Download CURRICULUM OF THE BLOCK

Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
CONTENTS
………..…………………………………………………………….
2
Introduction …………………………………………………………………………………….
3
Curriculum ………………………………………………………………………………………
4
Block Team ………………………………………………………………………...................
6
Facilitators ………………………………………………………………………………………
7
Time Table ………………….……………………………………………………………………
8
Meeting of Students representatives …………………………………………………………
17
Meeting of The Facilitators………………………………………………………………….
17
Assessment method …………………………………………………………………………...
17
Student Project ………………………………………………………….....………………….
18
Learning Program ……………………………………………………………………………..
20
Curriculum Mapping …………………………………………………………………………...
75
Reference ………………………………………………………………………………………
76
Table of contents
Udayana University Faculty of Medicine, DME, 2016
1
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
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 book aims to give general information for medical students about infections and
infectious diseases and important for facilitators and resource person while facilitating 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 38 days starts from
September, 1st 2016 as shown in the Time Table. The examination for Basic Microbiology
and Parasitology will be conducted on 30th of September 2016, followed by lecture of
infection and infectious disease. Examination for infection and infectious disease will be
held on 31st of October 2016. Final mark of this block is combination between result of basic
and clinical examination. During the 38 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 assessment).
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
Udayana University Faculty of Medicine, DME, 2016
2
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
CURRICULUM OF THE BLOCK
AIMS




To comprehend the biology of the infectious diseases
To apply and interpret common laboratory diagnosis of infectious diseases
To diagnose and manage common infectious diseases
To carry out basic immunization in children
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
 Diagnose and manage common bacterial infections (common Gram positive and
negative, spirochetal)
 Diagnose and manage common parasitic infections (common nematode,
trematode, cestode, and protozoal infections)
 Diagnose and manage common fungal infections
 Clinically diagnose and manage common viral infections (caused by common
respiratory virus, herpesvirus, arbovirus)
 Clinically diagnose and manage Infection in pregnancy (TORCH)
CURRICULUM CONTENT
1. The biology of infection: bacterial, viral, fungal and parasitic.
a. Principles of bacterial infections such as Staphylococci, Streptococci,
Neisseria, Salmonella, Vibrio, anaerobic bacteria¸ Leptospira, Mycobacteria,
Gram positive bacilli)
b. Principles of viral infections such as respiratory virus (influenza virus,
mumps, measles), retrovirus (HIV), herpesvirus (HSV 1, HSV 2, VZV,
arbovirus (dengue virus, Japanese B encephalitis virus).
c. Principles of fungal infections such as Candida, Pneumocytis jiroveci,
Histoplasma, Cryptococcus
d. Principles of parasitic infections such as Plasmodium, Toxoplasma gondii,
Entamoeba histolytica and soil transmitted helminthes.
2. General approach to the patients with infection such as:
a. Clinical manifestations (local and systemic infections)
b. Laboratory examination to support diagnosis of infections i.e. Microbiological
examination, Parasites examination, Clinical pathology examination,
Pathology examination and Imaging examination
3. Management patients with infection such as:
a. Common bacterial infections such as bacterial meningitis, typhoid fever,diarrhea,
endocarditis, diphtheria, tetanus, food poisoning, genital gonorrhoeae, non
gonococcal urethritis, etc.
b. Common parasitic infections such as malaria, amoebiasis, toxoplasmosis.
c. Common fungal infection such as dermatophytosis, systemic candidiasis,
histoplasmosis, cryptococcosis, pneumocytis jiroveci pneumonia.
Udayana University Faculty of Medicine, DME, 2016
3
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
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.
5. Infection in pregnancy
Udayana University Faculty of Medicine, DME, 2016
4
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
PLANNERS TEAM
No
Name
Departement
Phone
Internal Medicine
08123815025
1
dr. Made Susila Utama, Sp.PD-KPTI
2
dr. Putu Yuliandari, S.Ked
Microbiology
089685415625
3
dr NN Dwi Fatmawati, Sp.MK, Ph.D
Microbiology
087862200814
4
Dr. dr. Made Sudarmaja, M.Kes
Parasitology
08123953945
5
dr. Putu Gede Sudira, Sp.S
DME
081805633997
LECTURERS
NO
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
NAME
Prof. Dr. dr. Tuti Parwati Merati, SpPD,
KPTI-FINASIM
Prof.Dr. dr. Raka Sudewi, Sp.S (K)
dr. Made Susila Utama, Sp.PD
dr. Agus Somia, SpPD
dr. AA Yuli Gayatri, Sp.PD
dr. Ni Made Dewi Dian Sukmawati,
Sp.PD
dr W. Gustawan,M.Sc., Sp.A
dr. Made Bagiada, Sp.PD-KP
Dr. dr. Wayan Sudhana, SpPD-KGH
dr. Ratih Karna, Sp.KK
Dr. dr. IB Fajar Manuaba, SpOG
dr. Luh Ariwati
dr. Kadek Swastika, M.Kes
Dr. dr. Made Sudarmaja, M.Kes
dr NN Dwi Fatmawati, Sp.MK, Ph.D
Dr. dr. Sri Budayanti, Sp.MK
Dr. dr. I Dewa Made Sukrama, M.Si,
Sp.MK (K)
dr. Made Agus Hendrayana, M.Ked
I.B. Nyoman Putra Dwija, S.Si,
M.Biotech
Udayana University Faculty of Medicine, DME, 2016
DEPT
Internal Medicine
(Tropical Disease)
Neurology
Internal Medicine
(Tropical Disease)
Internal Medicine
(Tropical Disease)
Internal Medicine
(Tropical Disease)
Internal Medicine
(Tropical Disease)
Pediatri
Pulmonology
Internal Medicine
(Nefrology)
Dermatology &
Venerology
Obstetric &
Gynecology
Parasitology
Parasitology
Parasitology
Microbiology
Microbiology
PHONE
08123806626
0816710244
08123815025
08123989353
08123803985
081805656501
08123848241
08123607874
08123914095
081337808844
081558101719
08123662311
08124649002
08123953945
087862200814
08583711398
Microbiology
081338291965
Microbiology
08123921590
Microbiology
08179747502
5
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
FACILITATORS
(REGULAR CLASS)
NO
1
NAME
dr. Ni Made Susilawathi, Sp.S
GROUP
1
DEPT
Neurology
PHONE
08124690137
2
dr. Ketut Agus Somia, Sp.PDKPTI
dr. Tjok Istri Anom Saturti,
Sp.PD
dr. Putu Sudira, Sp.S
2
089617587075
4
Internal
Medicine
Internal
Medicine
DME
dr. Agus Roy Rusly HH, Sp.BERE
dr. IA Dewi Wiryanthini,
M.Biomed
dr. IN Gede Wardana, M.
Biomed
Prof. Dr. dr. I Putu Adiatmika,
M.Ked
dr. I Wayan Juli Sumadi, Sp.PA
5
Surgery
081239990399
6
Biochemistry
081239990399
7
Anatomy
087860405625
8
Physiology
08123811019
9
082237407778
dr. IA Kusuma Wardani, Sp.KJ,
MARS
10
Patology
Anatomy
Psychiatry
3
4
5
6
7
8
9
10
3
082145854167
081805633997
08123813831
VENUE
3nd floor:
R.3.09
3nd floor:
R.3.10
3nd floor:
R.3.11
3nd floor:
R.3.12
3nd floor:
R.3.13
3nd floor:
R.3.14
3nd floor:
R.3.15
3nd floor:
R.3.16
3nd floor:
R.3.17
3nd floor:
R.3.19
FACILITATORS
(ENGLISH CLASS)
NO
GROU
P
1
DEPT
PHONE
VENUE
ENT
081338701878
2
Forensik
08123988486
3
Surgery
08179201958
4
Pediatry
081337072141
5
dr. I Wayan Niryana, Sp.BS,
M.Kes
dr. Ni Nyoman Metriani Nesa,
Sp.A, M.Sc
Dr. dr. BK Satriyasa, M.Repro
5
Pharmacology
087777790064
6
Dr. dr. GN Indraguna P
6
IKK IKP
08123816424
7
7
Cardiology
8
dr. Made Satria Yudha
Dewangga, SpJP
dr. I Wayan Sugiritama, M.Kes
8
Histology
081805057315/
082163500096
08164732743
9
dr. Tjahya Aryasa EM, Sp.An
9
Anesthesiology
081339713553
10
Desak Ernawati, S.Si
PGPharm, M.Pharm,Ph.D
10
Pharmasi
081237753646
3nd floor:
R.3.09
3nd floor:
R.3.10
3nd floor:
R.3.11
3nd floor:
R.3.12
3nd floor:
R.3.13
3nd floor:
R.3.14
3nd floor:
R.3.15
3nd floor:
R.3.16
3nd floor:
R.3.17
3nd floor:
R.3.19
1
2
3
4
NAME
dr. Komang Andi Dwi Saputra,
Sp.THT-KL
dr. Henky, Sp.F, M.Beth
Udayana University Faculty of Medicine, DME, 2016
6
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
TIME-TABLE
(Block Basic Microbiology, Parasitology, Infection and infectious
Diseases)
DAY/ DATE
1
Thursday
Sept 1st 2016
2
Friday,
Sept 2nd
2016
3
Monday,
Sept 5th 2016
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
14.00-14.30
15.00-15.30
14.30-15.00
15.30-16.00
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
14.00-14.30
Topic
Lecture 1
Introduction of block
Basic Infection and
Infectious Diseases
Lecture 2
General Parasitology
Learning
situation
Introduction of
the Block
Individual
learning
Small group
discussion
Individual
learning
Plenary
Session
Place
PIC
Class room
Prof. Dr. dr.
