Beruflich Dokumente
Kultur Dokumente
CONTENTS
Introduction .
Curriculum
Facilitators
10
10
20
20
20
Learning Program ..
25
Lecture .
25
57
Reference
58
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 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
PLANNERS TEAM
No
1
Name
Departement
Internal Medicine
Phone
08123806626
Pharmacology
08123687288
Internal Medicine
08123989353
Parasitology
08123953945
2
3
Pharmacology
081237166686
Microbiology
081338291965
Neurology
0816710244
Dermatology and
Venereology
081338044921
LECTURER
NO
2
3
4
NAME
Prof. Dr. dr. Tuti Parwati Merati, SpPD,
KPTI
Prof.Dr. dr. Raka Sudewi, Sp.S (K)
Prof.Dr.dr. I.B. Rai, SpP (K)
dr. Agus Somia, SpPD
10
11
12
13
8
9
DEPT
Internal Medicine
Neurology
Pulmonology
Internal Medicine
Dermatology &
Venereology
Dermatology &
Venereology
Dermatology &
Venereology
Child Health
Dermatology &
Venereology
Microbiology
PHONE
08123806626
0816710244
08123804579
08123989353
081338645288
08123828548
08155735977
08125684656/
08123848241
081338044921
Parasitology
Clinical Pathology
081338675344
08123662311
081337165577
Pharmacology
08123687288
14
Pharmacology
081237166686
15
Parasitology
08124649002
Parasitology
08113804500
17
Pharmacology
081338770650
18
Microbiology
08583711398
19
Parasitology
Internal Medicine
081392017107
16
20
08123815025
21
22
24
25
26
27
28
29
23
Microbiology
08123921590
ENT
08113809882
Pharmacology
081337991177
Microbiology
08123831710
Pharmacology
Obstetrics &
Gynecology
Microbiology
08179787972
081339550423
Parasitology
085338565783
dr.Made Sudarmaja,M.Kes
Parasitology
08123953945
08179747502
~ FACILITATORS ~
REGULAR CLASS
NO
1
2
3
4
5
6
7
8
9
10
11
12
NAME
dr. Made Widhi Asih, Sp.Rad
dr. Muliani , M Biomed
dr. Ni Gusti Ayu Putri Mayuni, S.Ked
dr. Nyoman Suryawati , M.Kes, Sp.KK
dr. Ni Luh Ariwati
dr. Ni Luh Putu Ratih Vibriyanti Karna,
Sp.KK
dr. Ni Made Adi Tarini, Sp.MK
dr. Ni Made Dewi Dian Sukmawati,
Sp.PD
dr. I G.A. Indah Ardani, Sp.KJ
dr. Ni Nengah Dwi Fatmawati ,
Sp.MK, Ph.D
dr. Ni Nyoman Margiani, Sp.Rad
dr. Ni Putu Sriwidyani , Sp.PA
ENGLISH CLASS
NO
NAME
1
2
3
4
5
6
7
8
9
10
11
12
GROUP
1
2
3
4
5
6
7
8
9
10
11
12
GROUP
1
2
3
4
5
6
7
8
9
10
11
12
DEPT
PHONE
Radiology
081916442626
Anatomy
08123930767
Andrology
081933113003
Dermatology
0817447279
Parasitology
08123662311
Dermatology
081337808844
Microbiology
081338675344
Interna
081805656501
Psychiatry
0361 8810404
Microbiology
087862200814
Radiology
081337401240
Anatomy
Pathology
081337115012
DEPT
PHONE
Pharmacology
081337991177
Clinical
Pathology
08155237937
Interna
08123837372
Clinical
Pathology
08123647413
Public Health
082140517310
Clinical
Pathology
08155735034
Pharmacology
081237166686
Anasthesi
08123661312/
08113800107
Interna
081805530196
Psychiatry
08123806397
Anatomy
08123921765
Anatomy
Pathology
085338565783
VENUE
3nd floor:
R.3.01
3nd floor:
R.3.02
3nd floor:
R.3.03
3nd floor:
R.3.04
3nd floor:
R.3.05
3nd floor:
R.3.06
3nd floor:
R.3.07
3nd floor:
R.3.08
