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
========================================================
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
===============================================================

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
========================================================

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
=================================================
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,Toxoplasmosis, Trichomoniasis)
Oleh:
dr.Dewa Ayu A. Sri Laksmi,M.Sc, M.Kes
dr. Putu Astri Damayanti,M.Kes

ABSTRACT

Protozoa are unicellular organisms that have trophozoite form with one or more nuclei containing nucleoli or karyosome and bounded by a nuclear membrane and the usual eukaryotic cytoplasmic organelles including mitochondria ribosomes and endoplasmic reticulum. Trophozoite have a cell membrane but not cell wall. Most intestinal Protozoa also develop cyst that are more resistant than the fragile trophozoite to drying, cold or other environmental stresses.
Malaria and Toxoplasmosis well known as parasitic disease and have great impact due to their worldwide distribution. Human malarial parasite were first seen in 1880 and their development both in the anopheline mosquito and in the human blood stream was well understood by 1900, however Several clinical syndromes known to be caused by infection of malaria parasites were first recognized centuries before the discovery of their pathogens.Consequently the diseases were referred to the type of febrile cycle. Quotidian, tertian and quartan fevers denoted respectively 24-,48- and 72 hour cycles of fever. The modern tendency is to refer the various types of malaria by the name of the agent.
Toxoplasma is caused by a coccidian parasite, Toxoplasma gondii. It has a worldwide distribution and shows a broad host range from warm blooded animals to birds and reptiles. Man acquires the infection indirectly by ingesting oocysts from contaminated environments, by consuming Toxoplasma cysts from tissues of other intermediate hosts such as cow, goat, chicken, duck, rabbit, by blood transfusion or transplantation, or directly by transplacental infection
Human infection is generally asimptomatic and self limited except in immunocompromised host, infection can disseminated and fatal. The prevalence of antibody to toxoplasma in human and animal ranged from 2% to 75% in Southeast Asian Countries. Cats are the definitive host of T. gondii; they are the only animals that pass oocysts in their feces .

LEARNING TASKS PROTOZOA INFECTION
1. Case:
A 35 year old man present to primary public health service with one week history of headache, fever, chills, sweats and myalgia. Patient history reveals that he just returned from West Papua after 2 months lived there. He took chloroquine malarial prophylactic irregularly. Physical examination showed raised body temperature (400C), a rapid pulse rate, and generalized sweating. Complete Blood Count was ordered and demonstrated intra erythrocyte organism.
a. Describe the laboratory examinations to define the diagnosis
b. When in blood smear demonstrate normal size erythrocyte containing crescent shape gametocytes and multiple ring form within the blood cell,
* What is the most likely diagnosed in this patient?
* what is etiology of this cases and describe this parasite life cycle
c. Describe the pathogenesis of this disease
2. Please compare the morphology characteristic of 4 type of plasmodium in human.
3. Describe briefly about chagas’ disease.
4. Describe the life cycle of Trypanosoma cruzi and Leishmania donovani
5. Case
A previously healthy 28-year old man, who had recently returned from a trip to Lombok, was seen by his family physician for crampy abdominal pain, malaise, slight fever and bloody, mucoid diarrhea. Liquid stool specimens were collected and submitted for culture for enteric bacterial pathogens as well as parasites. Stool cultures were negative for bacterial pathogens, examination for ova and parasites was positive for motile trophozoites in the saline wet amount, and ameboid trophozoites with finely granular cytoplasm and ingested red blood cells in the permanent trichrome stain.
a. Describe the life cycle of parasites above !
b. Explain the pathogenesis of parasite above!
c. Describe infective stages of parasite above!
6. Describe the life cycle of Trichomonas vaginalis
7. Describe infective stages of Trichomonas vaginalis
8. Explain what the differences of Entamoeba histolytica and Giardia lamblia life cycle?
9. Describe the life cycle of Toxoplasma gondii
10. Explain transmission of Toxoplasma gondii infection
11. Explain why toxoplasma infection became latency?

Lecture 23
Protozoa Infection II (Management of protozoa Infections)

dr Yuli Gayatri, Sp.PD

Objectives
* To describe name the 4 important members of the Genus Plasmodium
* To known which from of Malaria is most dangerous and why.
* To describe disease that Malaria most commonly mimic
* To understand how Malaria is diagnosed
* To describe the current recommendation for Malaria treatment and what factors dictate the regimen of choice
* Recognized when should chemoprofilaxis be begun and how long after completion of a trip to an endemic area should preventive therapy be continued
* To describe clinical presentation of Amoebiasis/ Toxoplasmosis/ Trichomoniasis
* To know how Amoebiasis / Toxoplasmosis/ Trichomoniasis
Is diagnosed?
* To describe what are the treatment of choice of Amoebiasis Toxoplasmosis/ Trichomoniasis

