
dr. Dharma putra, Sp.KK
08.30-09.00 09.30-10.00 Lecture 17: Antimycobacterial Drugs ( anti TBC, Anti lepra) (PD/PK) Lecture Class room dr. IB Ngurah, M.For 09.00-10.30 12.00-13.30 Individual Learning 10.30-12.00 13.30-15.00 Small group discussion Disc. Room Facilitator 12.30-14.00 10.00-11.30 Student Project Class room dr. Dharma putra, Sp.KK
dr. IB Ngurah, M.For 14.00-15.00 15.00-16.00 Plenary Class room dr. Dharma putra, Sp.KK
dr. IB Ngurah, M.For 11
Wednesday
Des.11th13 08.00-08.30
09.00-093.0
Lecture 18:
Control of microorganism (infection control) Lecture Class room dr. N Dwi Fatmawati, Sp.MK, Ph.D 08.30-09.00 09.30-10.00 Lecture 19:
Immunization in child Lecture Class room dr. Dwi Lingga, sp.A/ dr. W. Gustawan,Sp.A
09.00-10.30 12.00-13.30 Lecture 20 : infections in upper respiratory tract (faringits, tonsillitis, laringits, otitis, mastoditis, rhinitis, sinusitis, furunkelitis) Lecture Dr Lely 10.30-12.00 13.30-15.00 Small group discussion Disc. Room Facilitator 12.30-14.00 10.00-11.30 Student Project Class room dr. N Dwi Fatmawati, Sp.MK, Ph.D
dr. Dwi Lingga, sp.A/ dr. W. Gustawan,Sp.A 14.00-15.00 15.00-16.00 Plenary Class room dr. N Dwi Fatmawati, Sp.MK, Ph.D
dr. Dwi Lingga, sp.A/ dr. W. Gustawan,Sp.A 12
Thusday
Des.12th13
08.00-08.30
09.00-093.0
Lecture 20
Antiseptic and disinfectant Lecture Class room Dr.dr.B.K. Satriyasa,M.Repro 08.30-09.00 09.30-10.00 Lecture 21
Universal Precaution Lecture Class room dr Agus Somia,Sp.PD 09.00-10.30 12.00-13.30 Individual learning – – 10.30-12.00 13.30-15.00 Small group discussion Disc. Room Facilitator 12.30-14.00 10.00-11.30 Student Project Class room Dr.dr.B.K. Satriyasa,M.repro
dr Agus Somia,Sp.PD 14.00-15.00 15.00-16.00 Plenary Class room Dr.dr.B.K. Satriyasa,M.repro
dr Agus Somia,Sp.PD 13
Friday
Des.13th13 08.00-09.00 09.00-10.00 Lecture 22
Protozoa Infection I (Malaria, Amoebiasis, Leismaniasis,Tripanosomiasis,Toxoplasmosis, Trichomoniasis) Lecture Class room dr.Dewa Ayu A. Sri Laksmi,M.Sc, M.Kes
dr. Putu Astri Damayanti,M.Kes 09.00-10.30 12.00-13.30 Individual learning 10.30-12.00 13.30-15.00 Small group discussion 12.30-14.00 10.00-11.30 Student Project dr.Dewa Ayu A. Sri Laksmi,M.Sc, M.Kes
dr. Putu Astri Damayanti,M.Kes 14.00-15.00 15.00-16.00 Plenary dr.Dewa Ayu A. Sri Laksmi,M.Sc, M.Kes
dr. Putu Astri Damayanti,M.Kes 12.00-13.30 Middle block meeting 14
Monday
Des.16th13 08.00-08.30
09.00-093.0
Lecture 23
Protozoa Infection II (Management of protozoa Infections) Lecture Class room dr Yuli Gayatri, Sp.PD
08.30-09.00 09.30-10.00 Lecture 24
Infection of Enterobacter (Thypoid, C. botulinum) Lecture Class room dr Agus Somia,Sp.PD 09.00-10.30 12.00-13.30 Individual learning 10.30-12.00 13.30-15.00 Small group discussion Disc. Room Facilitator 12.30-14.00 10.00-11.30 Student Project Class room dr Yuli Gayatri, Sp.PD
dr Agus Somia,Sp.PD 14.00-15.00 15.00-16.00 Plenary Class room dr Yuli Gayatri, Sp.PD
dr Agus Somia,Sp.PD 15
Tuesday
Des.17th13 08.00-08.30
09.00-093.0
Lecture 25
Sepsis and Bacteremia Lecture Class room dr. Made Susila utama, Sp.PD 08.30-09.00 09.30-10.00 Lecture 26
Cutaneous Viral Infection (Varicella, Zoster, Herpes) Lecture Class room dr.IGA Sumedha Pindha, Sp.KK/dr. Elis Indira,Sp.KK
09.00-10.30 12.00-13.30 Individual learning 10.30-12.00 13.30-15.00 Small group discussion Disc. Room Facilitator 12.30-14.00 10.00-11.30 Student Project Class room dr. Made Susila utama, Sp.PD
dr.IGA Sumedha Pindha, Sp.KK/dr. Elis Indira,Sp.KK 14.00-15.00 15.00-16.00 Plenary Class room dr. Made Susila utama, Sp.PD
dr.IGA Sumedha Pindha, Sp.KK/dr. Elis Indira,Sp.KK
16
Wednesday
Des.18th13 08.00-08.30
09.00-093.0
Lecture 27
Retroviral Infection (HIV) Lecture Class room Prof. Dr. dr. Tuti Parwati Merati, SpPD, KPTI 08.30-09.00 09.30-10.00 Lecture 28
Influenza Lecture Class room Prof. Dr. dr. Tuti Parwati Merati, SpPD, KPTI 09.00-10.30 12.00-13.30 Individual learning 10.30-12.00 13.30-15.00 Small group discussion Disc. Room Facilitator 12.30-14.00 10.00-11.30 Student Project Class room Prof. Dr. dr. Tuti Parwati Merati, SpPD, KPTI 14.00-15.00 15.00-16.00 Plenary Class room Prof. Dr. dr. Tuti Parwati Merati, SpPD, KPTI 17
Thursday
Dec.19 th13 08.00-08.30
09.00-093.0
Lecture 29
Infection in children (DBD, Difteri, sepsis, Campak) Lecture Class room dr. Dwi Lingga, sp.A/ dr. W. Gustawan,Sp.A
08.30-09.00 09.30-10.00 Lecture 30
infections in upper respiratory tract (faringits, tonsillitis, laringits, otitis, mastoditis, rhinitis, sinusitis, furunkelitis) Lecture Class room dr. Lely, Sp.THT 09.00-10.30 12.00-13.30 Individual learning 10.30-12.00 13.30-15.00 Small group discussion Disc. Room
Facilitator 12.30-14.00 10.00-11.30 Student Project Class room dr. Dwi Lingga, sp.A/ dr. W. Gustawan,Sp.A
dr. Lely, Sp.THT 14.00-15.00 15.00-16.00 Plenary Class room dr. Dwi Lingga, sp.A/ dr. W. Gustawan,Sp.A
dr. Lely, Sp.THT 18
Friday
Des.20th13 08.00-09.00 09.00-10.00 Lecture 31
