Study guide Infection Semester III 10 Nopember 2015

Table of contents ………..……….

1

Introduction ………. 2

Curriculum ……… 3

Block Team ………... 7

Facilitators ……… 9

Time Table Regular Class ……… 10

Time Table English Class ……….. 10

Meeting of Students representatives ……… 20

Meeting of The Facilitators………. 20

Assessment method ………... 20

Learning Program ……….. 25

 Lecture ………. 25

 Learning Task and Self Assessment……….25

Curriculum Mapping ………... 58

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 10th _of November 2015 as shown in the Time Table. The final examination will be conducted on 28th of Desember 2015. 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.

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 managepuerperial 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

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

1 Prof. Dr. dr. Tuti Parwati Merati, SpPD, _{KPTI (Coordinator)} Internal Medicine 08123806626 2 Dr. dr. Bagus Komang Satriyasa, _{M.Repro (Secretary)} Pharmacology 087777790064

081237166686 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. Surya candr, Mkes Pharmacology 81337991177 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. Surya Candra, M.Kes Pharmacology 081337991177 14. _{Dr. dr. Bagus Komang Satriyasa, M.Repro Pharmacology}

087777790064 15. _{dr. Kadek Swastika, M.Kes Parasitology}

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, SpTHT THT 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.Bayu Mehendra 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.

FACILITATORS

(REGULAR CLASS)

N

O

NAME

GROUP

DEPT

PHONE

VENUE

1 dr. Sri Laksminingsih Sp. Rad 1 Radiology _08164745561 3nd floor: R.3.09 2 dr. Ida Bagus Sutha, Sp.P-K 2 Pulmonology _08123990362 3nd floor:

R.3.10 3 dr. Putu Andrika, Sp.PD-KIC 3 Interna 08123989192 3nd floor:

R.3.11 4 dr. I Gusti Ngurah Purna Putra,

Sp.S (K)

4 Neurology _08123915763 3nd floor: R.3.12 5 dr. I Gede Eka Wiratnaya, ,

Sp.OT

5 Orthopedy _081338493832 3nd floor: R.3.13 6 dr. I Ketut Wibawa Nada, Sp.An 6 Anasthesi

087860602995 3nd floor:_R.3.14 7 dr.Kumara Tini, Sp.S 7 Neurology 081238701081 3nd floor: R.3.15 8 Dr.dr. I B G Fajar Manuaba,

Sp.OG, MARS

8 Obgyn 081558101719 3nd floor: R.3.16 9 dr. I Made Gotra, Sp.PA 9 Anatomy

Pathology

08123819233 3nd floor: R.3.17 10 dr. I Ketut Suanda, Sp.THT- KL 10 ENT 081337788377 3nd floor:

R.3.19

FACILITATORS (ENGLISH CLASS)

NO NAME GROUP DEPT PHONE VENUE

1 dr. Pande Kurniari, Sp.PD 1 Interna 082146179796 3nd floor: R.3.09 2 Dr.dr. Ni Nyoman Sri Budayanti,

Sp.MK(K)

2 Microbiology 08553711398 3nd floor: R.3.10 3 Dr. dr. Bagus Komang Satriyasa,

M.Repro

3 Pharmacology 081805368922 3nd floor: R.3.11 4 dr. I Gusti Ayu Agung Elis Indira , 4 Dermato- 081338718384 3nd floor:

Sp.PK Pathology R.3.14 7 dr. Ni Nengah Dwi Fatmawati ,

Sp.MK, Ph.D

7 Microbiology 087862200814 3nd floor: R.3.15 8 Dr. dr. I Wayan Putu Sutirta

Yasa, M.Si

8 Clinical Pathology

08123953344 3nd floor: R.3.16 9 Dr.dr. I Made Jawi, M.Kes 9 Pharmacology 08179787972 3nd floor:

R.3.17 10 dr. Ketut Rai Purnami, Sp.PD 10 Interna 0818350703 3nd floor:

Regular Class English Class 1 Tuesday Nov. 10th ₁₅

08.00-08.30 09.00-09.30 Lecture 1

Introduction to the block (Agent ,HostEnvironment, 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

bacterialclassification 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

Wednesday Nov. 11th ₁₅

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 RoomClass dr. Agus Hendrayana, M.Ked 14.00-15.00 15.00-16.00 Plenary Class

Room dr. Agus Hendrayana, M.Ked 3

Thursday Nov. 12th₁₅

08.00-08.30 09.00-093.0 Lecture 4

Viral classification Lecture RoomClass 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 Friday Nov. 13th₁₅

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 Dr.dr Made Sudarmaja, 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 12.30-14.00 10.00-11.30 Student

Project dr.Agus somiaSp.PD Dr.dr Made Sudarmaja, M.Kes 14.00-15.00 15.00-16.00 Plenary Class room dr.Agus

somiaSp.PD Dr.dr Made Sudarmaja, M.Kes 5 Monday Nov. 16th₁₅

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

Tuesday Nov. 17th₁₅

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.Repr o

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.Repr o

14.00-15.00 15.00-16.00 Plenary

Session Class room Dr.dr. B.K. Satriyasa,M.Repr o

7 Wednesday

Nov. 18th₁₅

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 adiTarini, 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