Case 1:
A 21-years-old man complained with fever for 6 days prior to admission, relapsing chills, muscle eches and lost of appetite. He took several day trip to Lombok island. They noted some mosquito bites and ate some fruits on the island. About 3 days into the illness He became jaundice and began passing dark urine. They sought treatment from local Lombok physician, who diagnosed hepatitis secondary to ingestion of toxic food. Two days later He was referred to Sanglah Hospital for intensive treatment. Based on an initial examination, patient was conscious, look pale and icteric, body temperature was 38,5 °C.
Learning task:
1. Find key words related to this case
2. Describe condition related to key words
3. Define organ system that involved in this condition and find probably cause of the key words
4. Define differential diagnosis and other examinations to support the diagnosis
5. Describe kinds of laboratory examination to diagnose malaria e.q. blood smear, thick smear, rapid test, etc
6. Define management of this case
7. Define complication and prognosis
8. Define prevention based on individual, family, and community
Self assessment:
1. Describe kinds of plasmodium
2. Describe pathogenesis of malaria
3. Describe diagnosis of malaria
4. Describe pathogenesis of complication
5. Define management of uncomplicated malaria
6. Define management of malaria with severe complicatio
Lecture 24
Infection of Enterobacter (Thypoid, C. botulinum)
dr Agus Somia,Sp.PD

Case 1
A 22-year-old male, with feeling generally unwell with fever, headache, malaise and diarrhea. the onset of fever since 7 days ago. His body temperature was 39 degree celcius, blood pressure 120/80 mmHg, Pulse rate 100 beat per minute.

Learning Task:
5. Define and describe others symptoms related to the patients that should be asked to this patient
6. Describe physical examination to support diagnosis of this patient.
7. What is possibly diagnosis of this patient?
8. Describe differential diagnosis of this case
9. Describe laboratory and other examination to support the diagnosis
10. Describe management of this patient
11. Describe how to explain to this patient about prognosis of patient`s disease

Case 1:
A 42-year-old man complained with diarrhea since last night. His diarrhea was 10 times. Diarrhea has accompanied with nausea, abdominal pain, and malaise. No history of fever and stomachache. He is a salesman. He took medicine to retrieve his diarrhea, but it does not work.
Learning task:
1. Define other sign and symptoms from this patient
2. Describe physical examination must be done to this patient
3. Describe laboratory examination and other examination must be done to support diagnosis
4. Describe management of this patient
5. Describe plan of therapy based on priority on this patient

Self assessment:
3. Explain pathogenesis of:
a. Bacillare Dysentriae
b. Typhoid fever
c. Cholera
d. Clostridium difficile associated diarrhea
4. Describe and interpret cerebrospinal fluid (CSF) examination in bacterial meningitis, viral meningitis, tuberculous meningitis, and streptococcal meningitis.
5. Define signs and symptoms of:
a. Typhoid fever
b. Bacillare dysentriae
c. Cholera
d. Clostridium difficile associated diarrhea
6. Differentiate clinical sign and symptoms of diarrhea caused by bacillare dysentriae, cholera and Clostridium associated diarrhea
7. Describe steps for how we doing rehydraton
8. Define management of these patients:
a. Typhoid fever
b. Bacillare dysentriae
c. Cholera
d. Clostridium difficile associated diarrhea
9. Describe about complication of
a. Typhoid fever
b. Bacillare dysentriae
c. Cholera
d. Clostridium difficile associated diarrhea
Lecture 25
Sepsis and Bacteremia
dr. Made Susila utama, Sp.PD
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Lecture 26
Cutaneous Viral Infection (Varicella, Zoster, Herpes)
Oleh:
dr.IGA Sumedha Pindha, Sp.KK/dr. Elis Indira,Sp.KK

Learning task

An adult woman, 45 years old came to clinic with chief complaints group of small blister in right side of the back since 3 day ago then the lession spread to the right waist and right chest. This complain is accompanied with burning sensation. One day before the blister appeared patient had fever. History of the same disease was denied. History of taking medicine before was denied.

1. What should we asked to the patient in the anamnesis ?
2. Describe the effloresensi in physical examination.
3. What are the differential diagnosis in this patient ?
4. What Laboratory tests is needed to confirm diagnosis of this case?
5. What is the diagnosis of this patient ?
6. Mention about complication of this disease
7. What is the prognosis of the disease ?
8. What is the treatment of this case?
9. What advice we can give to the patient ?

Self Assasement

1. What kind of diseased that can caused by the herpes virus group and what is the nature
virus of this group?
2. What is the majority characteristic of these group of virus?
3. What is clinical manifestation of varicella ?
4. How is pathogenesis of Herpes Zoster infection?
5. Mention about trigger factor the emergence of lesions in herpes simplex
6. What are the complication that occurs in Herpes Zoster?
7. Mention about complication that could occur happens when pregnant women suffer from varicella
8. What is the management of skin diseases caused by viruses?
Lecture 27
Retroviral Infection (HIV)
Oleh:
Prof. Dr. dr. Tuti Parwati Merati, SpPD, KPTI
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Lecture 28
Influenza
Oleh:
Prof. Dr. dr. Tuti Parwati Merati, SpPD, KPTI