Zoonosis Infection (Rabies, Leptospirosis) Lecture Class room Prof.Dr. dr. Raka Sudewi, Sp.S (K)
Dr. dr. Sri Budayanti, Sp.MK
09.00-10.30 12.00-13.30 Individual learning 10.30-12.00 13.30-15.00 Small group discussion Disc. Room Facilitator 12.30-14.00 10.00-11.30 Student Project Class room Prof.Dr. dr. Raka Sudewi, Sp.S (K)
Dr. dr. Sri Budayanti, Sp.MK 14.00-15.00 15.00-16.00 Plenary Class room Prof.Dr. dr. Raka Sudewi, Sp.S (K)
Dr. dr. Sri Budayanti, Sp.MK 19
Monday
Des.23th13 08.00-030.00 09.00-09.30
Lecture 32
Principles of Fungal Infection (Morphology of Fungal) Lecture Class room dr. Luh Ariwati 08.300-09.00 09.30-10.00 Lecture 33:
superficial fungal Infections (Tinea, Tinea versikolor, kadidiasis mukokutaneous)
Lecture Class room Prof. M. Swastika Adiguna
09.00-10.30 12.00-13.30 Individual learning 10.30-12.00 13.30-15.00 Small group discussion Disc. Room 12.30-14.00 10.00-11.30 Student Project Class room dr. Luh Ariwati
Prof. M. Swastika Adiguna
14.00-15.00 15.00-16.00 Plenary Class room dr. Luh Ariwati
Prof. M. Swastika Adiguna 20
Tuesday
Des.24th13 08.00-08.30 09.00-09.30 Lecture 34
Deep Fungal Infection Lecture Class room Prof.Dr.dr Tuti Parwati,Sp.PD 08.30-09.00 09.30-10.00 Lecture 35
Treatment of Fungal Infection (PD/PK) Lecture Class room dr.I B.Ngurah, M.For/dr. wiwiek Indrayani, M.Kes 09.00-10.30 12.00-13.30 Individual learning 10.30-12.00 13.30-15.00 Small group discussion Disc. Room Facilitator 12.30-14.00 10.00-11.30 Student Project Class room Prof.Dr.dr Tuti Parwati,Sp.PD
dr.I B.Ngurah, M.For/dr. wiwiek Indrayani, M.Kes 14.00-15.00 15.00-16.00 Plenary Class room Prof.Dr.dr Tuti Parwati,Sp.PD
dr.I B.Ngurah, M.For/dr. wiwiek Indrayani, M.Kes 21
Friday
Des.27th13 08.00-08.30 09.00-09.30 Lecture 36
Helminthes Infection Lecture Class room Dr. dr. I Made Sudarmaja, M.Kes 08.30-09.00 09.30-10,00 Lecture 37
Infection of Nematoda, Cestoda and Trematoda Lecture Class room dr. Kadek Swastika,M.Kes 09.00-10.30 12.00-13.30 Individual learning 10.30-12.00 13.30-15.00 Small group discussion Disc. Room Facilitator 12.30-14.00 10.00-11.30 Student Project Class room dr. I Made Sudarmaja, M.Kes
dr. Kadek Swastika,M.Kes 14.00-15.00 15.00-16.00 Plenary Class room dr. I Made Sudarmaja, M.Kes/Staff
22
Monday
Des.30th13 08.00-08.30 09.00-09.30 Lecture 38
Filariasis Lecture Class room dr. K. Agus Somia, Sp.PD 08.30-09.00 09.30-10.00 Lecture 39
Dengue Viral Infection Lecture Class room dr. Made Susila Utama, Sp,PD 09.00-10.30 12.00-13.30 Individual learning 10.30-12.00 13.30-15.00 Small group discussion Disc. Room Facilitator 12.30-14.00 10.00-11.30 Student Project Class room dr. K. Agus Somia, Sp.PD
dr. Made Susila Utama, Sp,PD 14.00-15.00 15.00-16.00 Plenary Class room dr. K. Agus Somia, Sp.PD
dr. Made Susila Utama, Sp,PD 23
Tuesday
Des.31th13 08.00-09.00 09.00-10.00 Lecture 40
Treatment of Helminthes Infection (PK/PD) Lecture
Class room Dr.dr. B.K.Satriyasa,M.Rrepro 09.00-10.30 12.00-13.30 Individual learning Class room 10.30-12.00 13.30-15.00 Small group discussion Facilitator 12.30-14.00 10.00-11.30 Student Project Class room Dr.dr. B.K.Satriyasa,M.Rrepro 14.00-15.00 15.00-16.00 Plenary Session Class room Dr.dr. B.K.Satriyasa,M.Rrepro 24
Wednesday
Jan.1st14 08.00-09.00 09.00-10.00 Lecture 41
Overview of Puerperal Infection Lecture
Class room dr.I Nym Bayu Mahendra,Sp.OG 09.00-10.30 12.00-13.30 Individual learning 10.30-12.00 13.30-15.00 Small group discussion Disc. Room Facilitator 12.30-14.00 10.00-11.30 Student Project Class room dr.I Nym Bayu Mahendra,Sp.OG 14.00-15.00 15.00-16.00 Plenary Session Class room dr.I Nym Bayu Mahendra,Sp.OG 25
Thusday
Jan.2nd14 08.00-09.00 09.00-10.00 Lecture 42
Overview of Sexually Transmitted Infection Lecture
Class room Dr. dr. A.A.G.P. Wiraguna, Sp.KK (K), FINSDV 09.00-10.30 12.00-13.30 Individual learning 10.30-12.00 13.30-15.00 Small group discussion Disc. Room Facilitaor 12.30-14.00 10.00-11.30 Student Project Class room dr. A.A.G.P. Wiraguna, Sp.KK 14.00-15.00 15.00-16.00 Plenary Session Class room dr. A.A.G.P. Wiraguna, Sp.KK 26
Friday
Jan.3rd14 08.00-15.00 09.00-16.00 Practice 1 : Laboratory diagnosis of Microbial infection
Laboratory I.B. Nyoman Putra Dwija, S.Si, M.Biotech
27
Monday
Jan.6th14 08.00-15.00 09.00-16.00 Practice 2 : Laboratory diagnosis of Microbial infection
Laboratory I.B. Nyoman Putra Dwija, S.Si, M.Biotech 28
Tuesday
Jan.7th14 08.00-15.00 09.00-16.00 Practice 3 : Laboratory Diagnosis of Clinical Pathology
Laboratory Dr Nyoman Mahartini SpPK
29
Wednesday
Jan.8th14 08.00-15.00 09.00-16.00 Practice 4 : Laboratory Examination of parasitic infectious
dr. Kadek Swastika, M.Kes 30
Thusday
Jan.9th14 08.00-15.00 09.00-16.00 Practice 5 : Laboratory Examination of parasitic infectious ()
dr. Kadek Swastika, M.Kes 31
Friday Jan.10th14
Silent Day 32
Monday
Jan.13th14
EXAMINATION BLOCK TEAM
MEETING OF STUDENT REPRESENTATIVES