Thursday Nov. 19th₁₅

08.00-08.30 09.00-093.0 Lecture 12: Response 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. I G A Artini 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

Friday Nov. 20th₁₅

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 Monday Nov. 23th₁₅

08.00-08.30 09.00-093.0 Lecture 16: Infection of Mycobacterium (Leprosy)

Lecture Class room dr. Darmada, Sp.KK/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. Surya candra, tropika, 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. Darmada, Sp.KK/dr. Dharma putra, Sp.KK

dr. Surya candra, tropika, M.Kes 14.00-15.00 15.00-16.00 Plenary Class room dr. Darmada,

Sp.KK/dr. Dharma putra, Sp.KK

dr. Surya candra, tropika, M.Kes 11

Tuesday Nov. 24th₁₅

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 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

Wednesday Nov. 25th₁₅

08.00-08.30 09.00-093.0 Lecture 20 Antiseptic and disinfectant

Lecture Class room Dr.dr.B.K. Satriyasa,M.Repr o

08.30-09.00 09.30-10.00 Lecture 21

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

Thursday Nov. 26th₁₅

08.00-09.00 09.00-10.00 Lecture 22

Protozoa Infection I (Malaria, Amoebiasis, Leismaniasis,Tripano somiasis,Toxoplasmo sis, 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 Friday Nov. 27th₁₅

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/dr. Dewi Dian, Sp.PD 09.00-10.30 12.00-13.30 Individual

10.30-12.00 13.30-15.00 Small group

discussion RoomDisc. Facilitator 12.30-14.00 10.00-11.30 Student

Project Class room dr Yuli Gayatri, Sp.PD dr Agus

Somia,Sp.PD/dr. Dewi Dian, Sp.PD 14.00-15.00 15.00-16.00 Plenary Class room dr Yuli Gayatri,

Sp.PD dr Agus

Somia,Sp.PD/dr. Dewi Dian Sp.PD 15

Monday Nov.30th₁₅

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 RoomDisc. 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 Tuesday Des. 1st₁₅

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 RoomDisc. 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 Des. 3th₁₅

08.00-08.30 09.00-093.0 Lecture29

Infection in children (DBD, Difteri, sepsis, Campak, Tetanus, Pertusis)

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. 4th₁₅

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.Dewi Dian, Sp.PD

09.00-10.30 12.00-13.30 Individual learning 10.30-12.00 13.30-15.00 Small group

discussion RoomDisc. Facilitator 12.30-14.00 10.00-11.30 Student

Project

Class room Prof.Dr. dr. Raka Sudewi, Sp.S (K) Dr.Dewi Dian, Sp.PD

14.00-15.00 15.00-16.00 Plenary Class room Prof.Dr. dr. Raka Sudewi, Sp.S (K) Dr.Dewi Dian, Sp.PD

19 Monday Des. 7th₁₅

08.00-030.00 09.00-09.30 Lecture 32

Principles of Fungal Infection (Morphology of Fungal)

Lecture Class room Dr.dr. I Made Sudarmaja, M.Kes/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

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. I Made Sudarmaja, M.Kes/dr. Luh Ariwati

Prof. M. Swastika Adiguna

14.00-15.00 15.00-16.00 Plenary Class room Dr.dr. I Made Sudarmaja, M.Kes/dr. Luh Ariwati

Prof. M. Swastika Adiguna

20 Tuesday Des. 8th₁₅

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. Surya candra trapika, M.kes 09.00-10.30 12.00-13.30 Individual

learning 10.30-12.00 13.30-15.00 Small group

discussion RoomDisc. Facilitator 12.30-14.00 10.00-11.30 Student

Project Class room Prof.Dr.dr Tuti Parwati,Sp.PD dr. Surya candra trapika, M.kes 14.00-15.00 15.00-16.00 Plenary Class room Prof.Dr.dr Tuti

Parwati,Sp.PD dr. Surya candra trapika, M.kes 21

Wednesday Des. 9th₁₅

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 RoomDisc. Facilitator 12.30-14.00 10.00-11.30 Student

Project Class room Dr.dr. I Made Sudarmaja, M.Kes dr. Kadek Swastika,M.Kes 14.00-15.00 15.00-16.00 Plenary Class room Dr. dr. I Made

Sudarmaja, M.Kes/Staff 22 08.00-08.30 09.00-09.30 Lecture 38Filariasis Lecture Class room dr. K. Agus Somia, Sp.PD

Thursday

Des. 10th₁₅ 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 RoomDisc. 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

Friday Des. 11th₁₅

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 Monday Des. 14th₁₅

08.00-09.00 09.00-10.00 Lecture 41

Overview of Puerperal Infection

Lecture Class room dr. Hariyasa Sanjaya,Sp.OG

09.00-10.30 12.00-13.30 Individual learning 10.30-12.00 13.30-15.00 Small group

discussion RoomDisc. Facilitator 12.30-14.00 10.00-11.30 Student

Project

Class room dr. Hariyasa Sanjaya,Sp.OG 14.00-15.00 15.00-16.00 Plenary

Session Class room dr. Hariyasa Sanjaya,Sp.OG 25

Tuesday Des. 15th₁₅

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 RoomDisc. 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