INFLUENZA
Abstract
Influenza virus infection, one of the most common infectious diseases, is a highly contagious airborne disease that causes an acute febrile illness and results in variable degrees of systemic symptoms, ranging from mild fatigue to respiratory failure and death. These symptoms contribute to significant loss of workdays, human suffering, mortality, and significant morbidity. Accurately diagnosing influenza A or B infection based solely on clinical criteria is difficult because of the overlapping symptoms caused by the various viruses associated with upper respiratory tract infection (URTI). In addition, several serious viruses, including adenoviruses, enteroviruses, and paramyxoviruses, may initially cause influenza like symptoms. The early presentation of mild or moderate cases of flavivirus infections (eg, dengue) may initially mimic influenza. For example, some cases of West Nile fever acquired in New York in 1999 were clinically misdiagnosed as influenza. Patients with influenza frequently present with various symptoms shared by many other viral infections. In the northern and southern hemispheres, these symptoms are more common in the winter months.Influenza virus is a single-stranded RNA virus, divided into type A, B, and C where structurally and biologically similar but vary antigenically. It is family of Orthomyxoviridae. The most common prevailing influenza A subtypes that infect humans are H1N1 and H3N2. Each year, the trivalent vaccine used worldwide contains A strains from H1N1 and H3N2, along with an influenza B strain. Influenza virus infection occurs after transfer of respiratory secretions from an infected individual to a person who is immunologically susceptible. If not neutralized by secretory antibodies, the virus invades airway and respiratory tract cells. Once within host cells, cellular dysfunction and degeneration occur, along with viral replication and release of viral progeny. Systemic symptoms result from inflammatory mediators, similar to other viruses. Influenza A is generally more pathogenic than influenza B. Recently, mutation of influenza A virus cause the emergence of new strain of virus which cause specific influenza such as Birds flue (H5N1) and Swine flue or Novel H1N1.
Case:
A man of 40 year-old came to hospital complaining fever, headache, sore throat and myalgia since 4 days . He just come from Hong Kong about a week ago. He also had cough, and feeling very weak.

Lecture 29
Infection in children (DBD, Difteri, sepsis, Campak)
dr. Dwi Lingga, sp.A/ dr. W. Gustawan,Sp.A
Case 1
A boy, 6 years 6 months has come to our clinic with swelling and pain on the cheek under right ear since 2 days ago. He has fever since 4 days ago. He hasn’t coryza, cough and cold. His appetite was decrease. His friends on the school have the same complaint.

1. What is the close diagnosis of this case?
2. What is the differential diagnosis?
3. What is the laboratory support needed?
4. What is the therapy?
5. What are the complications of this case?

Case 2
A boy comes to my clinic with five days of fever as the chief complaint. He was currently 6 years and 10 months old and a first grade of elementary school student. Fever was speaking immediately and has resolved one day before the doctor visited. This morning the fever reappears, giving a pattern of saddle back fever, which is accompanied with headache, muscular pain, articular and vertebra pain, retro orbital pain, nausea, vomiting and skin rashes. The skin rash appeared at the beginning of the disease, but subsequently vanished without any marks. In physical examination, the child looked compos mentis, mildly ill with fever of 38.8 0C. Dermatological examination reveals skin rash, mainly on the legs, foot soles and palms, the pharynx was slightly hyperemic and there is no palpable enlarge lymph nodes on the neck. Auscultator finding of the heart and lungs were within normal limits. Abdominal examination revealed epigastrial and right upper quadrant tenderness on palpation. There was no liver enlargement. No significant finding existed on the extremities, except for the positive tourniquets test.
1. What is the close diagnosis of this case?
2. What is the differential diagnosis?
3. What is the laboratory support needed?
4. What is the therapy?
5. What are the complications of this case?

Case 3
A girl, 2 years, comes to clinic with fever and rash as the chief complaint. Fever was appear from 5 days ago and rash appear since yesterday, which is accompanied with headache, cough, muscular pain, nausea, vomiting and red of her eyes. The rash phase is accompanied by high fever. The macular rash begins on the head (above the hairline) and spreads over of the body in 24 hours in a descending fashion.
1. What is the close diagnosis of this case?
2. What is the differential diagnosis?
3. What is the laboratory support needed?
4. What is the therapy?
5. What are the complications of this case?
Case 4
A boy, 3 years, comes to emergency department with unconsciousness since 2 hours ago. This complaint suddenly occurs when his mother talk to him. He is no response to talk, no move, and his eye look opened. He had fever since 5 days ago and still high until now. His temperature was unstable, it was decrease after drink parasetamol, and increase again few hour after that. The earliest symptoms are weakness, nausea or abdominal pain, and headache.
1. What is the differential diagnosis?
2. What is the other data needed to complete this case?
3. What is the laboratory support needed?
4. What is the therapy?
5. What are the complications of this case?

Lecture 30
Zoonosis Infection (Rabies, Leptospirosis, Listeriosis)
Prof.Dr. dr. Raka Sudewi, Sp.S (K)
dr. Sri Budayanti, Sp.MK
Infections in central nervous system have certain unique characteristics. First, they occur within an anatomic closed space. Secondly, the natural history of illnesses due to CNS infection often differs strikingly from that of those due to infection at other sites, even when caused by the same organism. Thirdly, many CNS infections cause high mortality the patients survives, serious sequelae after resolution of the acute infections.
There are four cardinal manifestation of NS infection are: fever, headache, alteration of mental status, and focal neurologic signs. Sometimes, these signs can be found in noninfectious CNS syndromes. The time course of disease is especially important in the evaluation of disease affecting the CNS. The date of onset, temporal relationship to presdiposing factors, rate of progression, time to reach the peak of severity, time needed to respond to treatment, and rate of resolution are all highly informative.
Infections of CNS can be caused by bacteria (pyrogenic infections), fungal, spirochetal, parasitic, and sarcoid. Pyrogenic infections of CNS such as bacterial meningitis, septic thromboplebitis, brain abscess, epidural abscess, and subdural empyema. The granulomatous infections of CNS such as tuberculosis, syphilis, and other spirochetal infections, and fungal infections.
Case 1
A 27 year-old man, Balinese, Hindu with unconciousness in emergency room Sanglah Hospital. From his family told that it was convulsion at least for 3 hours before arrived in hospital. From physical examination, axillary temperature 39,50C.