In the middle of block period, a meeting is designed among the student representatives of every small group discussion, facilitators and source person of the block. The meeting discuss about the ongoing teaching and learning process, quality of facilitator and lectures as a feedback to improve the next process.
MEETING OF THE FACILITATORS
All facilitators are invited to discuss all block activities with block contributors 1 week after meeting of student representatives.
ASSESSMENT METHOD
1. Assessment will be held on 25th day of the block period. The time provision is 100 minutes. The number of MCQ is 100 with passing point ? 70.
2. Assessment in this block consists of:
SGD : 5%
Student Project (Paper) : 10%
Final exam : 85%
STUDENT PROJECT
TITLE
(Subject/topic: choose from competency list)
Name:
NIM:
Faculty of Medicine, Udayana University
2011
1. Introduction (Pendahuluan)
2. Content (Isi sesuai dengan judul paper)
3. Summary (Ringkasan)
4. References (Daftar pustaka): VanCouver style
5. Pages: 6-10, Spasi: 1.5, Time New Roman:12
Student Project
No Topic Kompetensi
1 Staphylococcus bacteremia
1. Staphylococcus: microbiologis aspect
2. Clinical spectrum of staphylococcus infection
3. How are staphylococcus infection diagnosed
4. Complication of staph infection
5. Treatment and prevention of staph infection 2 2 Sinusitis
1. etiopathogenesis of sinus infection
2. clinical symptoms and sign of sinus infection
3. management of sinus infection
4. complication of sinus infection 2 3 Otitis Media
1. Otitis media acute: etiopathogenesis
2. Otitis media acute: management
3. Otitis media purulenta
4. Otitis media khronic suppurative
5. Complication of acute titis media 2 4 Mastoiditis
1. etiologi
2. pathogenesis
3. diagnosis
4. management
5. complication 2 5 Peritonsilar abses
1. etiopathogenesis
2. clinical manifestation
3. diagnosis
4. management
2 6 Rheumatic fever
1. etiologi
2. pathogenesis
3. diagnosis
4. management
5. complication 2 7 Rheumatic disease
1. etiopathogenesis
2. clinical manifestation
3. management
4. complication 2 8 Meningitis Purulenta
1. ethiopathogenesis
2. clinical manifestation
3. diagnosis
4. management
5. complication 1 9 Meningitis serosa
ethiopathogenesis
clinical manifestation
diagnosis
management
complication
2 10 Plaque (Pes)
Etiologi
Transmisi
Management
Complication 2 11 Actinomycosis
Diagnosis (microbiology)
Clinical manifestation
Management 1 12 Chromoblastomycosis
Diagnosis (microbiology)
Clinical manifestation
Management
1 13 Maduromycosis
Diagnosis (microbiology)
Clinical manifestation
Management 1 14 Fever
– Patogenesis of fever
– Metabolic respon of fever
– How to measure body temperature and fever pattern
– Algorithm management of acute fever illness
– Management of fever 15 CMV
– CMV: virology
– Clinical spectrum of CMV
– CMV in immunocompetent
– CMV infection in immunocompromized
– Management of CMV
3A 16 Malaria
– etiopatogenesis of severe malaria
– clinical spectrum of severe malaria
– malaria cerebral
– clinical approach management of severe malaria
– malaria in pregnant 4 17 Dengue infection
– How to know warning simptom and sign
– severe dengue
– management of severe dengue
– management 4
18 Typhoid fever
– typhoid toxic
– Typhoid fever: intestinal complication
– 4 19 HIV/AIDS
– stigma of HIV/AIDS
– VCT
– PICT
– CST (care support treatment)
– ARV 3A 20 Influenza
– seasonal influenza
– swine influenza
– Avian influenza
– Management
– Prevention 4 21 Acute Gastroenteritis
– watery diarrhea:
– inflammatory diarrhea
– how to assement of severity of dehydration
– how to do rehydration
– how to do rectal swab 4 22 Yaws (patek)
– etiopatogenesis
– clinical picture
– laboratory confirmation
– Management
– Prevention 4 23 Rabies
– etiopatogenesis of rabies
– clinical picture of rabies
– laboratory confirmation of rabies
– how to manage dog bite
– how to giving vaccination (IM and subcutans) 4 24 Candidiasis
– clinical spectrum of candida infection
– Laboratory confirmation
– Management 25 Leptospirosis
– etiopatogenesis
– clinical picture
– laboratory confirmation
– Management
– Prevention 3B 26 Emerging and reemerging disease: legionalle
Clinical manifestation
Diagnosis microbiology
Management
27 Emerging and reemerging disease: Enterovirus 71 (HFMD)
Clinical manifestation
Diagnosis microbiology
Management 28 Emerging and reemerging disease: Coronavirus (SARS)
Clinical manifestation
Diagnosis microbiology
Management 29 Emerging and reemerging disease: Bunyaviruses (Hantavirus)
Clinical manifestation
Diagnosis microbiology
Management 30 Infeksi nosokomial
Definition
Manifestation
Management
Prevention 31 Antibiotic resisten
Mechanism of resistence
Rationale of using antibiotica
Prevention 32 How to using prudent antibiotic
Profile of antibiotic
LEARNING PROGRAM
LECTURE 1
Introduction to the block (Agent ,Host Environment, and infection manifestation)
Oleh:
Prof. Dr. dr. Tuti Parwati Merati, SpPD, KPTI
================================================
Lecture 2:
Bacterial classification
Oleh:
dr. K.Januartha P. Pinatih, Mkes
1. Describe relationship between microbes and human in health and disease
2. Explain normal human flora and opportunistic infections
3. Describe the establishment of microbial infection
4. Explain the difference between Gram-positive and Gram-negative bacterial cell wall !
5. Classify the spherical bacteria (cocci) into Gram-positive and negative group. List their virulence factors and related diseases caused by them !
6. Classify the rod bacteria (bacilli) into Gram-positive and negative group. List their virulence factors and related diseases caused by them !
7. List the important enteric bacteria (Enterobacteriaceae), their virulence factors and related diseases !
8. Classify the anaerobic bacteria according to their capabilities to form spores. List their virulence factors and related diseases caused by them !
9. Explain the spesific characteristic of Mycobacteria cell-wall and the implication to their natural resistance !
10. Explain the virulence factors and pathogenesis of infection caused by Mycobacteria !
Lecture 3:
PATHOGENESIS OF BACTERIAL INFECTION
Made Agus Hendrayana
ABSTRACT
The pathogenesis of bacterial infection includes initiation of the infectious process and the mechanisms that lead to the development of signs and symptoms of disease. Characteristics of bacteria that are pathogens include transmissibility, adherence to host cells, invasion of host cells and tissues, toxigenicity, and ability to evade the host’s immune system. Many infections caused by bacteria that are commonly considered to be pathogens are inapparent or asymptomatic. Disease occurs if the bacteria or immunologic reactions to their presence cause sufficient harm to the person.
Bacteria (and other microorganisms) adapt to the environment, including animals and humans, where they normally reside and subsist. In doing so, the bacteria ensure their survival and enhance the possibility of transmission. By producing asymptomatic infection or mild disease, rather than death of the host, microorganisms that normally live in people enhance the possibility of transmission from one person to another.
Some bacteria that commonly cause disease in humans exist primarily in animals and incidentally infect humans. Other bacteria produce infection of humans that is inadvertent, a mistake in the normal life cycle of the organism; the organisms have not adapted to humans, and the disease they produce may be severe.
The clinical manifestations of diseases (eg, diarrhea, cough, genital discharge) produced by microorganisms often promote transmission of the agents.
Many bacteria are transmitted from one person to another on hands. A person with S aureus carriage in the anterior nares may rub his nose, pick up the staphylococci on the hands, and spread the bacteria to other parts of the body or to another person, where infection results. Many opportunistic pathogens that cause nosocomial infections are transmitted from one patient to another on the hands of hospital personnel.
The most frequent portals of entry of pathogenic bacteria into the body are the sites where mucous membranes meet with the skin: respiratory (upper and lower airways), gastrointestinal (primarily mouth), genital, and urinary tracts. Abnormal areas of mucous membranes and skin (eg, cuts, burns, and other injuries) are also frequent sites of entry. Normal skin and mucous membranes provide the primary defense against infection. To cause disease, pathogens must overcome these barriers.
Once in the body, bacteria must attach or adhere to host cells, usually epithelial cells. After the bacteria have established a primary site of infection, they multiply and spread directly through tissues or via the lymphatic system to the bloodstream. This infection (bacteremia) can be transient or persistent. Bacteremia allows bacteria to spread widely in the body and permits them to reach tissues particularly suitable for their multiplication and cause the diseases.
Learning Task
Case :
A 35 years old female, a secretary at private company come to general practician complained that she has unreasonable pain when urinate since 5 days. She feels pain too at lower abdominal. The urine color is dark yellow and little bit cloudy. Other physical examination results are normal. The practician ask for laboratory examination for urine analysis and urine culture. After few days, the urine analysis shown that she has urinary tract infection. The urine culture shown colonies of Escherichia coli bacteria and significant as agent of infection.
Questions :
1. In this case, Escherichia coli as a pathogen bacteria. When is Escherichia coli called as colonization bacteria?
2. Explain the differentiation between true pathogen and opportunistic pathogen!
3. Explain the pathogenesis how Escherichia coli can infect the urinary tract (from transmission until infection and cause the disease) !
4. What are Escherichia coli’s virulence factors that can cause urinary tract infection?
5. Explain the microbial virulence factors that you know!
6. Explain the differentiation between exotoxins and endotoxin !
7. Describe how several pathogens are able to survive inside the macrophages !
8. Explain the routes of transmission that you know and give examples of each !
Self Assessment
1. Explain the meaning of this term above :
A. Contamination
B. Colonization
C. Invasion
D. Infection
E. Pathogen
F. Carrier
G. Nonpathogenic
H. Opportunistic pathogen:
I. Pathogenicity:
J. Toxigenicity:
K. Virulence:
L. Symbiosis
M. Commensalism
N. Parasitism
O. Zoonoses
2. Give examples of attachment mechanism !
Reff :
Jawetz, Melnick, Adelberg. 2010. Chapter 9. Pathogenesis of Bacterial Infection in Medical Microbiology, 25th Edition by Vishal . The McGraw-Hill Companies. Lange Microbiology.