Tuti Parwati
Merati, SpPD,
KPTI
Dr. dr. Made
Sudarmaja,
M.Kes
Disc. Room
Facilitator
Class room
Prof. Dr. dr. Tuti
Parwati Merati,
SpPD, KPTI
Dr. dr. Made
Sudarmaja,
M.Kes
Dr. dr. I Dewa
Made
Sukrama, M.Si,
Sp.MK
dr. Made Agus
Hendrayana,
M.Ked
Plenary
Session
Class room
Lecture 3
Introduction of
Microbiology
Lecture
Class room
Lecture 4
Patogenesis of
bacterial infection
Lecture
Class room
Disc. Room
Facilitator
15.00-15.30
Individual
learning
Small Group
Discussion
Individual
learning
Plenary
Class Room
14.30-15.00
15.30-16.00
Plenary
Class Room
08.00-08.30
09.00-09.30
Lecture 5
Diagnosis of Malaria
Lecture
Class Room
08.30-09.00
09.30-10.00
Lecture 6
Diagnosis of Filariasis
Lecture
Class room
Dr. dr. I Dewa
Made Sukrama,
M.Si, Sp.MK
dr. Agus
Hendrayana,
M.Ked
Dr. dr. Made
Sudarmaja,
M.Kes
Dr. dr. Made
Sudarmaja,
M.Kes
09.00-10.30
12.00-13.30
10.30-12.00
13.30-15.00
Disc. Room
12.30-14.00
10.00-11.30
Individual
Learning
Small group
discussion
Individual
Udayana University Faculty of Medicine, DME, 2016
Facilitator
7
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
DAY/ DATE
4
Friday
Sept 9th 2016
5
Tuesday,
Sept 13th
2016
6
Wednesday,
Sept 14th
2016
7
Thursday
Sept 15th
2016
8
Monday,
Sept 19th
2016
Time
Regular
Class
English
Class
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
08.00-09.00
15.00-16.00
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
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
13.30-15.00
10.30-12.00
10.00-11.30
12.30-14.00
15.00-16.00
08.00-09.00
09.00-10.00
Topic
Lecture 7,8,9
Toxoplasmosis,
amoebiasis, and
systemic fungal
infection
Lecture 10, 11
Ascariasis,
Trichuriasis
Lecture 12,13,14
Hookworm infection,
Strongyloidiasis,
Enterobiasis
Learning
situation
Place
PIC
learning
Plenary
Class room
Lecture
Class Room
Dr. dr. Made
Sudarmaja,
M.Kes
dr. Luh Ariwati
Disc. Room
Facilitator
Class room
Class room
dr. Luh Ariwati
dr. Luh Ariwati
Individual
Learning
Small group
discussion
Individual
learning
Plenary
Lecture
Individual
learning
Small group
discussion
Individual
learning
Plenary
Session
Lecture
Individual
learning
Small group
discussion
Individual
learning
Plenary
Session
Lecture 15,16
Larva migrans,
Pediculosis
Lecture 17,18,19
Schistosomiasi,
Taeniasis,
Sistisercosis
Udayana University Faculty of Medicine, DME, 2016
Disc. Room
Facilitator
Class room
dr. Luh Ariwati
Class room
Dr. dr. Made
Sudarmaja,
M.Kes
Disc. Room
Facilitator
Class room
Dr. dr. Made
Sudarmaja,
M.Kes
dr. Kadek
Swastika,
M.Kes
Facilitator
Individual
learning
Small group
discussion
Individual
learning
Plenary
Session
Disc. Room
Lecture
Class room
Class room
dr. Kadek
Swastika,
M.Kes
dr. Kadek
Swastika,
M.Kes
8
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
DAY/ DATE
9
Tuesday
Sept 20th
2016
10
Tuesday
Sept 21st
2016
11
Thursday,
Sept 22nd
2016
12
Friday,
Sept 23rd
2016
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
08.00-16.00
08.00-16.00
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
14.00-14.30
15.00-15.30
14.30-15.00
15.30-16.00
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
10.30-12.00
13.30-15.00
Topic
Learning
situation
Individual
learning
Small group
discussion
Individual
learning
Plenary
Session
STUDENT PROJECT
(REGULER CLASS)
Lecture 20, 21
Gram positive and
negative bacteria
Lecture 22:
Mycobacterium
Lecture 25, 26
RNA virus,
Zoonosis
Udayana University Faculty of Medicine, DME, 2016
Facilitator
Class room
dr. Kadek
Swastika,
M.Kes
Evaluator &
Fasilitator
Teather
Room
Class room
Lecture
Class room
Facilitator
Class room
dr. Made Agus
Hendrayana,
M.Ked
IB Nyoman
Putra Dwija,
S.Si, M.Biotech
Dr. dr. Ni
Nyoman Sri
Budayanti,
Sp.MK
Class room
Lecture
Class room
Lecture
Individual
learning
Small group
discussion
dr. Made Agus
Hendrayana,
M.Ked
IB Nyoman
Putra Dwija,
S.Si, M.Biotech
Disc. Room
Plenary
Session
Individual
learning
Small group
discussion
Individual
learning
Plenary
PIC
Disc. Room
Lecture
Individual
learning
Small group
discussion
Individual
learning
Plenary
Session
Lecture 23, 24
Pathogenesis of viral
infection,
DNA virus
Place
Disc. Room
Facilitator
Class room
Dr. dr. Ni
Nyoman Sri
Budayanti,
Sp.MK
Dr. dr. Ni
Nyoman Sri
Budayanti,
Sp.MK
Class room
Disc. Room
Facilitator
9
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
DAY/ DATE
13
Monday,
Sept 26th
2016
14
Tuesday,
Sept 27th
2016
15
Wednesday,
Sept 28th
2016
Time
Regular
Class
English
Class
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
09.00-09.30
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
14.00-14.30
15.00-15.30
14.30-15.00
15.30-16.00
08.00-09.00
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
Learning
situation
Topic
Lecture 27, 28
Specimen collection
Microbial
identification &
Antimicrobial
Sensitivity Test (AST)
Place
PIC
Individual
learning
Plenary
Class room
Lecture
Class room
Dr. dr. Ni
Nyoman Sri
Budayanti,
Sp.MK
dr. Ni Nengah
Dwi Fatmawati,
Sp.MK, Ph.D
Individual
learning
Small group
discussion
Disc. Room
Facilitator
MIDDLE BLOCK MEETING
Plenary
Lecture 29
Mechanism of action
and resistance of
antibiotic
Lecture 30
Biosafety &
Biosecurity
Lecture
Class room
IB Nyoman
Putra Dwija,
S.Si, M.Biotech
Disc. Room
Facilitator
Plenary
Class room
dr. Ni Nengah
Dwi Fatmawati,
Sp.MK, Ph.D
Plenary
Class room
IB Nyoman
Putra Dwija,
S.Si, M.Biotech
Lecture
Class room
Dr. dr. I Dewa
Made
Sukrama, M.Si,
Sp.MK
Disc. Room
Facilitator
Lecture
Individual
learning
Small group
discussion
Individual
learning
Lecture 31, 32
Health careassociated infection
Anaerob bacteria &
Spirochaeta
Udayana University Faculty of Medicine, DME, 2016
dr. Ni Nengah
Dwi Fatmawati,
Sp.MK, Ph.D
dr. Ni Nengah
Class room
Dwi Fatmawati,
Sp.MK, Ph.D
Individual
learning
Small group
discussion
Individual
learning
10
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
DAY/ DATE
Thursday,
Sept 29th
2016
Friday,
Sept 30th
2016
16
Monday,
Oct 3rd 2016
17
Tuesday,
Oct 4th 2016
18
Wednesday,
Oct 5th 2016
19
Thursday,
Oct 6th 2016
Time
Regular
Class
English
Class
14.00-15.00
15.00-16.00
Learning
situation
Topic
Plenary
Place
PIC
Class room
Dr. dr. I Dewa
Made Sukrama,
M.Si, Sp.MK
SILENT DAY
BASIC MICROBIOLOGY & PARASITOLOGY EXAMINATION
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
10.30-12.00
13.30-15.00
12.30-14.00
10.00-11.30
14.00-15.00
15.00-16.00
08.00-16.00
08.00-16.00
08.00-09.00
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
Lecture 33
Host response to
infection
(viral, bacterial,
fungal, parasite)
Lecture
Individual
learning
Small group
discussion
Individual
learning
Plenary
Lecture 34, 35, 36
Hematology &
Immunology infection
(dengue fever,
dengue hemorrhagic
fever, dengue shock
syndrome)
Lecture
Individual
learning
Small group
discussion
Individual
learning
Plenary
STUDENT PROJECT
(ENGLISH CLASS)
Lecture 37
Infection in
pregnancy (TORCH in
pregnancy)
Udayana University Faculty of Medicine, DME, 2016
Class room
Prof. Dr. dr.
Tuti Parwati
Merati, SpPD,
KPTI
Disc. Room
Facilitator
Class room
Prof. Dr. dr. Tuti
Parwati Merati,
SpPD, KPTI
dr Dewi Dian
Sukmawati,
SpPD
Class room
Disc. Room
Facilitator
Class room
dr Dewi Dian
Sukmawati,
SpPD
Evaluator &
Fasilitator
Teather room
Lecture
Class room
DR Dr IB Fajar
Manuaba,
SpOG
Individual
learning
Small group
discussion
Individual
Disc. Room
Facilitator
11
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
DAY/ DATE
20
Friday,
Oct 7th 2016
21
Monday,
Oct 10th
2016
22
Tuesday,
Oct 11st
2016
23
Wednesday,
Oct 12nd
2016
Time
Regular
Class
English
Class
Topic
Learning
situation
Place
learning
Plenary
Class room
DR Dr IB Fajar
Manuaba,
SpOG
dr Susila
Utama, SpPDKPTI
dr Agus Somia,
SpPD-KPTI
14.00-15.00
15.00-16.00
08.00-08.30
09.00-09.30
Lecture 38
Malaria
Lecture
Class room
08.30-09.00
09.30-10.00
Lecture 39
Leptospirosis
Lecture
Class room
09.00-10.30
12.00-13.30
10.30-12.00
13.30-15.00
12.30-14.00
10.00-11.30
14.00-14.30
15.00-15.30
Individual
learning
Small group
discussion
Individual
learning
Plenary
14.30-15.00
15.30-16.00
Plenary
Class room
08.00-09.00
09.00-10,00
Lecture
Class room
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
09.30-10.00
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
Lecture 40
Skin infection
Individual
learning
Small group
discussion
Individual
learning
Plenary
Lecture 41
Central nervous
system infection
(meningitis,
encephalitis)
Lecture
Individual
learning
Small group
discussion
Individual
learning
Plenary
Lecture 42
Child Immunization
Udayana University Faculty of Medicine, DME, 2016
PIC
Disc. Room
Facilitator
Class room
dr Susila
Utama, SpPDKPTI
dr Agus Somia,
SpPD-KPTI
dr Ratih Karna,
SpKK
Disc. Room
Facilitator
Class room
Class room
dr Ratih Karna,
SpKK
Prof DR Dr
Raka Sudewi,
SpS(K)
Disc. Room
Facilitator
Class room
Prof DR Dr
Raka Sudewi,
SpS(K)
dr W.
Gustawan, SpA
Lecture
Class room
Individual
learning
Small group
discussion
Individual
learning
Plenary
Class room
Facilitator
Class room
dr W.