3nd floor:
R.3.20
3nd floor:
R.3.21
3nd floor:
R.3.22
3nd floor:
R.3.23
VENUE
3nd floor:
R.3.01
3nd floor:
R.3.02
3nd floor:
R.3.03
3nd floor:
R.3.04
3nd floor:
R.3.05
3nd floor:
R.3.06
3nd floor:
R.3.07
3nd floor:
R.3.08
3nd floor:
R.3.20
3nd floor:
R.3.21
3nd floor:
R.3.22
3nd floor:
R.3.23
Topic
Time
Regular
Class
English
Class
08.00-08.30
09.00-09.30
08.30-09.00
09.30-10.00
09.00-10.30
12.00-13.30
10.30-12.00
13.30-15.00
12.30-14.00
10.00-11.30
14.00-15.00
15.00-16.00
08.00-09.00
09.00-10.00
09.00-10.30
12.00-13.30
10.30-12.00
13.30-15.00
12.30-14.00
10.00-11.30
14.00-15.00
15.00-16.00
08.00-08.30
09.00-093.0
Thursday
Nov. 13th14
08.30-09.00
09.30-10.00
09.00-10.30
12.00-13.30
10.30-12.00
13.30-15.00
12.30-14.00
10.00-11.30
14.00-15.00
15.00-16.00
08.00-08.30
09.00-093.0
1
Tuesday
Nov. 11th 14
2
Wednesday
Nov. 12th 14
Lecture 1
Introduction to the
block (Agent ,Host
Environment, and
infection
manifestation)
Lecture 2
bacterial
classification
Learning
situation
Introduction to
the Block
Disc. Room
Class room
Lecture
Class room
Lecture
Lecture
Individual
Learning
Small group
discussion
Student
Project
Plenary
Lecture 6
Manifestation of virus
Plenary
Session
Individual
learning
Small Group
Discussion
Student
Project
Plenary
Lecture 4
Viral classification
Lecture 5
Mechanism of Viral
Pathogenesis
Class room
PIC
dr. K. Januarta,
M.Kes
Individual
learning
Small group
discussion
Student
Project
Lecture 3
Mechanism of
bacterial
Pathogenesis
Place
Lecture
Class
Room
Class
Room
Class
Room
Class room
Facilitator
Prof. Dr. dr. Tuti
Parwati Merati,
SpPD, KPTI dr. K.
Januarta, M.Kes
Prof. Dr. dr. Tuti
Parwati Merati,
SpPD, KPTI dr. K.
Januarta, M.Kes
dr. Agus
Hendrayana, M.Ked
dr. Agus
Hendrayana, M.Ked
dr. Agus
Hendrayana, M.Ked
Dr. dr. Sri
Budayanti, Sp.MK
Dr.dr. Sri Budayanti,
Sp.MK
Disc. Room
Class room
Class
Room
dr.Agus somia,
Sp.PD
10
DAY/ DATE
Topic
Time
Regular
Class
English
Class
08.30-09.00
09.30-10.00
09.00-10.30
12.00-13.30
10.30-12.00
13.30-15.00
12.30-14.00
10.00-11.30
14.00-15.00
15.00-16.00
08.00-09.00
09.00-10.00
Monday
Nov. 17th14
09.00-10.30
12.00-13.30
10.30-12.00
13.30-15.00
12.30-14.00
10.00-11.30
14.00-15.00
15.00-16.00
08.00-09.00
09.00-10.00
Friday
Nov. 14th14
6
Tuesday
Nov. 18th14
7
Wednesday
Nov. 19th14
Lecture
Individual
Learning
Small group
discussion
Student
Project
Lecture 8
Treatment of Viral
Infection (PK/PD)
Lecture 9
Treatment of
Microbacterial
Infections I (Type of
antimicrobacterial)
(PK/PD)
09.00-10.30
12.00-13.30
10.30-12.00
13.30-15.00
12.30-14.00
10.00-11.30
14.00-15.00
15.00-16.00
08.00-08.30
09.00-10.00
Lecture 10
Treatment of
Microbacterial
Infections II
(Resistance, rational
treatment, and drug
combination)
08.30-09.00
12.00-13.30
Lecture 11
Antimicrobial
susceptibly
Learning
situation
Place
Class room
Disc. Room
Plenary
Class room
Lecture
Class room
Individual
learning
Small group
discussion
Student
Project
Plenary
Session
Lecture
PIC
dr.Agus
somiaSp.PD
Prof. dr. D.P.