Lecture 4
Viral classification
Oleh:
dr. Sri Budayanti, Sp.MK
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Lecture 5
Mechanism of Viral Pathogenesis
Oleh:
dr. Sri Budayanti, Sp.MK
=======================================
Lecture 6
Manifestation of virus and bacterial infection
dr.Agus somia, Sp.PD
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Lecture 7
Basic concept of Parasitic Infections
Oleh:
Prof. dr. D.P. Widjana, DAP&E, Sp.Par.K
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Lecture 8
Treatment of Viral Infection (PK/PD)
Prof. dr. IGM Aman, Sp.FK
Most of antiviral agents exerts their actions on viral replication, at the stage of nucleic acid synthesis ot the stage of late protein synthesis and processing. Most of antiviral agents active against herpes viruses and against the Human Immunodeficiency Virus (HIV) are antimetabolites, so that it must first undergo conversion to active forms, usually triphosphate derivatives. One of the most important recent trends in viral chemotherapy has been combination therapy, where treatment with combination result in greater effectiveness and prevent or delay the emergence of resistance, especially in the treatment of HIV disease. Such combination usually include two Nucleoside Reverse Transcriptase Inhibitor (NRTIs) plus Protease inhibitor. In some combination regimens, a non nucleoside reverse transcriptase inhibitor (NNRTI) has been used place of Protease inhibitor. Highly active antiretroviral therapy (HAART) is recommended for AIDS patients.
Learning Task
A male patient, 30 year old, is HIV-positive, has a CD4 count 300/ul and a viral RNA load 500 copies/ml. The physician give him antiviral drug. Two weeks later he complained anorexia, nausea, vomiting, and abdominal pain. His abdomen was tender in the epigastric area. Finally the physician diagnose him as acute pancreatitis.
1. List drugs that have cross resistance with acyclovir, and explain the reason why cross resistance happened? (Katzung p.824)
2. List and describe the drugs preserved for acyclovir resistant strain. (Katzung p.824)
3. In the treatment of HIV disease, the combination of antiviral is needed. Explain the adventages of drug combination. In the case what’s likely antiviral drug given by the doctor.
4. How do you manage this patient?
Self assessment:
1. A patient suffering from herpes simplex, treated with acyclovir. But HSV is resistant to acyclovir. The alternative drug can choose:
1. Ganciclovir
2. Valaciclovir
3. Famciclovir
4. Cidofovir
2. As antiviral, the clinical use of acyclovir are as follow:
1. Varicella
2. Retinitis by CMV (cytomegalovirus)
3. Herpes zoster
4. Reccurent herpes labialis
3. The antiviral that are good for treating hepatitis patient are:
1. Lamivudin
2. Ribavirin
3. Interferon
4. Stavudin
4. For treated AIDS patient a combination of antiviral are needed. The combination that are effective for this patient are:
1. Indinavir + Didanosine + Lamivudin
2. Acyclovir + Amantadine + Zidovudine
3. Zidovudine + Didanosine + Nevirapine
4. Ganciclovir + Sorivudine + Cidofovir
Lecture 9
Treatment of Microbacterial Infections I (Type of antimicrobacterial) (PK/PD)
Oleh:
Dr.dr. B.K. Satriyasa,M.Repro
Abstract
Many of microorganism are classified as either Gram-positive or Gram-negative. Both of them could be differentiated by several respect, not least in the structure of the cell wall, which has implications for the action of antibiotics. The cell wall of Gram-positive organisms is a relatively simple structure and it consist of 50% peptidoglycan. The cell wall of Gram-negative organisms is much complex, so more difficult in penetrating by some antibiotics. Antibiotic for which penetration is a problem include benzylpenicillin, methicillin, macrolides, vancomycin, bacitracin, and novobiocin. There are many mechanisms of action of antibiotics or antimicrobial drugs in killing or inhibited the bacterial growth such as: inhibit cell wall synthesis, inhibit protein synthesis, as a antimetabolites, and inhibit microbial nucleic acid metabolism. The emergence of microbial resistance pose a constant challenge to the use of antimicrobial drugs. Mechanism of underlying microbial resistance to the cell wall synthesis inhibitors include the production of antibiotic-inactivating enzymes, change in the structure of target receptors, increased efflux via drugs transporters, and decreases in the permeability of microbes cellular membranes to antibiotics. Strategies designed to combat microbial resistance include the use of adjunctive agents that can protect against antibiotic inactivation, the use of antibiotic combination and avoid the misuse of antibiotic.
Learning Task
A-36-year old woman recently treated for leukemia is admitted to the hospital with malaise, chills, and high fever. Bram stain of blood reveals the presence of Gram negative bacilli. The initial diagnosis is bacteremia. The records of the patient reveal that she had a severe urticarial rash after oral penicillin V.
a. If you a medical doctor what antibiotic would you choose for this woman?
b. Explain the mechanism of action and adverse reaction of the drugs that you choosed
c. In your opinion is there appropriate if that pasien treated by Chloramphenicol? Explain your answer.
Self assessment:
1. Which one of the following item is beta lactamase inhibitors:
a. Mafenide
b. Penicillin V
c. Clavulanic acid
d. Amoxycillin
e. Ofloxacin
2. Ciprofloxacin and the other fluoroquinolone mechanism of action is by:
a. Inhibiting the synthesis of bacterial protein
b. Inhibiting an enzyme deoxyribonucleic acid (DNA) gyrase
c. Interfering cell wall synthesis
d. Inhibiting the production of mycolic acid
e. Inhibiting enzyme dehydrofolate reductase
3. The following antibiotics inhibit bacterial protein synthesis and are considered as bacteriostatic:
a. Azithromycin
a. Ofloxacin
b. Chlarithromycin
c. Ciprofloxacin
4. The following drugs are used for topical application:
a. Mafenide
b. Sulfasalazine
c. Silversulfadiazine
d. Penicillin
5. Which ones are the contraindication of tetracycline:
a. Producing a yellow discoloration of teeth
b. Growth retardation in relation to infant skeletal development
c. Depression of bone growth
d. Crystalluria
6. These statements are true about chloramphenicol:
a. It is a potent inhibitor of microbial protein synthesis
b. It binds reversibly to the p450 as sub unit of bacterial ribosomal
c. It inhibits the peptidyl transferase step of protein synthesis
d. It is a bacteriostatic broad spectrum antibiotic
7. Antibiotic that has ototoxic and nephrotoxic effect is:
a. Erythromycin
b. Streptomycin
c. Chloramphenicol
d. Amoxycillin
e. Clindamycin
Textbook
Source :