12
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
DAY/ DATE
24
Thursday,
Oct 13rd 2016
25
Friday,
Oct 14th
2016
26
Monday,
Oct 17th
2016
Time
Regular
Class
English
Class
Topic
Learning
situation
Place
PIC
Session
Lecture
Class room
Gustawan, SpA
dr Agus Somia,
SpPD-KPTI
Lecture
Class room
dr Yuli Gayatri,
SpPD
08.00-08.30
09.00-10.00
Lecture 43
Thypoid fever
08.30-09.00
09.30-10.00
Lecture 44
Acute gastroenteritis
09.00-10.30
12.00-13.30
Individual
learning
10.30-12.00
13.30-15.00
Disc. Room
Facilitator
12.30-14.00
10.00-11.30
Small group
discussion
Individual
learning
14.00-14.30
15.00-15.30
Class room
14.30-15.00
15.30-16.00
08.00-08.30
09.00-09.30
Lecture 45
Urinary Tract
Infection (acute
pyelonephritis, lower
urinary tract infection)
Plenary
Session
Plenary
Session
Lecture
dr Agus Somia,
SpPD-KPTI
dr Yuli Gayatri,
SpPD
DR Dr Wayan
Sudhana,
SPPD-KGH
08.30-09.00
09.30-10.00
Lecture 46
Lower respiratory
tract infection
(pneumonia, acute
bronchitis)
Lecture
Class room
dr. Made
Bagiada, SpPDKP
09.00-10.30
12.00-13.30
10.30-12.00
13.30-15.00
Disc. Room
Facilitaor
12.30-14.00
10.00-11.30
Individual
learning
14.00-14.30
15.00-15.30
Plenary
Session
Class room
14.00-14.30
15.00-15.30
Plenary
Session
Class room
08.00-08.30
09.00-09.30
Lecture
Class room
08.30-09.00
09.30-10.00
Lecture
Class room
DR Dr Wayan
Sudhana,
SPPD-KGH
dr. Made
Bagiada, SpPDKP
dr Yuli Gayatri,
SpPD
dr Dewi Dian
Sukmawati,
SpPD
09.00-10.30
12.00-13.30
10.30-12.00
13.30-15.00
12.30-14.00
10.00-11.30
14.00-14.30
15.00-15.30
Individual
learning
Small group
discussion
Lecture 47
Toxoplasmosis
Lecture 48
Filariasis
Udayana University Faculty of Medicine, DME, 2016
Individual
learning
Small group
discussion
Individual
learning
Plenary
Session
Class room
Class room
Disc. Room
Facilitaor
Class room
dr Yuli Gayatri,
SpPD
13
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
DAY/ DATE
27
Tuesday,
Oct 18th
2016
28
Wednesday
Oct 19th
2016
29
Thursday,
Oct 20th
2016
30
Friday,
Oct 21st
Time
Topic
Learning
situation
Place
PIC
Plenary
Session
Class room
Lecture
Class room
dr Dewi Dian
Sukmawati,
SpPD
Prof DR Dr Tuti
Parwati, SpPDKPTI
Regular
Class
English
Class
14.30-15.00
15.30-16.00
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
10.30-12.00
13.30-15.00
12.30-14.00
10.00-11.30
Individual
learning
14.00-15.00
15.00-16.00
08.00-08.30
09.00-09.30
Lecture 52
Parotitis
08.30-09.00
09.30-10.00
Lecture 53
Bacteremia, Sepsis
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
Individual
learning
14.00-14.30
15.00-15.30
14.30-15.00
15.30-16.00
08.00-08.30
09.00-09.30
Lecture 49
HIV infection
(pathogenesis &
opportunistic
infection)
Individual
learning
Small group
discussion
Individual
learning
Plenary
Session
Lecture 50, 51
Avian influenza,
SARS
Lecture
Individual
learning
Small group
discussion
Lecture 54
Rabies
Udayana University Faculty of Medicine, DME, 2016
Disc. Room
Facilitaor
Class room
Prof DR Dr Tuti
Parwati, SpPDKPTI
dr Agus Somia,
SpPD-KPTI
Class room
Disc. Room
Facilitaor
Plenary
Session
Lecture
Class room
Lecture
Class room
dr Agus Somia,
SpPD-KPTI
dr Dewi Dian
Sukmawati,
SpPD
dr Susila
Utama, SpPDKPTI
Class room
Disc. Room
Facilitaor
Plenary
Session
Class room
Plenary
Session
Class room
Lecture
Class room
dr Dewi Dian
Sukmawati,
SpPD
dr Susila
Utama, SpPDKPTI
dr Susila
Utama, SpPDKPTI
14
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
DAY/ DATE
2016
31
Monday,
Oct 24th
2016
32
Tuesday,
Oct 25th
2016
33
Wednesday,
Oct 26th
2016
34
Thursday,
Oct 27th
2016
Friday,
Oct 28th
2016
Monday,
Oct 31st
2016
Time
Learning
situation
Topic
Place
PIC
Regular
Class
English
Class
08.00-09.00
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
12.30-14.00
10.00-11.30
Individual
learning
14.00-14.30
15.00-15.30
14.30-15.00
15.30-16.00
08.00-15.00
09.00-16.00
Laboratory Practice 1:
Gram Stain
Laboratory
Microbiology
Team
08.00-15.00
09.00-16.00
Laboratory Practice 2:
ZN stain
Laboratory
Microbiology
Team
08.00-15.00
09.00-16.00
Laboratory Practice 3:
Fecal examination
Parasitology
Team
08.00-15.00
09.00-16.00
Laboratory Practice 4:
Parasit identification
Parasitology
Team
Lecture 55
Tetanus
Lecture
Class room
dr Yuli Gayatri,
SpPD
Disc. Room
Facilitaor
Plenary
Session
Class room
Plenary
Session
Class room
dr Susila
Utama, SpPDKPTI
dr Yuli Gayatri,
SpPD
SILENT DAY
INFECTION & INFECTIOUS DISEASES EXAMINATION
Udayana University Faculty of Medicine, DME, 2016
15
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
MEETING OF STUDENT REPRESENTATIVES
In the middle of block period, a meeting is designed among the student representatives of
every small group discussion, facilitators and source person of the block. The meeting
discuss about the ongoing teaching and learning process, quality of facilitator and lectures
as a feedback to improve the next process.
MEETING OF THE FACILITATORS
All facilitators are invited to discuss all block activities with block contributors 1 week after
meeting of student representatives.
ASSESSMENT METHOD
1. Assessment will be held twice, for basic microbiology & parasitology and infection &
infectious diseases. Final mark is combination beteween this mark. 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%
Exam (basic & clinical)
: 85%
Udayana University Faculty of Medicine, DME, 2016
16
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
STUDENT PROJECT
Regulation:
TITLE
Name:
NIM:
Faculty of Medicine, Udayana University
2016
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
TOPIC Regular Class (Class A)
GROUP DATE & TIME
TITLE
6
Tuesday,
Cerebral abses
Sept
20th
2016,
08.30-09.00
09.00-09.30
Cerebral
toxoplasmosis
09.30-10.00
Multi drug
resisten (MDR)
TB
10.00-10.30
Spondilitis TB
10.30-11.00
Acute infection
pancreatitis
11.00-11.30
Pes
7
11.30-12.30
12.30-13.00
BREAK
Leishmaniasis
8
13.00-13.30
Tripanosomiasis
9
13.30-14.00
10
14.00-14.30
Cytomegalovirus
infection
Squamous cell
carcinoma
(associated with
HPV infection)
1
2
3
4
5
Udayana University Faculty of Medicine, DME, 2016
PEMBIMBING/
FASILITATOR
dr. Ni Made Susilawathi,
Sp.S
dr. Ketut Agus Somia,
Sp.PD-KPTI
dr. Tjok Istri Anom
Saturti, Sp.PD
dr. Putu Sudira, Sp.S
dr. Agus Roy Rusly HH,
Sp.BE-RE
dr. IA Dewi Wiryanthini,
M.Biomed
dr. IN Gede Wardana,
M. Biomed
Prof. Dr. dr. I Putu
Adiatmika, M.Ked
dr. I Wayan Juli Sumadi,
Sp.PA
dr. IA Kusuma Wardani,
Sp.KJ, MARS
EVALUATOR
Prof DR Dr Raka
Sudewi, SpS(K)
dr. Made
Bagiada, SpPDKP
dr. Agus Somia,
SpPD-KPTI
Dr. dr. Made
Sudarmaja,
M.Kes
dr. NN Dwi
Fatmawati,
Sp.MK, Ph.D
17
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
TOPIC English Class (Class B)
GROUP
DATE & TIME
TITLE
2
Wednesday,
Oct 5th 2016,
08.30-09.00
09.00-09.30
3
09.30-10.00
4
10.00-10.30
5
10.30-11.00
6
11.00-11.30
Carcinoma servik
(associated with HPV
infection)
Penyakit jantung
rematik
Endoftalmitis
7
11.30-12.30
12.30-13.00
BREAK
Hepatitis C
8
13.00-13.30
Abses payudara
9
13.30-14.00
Epididimitis
10
14.00-14.30
Herpes genital tipe 2
1
Nasopharyngeal
carcinoma (associated
with EBV infection)
Hairy leukoplakia
(associated with EBV
infection)
Korioretinitis
Udayana University Faculty of Medicine, DME, 2016
PEMBIMBING/
FASILITATOR
dr. Komang Andi
Dwi Saputra,
Sp.THT-KL
dr. Henky, Sp.F,
M.Beth
EVALUATOR
dr. Made Agus
Hendrayana,
M.Ked
dr. I Wayan
Niryana, Sp.BS,
M.Kes
dr. Ni Nyoman
Metriani Nesa,
Sp.A, M.Sc
Dr. dr. BK
Satriyasa, M.Repro
Dr. dr. GN
Indraguna P
dr. Kadek
Swastika,
M.Kes
dr. IA Rangga W,
Sp.JP, FIHA,
M.Biomed
dr. I Wayan
Sugiritama, M.Kes
dr. Tjahya Aryasa
EM, Sp.An
Desak Ernawati,
S.Si PGPharm,
M.Pharm,Ph.D
dr. Ni Made
Dewi Dian
Sukmawati,
Sp.PD
dr W.
Gustawan,
SpA
dr. Ratih
Karna, SpKK
18
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
LEARNING PROGRAM
LECTURE 1
INTRODUCTION OF BLOCK BASIC INFECTION AND INFECTIOUS DISEASES
Prof. Dr. dr. Tuti Parwati Merati, SpPD, KPTI
Abstract
Infections and infectious diseases are a great burden on many societies, including
Indonesia. To reduce that burden an integrated approach is required, combining health
promotion, disease prevention and patient treatment. The prerequisite for success in this
fight is the participation of all health care professionals. Should know and understand
terminology commonly use in the context of infectious disease.
Infectious diseases are disorders or diseases caused by organisms — such as bacteria,
viruses, fungi or parasites. Many organisms live in and on our bodies. They're normally
harmless or even helpful, which we called them normal flora; but under certain conditions,
some organisms may cause disease. This organisms called as pathogen as they can
produced pathology to the body.
Infectious diseases are one of the leading causes of death worldwide. Infectious diseases
can be spread directly or indirectly . Some infectious diseases can be passed from person
to person. Some are transmitted by bites from insects or animals. And others are acquired
by ingesting contaminated food or water or being exposed to organisms in the environment.
Many infectious diseases become difficult to control if the infectious agents evolve
resistance to commonly used drugs: For example, bacteria can accumulate mutations in
their DNA or acquire new genes that allow them to survive contact with antibiotic drugs that
would normally kill them.
Signs and symptoms vary depending on the organism causing the infection, but often
include fever and fatigue. Mild infections may respond to rest and home remedies, while
some life-threatening infections may require hospitalization.
Many infectious diseases, such as measles and chickenpox, can be prevented by vaccines
but many other still do not have vaccine available. Other prevention mean such as
frequent and thorough hand-washing helps protect from most infectious diseases.
Symptoms
Each infectious disease has its own specific signs and symptoms. General signs and
symptoms common to a number of infectious diseases include: fever, fatigue, muscle
aches, coughing and diarrhea
Transmission: an infection can be spread through direct and indirect contact
Direct contact
An easy way to catch most infectious diseases is by coming in contact with a person or
animal who has the infection. Three ways infectious diseases can be spread through direct
contact are:
Person to person. A common way for infectious diseases to spread is through the direct
transfer of bacteria, viruses or other germs from one person to another. This can occur
when an individual with the bacterium or virus touches, kisses, or coughs or sneezes on
someone who isn't infected. These germs can also spread through the exchange of body
fluids from sexual contact. The person who passes the germ may have no symptoms of the
disease, but may simply be a carrier.