Learning Task:
12. Define and describe others symptoms related to the patients that should be asked to his family
13. Describe physical examination to support diagnosis of this patient.
14. What is possibly diagnosis of this patient?
15. Describe differential diagnosis of this case
16. Describe laboratory and other examination to support the diagnosis
17. Describe management of this patient
18. Describe how to explain to his family about prognosis of patient`s disease

Self assessment:
10. Describe about:
a. Meningitis
b. Encephalitis
c. Meningoencephalitis
d. Myelitis
e. Cerebral abscess
11. Explain pathogenesis of bacterial meningitis
12. Describe and interpret cerebrospinal fluid (CSF) examination in bacterial meningitis, viral meningitis, tuberculous meningitis, and streptococcal meningitis.
13. Define signs and symptoms of:
a. Meningitis
b. Cerebral abscess
c. Acute Anterior Poliomyelitis
d. AIDS Dementia Complex
e. Cerebral cysticercosis
14. Differentiate clinical sign and symptoms of bacterial meningitis, viral meningitis, tuberculous meningitis, and streptococcal meningitis
15. Define management of these patients:
a. Herpes Simplex Encephalitis
b. Tuberculous meningitis
c. Cerebral abscess
16. Define prognosis of:
a. Acute anterior poliomyelitis
b. Tuberculous meningitis
c. Cerebral abscess
17. Describe kinds or types of neurosyphilis
18. Describe about tabes dorsalis

Lecture 31
Principles of Fungal Infection (Morphology of Fungal)
dr. Luh Ariwati
Abstract :

Fungi are eukaryotic micro-organism, have a nucleus containing their DNA and a RNA nucleolus, and cytoplasma. Surrounding them is plasmalemma which containing ergosterol and out side plasmalemma is a rigid cell wall. Fungi do not contain chlorophyl and cannot synthesize macro molecules from carbon dioxide and energy derived from light rays, therefore all fungi lead a heterotrophic existence in nature as saprobes, commensals or parasites.
Fungi can be divided into two basic morphologic form: yeast and hyphae.
Yeast are unicellular and reproduce asexually by budding and most fungi have branching, threadlike tubular filaments called hyphae. Dimorphic fungi exist in both form. All fungi reproduce by asexual processes and most can reproduce by sexual mechanism.
The fungi contribute to food spoilage, destroy textile, etc. As saprobe, they share with bacteria in the decay of complex plant and animal remains in the soil. Fungi used in production of antibiotics, products of fermentation such as beverages, soy sauce etc. Fungi are free living and abundant in nature and a few live in normal flora of humans. Thousands of species have been known, but less than 100 are cause diseases in humans. The effects of fungi on humans are numerous such as mycotoxicosis, hypersensitivity and colonization of fungi with resultant diseases.
Humans have good barriers against fungal infection such as intact skin, mucosal surfaces, saliva, normal bacterial flora etc. Healthy, immunocompetent people have a high innate resistant to fungi even though they are constantly exposed to the propagules of fungi. Infections and diseases occur when there are disruptions in the protection barrier of skin and mucus membrane or defect in immunity system. The characteristic of fungal pathogens categorized into groups according to tissue that they colonize: superficial, cutaneous, subcutaneous and systemic mycosis. Fungal infections that occur only because of compromising situations are categorized as opportunistic mycosis.
Learning task:

1. Describe the structure of fungi
2. Explain terms used in medical mycology : yeast, hyphae, mycelium and dimorphic fungi.
3. Describe the mechanisms of fungal pathogenesis
4. Describe the effect (medical importance) of fungi on humans
5. Describe the laboratory diagnosis of fungal diseases
Lecture 32:
superficial fungal Infections (Tinea, Tinea versikolor, kadidiasis mukokutaneous)
Prof. M. Swastika Adiguna
Male 35 years old came to Dermatology Clinic with chief complain itching in the sites of neck, upper, lower extremitas, trunk, and inner surfaces of the thigh especially during the hot climate. It began as a small erythematous and scaling or vesicular and crusted patch that spreads peripherally and partly clear in the centre. These lesion may be slightly elevated particularly at the border, where they more inflamed and scaly.

1. Please explore another history to complete anamnesis
2. What kind of clinical examination will you do?
3. What kind of laboratory examination will you do.
4. What was the diagnosis of this patient?
5. Describe your planning therapy for this patient.
6. Describe your planning education for this patient.