1. Katzung, B.G. 2001. Basic and Clinical Pharmacology. Eight Edition. Lange Medical Books/McGraw -Hill.
2. Katzung and Trevor’s. Pharmacology Examination and Board Review. Sixth Edition.Lange Medical Books/McGraw-Hill.
Lecture 10
Treatment of Microbacterial Infections II (Resistance, rational treatment, and drug combination)
Oleh: Dr. Made Jawi, M.Kes
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Lecture 11
Antimicrobial susceptibly
Oleh: dr. Ni Made Adi Tarini, Sp.MK
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Lecture 12:
Respond Host against parasitic and clinical manifestation
dr. I Made Susila Utama,Sp.PD
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Lecture 13
Treatment of parasitic infection (PK/PD)
dr. A. Wiwiek Indrayani, M.Kes
Abstract
Malaria is the most important protozoal disease in tropical medicine. It is responsible for 2 million deaths per year and much morbidity in the 200 million people worldwide who are infected. Malaria is caused by four species of plasmodial parasites that are transmitted by female anophelene mosquitoes. Anti malarial drugs are usually classified in terms of their action against different stages of the parasite. They are used to prevent transmission or cure malaria. The aim of prophylactic use is to prevent the occurrence of infection in a previously healthy individual who is at potential exposure risk. Suppressive prophylaxis involves the use of blood schizonticides to prevent acute attacks; causal prophylaxis involves the use of tissue schizonticides or drugs against the sporozoite to prevent the parasite established in the liver. Anti malarial drugs can be used curatively (therapeutically) against an established infection. Suppressive treatment aims to control acute attacks, usually with blood schizonticides; radical treatment aims to kill dormant liver forms, usually with a hypnozonticide, to prevent relapsing malaria. Several classes of antimalarial drugs such as chloroquine, amodiaquine, quinine, quinidine, mefloquine, primaquine, fansidar, proguanil, artemisin, and atovaquone-proguanil. The effectiveness of anti malarial agents varies between parasite species . In addition, drug resistance is an important therapeutics problem, most notably with P falciparum.
Amoebic dysentery is caused by infection with Entamoeba histolytica, which is ingested in a cystic form. Dysentery results from invasion of the parasite in the intestinal wall. Occasionally, the organism insists in the liver, forming abscesses. E. Histolytica can cause asymptomatic intestinal infection, mild to moderate colitis, severe intestinal infection, ameboma, liver abscess and other extra intestinal infections. The choice of drugs for amoebiasis depends on the clinical presentation. Drugs of choice for asymptomatic intestinal infection are luminal agent such as diloxanide furoate, iodoquinol and paromomycin; for mild to moderate intestinal infection are metronidazole plus luminal agent; for severe intestinal infection and hepatic abscess are metronidazole plus luminal agent .
Toxoplasmosis is an infection caused by toxoplasma gondii parasite. Most people have no symptoms because their immune system keeps the parasite from causing illness. However, in people who have a weak immune system, toxoplasmosis can cause serious medical problems, such as damage the eyes and brain. The immune system can become weak for a number of reasons.The drug of choice for toxoplasmosis are pyrimethamine plus clindamycin plus folinic acid
Learning Task
1. Ms. Dewi, a 25 year old student, presents with a four day history of high fever (40 C), general malaise , feeling intensely cold and shaking followed by profuse sweating. He returned from Lombok island 3 weeks ago. She takes drugs for malaria. Today she feel dizziness, nausea, diarrhea, tinnitus, blurred vision , flushed, sweaty skin and impaired hearing.
Ouestions :
1. Which of the following antimalarial drugs causes a dose dependent toxicity ?
2. Describe the pharmacodynamic and pharmacokinetic properties of the major antimalarial drugs (chloroquine, mefloquine, quinine, primaquine, and the antifolate agents)!
The five star hotel usually has screening their food handler s every six months. Mr. Andi had positive cysts amoebiasis without dysentery symptom.
Ouestions
1. Which of the following anti amoebiasis drugs can use to treat Mr. Andi ?
2. Describe the pharmacodynamic and pharmacokinetic properties of the major amebicides (diloxanide, emetine, iodoquinol, and metronidazole) !
Mrs Ratna, a 28 years old, come to hospital policlinic with chief complaints had abortus for 3 times. She usually eat steak or satay and has many cat in her house. Doctor suspect she had infected by toxoplasma gondii.
Ouestions
1. Identify the drugs useful for prophylaxis and treatment toxoplasmosis and know their toxic effects !
Self -assesment questions
1. Which of the following antimalarial drugs should be used for prophylaxis for travel to the East of Lombok island ?
A. Chloroquine
B. Primaquine
C. Mefloquine
D. Hydroxychloroquine
E. Pyrimethamine
2. Which of the following drugs has a major side effect of hemolysis in persons with G6PD deficiency?
A. Chloroquine
B. Primaquine
C. Mefloquine
D. Pyrimethamine
E. Doxcycline
3. Which of the following drugs is recommended as a single agent for oral treatment of uncomplicated malaria due to chloroquine-resistent P falciparum strains ?
A. Doxycline
B. Iodoquinol
C. Primaquine
D. Proguanil
E. Quinine
4. Which of the following drigs is effective against E. histolytica and other protozoa that live under anaerobic conditions?
A. Metronidazole
B. Pentamidine isethionate
C. Quinine
D. Eflornithine
E. Chloroquine
5. Which one of the following statements about amebicides is least accurate?
A. Diloxanide furoate is a luminal amebicide
B. Emetine is contraindicated in pregnancy and in patients with cardiac disease
C. Metronidazole has little activity in the gut lumen
D. Paromomycin is effective in extraintestinal amebiasis
E. Systemic use of iodoquinol may cause thyroid enlargement and peripheral neuropathy
Textbook
Source :
3. Katzung, B.G. 2001. Basic and Clinical Pharmacology. Eight Edition. Lange Medical Books/McGraw -Hill.
4. Katzung and Trevor’s. Pharmacology Examination and Board Review. Sixth Edition.Lange Medical Books/McGraw-Hill.
Lecture 14:
The Role of Immunity to infection (Basic)
Oleh:
Dr.dr. Dewa Made Sukrama, M.Si, Sp.MK
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Lecture 15:
Infection of Mycobacterium (TBC)
Prof Dr.dr. IB Rai,Sp.P
========================================================
Lecture 16:
Infection of Mycobacterium (Leprosy)
Dr. Dharma putra, Sp.KK
Morbus Hansen is an infectious disease primary affected the periphery nerve and secondary affected skin and the other organ caused by Mycobacterium leprae. Readley and Jopping classification is Tuberculoid-Tuberculoid (TT), BorderlineTuberculoid (BT), Borderline-Borderline (BB), Borderlline-Lepromatous (BL), and Lepromatous-Lepromatous (LL).