Udayana University Faculty of Medicine, DME, 2016
19
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
Animal to person. Being bitten or scratched by an infected animal — even a pet — can
make you sick and, in extreme circumstances, can be fatal. Handling animal waste can be
hazardous, too. For example, you can acquire a toxoplasmosis infection by scooping your
cat's litter box.
Mother to unborn baby. A pregnant woman may pass germs that cause infectious
diseases to her unborn baby. Some germs can pass through the placenta. Germs in the
vagina can be transmitted to the baby during birth.
Indirect contact
Touching : Disease-causing organisms also can be passed by indirect contact. Many
germs can linger on an inanimate object, such as a tabletop, doorknob or faucet handle.
When you touch a doorknob handled by someone ill with the flu or a cold, for example, you
can pick up the germs he or she left behind. If you then touch your eyes, mouth or nose
before washing your hands, you may become infected.
Vectors/insect bites - Some germs rely on insect carriers — such as mosquitoes, fleas,
lice or ticks — to move from host to host. These carriers are known as vectors. Mosquitoes
can carry the malaria parasite or West Nile virus, and deer ticks may carry the bacterium
that causes Lyme disease.
Food/water
contamination : disease-causing germs can infect you is through
contaminated food and water. This mechanism of transmission allows germs to be spread
to many people through a single source. E. coli, for example, is a bacterium present in or on
certain foods — such as undercooked hamburger or unpasteurized fruit juice.
Risk factors
Anyone can catch infectious diseases easier than other people because the body immune
system is not work well. This may occur if there are primary or secondary immune
deficiency , such as : Taking steroids or other medications that suppress immune system,
such as anti-rejection drugs for a transplanted organ, certain types of cancer or other
disorders that affect the immune system, infection by HIV or AIDS. In addition, certain
other medical conditions may predispose you to infection, including implanted medical
devices, malnutrition and extremes of age, among others.
Complications
Most infectious diseases have only minor complications. But some infections — such as
pneumonia, AIDS and meningitis — can become life-threatening. A few types of infections
have been linked to a long-term increased risk of cancer: hepatitis B and C have been
linked to liver cancer, human papillomavirus is linked to cervical cancer, Helicobacter pylori
is linked to stomach cancer and peptic ulcers and In addition, some infectious diseases may
become silent, only to appear again in the future — sometimes even decades later. For
example, someone who's had a chickenpox infection may develop shingles much later in
life.
Diagnosis
Diagnosis can be made with clinical symptoms and signs. Because many of infectious
disease have a very similar symptoms and signs, usually laboratory or imaging test would
be needed to confirmed the diagnosis
Laboratory tests
Many infectious diseases have similar signs and symptoms. Samples of body fluids can
sometimes reveal evidence of the particular microbe that's causing illness. Samples can
Udayana University Faculty of Medicine, DME, 2016
20
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
get from blood, urine, throat swabs, stool sample, spinal tap (lumbar puncture). A
technician obtains a sample with a standard procedure from each.
Imaging scans
Imaging procedures — such as X-rays, computerized tomography and magnetic resonance
imaging — can help pinpoint diagnoses and rule out other conditions that may be causing
the symptoms.
Biopsies
During a biopsy, a tiny sample of tissue is taken from an internal organ for testing. For
example, a biopsy of lung tissue can be checked for a variety of fungi that can cause a type
of pneumonia.
Treatment
Knowing what type of germ is causing the illness makes it easier to choose appropriate
treatment such as : antibiotics, anti viral, anti fungal, and anti-parasitics.
However, the use of those agents should be use appropriately. The overuse of antibiotics
has resulted in several types of bacteria developing resistance to one or more varieties of
antibiotics. This makes these bacteria much more difficult to treat
As an alternative medicine, a number of products have been purported to help fend off
common illnesses, such as the cold or flu. Cranberry, echinacea, garlic, ginseng, vitamin C,
D and zinc are among other.. While some of these substances have appeared promising in
early trials, follow-up studies may have had negative or inconclusive results. More research
needs to be done.
Prevention
Infectious diseases can be prevented by vaccines but many other still do not have vaccine
available. Prevention to infectious disease transmission with no vaccine available should
use another approach. Personal protected equipment such as gown, masker, google,
gloves, and shoes boot. Infectious disease transmitted by vectors should avoid to being
bitten by mosquitoes or other insects may be useful, such as wearing long sleeve shirt,
and putting mosquitos repellent. Other prevention means such as frequent and thorough
hand-washing helps protect from most infectious diseases.
Learning tasks:
1. How do we know that a patient in our hospital is suffering from a kind of infectious
disease?
2. How he or she can get it?
3. What prevention do we need to do to avoid of getting any infectious diseases?
Self assessment:
1. Describe all common terminology use in the context of infectious diseases.
2. Describe general clinical manifestation of infectious diseases.
3. Describe pathogenesis of general symptoms of infectious disease.
Udayana University Faculty of Medicine, DME, 2016
21
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
LECTURE 2
GENERAL PARASITOLOGY
Dr. dr. Made Sudarmaja, M. Kes
Abstract
Parasitology: The study of PARASITES and their relationships to their HOSTS. Parasite : A
living organism which receives nourishment and shelter from another organism where it
lives. Host : An organism which harbours the parasites. Parasite depend on its location of
infection divided into ectoparasites and endoparasites. Some term of parasites : facultative
parasites, obligate parasites, incidental parasites, temporary parasites, permanent
parasites, pathogen parasites and pseudoparasite. Host divided into definitive host and
intermediate host. The study of Parasitology consist several aspect such as : epidemiology,
habitat, morphology, life cycle, pathogenic effect, sign & symptom, diagnosis & laboratory
diagnosis, treatment and prophylaxis. In The Indonesian Standard Competency of Doctor
(SKDI = Standar Kompetensi Dokter Indonesia) shown that several diseases that caused by
parasites must be competence by general practioner such as : Malaria, Filariasis,
Toxoplasmosis, mikosis, Hookworm infection, Amoebiasis, Ascariasis, Trichuriasis,
Enterobiasis, Strongyloidiasis, Schistosomiasis, Taeniasis, Scabies, Pediculosis capitis and
Pthiriasis pubis
Learning task:
1. Explain differentiation between Hospes definitive and Hospes intermediate and give
example hospes definitive and hospes intermediate!
2. Mention and explain the infective stage of several parasites that caused diseases in
human
3. The preventive and control the parasites disesase must be based on life cycle of
parasites. Why?
Self-Assessment
1. Amoebic dysentri caused by:
A. Ascaris lumbricoides
B. Necator americanus
C. Trichuris trichiura
D. Brugia malayi
E. Entamoeba histolytica
2. Tapeworm that transmitted with pork
A. Taenia saginata
B. Taenia solium
C. Hymenolepis nana
D. Hymenolepis diminuta
3. Nematode that include of soil transmitted helminthes:
A. Enterobius vermicularis
B. Taenia saginata
C. Trichinella spiralis
D. Brugia malayi
E. Trichuris trichiura
Udayana University Faculty of Medicine, DME, 2016
22
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
LECTURE 3
INTRODUCTION OF MICROBIOLOGY
Dr. dr. I Dewa Made Sukrama, M. Si, Sp.MK
ABSTRACT
The discipline of bacteriology evolved from the need of physicians to test and apply the
germ theory of disease and from economic concerns relating to the spoilage of foods and
wine. The initial advances in pathogenic bacteriology were derived from the identification
and characterization of bacteria associated with specific diseases. During this period, great
emphasis was placed on applying Koch's postulates to test proposed cause-and-effect
relationships between bacteria and specific diseases. Today, most bacterial diseases of
humans and their etiologic agents have been identified, although important variants
continue to evolve and sometimes emerge, e.g., Legionnaire's Disease, tuberculosis and
toxic shock syndrome.
Major advances in bacteriology over the last century resulted in the development of many
effective vaccines (e.g., pneumococcal polysaccharide vaccine, diphtheria toxoid, and
tetanus toxoid) as well as of other vaccines (e.g., cholera, typhoid, and plague vaccines)
that are less effective or have side effects. Another major advance was the discovery of
antibiotics. These antimicrobial substances have not eradicated bacterial diseases, but they
are powerful therapeutic tools. Their efficacy is reduced by the emergence of antibiotic
resistant bacteria (now an important medical management problem) In reality,
improvements in sanitation and water purification have a greater effect on the incidence of
bacterial infections in a community than does the availability of antibiotics or bacterial
vaccines. Nevertheless, many and serious bacterial diseases remain.
LEARNING TASK:
1. Define and apply major taxonomic group when classifying microorganisms (bacteria,
fungi, parasites, and viruses)
2. Relate microbial cell structure and processes to growth, disease, survival, or other
relevant phenotypes.
3. Be able to describe the principle of Koch’s postulate.
LECTURE 4
PATHOGENESIS OF BACTERIAL INFECTION
dr. Made Agus Hendrayana, M. Ked
ABSTRACT
Pathogenesis is a multi-factorial process which depends on the immune status of the host,
the nature of the species or strain (virulence factors) and the number of organisms in the
initial exposure. A limited number of bacterial species are responsible for the majority of
infectious diseases in healthy individuals. Due to the success of vaccination, antibiotics, and
effective public health measures, until recently, epidemics were felt to be a thing of the past.
Due to the development of antibiotic resistant organisms, this situation is changing rapidly.
All humans are infected with bacteria (the normal flora) living on their external surfaces
Udayana University Faculty of Medicine, DME, 2016
23
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
(including the skin, gut and lungs). We are constantly also exposed to bacteria (including air,
water, soil and food). Normally due to our host defenses most of these bacteria are
harmless.
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. The
biochemical, structural, and genetic factors that play important roles in bacterial
pathogenesis are introduced in this chapter and may be revisited in the organism-specific
sections. Characteristics of bacteria that are pathogens include transmissibility, adherence
to host cells, persistence, invasion of host cells and tissues, toxigenicity, and the ability to
evade or survive the host's immune system. Resistance to antimicrobials and disinfectants
can also contribute to virulence, or an organism's capacity to cause disease. Many
infections caused by bacteria that are com-monly 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.
Learning Task
Case:
A 15 years old female, a student at Junior High School, come to general practician
complained that she has fever since 6 days. The fever is intermitten, commonly arise when
aftenoon till night, but back to normal in the morning. She feels slightly discomfort at the
abdominal. She also complained that not defecated since 4 days. Other physical
examination results are normal. The practician ask for laboratory examination and culture.
After few days, the laboratory analysis shown that she has typoid fever. The culture shown
colonies of Salmonella typhi bacteria and significant as agent of infection.
1.
What are Salmonella typhi’s virulence factors that can cause infection?
2.
Explain the microbial virulence factors that you know!
3.
What are Salmonella typhi ’s virulence factors that can cause infection?
4.