Widjana, DAP&E,
Sp.Par.K
dr.Agus
somiaSp.PD
Prof. dr. D.P.
Widjana, DAP&E,
Sp.Par.K
Prof. IGM Aman,
Sp.FK
Disc. Room
Class room
Facilitator
Prof. IGM Aman,
Sp.FK
Prof. IGM Aman,
Sp.FK
Class room
Dr.dr. B.K.
Satriyasa,M.Repro
Individual
learning
Small group
discussion
Student
Project
Plenary
Session
Lecture
Individual
learning
Disc. Room
Class room
Class room
Dr.dr. B.K.
Satriyasa,M.Repro
Dr.dr. B.K.
Satriyasa,M.Repro
dr. Made Jawi,
M.Kes
11
DAY/ DATE
Topic
Time
Regular
Class
English
Class
09.00-10.30
13.30-15.00
10.30-12.00
10.00-11.30
12.30-14.00
15.00-16.00
08.00-08.30
09.00-093.0
08.30-09.00
09.30-10.00
09.00-10.30
12.00-13.30
10.30-12.00
13.30-15.00
12.30-14.00
10.00-11.30
14.00-15.00
15.00-16.00
08.00-08.30
09.00-093.0
Friday
Nov. 21th14
08.30-09.00
09.30-10.00
09.00-10.30
12.00-13.30
10.30-12.00
13.30-15.00
12.30-14.00
10.00-11.30
14.00-15.00
15.00-16.00
8
Thursday
Nov. 20th14
Lecture 12:
Respond Host against
parasitic and clinical
manifestation
Lecture 13
Treatment of
parasitic infection
(PK/PD)
Learning
situation
PIC
Small group
discussion
Student
Project
Disc. Room
Facilitator
Class room
Plenary
Session
Lecture
Class room
Lecture
Class room
Disc. Room
Facilitator
Class room
Individual
learning
Small group
discussion
Student
Project
Lecture 14:
The Role of Immunity
to infection (Basic)
Lecture 15: Infection
of Mycobacterium
(TBC)
Place
Class room
Plenary
Session
Class room
Lecture
Class room
Lecture
Class room
Individual
learning
Small group
discussion
Student
Project
Plenary
Session
Disc. Room
Class room
Class room
12
DAY/ DATE
10
Topic
Time
Tuesday
Nov. 25th14
12
Place
PIC
Regular
Class
English
Class
08.00-08.30
09.00-093.0
Lecture
Class room
08.30-09.00
09.30-10.00
Lecture 17:
Antimycobacterial
Drugs ( anti TBC, Anti
lepra) (PD/PK)
Lecture
Class room
09.00-10.30
12.00-13.30
10.30-12.00
13.30-15.00
Disc. Room
Facilitator
12.30-14.00
10.00-11.30
Class room
14.00-15.00
15.00-16.00
08.00-08.30
09.00-093.0
08.30-09.00
09.30-10.00
09.00-10.30
12.00-13.30
10.30-12.00
13.30-15.00
12.30-14.00
10.00-11.30
14.00-15.00
15.00-16.00
08.00-08.30
09.00-093.0
Monday
Nov. 24th14
11
Learning
situation
Wednesday
Individual
Learning
Small group
discussion
Student
Project
Plenary
Class room
Lecture 18:
Control of
microorganism
(infection control)
Lecture 19:
Immunization in child
Lecture
Class room
Lecture
Class room
Lecture 20 : infections
in upper respiratory
tract (faringits,
tonsillitis, laringits,
otitis, mastoditis,
rhinitis, sinusitis,
furunkelitis)
Lecture
Lecture 20
Antiseptic and
disinfectant
Small group
discussion
Student
Project
Disc. Room
Facilitator
Class room
Plenary
Class room
Lecture
Class room
dr. N Dwi
Fatmawati, Sp.MK,
Ph.D
dr. Dwi Lingga,
sp.A/ dr. W.