Self assessment:
1. What in the definition of dermatophytosis (tinea or ring worm)
2. Please, describe the fungi of dermatophytes
3. what is the differential diagnosis of dermatophytosis

Please describe the antifungal therapy

Lecture 33
Deep Fungal Infection
Oleh:
Prof.Dr.dr Tuti Parwati,Sp.PD

Abstract

Fungal infections have become increasingly frequent especially in immune compromised host such as AIDS, cancer patients, organ transplantation , and also as a consequent of the availability of advanced medical technology which allow to do more invasive treatment using more invasive instruments. Systemic fungal infections (SFI) or invasive fungal infection are a significant cause of morbidity and mortality among immune compromised patients, such as HIV-infected individuals, cancer patients, neonates and patients in the intensive care unit.
The infections considered as nosocomial infections in the hospital for patients who have risk factors such as immune compromised patients. The aetiology are : Predominant fungi : Candida (C): such as C. Albicans, C. glabrata, C. tropicalis and C.parapsilopsis, Aspergillus spp.and Cryptococcus spp., Emerging fungi : Fusarium spp., and Rhizopus spp. and Endemic fungi : Histoplasma capsulatum, Blastomyces dermatitidis and Coccidioides immitis

Clinical Diagnosis: There is no specific sign and symptoms of systemic fungal infection. That is why suspected clinical diagnosis of systemic fungal infection is frequently late. Its resemble bacterial infections, such as severe sepsis, septic shock and multi organ failure. Alertness to this infection will comes late though sign and symptoms appear early. In many cases the diagnosis was done per exlusionem. Diagnosis should be considered in patient with risk factors has the signs of systemic infection despite adequate antibiotics.
Risk Factors : Patients at the Intensive Care Unit (ICU), Colonization of skin and mucous membranes with Candida, Alteration of natural host barriers (wounds, surgery), The colonized Candida might enter the blood stream when microbes balance disturbed by antibiotics and the barrier altered, eg. Indwelling central/peripheral catheter, Neutropenia (hematology disorders), Malignancy, Post chemo/radiation therapy, Organ Transplant patients, HIV infection.
Portal entry : Gastro Intestinal tract, skin, urogenital tract, Catheter related
Case study:
Female 65 year-old consulted from a private hospital with chief complain : fever since 5 days ago. Other complain: coughing -7 days, has been treated with AB injection, improved , but worsening in the last 2 days. History of chronic diarrhoea, but not now. Loss of appetite and Slight odinophagia. Physical examination : decreased of consciousness, high fever (39,8 C), BP: 100/60 mm Hg, Pulse 108/min, RR 24/min. Heart : WNL, Ronchi +/+
Learning Task
What is DD of this patients?
Chest X ray : infiltrates on both middle and lower lung, increased hilar marking and emphysematous lung. Lab. Test : CBC : Hb 7,2 g/dl, PLT 140, TLC 0,7 x 103 /ml, WBC 4,5 x 1000/ml, Other physical examination revealed : oral mucosa !! , tounge : coated.
What lab test do you suggest ?

Lecture 34
Treatment of Fungal Infection (PK/PD)
dr.I B.Ngurah, M.For/dr. wiwiek Indrayani, M.Kes
Abstract

Chemotherapy that are used as antifungal agents difficult to treat fungal infection particularly in the immunocompromised or neutropenic patient. Drugs for systemic fungal infections are amphotericin B, fluocytosine, and azole antifungal agents. Systemic drugs for superficial fungal infections are griseofulvin, terbinafine, and azoles. Topical drugs for superficial fungal infections are nystatin, miconazole, clotrimazole, haloprogin, tolnafnate, and undecylenic acid. Only few drugs are available for tretament of systemic fungal infections. Ergosterol is a sterol that is unique to the fungal cell membrane. The predominant sterol of human cells is cholesterol.

A 25-year old woman with she feel itchy since 2 weeks ago and changes brown nail colour. The physician diagnosed as dermatophytes of the nail.
1. What kind of antifungal the best to be used.
2. How is the mechanism of action of the drug?
3. Describe the pharmacokinetic of the drug
4. What will be happened if the drug is given concomitanly with coumarin?

Self assessment:
1. List the systemic antifungals for systemic fungal infections and superficial fungal infections
2. List the topical drugs for superficial fungal infections
3. Explain the mechanism of action systemic antifungals and superficial antifungals
4. Explain the pharmacokinetics of amphotericin B, fluocytosine, fluconazole, itraconazole, ketokonazole, griseofulvin, and terbinafine.
5. describe the clinical uses of systemic antifungals and superficialis antifungals.
6. Describe the toxic effects of systemic antifungal and superficial antifungals.
Lecture 35
Helminthes Infection

dr. I Made Sudarmaja, M.Kes

In the National Standard of Competency of Undergraduate Medical Education, the core content of curriculum related to helminthic infections has been identified. This core must be well mastered by the students. Although hundred or more species are identified as a helminthes of medical importance, however, only a few of those are considered as core. The core species are: (1) Ascaris lumbricoides (2) Trichiuris trichiura, (3) Hookworm spp, (4) Strongyloides stercoralis; (5) Enterobius vermicularis; (6) Species causing cutaneous larva migrant; (7) Filaria spp; (8) Schistosoma spp; and (8) Taenia spp. For those species, the fourth level of student’s competency has been formulated, in which students must be able to perform clinical diagnosis based on physical examination and other additional examinations (such as simple laboratory and X ray examination). Instead of just making clinical diagnosis, the students should also be able to manage all related problems completely and individually. The students must therefore be familiar with the life cycle, epidemiology, pathogenesis, clinical manifestations, diagnosis as well as treatment procedures of all the above mentioned helminthic infections, otherwise the four level of student competency can not be achieved.