Explain the pathogenesis how Salmonella typhi can infect the human (from
transmission until infection and cause the disease)!
5.
Whether the virulence factors of each microbial is the same? Why?
6.
When any bacteria called as colonization bacteria?
7.
Explain the differentiation between true pathogen and opportunistic pathogen!
8.
Explain the differentiation between exotoxins and endotoxin !
9.
Describe how several pathogens are able to survive inside the macrophages !
10. Explain the routes of transmission that you know and give examples of each !
11. Explain why are important to know about the bacteria virulence factors
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:
Udayana University Faculty of Medicine, DME, 2016
24
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
J. Toxigenicity:
K. Virulence:
L. Symbiosis
M. Commensalism
N. Parasitism
O. Zoonoses
2. Give examples of attachment mechanism !
Reff :
Jawetz, Melnick, Adelberg. 2013 Chapter 9. Pathogenesis of Bacterial Infection in Medical
Microbiology, 26th Edition by Vishal . The McGraw-Hill Companies. Lange Microbiology.
LECTURE 5
DIAGNOSIS OF MALARIA
Dr. dr. Made Sudarmaja, M.Kes
Abstract
Malaria remains a global health problem and also in Indonesia and can cause death,
especially in high-risk such as infants, toddlers and pregnant women. Malaria Diagnosis is
made by anamnesis, physical examination and laboratory tests. To get a definite diagnosis
of malaria should be performed laboratory tests to find the malaria parasite in the blood.
Examination and detection of the parasite causing-malaria in blood can be done by: a
microscopic examination (blood smear), Rapid Diagnostic Test (RDT) and examination by
PCR.
Blood smear using microscopic examination is the gold standard for the diagnosis of
malaria. Examination of blood smear can be developed thick and thin blood smear.
Examination of blood smear aims to found the Plasmodium (malaria parasite), plasmodium
determine species and stage and parasite density. Examination using RDT aims to detect
the presence of malaria parasite antigens using immunochromatography. PCR can only be
done in health facilities that have the equipment for inspection biomoleculer.
Learning task
1. How to distinguish species of malaria by peripheral blood smear examination?
LECTURE 6
DIAGNOSIS OF FILARIASIS
Dr. dr. Made Sudarmaja, M.Kes
Abstract
The infection of filariasis affects 120 million people living in 73 countries, leaving some 40
million profoundly disfigured and incapacitated.The diagnosis of filariasis enforced through
anamnesis, physical examination and investigation of the examination of blood smears for
the presence of microfilaria in the peripheral blood. The microfilariae that cause lymphatic
Udayana University Faculty of Medicine, DME, 2016
25
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
filariasis circulate in the blood at night (called nocturnal periodicity). Blood collection should
be done at night to coincide with the appearance of the microfilariae, and a thick smear
should be made and stained with Giemsa or hematoxylin and eosin.
Learning task
1. How to differentiated species caused filariasis in the examination of blood smears?
Self Assessment
1. Sexual reproduction of P vivax take place in:
A. Human gut
B. Red blood cells
C. Mosquito
D. Liver cell
E. Human Leucocyts
2. The species of plasmodium is characterized by cressent shaped gametocytes and
multiple ring forms whitin RBC:
A. P vivax
B. P falciparum
C. P ovale
D. P malariae
E. P knowlesi
3. The dormant parasite forms found in patient with vivax malaria are called:
A. Thropozoites
B. Sporozoites
C. Hypnozoites
D. Gametocytes
E. Merozoites
4. Sheated microfilaria, described as having two discrete nuclei in the tip of a pointed
tail
A. W bancrofti
B. B malayi
C. Loa loa
D. Onchocerca volvulus
LECTURE 7, 8
TOXOPLASMOSIS & AMOEBIASIS
dr. Luh Ariwati
Entamoeba histolytica is a protozoan parasite responsible for a disease called
amoebiasis. It occurs usually in the large intestine and causes internal inflammation as its
name suggests (histo = tissue, lytic = destroying). 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.
Udayana University Faculty of Medicine, DME, 2016
26
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
Amoebiasis is diagnosed under a microscope by finding cysts and (rarely trophozoites)
from a stool sample. The results are usually said to be negative, if Entamoeba histolytica is
not found in three different stool samples. But it still does not necessarily mean that you are
not infected because the microscopic parasite is hard to find and it might not be present the
particular samples. A blood test might also be available but is only recommended, if your
health care provider believes that the infection could have spread to other parts of the body.
Trophozoites can be identified under a microscope from biopsy samples taken during
colonoscopy or surgery.
Toxoplasmosis well known as parasitic disease and have great impact due to their
worldwide distribution. 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
A previously healthy 28-year old man, who had recently returned from a trip to
Lombok, was seen by his family physician for crampy abdominal pain, malaise, slight fever
and bloody, mucoid diarrhea. Liquid stool specimens were collected and submitted for
culture for enteric bacterial pathogens as well as parasites. Stool cultures were negative for
bacterial pathogens, examination for ova and parasites was positive for motile trophozoites
in the saline wet amount, and ameboid trophozoites with finely granular cytoplasm and
ingested red blood cells in the permanent trichrome stain.
a. Describe the life cycle of parasites above !
b. Explain the pathogenesis of parasite above!
c. Describe infective stages of parasite above!
1. Describe the life cycle of Toxoplasma gondii
2. Explain transmission of Toxoplasma gondii infection
3. Explain why toxoplasma infection became latency
LECTURE 9
SYSTEMIC FUNGAL INFECTION
dr. Luh Ariwati
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.
Udayana University Faculty of Medicine, DME, 2016
27
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
Infections and diseases occur when there are disruptions in the protection barrier of skin
and mucus membrane or defect in immunity system. The characteristic of fungal pathogens
categorized into groups according to tissue that they colonize: superficial, cutaneous,
subcutaneous and systemic mycosis. Fungal infections that occur only because of
compromising situations are categorized as opportunistic mycosis.
Systemic 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. The aetiology are : Predominant fungi
: Candida (C): such as C. Albicans, C. glabrata, C. tropicalis and C.parapsilopsis,
Aspergillus spp.and Cryptococcus spp., Emerging fungi : Fusarium spp., and Rhizopus
spp. and Endemic fungi : Histoplasma capsulatum, Blastomyces dermatitidis and
Coccidioides immitis
There is no specific sign and symptoms of systemic fungal infection. That is why suspected
clinical diagnosis of systemic fungal infection is frequently late. Its resemble bacterial
infections, such as severe sepsis, septic shock and multi organ failure. Alertness to this
infection will comes late though sign and symptoms appear early. In many cases the
diagnosis was done per exlusionem. Diagnosis should be considered in patient with risk
factors has the signs of systemic infection despite adequate antibiotics.
Learning Tasks:
1. Describe the cause and the risk factors of Systemic Fungal Infection
2. Describe the Laboratory diagnosis of candidiasis
3. Describe the morphologic different between Candida and Cryptococcus sp in direct
microscopic examination
LECTURE 10, 11
ASCARIASIS & TRICHURIASIS
dr. Luh Ariwati
Infections with soil-transmitted helminths (STHs: Ascaris, Trichuris, Hookworm and
Strongiloides), which are intestinal worms transmitted through contaminated soil, are the
most common infections worldwide. Globally, more than 1 billion people are infected with
one or more STHs, mainly in areas with warm and moist climates where sanitation and
hygiene are poor. Infection with STH contributes to anemia, vitamin A deficiency,
malnutrition and impaired growth, delayed development, and intestinal blockages.
Ascariasis is a Soil-transmitted helminthiasis (STH) infection caused by the
roundworm Ascaris lumbricoides (A. lumbricoides). Ascariasis, one of the most common
STH infections, affects an estimated 1 billion people worldwide. About half of the
populations in tropical and subtropical areas are infected with this parasite, which causes an
estimated 20,000 deaths each year. While mild cases of ascariasis often show no
symptoms, heavy infections can cause intestinal blockage and impair growth in children.
Ascariasis infection is highly prevalent and geographically widespread. Many factors,
including the large number of eggs produced by a female worm, the properties of the eggs,
Udayana University Faculty of Medicine, DME, 2016
28
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
environmental conditions, and poor socioeconomic settings facilitate the spread of the
parasite and thus determine the geographic distribution of the disease.
Children, especially those suffering from malnutrition, are infected more often than adults,
with the most common age group being 3 to 8 year olds. Children often become infected by
playing in contaminated soil, but eating uncooked food grown in contaminated soil or
irrigated with inadequately treated wastewater is another frequent avenue of infection.
Whipworm (Trichuris trichiura) is the third most common roundworm found in
humans. The name "whipworm" refers to the shape of the worm; the worms look like whips
with wider "handles" at the posterior end. Globally, nearly 800 million people are infected
with whipworms, which are highly prevalent in children. Heavy infections could lead to shortterm symptoms such as diarrhea and anemia and longer-term symptoms such as growth
retardation and impaired cognitive development. Coinfection of whipworm with Giardia,
Entamoeba histolytica, Ascaris lumbricoides, and hookworm is common.
Whipworm infection, known as trichuriasis, is prevalent in both temperate and tropical zones
of the world. However, infections follow a clustered distribution and are more frequently
found in areas with tropical weather and poor sanitation practices. Whipworm infection
occurs through ingestion of whipworm eggs, which can be found in fecally contaminated dry
goods, such as beans, rice, and various grains, and in crops grown in soil fertilized with
sewage. Humans are infected when such produce is consumed raw or food is contaminated
by handlers.
Learning Tasks:
1. Differentiate the morphological characteristics of A.lumbricoides and T. trichiura
2. Describe their life cycles and identify each of their infective stages
3. Describe their pathogenesis and clinical manifestations
4. Identify their stages of development which are useful from the viewpoint of diagnosis
purpose and try to figure their morphological characteristics
5. Define their epidemiological standpoints and list the factors that are closely related to
the transmission of the infections
6. Manage appropriately the diagnosis, treatment, and prevention measures.
LECTURE 12, 13, 14
HOOKWORM INFECTION, STRONGYLOIDIASIS AND ENTEROBIASIS
Dr. dr. Made Sudarmaja, M.Kes
Abstract
Hookworm infection is an infection by a parasitic blood sucking roundworm Ancylostoma
duodenale and Necator americanus. Hookworm infection is a soil-transmitted helminthiasis
and therefore classified as a neglected tropical diseases.These worms live in the small
intestine of human. Hookworm infection affects more than half a billion people in the world.
In developing countries, hookworm infection is rarely fatal, but anemia can be significant in
a heavily infected individual. Ancylostomiasis is the disease caused when
Ancylostomaduodenale hookworms, present in large numbers, produce an iron deficiency
anemia by sucking blood from the host's intestinal walls.Diagnosis of Ancylostomiasis and
Udayana University Faculty of Medicine, DME, 2016
29
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
Necatoriasisdepends on finding characteristic worm eggs on microscopic examination of the
stools
Strongyloidiasis is a human parasitic disease caused by Strongyloidesstercoralis. This
intestinal worm can cause a number of symptoms in people, principally skin symptoms,
abdominal pain, diarrhea and weight loss. In some people, particularly those who require
corticosteroids or other immunosuppressive medication, Strongyloides can cause a
hyperinfection syndrome that can lead to death if untreated. The diagnosis is made by blood
and stool tests. The drug Ivermectin is widely used in the treatment of strongyloidiasis.