Gustawan,Sp.A
dr. N Dwi
Fatmawati, Sp.MK,
Ph.D
dr. Dwi Lingga,
sp.A/ dr. W.
Gustawan,Sp.A
Dr.dr.B.K.
Satriyasa,M.Repro
13
DAY/ DATE
Nov. 26th14
13
Topic
Time
PIC
English
Class
08.30-09.00
09.30-10.00
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
14.00-15.00
15.00-16.00
Plenary
Class room
08.00-09.00
09.00-10.00
Lecture
Class room
Dr.dr.B.K.
Satriyasa,M.repro
dr Agus
Somia,Sp.PD
Dr.dr.B.K.
Satriyasa,M.repro
dr Agus
Somia,Sp.PD
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
14.00-15.00
15.00-16.00
Plenary
Lecture 21
Universal Precaution
Lecture 22
Protozoa Infection I
(Malaria, Amoebiasis,
Leismaniasis,Tripano
somiasis,Toxoplasmo
sis, Trichomoniasis)
12.00-13.30
Friday
Nov. 28th14
Place
Regular
Class
Thursday
Nov. 27th14
14
Learning
situation
08.00-08.30
09.00-093.0
08.30-09.00
09.30-10.00
Lecture 23
Protozoa Infection II
(Management of
protozoa Infections)
Lecture 24
Infection of
Enterobacter
(Thypoid, C.
botulinum)
Lecture
Class room
dr Agus
Somia,Sp.PD
-
Class room
dr Yuli Gayatri,
Sp.PD
Lecture
Class room
dr Agus
Somia,Sp.PD
14
DAY/ DATE
Topic
Time
Learning
situation
Place
PIC
Regular
Class
English
Class
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
14.00-15.00
15.00-16.00
Plenary
Class room
dr Yuli Gayatri,
Sp.PD
dr Agus
Somia,Sp.PD
dr Yuli Gayatri,
Sp.PD
dr Agus
Somia,Sp.PD
15
08.00-08.30
09.00-093.0
Lecture 25
Sepsis and
Bacteremia
Lecture
Class room
Monday
Des. 1st 14
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
14.00-15.00
15.00-16.00
Plenary
Class room
08.00-08.30
09.00-093.0
Lecture 27
Retroviral Infection
(HIV)
Lecture
Class room
08.30-09.00
09.30-10.00
Lecture 28
Influenza
Lecture
Class room
09.00-10.30
12.00-13.30
10.30-12.00
13.30-15.00
Disc. Room
Facilitator
12.30-14.00
10.00-11.30
Class room
16
Tuesday
Des. 2nd 14
Individual
learning
Small group
discussion
Student
Project
15
DAY/ DATE
17
Wednesday
Des. 3th14
18
Topic
Time
Regular
Class
English
Class
14.00-15.00
15.00-16.00
08.00-08.30
09.00-093.0
08.30-09.00
09.30-10.00
09.00-10.30
12.00-13.30
10.30-12.00
13.30-15.00
12.30-14.00
10.00-11.30
14.00-15.00
15.00-16.00
08.00-09.00
09.00-10.00
09.00-10.30
12.00-13.30
10.30-12.00
13.30-15.00
12.30-14.00
10.00-11.30
14.00-15.00
15.00-16.00
08.00-030.00
09.00-09.30
08.300-09.00
09.30-10.00
Thursday
Des. 4th14
19
Friday
Des. 5th14
Lecture 29
Infection in children
(DBD, Difteri, sepsis,
Campak)
Lecture 30
infections in upper
respiratory tract
(faringits, tonsillitis,
laringits, otitis,
mastoditis, rhinitis,
sinusitis, furunkelitis)
Learning
situation
Place
PIC
Plenary
Class room
Lecture
Class room
Lecture
Class room
Individual
learning
Small group
discussion
Student
Project
Lecture 31
Zoonosis Infection
(Rabies,
Leptospirosis)
Class room
Plenary
Class room
Lecture
Class room
Individual
learning
Small group
discussion
Student
Project
Lecture 32
Principles of Fungal
Infection (Morphology
of Fungal)
Lecture 33:
superficial fungal
Infections (Tinea,
Tinea versikolor,
kadidiasis
mukokutaneous)
Disc. Room
Facilitator
dr. Dwi Lingga,
sp.A/ dr. W.