Learning Tasks
1. Differentiate the morphological characteristics of the class Nematode, Cestode and Trematode
2. Describe their life cycles and identify each of their infective stages
3. Define their epidemiological standpoints and list the factors that are closely related to the transmission of the infections
4. Identify their stages of development which are useful from the viewpoint of diagnosis purpose and try to figure their morphological characteristics
5. Describe their pathogenesis and clinical manifestations
6. Manage appropriately the diagnosis, treatment, and prevention measures.

Self evaluation
Ni Made Artini, a previously healthy 26 year old female medical student of the Faculty of Medicine University of Uadayana was admitted to the emergency room of Sanglah Hospital due to seizure. She was born in the Village of Ketewel, Sub-district of Sukawati, district of Gianyar. and attended primary and secondary high school at the same village. Her history was otherwise unremarkable, although she reported that she had been suffering from severe headache for a couple of months. Her neurological examination revealed no clear abnormalities. However, a computerized tomography scan (CT scan) of the head showed multiple calcified lesions in both cerebral hemispheres.
Questions
1. If it is a disease caused by parasitic infection, what parasite would you consider to be responsible for the patient’s condition?
2. How does man acquire this infection?
3. What are the factors that may predispose to this infection?
4. How would you diagnose this patient properly?
5. How would you treat this patient appropriately?

Lecture 37
Filariasis
dr. K. Agus Somia, Sp.PD
Lymphatic filariasis is the commonest lymphatic system infection that is occurred in community especially in eastern part of Indonesia. Lymphatic filariasis, onchocerciasis, and loiasis are the three most important filarial infections of humans. Lymphatic filariasis is caused by parasite transmitted by biting arthropods (mosquitoes). Almost 90% are caused by Wuchereria bancrofti, whose only in human and most of the remainder are caused by Brugia malayi. The major vectors for W. bancrofti are culicine mosquitoes in most urban and semiurban areas, anopheline mosquitoes in the more rural areas of Africa and Aedes spp in mnay of the endemic Pasific island.
A-35-year-old woman complaints her leg is swelling. The swollen is getting worst and pain since 2 weeks ago. Half of his swollen leg looks redness and felt pain. The patient lives in Bali and she comes from Kupang. She has been like this before and it is the 3rd times. She gets fevers, fatique, and headache.

Learning task:
1. Define other things that should be found from history taking of this patient.
2. Describe physical examination to diagnose this patient
3. Define other examination/ investigation to support the diagnosis
4. Define the invasive treatment should be done to this patient
5. Describe management/ treatment of this patient

Self assessment:

Choose RIGHT or WRONG of these statement
1. The possibly diagnosis is limfangitis
2. The most possibly diagnosis is filariasis with inflammation
3. It needs cell blood count and thick smear examination
4. Lymphograpy examination showed obstruction, atresia, or dilatation can helps to diagnose this disease
5. Diethylcarbamazine 2-3 mg/kg, 3 times a day is given for 2-3 weeks.
Lecture 38
Dengue Viral Infection
dr. Made Susila Utama, Sp,PD

Abstract
Dengue fever/dengue hemorrhagic fever caused by dengue viruses (type 1,2,3 and 4), transmission from human to human is by the mosquito Aedes aegypti. Clinical spectrum of dengue viral infections are wide variation, from undifferentiated fever, dengue fever, dengue hemorrhagic fever and dengue shock syndrome. There is plasma leakage in dengue hemorrhagic fever, so differentiated with dengue fever.
Dengue fever should be treated supportively. Dengue hemorrhagic fever/dengue shock syndrome is life threatening and requires immediate evaluation of vital sign, hemoconcentration, dehydration, urine output, electrolit imbalance.

Reference
Halstead SB. Dengue fever/ Dengue Haemorrhagic fever. Powderly WG.(Ed). Infectious disease. Second ed. 2004. P. 1681-4

Dengue infection
Case:
A Male, 34 years old, Balinese, came to the Sanglah Hospital. The chief of complain was fever since 2 days ago, he also complain about headache, joint pain, rash on the skin. The neighbored was admitted in the hospital with DHF

Learning task:
1. What the some specific factor in the history and examination suggest the need for making diagnose
2. what the laboratory examination the need for this patients
3. what the management for this patients
Self assessments
1. describe the clinical spectrum of dengue infection
1. describe the pathogenesis of DHF
2. describe the management approach for the dengue infections
References
1. Halstead SB. Dengue fever/ Dengue Haemorrhagic fever. Powderly WG.(Ed). Infectious disease. Second ed. 2004. P. 1681-4

Lecture 39
Treatment of Helminthes Infection (PK/PD)

Dr.dr. B.K.Satriyasa,M.Rrepro

Anthelmintic
Helminthic infections still as a problem on the world. There are many of anthelminthic drugs that can be used to eradicate the parasite in the intestinal tract or in the tissue of the body. Most anthelminthics in use today are active against specific parasites, and some are toxic. Therefore parasites must be identified before treatment is started. In this topic will be introduced the drugs for anthelmintic so after this program all of student be able to choose anthelmintic drugs for the patients in rationally.