Other drugs that are effective are albendazole and thiabendazole (25 mg/kg twice daily for 5
days—400 mg maximum (generally)).
Enterobiasis is an infection caused by Enterobiusvermicularis. Enterobiusvermicularis
(Oxyurisvermicularis) also called human pinworm habits in caecum or in large intestinal.
Adult females has lenght 8 to 13 mm, adult male: 2 to 5 mm. The infective stage of this
worm is embryonated egg. The infection will be occurs through 3 routes:
Self-infection occurs by transferring infective eggs to the mouth with hands that have
scratched the perianal area
Person-to-person transmission can also occur through handling of contaminated clothes or
bed linens. Enterobiasis may also be acquired through surfaces in the environment that are
contaminated with pinworm eggs (e.g. , curtains, carpeting). Some small number of eggs
may become airborne and inhaled. These would be swallowed and follow the same
development as ingested eggs. Following ingestion of infective eggs, the larvae hatch in the
small intestine
Retroinfection, or the migration of newly hatched larvae from the anal skin back into the
rectum, may occur but the frequency with which this happens is unknown.
Diagnostic: found specific egg using perianal swab (under microscope examination)
Learning task:
1. Please explain the life cycle of Hookworm, Strongyloides stercoralis and Enterobius
vermicularis!
2. Describe the prevention based on the life cucle from hookworm infections,
strongyloidiasis and enterobiasis!
3. Explain symptoms and sign of hookworm infections, strongyloidiasis and
enterobiasis!
Self Assessment:
1. The “scoth tape test” is used to diagnose infection with:
A. Ancylostoma duodenale
B. Strongyloides stercoralis
C. Necator americanus
D. Enterobius vermicularis
2. The parasite is capable of autoinfection with may leadto hyperinfection syndrome:
A. Ancylostoma duodenale
B. Strongyloides stercoralis
C. Necator americanus
D. Enterobius vermicularis
3. The eggs of this helmiths is planoconvex and contain tad pole like larva:
A. Ancylostoma duodenale
B. Strongyloides stercoralis
Udayana University Faculty of Medicine, DME, 2016
30
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
C. Necator americanus
D. Enterobius vermicularis
LECTURE 15, 16
LARVA MIGRANS & PEDICULOSIS
dr. Kadek Swastika, M.Kes
Abstract
Cutaneous larva migrans caused by the larvae of animal hookworms. Humans
normally become infected with the hookworm larvae by walking barefoot on a beach, or by
contact with soil that is contaminated with animal faeces Cutaneous larva migrans is most
commonly found in tropical and subtropical geographic areas and the southwestern United
States. It has become an endemic in the Caribbean, Central America, South America,
Southeast Asia, and Africa. However, the ease and the increasing incidence of foreign
travel by the world's population have no longer confined cutaneous larva migrans to these
areas. Cutaneous larva migrans is caused by the larvae of animal hookworms, of which
Ancylostoma braziliense is the species most frequently found in humans [2, 3]. These
hookworms generally live in the intestines of domestic pets such as dogs and cats and shed
their eggs via feces to soil (usually sandy areas of beaches or under houses). Humans are
infected in tropical and subtropical areas of endemicity by contact with contaminated soil.
The hookworm larva burrows through intact skin but remains confined to the upper dermis,
since humans are incidental hostsCreeping eruption usually appears 1–5 days after skin
penetration, but the incubation period may be ≥1 month. Typically, a serpiginous,
erythematous track appears in the skin and is associated with intense itchiness and mild
swelling. Usual locations are the foot and buttocks, although any skin surface coming in
contact with contaminated soil can be affected.
Pediculosis is an infestation of the hairy parts of the body or clothing with the eggs,
larvae or adults of lice. Lice infestation remains a major problem throughout the world,
making the diagnosis and treatment of louse infestation a common task in general medical
practice. Lice on human comprice three types, namely the body louse (Pediculus humanus),
the head louse (Pediculus capitis) and the pubic louse (Pthirus pubis). Head, body and
pubic lice are blood-sucking ectoparasites that are species of Anoplura. They are usually
transmitted directly, by person-to-person contact, but they may also be transmitted
indirectly, via the clothing, towelling and bedding of infested persons. Infestations occur
throughout the world, particularly where there is overcrowding. Poor hygiene tends to
increase the incidence of body lice infestations.
Head lice infestation is very common and is distributed worldwide. Preschool and
elementary-age children, 3 to 11 years of age are infested most often. Females are infested
more often than males, probably due to more frequent head to head contact. Body lice are
also cosmopolitan but are less common and usually seen in settings of poverty, war, and
homelessness.The majority of head lice infestations are asymptomatic. When symptoms
are noted they may include a tickling feeling of something moving in the hair, itching,
caused by an allergic reaction to louse saliva, and irritability. Secondary bacterial infection
may be a complication. Body lice can serve as vectors for Rickettsia prowazekii (epidemic
typhus), Bartonella quintana (trench fever), and Borrelia recurrentis (louse-borne relapsing
fever).
Udayana University Faculty of Medicine, DME, 2016
31
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
Learning task 1
A 10-year-old girl accompany by her family come to the health center complaining of itchy
head. Itching is already being felt since one month ago. Patients living in the dorms, some
of the children who lived there also had the same complaint. On physical examination was
found in scalp hair looks dull and contain white objects.
1. What is the etiology of that case?
2. Describe the life cycle that species!
3. Describe the mode of transmission of that case!
4. How to manage that case? Please explain the treatment and prevention.
Learning task 2
A man 30 years old came to the clinic with complaints of redness track appears in the skin
of left foot since 3 days ago. These symptom associated with intense itchiness and mild
swelling. Last week he went to beach and walking around without slippers. On local
examination found erythematous track on left foot.
1. What is the diagnosis of that case?
2. What are the possibility agents cause that case?
3. Describe the mode of transmission of that case
4. How to manage that case? Please explain the treatment and prevention
LECTURE 17, 18, 19
SCHISTOSOMIASIS, TAENIASIS, SISTISERKOSIS
dr. Kadek Swastika, M.Kes
Abstract
Schistosomiasis is an acute and chronic disease caused by parasitic worms.
Schistosomiasis is caused by digenetic blood trematodes. The three main species
infecting humans are Schistosoma haematobium, S. japonicum, and S. mansoni.
Estimates show that at least 258 million people required preventive treatment in 2014.
Preventive treatment, which should be repeated over a number of years, will reduce and
prevent morbidity. Transmission occurs when people suffering from schistosomiasis
contaminate freshwater sources with their excreta containing parasite eggs which hatch
in water. People become infected when larval forms of the parasite – released by
freshwater snails – penetrate the skin during contact with infested water. In the body, the
larvae develop into adult schistosomes. Adult worms live in the blood vessels where the
females release eggs. Some of the eggs are passed out of the body in the faeces or
urine to continue the parasite’s life-cycle. Others become trapped in body tissues,
causing immune reactions and progressive damage to organs. Schistosomiasis is
diagnosed through the detection of parasite eggs in stool or urine specimens. Antibodies
and/or antigens detected in blood or urine samples are also indications of infection. The
WHO strategy for schistosomiasis control focuses on reducing disease through periodic,
targeted treatment with praziquantel through the large-scale treatment (preventive
chemotherapy) of affected populations.
The cestodes, or tapeworms, constitute a class of phylum Platyhelminthes. The
adult tapeworms found in human all have a flat and ribbonlike body. Living worms are
white or yellowish. The cestode body consists of an anterior attachment organ, or scolex,
Udayana University Faculty of Medicine, DME, 2016
32
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
followed by a chain segments or proglottids also known as strobila. Three spesies of
human Taenia are recognized : Taenia solium, Taenia saginata and Taenia asiatica. All
three spesies are important public health problems in endemic areas as foodborne
zoonoses. The beef tapeworm occurs wherever people eat cured or undercooked beef
infected with taenia saginata, and the pork tapeworm occurs wherever people eat cured
or undercooked pork infected with taenia solium.Cysticercosis is caused by the larval
stage of tapeworm Taenia solium. Taenia solium is endemic in all area of world where
pigs are raised under conditions in which they have access to human fecal material.
Highly endemic area of Taeniasis/Cysticercosis are in Latin America, Eastern Europe,
sub-Saharan Africa, India, also recognized in Indonesia, Southeast Asia, China, Korea.
In Indonesia there are three endemic provinces for taeniasis/cysticercosis : Bali, Papua
and North Sumatra. Others provinces also reported this cases such as East Nusa
Tenggara, Lampung, North Sulawesi, Southeast Sulawesi, and West Kalimantan.
Learning Task
A man 47 years old came to Primary Health care with the complained discomfort on his
stomach since one month ago and sometimes accompanied with diarrhea, No fever. He is
a Balinese and work as a social worker. Physical examination found temperature 37,1 ° C,
Blood pressure 120/80 mmHg. Stool examination found an oval egg size 35 µm, with
radially striated brown sell and six hooked onchospere
1. What other information you need to complete the diagnosis?
2. What is the possibility diagnosis and how to manage this patient
3. What is additional examination you need to know the species?
4. On gravid proglotids found 11 uterine branch, Please Describe the life cycle of this
species!
5. What is possibility complication caused by this spesies? And how it can be occur?
LECTURE 20, 21
GRAM POSITIVE AND NEGATIVE BACTERIA
dr. Made Agus Hendrayana, M. Ked
ABSTRACT
Danish scientist Hans Christian Gram devised a method to differentiate two
types of bacteria based on the structural differences in their cell walls. In his test, bacteria
that retain the crystal violet dye do so because of a thick layer of peptidoglycan and are
called Gram-positive bacteria. In contrast, Gram-negative bacteria do not retain the violet
dye and are colored red or pink. Compared with Gram-positive bacteria, Gram-negative
bacteria are more resistant against antibodies because of their impenetrable cell wall.
These bacteria have a wide variety of applications ranging from medical treatment to
industrial use
In a Gram stain test, bacteria are washed with a decolorizing solution after being dyed with
crystal violet. On adding a counterstain such as safranin or fuchsine after washing, Gramnegative bacteria are stained red or pink while Gram-positive bacteria retain their crystal
violet dye. This is due to the difference in the structure of their bacterial cell wall. Grampositive bacteria do not have an outer cell membrane found in Gram-negative bacteria. The
Udayana University Faculty of Medicine, DME, 2016
33
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
cell wall of Gram-positive bacteria is high in peptidoglycan which is responsible for retaining
the crystal violet dye. 90-95% of Gram negative bacteria are pathogenic. On the other hand,
many Gram-positive bacteria are non-pathogenic. Not only do gram-negative bacteria tend
to be harmful to humans, they are also more resistant to antibiotics.
LEARNING TASK
Case:
A 25 years old male, collage student, come to clinic complained that there are infected
wound on his right foot. The wound is ooze yeloow pus. The wound obtained a week ago
due to fall while playing soccer. Four days ago he went to the doctor and been given some
medicine but is not getting better.