Gustawan,Sp.A
dr. Lely, Sp.THT
dr. Dwi Lingga,
sp.A/ dr. W.
Gustawan,Sp.A
dr. Lely, Sp.THT
Prof.Dr. dr. Raka
Sudewi, Sp.S (K)
Dr. dr. Sri
Budayanti, Sp.MK
Disc. Room
Facilitator
Class room
Plenary
Class room
Lecture
Class room
Lecture
Class room
Prof. M. Swastika
Adiguna
16
DAY/ DATE
Topic
Time
Regular
Class
English
Class
09.00-10.30
12.00-13.30
10.30-12.00
13.30-15.00
12.30-14.00
10.00-11.30
14.00-15.00
15.00-16.00
20
08.00-08.30
09.00-09.30
Monday
Des. 8th14
08.30-09.00
09.30-10.00
09.00-10.30
12.00-13.30
10.30-12.00
13.30-15.00
12.30-14.00
10.00-11.30
14.00-15.00
15.00-16.00
21
08.00-08.30
09.00-09.30
Tuesday
Des. 9th14
08.30-09.00
09.30-10,00
09.00-10.30
12.00-13.30
10.30-12.00
13.30-15.00
12.30-14.00
10.00-11.30
14.00-15.00
15.00-16.00
08.00-08.30
09.00-09.30
08.30-09.00
09.30-10.00
22
Learning
situation
Individual
learning
Small group
discussion
Student
Project
Lecture 34
Deep Fungal Infection
Lecture 35
Treatment of Fungal
Infection (PD/PK)
Disc. Room
dr. Luh Ariwati
Prof. M. Swastika
Adiguna
Plenary
Class room
Lecture
Class room
Lecture
Class room
Disc. Room
Facilitator
Class room
Prof.Dr.dr Tuti
Parwati,Sp.PD
dr.I B.Ngurah,
M.For/ dr. I Gusti
Made Surya Candra
Trapika, M.Sc
Prof.Dr.dr Tuti
Parwati,Sp.PD
dr.I B.Ngurah,
M.For/dr. wiwiek
Indrayani, M.Kes
Dr. dr. I Made
Sudarmaja, M.Kes
dr. Kadek
Swastika,M.Kes
Plenary
Class room
Lecture
Class room
Lecture
Class room
Individual
learning
Small group
discussion
Student
Project
Lecture 38
Filariasis
Lecture 39
Dengue Viral Infection
PIC
Class room
Individual
learning
Small group
discussion
Student
Project
Lecture 36
Helminthes Infection
Lecture 37
Infection of
Nematoda, Cestoda
and Trematoda
Place
Disc. Room
Facilitator
Class room
dr. I Made
Sudarmaja, M.Kes
dr. Kadek
Swastika,M.Kes
Plenary
Class room
Lecture
Class room
Lecture
Class room
dr. I Made
Sudarmaja,
M.Kes/Staff
dr. K. Agus Somia,
Sp.PD
dr. Made Susila
Utama, Sp,PD
17
DAY/ DATE
Wednesday
Des. 10th14
23
Thursday
Des. 11th14
24
Topic
Time
Place
PIC
Regular
Class
English
Class
09.00-10.30
12.00-13.30
10.30-12.00
13.30-15.00
12.30-14.00
10.00-11.30
14.00-15.00
15.00-16.00
08.00-09.00
09.00-10.00
09.00-10.30
12.00-13.30
10.30-12.00
13.30-15.00
12.30-14.00
10.00-11.30
14.00-15.00
15.00-16.00
08.00-09.00
09.00-10.00
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. Hariyasa
Sanjaya,Sp.OG
14.00-15.00
15.00-16.00
Plenary
Session
Class room
dr. Hariyasa
Sanjaya,Sp.OG
08.00-09.00
09.00-10.00
Lecture
Class room
09.00-10.30
12.00-13.30
Individual
learning
10.30-12.00
13.30-15.00
Small group
discussion
Disc. Room
Facilitaor
Friday
Des. 12th14
25
Learning
situation
Monday
Des. 15th14
Individual
learning
Small group
discussion
Student
Project
Lecture 40
Treatment of
Helminthes Infection
(PK/PD)
Lecture 41
Overview of Puerperal
Infection
Lecture 42
Overview of Sexually
Transmitted Infection
Disc. Room
Facilitator
Class room
Plenary
Class room
Lecture
Class room
Individual
learning
Small group
discussion
Student
Project
Class room
Plenary
Session
Class room
Lecture
Class room
Facilitator
Class room
Dr.dr.
B.K.Satriyasa,M.Rre
pro
Dr.dr.
B.K.Satriyasa,M.Rre
pro
dr. Hariyasa
Sanjaya,Sp.OG
18
DAY/ DATE
Learning
situation
Topic
Time
Place
PIC
Regular
Class
English
Class
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
08.00-15.00
09.00-16.00
Laboratory
Friday
Des. 19th14
27
Practice 1 :
Laboratory diagnosis
of Microbial infection
08.00-15.00
09.00-16.00
Laboratory
Monday
Des. 22th14
28
Practice 2 :
Laboratory diagnosis
of Microbial infection
08.00-15.00
09.00-16.00
Practice 3 :
Laboratory Diagnosis
of Clinical Pathology
Laboratory
Dr Nyoman
Mahartini SpPK
08.00-15.00