The 4 cardinal sign of Leprosy are: 1. Macula hypopigmented or erythematous skin, 2. Anaesthesi, 3. Enlargement of periphery nerve, 4. Acid Fast Bacilli (AFB) found from slit skin smear. Diagnosis of leprosy is based on finding two from three cardinal sign of leprosy or if only cardinal sign number 4.
There are two kind regimen therapy for leprosy i.e. the therapy for paucy bacillary leprosy (TT, BT with AFB (-) are rimfapicin 600 mg a month and dafson6% (DDS) 100 mg a day continuous for six month and for multi bacillary leprosy are rifampicin 600 mg a month, clofacimin (lamprene) 300 mg a month continuous with lamprene 50 mg a day and dafson (DDS) 100 mg a day continuous therapy for 12 months.
Kepustakaan
1. Andrews Diseases of the skin. Nine Ed
2. Leprosy. Third edition. Antony Bryceson
Intoroduction of Leprosy
1. Explain the etiology of leprosy ( My cobacterium leprae)
2. Explain the test for detection of M leprae : Zeihl-Neilsen staining test, histopathological examination, lepromin test, Gunawan test and anaesthetic test in supporting the diagnosis of leprosy
3. Explain the classification of leprosy
4. Explain the clinical sign and symptom of leprosy
5. Explain the complications of leprosy
6. Explain the management of leprosy and the complications
Kasus
Seorang wanita, 35 tahun mengeluh ada bercak merah pada punggung kiri dan kanan dengan batas tidak tegas, selain itu juga dijumpai bercak merah di wajah dan dada yg tersebar simetris, kecil-kecil. Bercak merah tersebut tidak gatal. Selain itu dijumpai penebalan pada cuping telinga kanan dan kiri serta alis mata rontok.
Pertanyaan :
a. Apa yang perlu ditanyakan lagi pada penderita tersebut?
b. Pemeriksaan apa saja yang diperlukan ?
c. Apa diferensial diagnosis Saudara ?
d. Apa diagnosa Saudara ?
Bagaimana penatalaksanaannya ?
Lecture 17:
Antimycobacterial Drugs ( anti TBC, Anti lepra) (PK/PD)
dr. IB Ngurah, M.For
The chemotherapy of infection caused by Mycobacterium tuberculosis is complicated because: limited information about the mechanism of drugs action, the development of resistance, the intracellular site of mycobacterial, the chronic mycobacterial disease and many drug drug toxicities, and patient compliance. Chemotherapy of tuberculosis always the use of drug combinations to delay of resistance and increased antituberculosis efficacy.
The 4 cardinal sign of Leprosy are: 1. Macula hypopigmented or erythematous skin, 2. Anaesthesi, 3. Enlargement of periphery nerve, 4. Acid Fast Bacilli (AFB) found from slit skin smear. Diagnosis of leprosy is based on finding two from three cardinal sign of leprosy or if only cardinal sign number 4.
There are two kind regimen therapy for leprosy i.e. the therapy for paucy bacillary leprosy (TT, BT with AFB (-) are rimfapicin 600 mg a month and dafson6% (DDS) 100 mg a day continuous for six month and for multi bacillary leprosy are rifampicin 600 mg a month, clofacimin (lamprene) 300 mg a month continuous with lamprene 50 mg a day and dafson (DDS) 100 mg a day continuous therapy for 12 months.
Case 1:
A 40-year old man got cough since one month, lost of appetite and sweating every night. After examination the physician diagnosed the patient as tuberculosis.
1. Describe the combination therapy for tuberculosis which used best
2. Explain the mechanism of action of each drugs
3. The therapy of tuberculosis need long time. Explain what is the reason.
4. Explain the interaction of isoniazid with phenytoin
5. Descrie the toxic effect of drugs for tuberculosis
6. List all drugs for leprosy
7. Describe the mechanism of action dapsose for leprosy
8. Describe why you use combination dapsone with rifampin and clofazimine for leprosy
9. Describe the toxic effects of dapsone and treatment for erythema nodosum
10. Describe the pharmacological aspects of rifampin for leprosy
11. Describe the pharmacological aspects of clofazimine for leprosy
Self assessment:
1. Compare the fate of isoniazid in slow asetilator patient and rapid asetilator patient.
2. Isoniazid for tuberculosis is usully combined with vitamin B6. Describe the reason
3. Why do you choose pyrazinamide as primary drug for tuberculosis.
Lecture 18:
Control of microorganism (infection control)
dr. Ni Made Aditarini Sp. MK
ABSTRACT
Microorganism like viruses, bacteria, fungi and protozoans reproduce directly within the host. They are usually small and have a short generation time. Recovery from infection usually gives immunity against re-infection; in the case of viral infections this may be lifelong. We know, the source of infection can be from community and hospital, while the transmission of infection varies to depending from microorganism. The principle prevention of infection must to know the kind of microorganism, transmission method and population of infection. Among various major factors contributing to the emergence of infectious diseases, the important ones are human demographics and behavior, industry and technology, economic development and land use, globalization and international travel, microbial adaptation and change, breakdown of public health measures, and economic disparity of have and have-nots
One of the great achievements of applied medical research has been its success in controlling so many infectious diseases; smallpox has been eradicated and other infections are now controlled effectively in many parts of the world. This control has been accomplished in three main ways by the use of chemotherapy, immunization and improving the environment (e.g. better sanitation, nutrition)
In general, chemotherapy is used to control infectious diseases in individuals, whereas immunization and environmental improvements are used for control in populations. Understanding the ways in which these diseases arise, spread and can be controlled requires detailed epidemiologic studies to provide an accurate basis for assessment of risks and for planning intervention. These studies are based on knowledge of the infectious agents and their patterns of association with their hosts, but require the collection and analysis of data, in conjunction with the use of mathematical models, to produce useful pictures of disease transmission and control. Where the causal links between a clinical condition and an infectious agent or its mode of transmission are unknown, epidemiologic investigations can establish this link and thus determine appropriate control strategies.