Anthelmintic
1. Discuss anthelmintic drugs that use to eradicate or reduce the number of helminthic parasites in the intestinal tract or tissue of the body
2. Discuss drugs of choice for the especially parasite and side effect of that drugs of the body
3. Discuss the mechanism of action of anthelmintic drugs that you know
4. Discuss the principle of treatment of patient according to the parasite that will be eradicated
Self assessment:
1. Drug of choice for Ascaris lumbricoides is:
a. Pyrantel pamoate
b. Albendazole
c. Piperazine
d. Levamisole
e. Praziquantel

2. Drug of choice for cutaneus larva migran is:
a. Pyrantel pamoate
b. Albendazole
c. Piperazine
d. Thiabendazole
e. Praziquantel

3. A patient suffered from taenia solium. Drug that can be used as drug of choice of this worm is:
a. Pyrantel pamoate
b. Albendazole
c. Piperazine
d. Levamisole
e. Praziquantel
Lecture 40
Overview of Puerperal Infection
dr. I Nyoman Bayu Mahendra,Sp.OG
1. Abstract:
Puerperal Infection – is a general term used to describe any bacterial infection of the genital tract after delivery along with preeclampsia and obstetrical hemorrhage puerperal infection formed the lethal triad of causes of maternal deaths because of effective antimicrobials, maternal deaths from infection have become uncommon

2. Learning task:
2.1. To understand definition of puerperial infection.
2.2. To understand definition and management of puerperial fever
2.3. To understand definition, predisposing factors, bacteriology and management of uterine infection.
2.4. To understand the complication of pelvic infection
2.5. To understand the pathogenesis, clinical course and treatment of infections of perineum, vagina and cervix.
2.6. To understand the toxic shock syndrome
2.7. To understand the prevention of puerperial infection

3. Case
A 25 year old woman (G1P1) presents to your clinic eight days postpartum, complaining of a temperature of at least 38.5 degrees Celsius over the past 3 days, and a foul-smelling vaginal discharge. She is in otherwise good health, and her baby, who was born by emergency Caesarian section in a rural clinic, is doing well. Physical examination of your patient reveals an oral temperature of 38.6 degrees Celsius, a clean and non-weeping abdominal wound, and pain of palpation of her uterus.
What is the differential diagnosis of the site of infection? What was most likely the source of this infection? What features of your patient’s history and delivery put her at higher risk for puerperal infection?
4. Self assessment:
1. How the student understand about definition, risk factors, pathogenesis, complication and management of puerperial infection?
2. How the student understand the definition of puerperial fever and the deferential diagnosis of puerperial fever?
3. How the student understand the prevention of puerperial fever?
Lecture 41
Overview of Sexual Transmitted Diseases
dr. A.A.G.P. Wiraguna, Sp.KK

Case 1:
A 27-year-old man had single painless ulcer on his glans penis 3 year ago. This ulcers disappear without treatment. One year ago, he got married with a 23-year-old woman and now his wife is pregnant for 4 months. His wife complain of having vaginal discharge with itchy and odor. This man now has rash on whole body and mucopurulent urethral discharge, they already went to a venereologist. The result of laboratories examinations shows VDRL 1:64 and doctor referred this couple to go to the Department Dermato-Venereology Sanglah Hospital.

Learning task/ questions:
1. What other history you need to find out from these patients?
2. What laboratories examination needs to be done for this couple?
3. What is your diagnosis for this man?
4. What is your diagnosis for his wife?
5. What could possibly happen with her pregnancy?
6. What could possibly happen with their baby?
7. How would you treat this man, his wife, and their baby based on their conditions?

Self assessment:
1. Describe the stages clinical manifestation of syphilis.
2. Describe the causes of genital ulceration.
3. Describe microorganism pathologic of urethral discharge.
4. Describe the risk factors of sexually transmitted infection patient
5. How to prevent management of STI.
6. Describe microorganism pathologic of vaginal discharge and the clinical manifestation
7. How to treat clinical manifestation of vaginal discharge, the dose, and for how long.