Wednesday Des. 16th₁₅

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 Thursday Des. 17th₁₅

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 Friday Des. 18th₁₅

08.00-15.00 09.00-16.00 Practice 3 :

Laboratory Diagnosis of Clinical Pathology

Laboratory Dr Nyoman Mahartini SpPK

29 Monday Des. 21th₁₅

08.00-15.00 09.00-16.00 Practice 4 : Laboratory Examination of parasitic infectious

dr. Kadek Swastika, M.Kes

30 Tuesday Des. 22th₁₅

08.00-15.00 09.00-16.00 Practice 5 : Laboratory Examination of parasitic infectious ()

dr. Kadek Swastika, M.Kes

32 Wednesday

Des. 23th₁₅ Pre-evaluation Break BLOCK TEAM

33 Monday

Des. 28th₁₅ Evaluation 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

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 2015

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

5. Treatment and prevention of staph infection

2 H F M D

1. Etiopathogenesis of infection 2. clinical symptoms and sign ofs

infection

3. management of infection 4. complication of infection

2

3 J E

1. etiopathogenesis

2. Clincal Symtom and sign 3. management

4. Complication

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

Complication 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

- seasonal influenza

- swine influenza

- Avian influenza

- Management

- Prevention 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: viral exanthema

Clinical manifestation

Diagnosis microbiology Management

28 Emerging and reemerging disease: Coronavirus (SARS)

(Hantavirus)

Clinical manifestation

Diagnosis microbiology Management

30 Healthcare assosiated infections (HAIs) 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

Oleh:

Prof. Dr. dr. Tuti Parwati Merati, SpPD, KPTI

TRIGGER 1 (patogenesis dan patofisiologi infeksi ) :

Seorang laki-laki usia 20 tahun datang ke dokter dengan keluhan panas badan sejak 1 mg tidak turun-turun dan terasa sakit pada paha saat bergerak. Setelah diperiksa oleh dokter trnyata didapatkan pembengkakan pada paha bagian dalam yang terlihat kemerahan, teraba panas, dan nyeri saat ditekan. Setelah itu diberikan obat oleh dokter dan diminta untuk kembali setelah 3 hari. Pada pemeriksaan saat kontrol ditemukan warna kemerahan pada paha semakin meluas, semakin membengkak dan dibagian tengahnya terdapat tumpukan nanah. Setelah pemeriksaan disimpulkan penderita ini mengalami suatu abses. Tugas:

1. Jelaskan bagaimana perjalanan penyakit sampai terjadinya abses 2. Jelaskan proses terjadinya panas pada penderita infeksi

3. Jelaskan jenis-jenis mikrobial penyebab infeksi

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

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?

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

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

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

==

Lecture 7

Basic concept of Parasitic Infections

Oleh:

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

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

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

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

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

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

==

Oleh:dr. Ni Made Adi Tarini, Sp.MK

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

Lecture 12:

Respond Host against parasitic and clinical manifestation

dr. I Made Susila Utama,Sp.PD

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

Lecture 13

Treatment of parasitic infection (PK/PD)

dr. I G A Artini, 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

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

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.

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. Darmada, Sp.KK/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

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. Surya Candra Tropika, M.Kes

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

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 infectiousdiseases, the important ones are human demographics and behavior, industryand technology, economic development and land use, globalization andinternational travel, microbial adaptation and change, breakdown of publichealth 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 :

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 380_{C. 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.

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

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:

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 (400_{C), a rapid pulse} rate, and generalized sweating. Complete Blood Count was ordered and demonstrated intra erythrocyte organism.

 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 ofparasite 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

 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

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:

1. Define and describe others symptoms related to the patients that should be asked to this patient

2. Describe physical examination to support diagnosis of this patient. 3. What is possibly diagnosis of this patient?

4. Describe differential diagnosis of this case

5. Describe laboratory and other examination to support the diagnosis 6. Describe management of this patient

7. 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:

1. Explain pathogenesis of: a. Bacillare Dysentriae b. Typhoid fever

c. Cholera

d. Clostridium difficile associated diarrhea

2. Describe and interpret cerebrospinal fluid (CSF) examination in bacterial meningitis, viral meningitis, tuberculous meningitis, and streptococcal meningitis.

3. Define signs and symptoms of: a. Typhoid 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

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. Hariyasa Sanjaya,Sp.OG

1. Abstract:

Puerperal Infection – is a general term used to describe any bacterialinfection of the genital tract after deliveryalong with preeclampsia and obstetrical

hemorrhage puerperal infectionformed the lethal triad of causes of maternal deathsbecause of effective antimicrobials, maternal deaths from infection havebecome 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

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.

~ CURRICULUM MAP ~

Smstr

Program or curriculum blocks

10

Senior Clerkship

9

Senior Clerkship

8

Senior clerksh

_ip

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)

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.