After physical examination, the doctor ask for laboratory examination as Gram staining for
the pus. After few minttes, the Gram staining result sight at the microscope is visible
colonies of blue bacteria, spherical shape and clusters like grapes fruit.
1. What bacteria that visible at the microscope for this case?
2. Explain the differences in the characteristics of gram-negative and gram-positive bacteria
!
3. Explain why each bacteria produce different colors in Gram staining !
4. Identify each five (5) examples of Gram Positive and Gram Negative Bacteria !
5. Describe the structure of Gram-negative bacteria cell wall !
6. . Describe the structure of Gram-positif bacteria cell wall !
7. Explain the benefits of knowing the classification of bacteria based on the results of gram
staining !
Self Assessment:
1. Explain the steps of Gram staining !
Reff :
Jawetz, Melnick, Adelberg. 2013 Chapter 3. Classification of Bacteria in Medical
Microbiology, 26th Edition by Vishal . The McGraw-Hill Companies. Lange Microbiology.
LECTURE 22
MYCOBACTERIUM
IB Nyoman Putra Dwija, S.Si, M. Biotech
ABSTRACT
Genus of Mycobacterium consist of many species that potentially pathogen such as
Mycobacterium complex (M.tuberculosis, M.bovis, M.africanum), M.leprae and M.ulcerans.
All the member of the genus has the similar properties Which is thin, slightly curved or
straight rod-shaped (0.2-0.4 X 2 – 10 µm), non motile, grow slowly, aerobe, non
sporoforming, non motile and pigment of the colony are varies from non pigmented to
pigmented.
Tuberculosis (Tb) is an ancient diseases that found more than 100 year ago, which
is still have a high number of cases. In a predicted as much as 9 million people are
infected and more than 2 million death annualy. Mycobacterium tuberculosis (M.Tb) is the
only agent of Tb, M.Tb was identified for the first time by Robert Koch in 1882, while he
Udayana University Faculty of Medicine, DME, 2016
34
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
was presenting his famous postulate. Mycobacteria spp have a different structure of cell
wall which contain N- glycolylmuramic and rich content of lipid. Because of this unusual cell
wall, mycobacteria are dificult to stain with basic anyline dye such as Gram staining, but
once the bacteria stained, it’s dificult to decolorization even with acidified alcohol (3% HCL),
and so called Acid fast bacilli. HIV Pandemic and emerging of MDR/XDR-TB is another
problem that treathed a human health.
Another member of genus of Mycobacterium is Mycobacterium leprae,the etiologic
agent of Leprosy (Hansen diseases). Majority of the cases found in South and Southeast
Asia, Africa and Latin America,with number of cases average 600.000-700.000 annualy.
Leprosy is a chronic, granulomatous and delibitating diseases. General manifestation is
anasthetic skin lesion and peripheral neuropathy with tickening of the nerve. Bacilli can be
found from few (Tuberculoid leprosy) to massive number of bacteria (Lepromatous leprosy).
Since the bacteria is dificult tu culture, diagnosis is based on finding of the diseases sign
with suported by AFB finding in the slit skin smear or biopsy, molecular detection as well.
LEARNING TASK
A 45 years old women come to the private clinic with productive cought,with blood on the
sputum since 2 weeks, sweating in the night, loses in body weight and loses of apetite
1. What is the posible diagnosis of this patient?
2. Explain the properties of the etiologic agent of deseases!
3. What is the best specimen must be collected for laboratory examination?
4. As a doctor what is your suggestion for this patient?
5. What is latent tuberculosis?
SELF ASSESSMENT:
1. What is the relationship between HIV and TB
2. What is MDR and XDR TB and How did it happen?
3. What is the role of the lipid rich of the wall on the staining?
4. What staining can be use to detect M. tuberculosis?
5. Explain about: Tubercolous tuberculosis, Non tuberculous tuberculosis, Tb
Extrapulmonal?
LECTURE 23
PATHOGENESIS OF VIRAL INFECTION
Dr. dr. Ni Nyoman Sri Budayanti, SpMK
Abstract
Viral pathogenesis is the process by which viruses produce disease in the host. The factors
that determine the viral transmission, multiplication, and development of disease in the host
involve complex and dynamic interactions between the virus and the susceptible host.
Viruses cause disease when they breach the host's primary physical and natural protective
barriers; evade local, tissue, and immune defenses; spread in the body; and destroy cells
either directly or via bystander immune and inflammatory responses. Pathogenic
Udayana University Faculty of Medicine, DME, 2016
35
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
mechanisms of viral disease include ; implantation of virus at the portal of entry, local
replication, spread to target organs (disease sites), and spread to sites of shedding of virus
into the environment. Factors that affect pathogenic mechanisms are accessibility of virus to
tissue, cell susceptibility to virus multiplication, and virus susceptibility to host defenses.
Learning Task
A 5-year old boy goes to emergency room because of fever, rash, cold and cough. On
physical examination was found Koplik spots on his bucosal mukosa
Question:
1. What is the meaning of Koplik spots
2. What kind of viruses can make Koplik spots
3. Describe how the virus can enter to the human body
4. Describe the complication of this disease
Self Assesment
1. Describe the clasification of viruses
2. Describe the simptoms and signs of viral infection
3. Describe how the viruses can enter to the human body
4. Describe the effect of viral infection in the cellular level
5. Describe the replication of viruses in general
6. Describe how the viruses can spread from human to human
LECTURE 24
DNA VIRUS
Dr. dr. Ni Nyoman Sri Budayanti, SpMK
Abstract
Viruses can be classified based on proteins encoded within the viral genetic material or
genomic. DNA virus is a virus that has DNA as its genetic mterial and replicates using DNAdependent DNA polymerase. In the appropriate cell, DNA viruses are able to program the
cell to replicate the virus using the genes contained within the viral DNA genome. There are
six different DNA virus families that infect and may cause significant disease in humans.
Viruses with small DNA genomes include human papillomavirus (HPV). HPV infects
epithelial cells of the skin. It causes common warts on hands and feet and in some cases is
important for the development of cervical cancer in woman. Hepatitis B is another small
DNA virus that infects the liver, causes hepatitis, and is associated with liver cancer.
Adenovirus, herpesvirus, and poxvirus are all examples of large DNA viruses that infect
humans. Adenovirus cause gastroenteritis and respiratory disease in humans.
Learning task
 Describe in detail the clasification of DNA viruses base on Baltimore’s clasification
and example of the viruses from each classes
 Explain in detail 3 viruses (Hepatitis virus, Herpes virus, Human papiloma virus)
which are belong to DNA viruses based on their :
o Baltimore’s clasification
o Structure of their virion
Udayana University Faculty of Medicine, DME, 2016
36
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
o
o
o
o
Replication
Route of shedding and spreading
Simptoms and signs
Complication
Self Assesment
A 30-year old woman goes to private clinic because of fever, fatique, malaise, jaundice and
dark urine. Her boy friend has addmited in hospital last month due to similar simptoms.
Question:
1. What kind virus as the causes of that illness.
2. Which Baltimore’s clasification is the virus belong to
3. How can the virus enter our body
4. How can the virus infect her
5. What kind treatment can be given to her
LECTURE 25
RNA VIRUS
Dr. dr. Ni Nyoman Sri Budayanti, SpMK
Abstract
An RNA virus is a virus that has RNA (ribonucleic acid) as the genetic material. Notable
human diseases caused by RNA viruses include Ebola, Hemorrhagic fever, SARS,
Influenza, Hepatitis C, Polio and measles. RNA generally have very high mutation rate
compare to DNA viruses, because virus RNA polymerase lact the proof-reading ability of
DNA polymerase. Classification is based on the type of genomes and gene number and
organitation.
Learning task
1. Describe the structure of RNA viruses
2. Describe classification RNA viruses based on their type of genome
3. Describe replication of RNA virus, particullary retroviruses
4. Explain 3 kinds of RNA viruses (rabies, influenza, polio) based on their :
 Structure of virion
 Replication
 Mode of transmition
 Pathogenesis
 Simptom and signs
 Treatment
Self assesment
A 5-year old boy come to emergency room because of panic, dificult to swallow, avoid light
and hidrofobi. His parent told that he has been bitten by dog 2 month ago and no
vaccination was given.
Question
 What kind simptom and sign were specific for this illness
Udayana University Faculty of Medicine, DME, 2016
37
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases


What kind virus is cause of this illnes
Explain in detail the vaccination should be receive to prevent this illness
LECTURE 26
ZOONOSIS
Dr. dr. Ni Nyoman Sri Budayanti, SpMK
Abstract
Any disease of infection that is naturally transmissible from vertebrate animals to humans
and vice versa is classified as a zoonosis. Zoonoses have been recognized for many
centuries. They are caused by all types of pathogenic agent including bacteria, parasites,
fungi and viruses. Zoonosis still represent significant publict health threats but many of them
a negleted i.e. they are not priotized by health system at national and international level.
They affect people especially in developing country although most of them can be prevent.
Learning task
1. Namely 5 diseases which are including in zoonosis diseases and explain why those
of them fit with zoonosis criteria.
2. Explain in detail why One Health approach is a good stategic to prevent and
overcome problem of zoonosis disease
Self assesment
A 23-year old man come to emergency room because of fever, hard to breathe since 2 days
ago. In 2 days he felt the simptom getting worse. He has history contacted with dead
chicken in his farm.
Question
 What kind disease has he suffering
 What kind microorganism as cause of that illness
 How to prevent that illness
LECTURE 27
SPECIMEN COLLECTION
dr. Ni Nengah Dwi Fatmawati, SpMK, Ph.D
Abstract
Infectious diseases are caused by microbes, including bacteria and viruses. Identification of
microbes as causative agents of infection is important to help in determining definitive
therapy. Clinical specimens from patients such as blood, sputum, urine, wound swab, etc.,
are needed for Clinical Microbiology assay for microbes identification and antimicrobial
susceptibility test. Correct and proper specimen must be collected for the assay. There are
considerations that must be concerned when collecting specimen for Clinical Microbiology
for example proper time collection, proper site of collection, volume or number of specimen,
Udayana University Faculty of Medicine, DME, 2016
38
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
avoid contamination, etc., therefore the results of assay will be reliable and can assist the
clinicians to treat the infectious diseases properly.
Learning Task:
Case 1:
A 30-year-old woman goes to private clinic because of dysuria, frequency, and urgency on
urination for 24 hours.
Questions:
1. What kind of specimen(s) must be collected from this patient?
2. How to collect the specimen(s) therefore get proper specimen?
3. How to transport and preserve the specimen(s)?
Case 2:
A-70-year old man admitted to ER with chief complain harsh, productive cough since 4 days
prior to being seen by a physician. The sputum is thick and yellow with blood streaks. He
had fever, shaking, chills and malaise along with the cough.
Questions:
1. What kind of specimen(s) must be collected from this patient?
2. How to collect the specimen(s) therefore get proper specimen?
3. How to transport and preserve the specimen(s)?
Self assesment:
1. Describe general considerations of clinical specimen collection for clinical
microbiology assay.