09.00-16.00
Practice 4 :
Laboratory
Examination of
parasitic infectious
08.00-15.00
09.00-16.00
Practice 5 :
Laboratory
Examination of
parasitic infectious ()
Tuesday
Des. 23th14
29
Wednesday
Des. 24th14
30
Monday
Des. 29th14
31
Tuesday
Des. 30th14
32
Wednesday
Des. 31th14
Silent Day
EXAMINATION
BLOCK TEAM
19
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.
2.
3.
4.
5.
Introduction (Pendahuluan)
Content (Isi sesuai dengan judul paper)
Summary (Ringkasan)
References (Daftar pustaka): VanCouver style
Pages: 6-10, Spasi: 1.5, Time New Roman:12
20
Student Project
No
Topic
Kompetensi
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
Sinusitis
1. etiopathogenesis of sinus infection
2. clinical symptoms and sign of sinus
infection
3. management of sinus infection
4. complication of sinus infection
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
Mastoiditis
1. etiologi
2. pathogenesis
3. diagnosis
4. management
5. complication
Peritonsilar abses
1. etiopathogenesis
2. clinical manifestation
3. diagnosis
4. management
Rheumatic fever
1. etiologi
2. pathogenesis
3. diagnosis
4. management
5. complication
Rheumatic disease
1. etiopathogenesis
2. clinical manifestation
3. management
4. complication
Meningitis Purulenta
1. ethiopathogenesis
2. clinical manifestation
3. diagnosis
4. management
5. complication
21
Meningitis serosa
ethiopathogenesis
clinical manifestation
diagnosis
management
complication
10
Plaque (Pes)
Etiologi
Transmisi
Management
Complication
Actinomycosis
Diagnosis (microbiology)
Clinical manifestation
Management
Chromoblastomycosis
Diagnosis (microbiology)
Clinical manifestation
Management
Maduromycosis
Diagnosis (microbiology)
Clinical manifestation
Management
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
CMV
- CMV: virology
- Clinical spectrum of CMV
- CMV in immunocompetent
- CMV infection in immunocompromized
- Management of CMV
11
12
13
14
15
16
17
18
Malaria
- etiopatogenesis of severe malaria
- clinical spectrum of severe malaria
- malaria cerebral
- clinical approach management of severe
malaria
- malaria in pregnant
Dengue infection
- How to know warning simptom and sign
- severe dengue
- management of severe dengue
- management
Typhoid fever
- typhoid toxic
3A
22
20
21
22
23
24
25
26
27
HIV/AIDS
- stigma of HIV/AIDS
- VCT
- PICT
- CST (care support treatment)
- ARV
Influenza
- seasonal influenza
- swine influenza
- Avian influenza
- Management
- Prevention
Acute Gastroenteritis
- watery diarrhea:
- inflammatory diarrhea
- how to assement of severity of
dehydration
- how to do rehydration
- how to do rectal swab
Yaws (patek)
- etiopatogenesis
- clinical picture
- laboratory confirmation
- Management
- Prevention
Rabies
- etiopatogenesis of rabies
- clinical picture of rabies
- laboratory confirmation of rabies
- how to manage dog bite
- how to giving vaccination (IM and
subcutans)
Candidiasis
- clinical spectrum of candida infection
- Laboratory confirmation
- Management
Leptospirosis
- etiopatogenesis
- clinical picture
- laboratory confirmation
- Management
- Prevention
Emerging and reemerging disease: legionalle
Clinical manifestation
Diagnosis microbiology
Management
3A
3B
23
29
30
31
32
24
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.
2.
3.
4.
5.
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
25
26
Contamination
Colonization
Invasion
Infection
Pathogen
Carrier
Nonpathogenic
Opportunistic pathogen:
Pathogenicity:
Toxigenicity:
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
======================================================
Faculty of Medicine UNUD,MEU
27