REFFRENCES

1. Spicer WJ. (200): Clinical Bacteriology, Mycology, and Parasitology, An Illustrated Colour Text. Churchill Livingstone, 14-19.
2. Clinical Bacteriology, Mycology and Parasitology : An Illustrated Colour Text. W. John Spicer. Churchill-Livingstone
3. Brooks et al. pathogenesis and Control of Viral Diseases. In: Lange Medical Microbiology. 23rd ed. McGraw Hill. International Ed. 2004. p. 394 – 413.(Principles of Viral Infection)
4. Levinson et al. Lange Medical Microbiology & immunology. Examination & Board review. 8th ed. McGraw Hill. International Ed. 2004. p. 186 – 220, 259-269, 244-250.(Principles of Viral Infection)
5. Roitt. I., Brostoff.J., Male. D. Immunology
6. Durack DT, Whitley RJ, and Scheld WM. Introduction: Approach to the Patient with Central nervous System Infection. In : Scheld WM, Whitley RJ, Durack DT, (eds). Infections of The Central Nervous System. Raven Press. New York. 1991 p. 1-4.
7. Victor M and ropper AH. Infections of the Nervous System (Bacterial, Fungal, spirochetal, Parasitic) and Sarcoid. In: Adams and Victors’ principles of the Neurology. 7th ed. McGraw-Hill. New York/Toronto. P. 734-780.
8. Ottesen EA. Filariasis.in Powderly WG. (ed). Infectious Diseases. 2nd ed. P.1607-13.
9. Ringsrud KM, Linne JJ. Urinalysis and Body Fluids A Colortext and Atlas. 1st ed. Mosby. St. Louis/ Toronto. 1995. p. 95-206.
10. Burtis CA. Tietz Fundamentals of Clinical Chemistry. 4th ed. WB Saunders Company. Philadelphia/ Tokyo. 1996. p. 558-561.
11. Simmons A. Statland BE. Hematology A combined Theoritical and technical Approach. 2nd ed. Buuterworth-Heinemann. Boston/ Singapore. 1997. p. 129-142.
12. Stites DP, Terr AI, Parslow TG. Medical Immunology. 9th ed. Prentice-Hall International. 1997. p. 264-269.
13. Kasper DL, Fauci AS, Longo DL, Braunwald E, et al. Harrison’s Principles of Internal Medicine. 16th ed. Vol 1. McGraw-Hill. New York/ Toronto. 2005. p. 981-1103.
14. Sutton D. Radiology and Imaging for Medical Students. Churchill Livingstone. 7th ed. 1998.
15. Grainger RG and Allison DJ. Diagnostic Radiology. Churchill Livingstone. 2nd ed. 1993.
16. McAdam AJ and Kumar S. Infectious Diseases in Kumar V, Contran RS and Robbins SL, Robbins Basic Pathology. P. 344-398.
17. Andrews. Diseases of The Skin. 9th ed.
18. Bryceson A. Leprosy. 3rd ed.
19. King & Nicole. Sexually Transmitted Diseases. 2003
20. Holmes KK, Spiring PF, Mirdh P. Sexually Transmitted Diseases. 3rd ed. McGraw-Hill. 1999.
21. McMillan A, Young H, Ogilvie MM, Scott GR. Clinical Practice in Sexually Transmissible Infection. Saunders. 2002.
22. Braunwald’s Heart Disease. Subacute bacterial endocarditis.

~ CURRICULUM MAP ~
Smstr Program or curriculum blocks 10 Senior Clerkship 9 Senior Clerkship 8 Senior clerkship 7 Medical Emergency
(3 weeks)

BCS (1 weeks) Special Topic:
-Travel medicine
(2 weeks) Elective Study III
(6 weeks) Clinic Orientation (Clerkship)
(6 weeks) 6 The Respiratory System and Disorders
(4 weeks)

BCS (1 weeks) The Cardiovascular System and Disorders
(4 weeks)

BCS (1 weeks) The Urinary System and Disorders
(3 weeks)
BCS (1 weeks) The Reproductive System and Disorders
(3 weeks)
BCS (1 weeks)
5 Elective Study II
(1 weeks) Alimentary
& hepato-
biliary systems
& disorders
(4 Weeks)

BCS (1 weeks) The Endocrine System, Metabolism and Disorders
(4 weeks)

BCS (1 weeks)
Clinical Nutrition and Disorders
(2 weeks)

BCS (1 weeks) Special Topic :
– Palliative medicine
-Compleme
ntary & Alternative Medicine
– Forensic
(3 weeks) Elective Study II
(1 weeks)
4 Musculoskeletal
system &
connective
tissue disorders
(4 weeks)

BCS (1 weeks) Neuroscience
and
neurological
disorders
(4 weeks)

BCS (1 weeks) Behavior Change
and disorders
(4 weeks)

BCS(1 weeks) The Visual
system &
disorders
(2 weeks)

BCS
(1 weeks) 3 Hematologic
system & disor-
ders & clinical
oncology
(4 weeks)

BCS (1 weeks) Immune
system &
disorders
(2 weeks)
BCS(1 weeks) Infection
& infectious
diseases
(5 weeks)
BCS (1 weeks) The skin & hearing system
& disorders
(3 weeks)
BCS(1 weeks) 2 Medical Professionalism
(2 weeks)

BCS (1 weeks) Evidence-based Medical Practice
(2 weeks)

Health System-based Practice
(3 weeks)

BCS (1 weeks) Community-based practice
(4 weeks) Special Topic
– – Ergonomi
– – Geriatri
(2 weeks) Elective Study I
(2 weeks) 1 Studium
Generale and Humaniora
(3 weeks) Medical
communication
(3 weeks)
BCS (1 weeks) The cell
as bioche-
mical machinery
(3 weeks)

BCS(1 weeks) Growth
&
development
(4 weeks)

BCS: (1 weeks) Pendidikan Pancasila & Kewarganegaraan (3 weeks)

Study Guide Infection and Infectious Diseases

1
Faculty of Medicine UNUD,MEU