Learning Task
1. Describe risk factors are influence to community infection and hospital infection
2. Describe how infections flow through a host population .
3. Describe some strategies for control of infectious diseases.
4. Describe some factors are influence to spread of infection.
5. Describe some factors are influence the success of vaccination.
Self Assesment
1. Comparison of chemotherapy and vaccination
2. Explain the meaning of this term above :
a. Susceptible host
b. Incubation period
c. Latent period
d. Generation time
3. Mention some factors are important at vaccination gift
Reference :
Mims. Medical Microbiologi, 4th Edition, Mosby Elsevier. 2008. p.445-457 & p. 551-568
Lecture 19:
Immunization in child
dr. Dwi Lingga, sp.A/ dr. W. Gustawan,Sp.A
Abstract
Immunization is the process of artificially inducing immunity or providing protection from disease. Active immunization is the process of stimulating the body to produce antibody and other immune responses through administration of a vaccine or toxoid. Passive immunization, the provision of temporary immunity by administration of preformed antibodies derived from humans or animals. Biologic agents used to induce active immunization include vaccines and toxoids. A vaccine is defined as a suspension of live (usually attenuated) or inactivated microorganisms, or fractions there of, which is administered to induce immunity and prevent infectious disease or its sequelae. There are some diseases that can prevent with immunization. Polio, diphtheria, tetanus, pertusis, tuberculosis, measles, hepatitis B, hepatitis A, influenza, meningitis caused by hemophilus influenza type B. All vaccines may cause side effects, and immunization safety is a real concern. Unlike most other medical interventions, vaccines are given to healthy people, and people are far less willing to tolerate vaccines’ adverse effects than adverse effects of other treatments. As the success of immunization programs increases and the incidence of disease decreases, public attention shifts away from the risks of disease to the risk of vaccination, and it becomes challenging for health authorities to preserve public support for vaccination programs.
Learning task
The baby, boy, 5 months old accompanied by his mother come to clinic to get immunization. His mother told to doctor that her baby had fever after the first DPT immunization. Her baby had fever until 380C. He has no seizure, no high crying but his mother worried about that experience.
1. What is the explanation that you must tell to his mother?
2. How about the next immunization schedule?
3. What is contraindication for next immunization?
Lecture 20
Antiseptic and disinfectant
Dr.dr.B.K. Satriyasa,M.Repro
Abstract:
Disinfectants are chemical agent that inhibit or kill microorganism in an inanimate environment. Antiseptics are disinfecting agent with sufficiently low toxicity for host cells that they can be used directly on skin, mucous membranes or wound. Antiseptics and disinfectants are extensively used in hospitals and other health care settings for a variety of topical and hard-surface applications. A wide variety of active chemical agents (biocides) are found in these products, many of which have been used for hundreds of years, including alcohols, phenols, iodine, and chlorine.
A wide variety of active chemical agents (or “biocides”) are found in these products, many of which have been used for hundreds of years for antisepsis, disinfection. Despite this, less is known about the mode of action of these active agents than about antibiotics. In general, biocides have a broader spectrum of activity than antibiotics, and, while antibiotics tend to have specific intracellular targets, biocides may have multiple targets. The widespread use of antiseptic and disinfectant products has prompted some speculation on the development of microbial resistance, in particular cross-resistance to antibiotics. The process of disinfectants prevent infection by reducing the number of potentially infective organism either by killing, removing, or diluting them.
Antiseptics are disinfecting agents with sufficiency low toxicity for host cells that can used directly in skin, mucous membrane, or wound. Disinfectants are strong chemical agents that inhibit or kill microorganisms in an inanimate environment. Disinfectant and antiseptics do not have selective toxicity, and their clinical use are therefore limited. Most antiseptics delay wound healing. User of antiseptics and disinfectants need to consider their short-term and long-term toxicity since they may general biocidal activity and may accumulate in the environment or the body of the patients.
Learning Task
1. List the Disinfectants and antiseptics (Katzung & Trevor’s, Katzung, BG)
2. Explain the mechanism of action disinfectants and antiseptics (Katzung & Trevor’s, Katzung, BG)
3. Describe the clinical use of disinfectants and antiseptics for nosocomial infection
4. Describe the side effect of disinfectants and antiseptics (Katzung & Trevor’s, Katzung, BG)
Self assessment
1. Which one the following antiseptics promote wound healing?
A. Iodine
B. Alcohol
C. Hexachlorophene
D. Chlorhexidine
E. None of the above
2. . Which one the following antiseptics and disinfectant derivates of oxidizing Agent?
A. Iodine
B. Alcohol
C. Hexachlorophene
D. Chlorhexidine
E. Hydrogen peroxide
3. Alcohols are not used as sterilants because they are. EXCEPT:
A. They are sporicidal
B. Do not penetrate protein-containing organic material
C. May not be active against hydrophilic viruses
D. Lack residual action
E. They evaporate completely
4. Mechanism of action of povidone-iodine is to
A. Inhibitor of arabinosyl tranferase
B Inhibitor of thymidilate syntetase
C Inhibitor of protein kinase
D Denature of protein
E. Denature of lipid
Lecture 21
Universal Precaution
dr Agus Somia,Sp.PD
Learning task
Case 1
A 22-year-old male, work as an interns doctor in emergency care unit, had a patient with suspected of HIV infection stage IV and Lung TB and chronic diarrhea. This doctor will do the history-taking, physical examination and giving first aid to the patient
Learning Task:
1. What is the type of exposure risk that may happen to this doctor?
2. What is specific precaution that this doctor have to do to prevent cross transmission?
3. What are the kind of body protector that this doctor have to wear ?
4. If this doctor have to take blood specimen with syringes needle to laboratory examination, how to recapping needles in order to prevent the infection?
Self assessment:
1. Describe about:
a. Nosocomial infection
b. Kinds of nosocomial infection
c. How to do hygienic hand washing
d. How is the preparation and procedure of using sterile gloves?
e. How is the preparation and procedure unleashing sterile gloves?
2. Explain pathogenesis of:
a. Nosocomial blood stream infection
Lecture 22
Protozoa Infection I (Malaria, Amoebiasis, Leismaniasis,Tripanosomiasis,Toxoplasm