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 whats 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
28
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 Gramnegative 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
29
30
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
======================================================
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 Gusti Made Surya Candra Trapika, M.Sc
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
31
32
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
33
Textbook
Source :
3. Katzung, B.G. 2001. Basic and Clinical Pharmacology. Eight Edition. Lange Medical
Books/McGraw Hill.
4. Katzung and Trevors. 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.
34
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.
35
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
36
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?
37
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 & Trevors, Katzung, BG)
2. Explain the mechanism of action disinfectants and antiseptics (Katzung & Trevors,
Katzung, BG)
3. Describe the clinical use of disinfectants and antiseptics for nosocomial infection
4. Describe the side effect of disinfectants and antiseptics (Katzung & Trevors,
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
38
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
39
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,
40
what is etiology of this cases and describe this parasite life cycle
c. Describe the pathogenesis of this disease
2.
3.
4.
5.
Lecture 23
Protozoa Infection II (Management of protozoa Infections)
dr Yuli Gayatri, Sp.PD
Objectives
41
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.
42
Lecture 25
Sepsis and Bacteremia
dr. Made Susila utama, Sp.PD
============================
43
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
===============================================
44
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.
Lecture29
Infection in children (DBD, Difteri, sepsis, Campak)
dr. Dwi Lingga, sp.A/ dr. W. Gustawan,Sp.A
Case 1
45
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?
46
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
47
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
48
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.
2.
3.
4.
5.
6.
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.
49
50
Lecture 34
Treatment of Fungal Infection (PK/PD)
dr.I B.Ngurah, M.For/ dr. I Gusti Made Surya Candra Trapika, M.Sc
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 students competency has been formulated, in which students must be able to
Faculty of Medicine UNUD,MEU
51
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
52
Define other things that should be found from history taking of this
Describe physical examination to diagnose this patient
Define other examination/ investigation to support the diagnosis
Define the invasive treatment should be done to this patient
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
53
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
54
Lecture 40
Overview of Puerperal Infection
dr. Hariyasa Sanjaya,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 patients 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?
55
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.
56
~ CURRICULUM MAP ~
Smstr
10
Senior Clerkship
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Medical
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57
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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.
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