2. Describe in detail how to collect, transport and preserve blood specimen.
3. Describe in detail how to collect, transport and preserve sputum specimen.
4. Describe in detail how to collect, transport and preserve urine specimen.
5. Describe in detail how to collect, transport and preserve wound aspiration specimen.
6. Describe in detail how to collect, transport and preserve wound swab specimen.
7. Describe in detail how to collect, transport and preserve throat swab specimen.
8. Describe in detail how to collect, transport and preserve cerebrospinal fluid (CSF)
specimen.
9. Determine proper specimen for diagnose:
a. Urinary tract infections
b. Pneumonia
c. Sepsis
d. Infected wound
e. Meningitis
f. Pharingitis
10. How to avoid normal flora contamination when collecting urine and sputum
specimen?
References:
Mahon et al., Textbook of Diagnostic Microbiology, Fourth Edition, Elsevier, 2011
Udayana University Faculty of Medicine, DME, 2016
39
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
LECTURE 28
MICROBIAL IDENTIFICATION & ANTIMICROBIAL SENSITIVITY TEST (AST)
dr. Ni Nengah Dwi Fatmawati, SpMK, Ph.D
Abstract
Proper clinical specimen is needed for reliable result of Clinical Microbiology Tests. After
collecting the specimen, specimen is subjected to several Clinical Microbiology
examinations or tests to identify the causative agents of infections. The specimen generally
will be subjected to staining (for example Gram staining, Ziehl Neelsen staining), culture,
biochemical tests for identification, or molecular biology tests for further identification. The
microbial (bacterial) identification is followed by antisusceptibility testing (AST) to determine
the susceptibility of tested bacteria to certain antibiotics. The bacterial identification and AST
can be done manually, semi automatically or automatically. The result of bacterial
identification and AST will help the clinicians to determine definitive therapy of antibiotics.
Learning task:
Case:
A-50-year old man admitted to ER with chief complain productive cough since 7 days prior
to being seen by a physician. The sputum is thick and yellow with blood streaks. He had
fever, shaking, chills and malaise along with the cough. Sputum specimen was taken.
Question:
1. Explain steps for bacterial identification for this patient.
2. Explain steps for the AST for this patient (using Kirby Bauer Disk Difussion).
Antibiotics that used for this case is Ciprofloxacin, Ampicillin, Amoxyxillin, Cefadroxil,
and Gentamicin.
3. Explain the result iof AST if the result showed like this.
Table from CLSI (only simulation)
Antibiotics’
name
Ciprofloxacin
Ampicillin
Amoxycillin
Cefadroxil
Gentamicin
Range for
Susceptible/S
(mm)
> 25
> 20
> 17
> 22
> 18
Range for
Intermediate/I
(mm)
15-25
11-20
10-17
15-22
11-18
Range for
Resistant/R
(mm)
< 15
< 11
< 10
< 15
< 11
Result of This
Case’s AST
(mm)
30
8
15
23
19
Self assesment:
1. Describe how to identify Staphylococcus (based on Gram staining, colony on
culture, and biochemical tests).
2. Describe how to identify Streptococcus (based on Gram staining, colony on culture,
and biochemical tests).
3. Explain or give examples of manual, semi-automatic, and automatic bacterial
identification.
Udayana University Faculty of Medicine, DME, 2016
40
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
4. Explain how to identify Mycobacterium tuberculosis (based on Ziehl Neelsen staining
and colony characteristic on culture)
5. Explain how to perform Kirby Bauer Disk Diffusion Tests and how to interpret the
result.
References:
Mahon et al., Textbook of Diagnostic Microbiology, Fourth Edition, Elsevier, 2011
LECTURE 29
MECHANISM OF ACTION AND RESISTANCE OF ANTIBIOTIC
dr. Ni Nengah Dwi Fatmawati, SpMK, Ph.D
Abstract
Antibiotics are therapy for bacterial infections. Antibiotics can be used as empirical,
definitive, and prophyoaxis therapy. There are several mechanism of action of antibiotics
i.e., Inhibition of Cell Wall Synthesis (Beta lactam, Vancomycin, Bacitracin), Inhibition of
Protein Synthesis (Aminoglycosides, Tetracyclin, Chloramphenicol, Macrolides,
Clindamycin), Alteration of Cell Membrane (Polymixins), Inhibition of Nucleic Acid Synthesis
(Quinolone, Metronidazole, Rifampin), and Antimetabolite Activity (TMP-SXT).
Considerations are needed for prudent use of antibiotics. Misuse of antibiotics will
encourage the resistance against the antibiotics. Several mechanism involve in bacterial
resistance.
Learning Task:
Case:
A 20-year-old woman goes to GP because of dysuria, frequency, and urgency on urination
for 24 hours. The bacterial identification of bacteria showed Escherichia coli (105 colony
count) and susceptible to Trimethoprim-Sulphametoxazole (TMP-SXT) and Ciprofloxacin.
Questions:
1. Explain the mechanism of action TMP-SXT and the resistance mechanism against
TMP-SXT.
2. Explain the mechanism of action Ciprofloxacin and the resistance mechanism of
Ciprofloxacin
3. Explain how the antimicrobial resistant genes are transferred via conjugation,
transduction, transformation and transposition
4. Explain other antibiotics that are classified as quinolone.
Self Asessment:
1. Explain classes of antibiotics and give examples of each clasess
2. Explain the mechanism of action of each antibiotic class
3. Explain the mechanism of resistance to each classes of antibiotics
4. Explain what are the empirical, definitive and prophylaxis antibiotics
5. Explain the consideration for prudent use of antibiotics
References:
Udayana University Faculty of Medicine, DME, 2016
41
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
Jawetz, Melnick & Adelberg’s Medical Microbiology. 26th Ed, 2013.
LECTURE 30
BIOSAFETY & BIOSECURITY
IB Nyoman Putra Dwija, S.Si, M. Biotech
ABSTRACT
Biosafety and biosecurity issues began to develop since the occurrence of some of the
pandemic in some countries of the world, such as bird flu, swine flu and the case envelopes
containing anthrax. Biosafety and biosecurity not just concenrn obout the biologic agent but
also concerned about the issue of bioterrorism, good laboratory practice, risk group of the
potentially pathogen and also the safety of the environment. Material transfer agreement
also become one of the study in the biosafety and biosecurity so that, the biological material
is not misused and there is an agreement between two parties in its management.
LEARNING TASK
A 23 years old man work as a cleaning service in the research laboratorium, he come to the
clinic because of feel afraid after sticking by needle in the bin while he work.
1. What is the posibility of misconduct in this cases?
2. Why we should keep our specimen in the special container?
3. What is the role of biosafety and biosecurity oon that case?
4. What is the role of standart operational procedure in the laboratory?
SELF ASSESSMENT
1. Explain about risk group of organism
2. What we need when we are working with M.tuberculosis?
3. What is containment? Please explain!
4. What is good laboratory practice?
LECTURE 31
HEALTH CARE-ASSOCIATED INFECTION
Dr. dr. I Dewa Made Sukrama, M. Si, Sp.MK
ABSTRACT
Health care-associated infection (HAI) — also known as nosocomial infection — is an
infection that is contracted from the environment or staff of a healthcare facility. It can be
spread in the hospital environment, nursing home environment, rehabilitation facility, clinic,
or other clinical settings. Infection is spread to the susceptible patient in the clinical setting
by a number of means. Health care staff can spread infection, in addition to contaminated
equipment, bed linens, or air droplets. The infection can originate from the outside
environment, another infected patient, staff that may be infected, or in some cases, the
source of the infection cannot be determined. In some cases the microorganism originates
from the patient's own skin microbiota, becoming opportunistic after surgery or other
procedures that compromise the protective skin barrier. Though the patient may have
Udayana University Faculty of Medicine, DME, 2016
42
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
contracted the infection from their own skin, the infection is still considered nosocomial
since it develops in the health care setting
In the United States, the Centers for Disease Control and Prevention estimated roughly 1.7
million hospital-associated infections, from all types of microorganisms, including bacteria
and fungi combined, cause or contribute to 99,000 deaths each year.[citation needed] In Europe,
where hospital surveys have been conducted, the category of gram-negative infections are
estimated to account for two-thirds of the 25,000 deaths each year. Nosocomial infections
can cause severe pneumonia and infections of the urinary tract, bloodstream and other
parts of the body. Many types are difficult to treat with antibiotics. In addition, antibiotic
resistance can complicate treatment.
Learning Task
1. Describe risk factors are influence hospital acquired infection
2. Describe some strategies for control of hospital acquired infection
3. Describe some factors are influence to spread of hospital acquired infection.
4. Explain the prevention hospital acquired infection
5. Explain the sources and routes of spread of Hospital Acquired Infection
LECTURE 32
ANAEROB BACTERIA & SPIROCHAETA
Dr. dr. I Dewa Made Sukrama, M. Si, Sp.MK
ABSTRACT
Anaerobic infections are caused by anaerobic bacteria. Obligately anaerobic bacteria do
not grow on solid media in room air (0.04% carbon dioxide and 21% oxygen); facultatively
anaerobic bacteria can grow in the presence or absence of air. Microaerophilic bacteria do
not grow at all aerobically or grow poorly, but grow better under 10% carbon dioxide or
anaerobically. Anaerobic bacteria can be divided into strict anaerobes that can not grow in
the presence of more than 0.5% oxygen and moderate anaerobic bacteria that are able of
growing between 2 and 8% oxygen. Anaerobic bacteria usually do not possess catalase,
but some can generate superoxide dismutase which protects them from oxygen. .The
frequency of isolation of anaerobic bacterial strains varies in different infectious sites.Mixed
infections caused by numerous aerobic and anaerobic bacteria are often observed in clinical
situations.
Anaerobic bacteria are a common cause of infections, some of which can be serious and
life-threatening. Because anaerobes are the predominant components of the normal flora of
the skin and mucous membranes, they are a common cause infections of endogenous
origin. Because of their fastidious nature, anaerobes are hard to culture and isolate and are
often not recovered from infected sites. The administration of delayed or inappropriate
therapy against these organisms may lead to failures in eradication of these infections. The
isolation of anaerobic bacteria requires adequate methods for collection, transportation and
cultivation of clinical specimens.The management of anaerobic infection is often difficult
because of the slow growth of anaerobic organisms, which can delay their identification by
the frequent polymicrobial nature of these infections and by the increasing resistance of
anaerobic bacteria to antimicrobials.
Udayana University Faculty of Medicine, DME, 2016
43
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
LEARNING TASK
1. Discrebe the anaerobic gram positive bacteria
2. Discrebe the gram negative anaerob bacteria
3. Be able to describe the genus clostridia and specific deseases
4. Explain how diagnosis microbiology anaerobic infection
LECTURE 33
HOST RESPONSE TO INFECTION
Prof. Dr. dr. Tuti Parwati Merati, SpPD, KPTI
Abstract
Infectious diseases are one of the leading causes of death worldwide. Many infectious
diseases become difficult to control if the infectious agents evolve resistance to commonly
used drugs, for example, bacteria can accumulate mutations in their DNA or acquire new
genes that allow them to survive contact with antibiotic drugs that would normally kill them.
Scientists are currently searching for new approaches to treat infectious diseases, focusing
on exactly how the pathogens change and drug resistance evolves. Understanding and
comprehend the host response to infection is important.
Infection process
After invading the body, microorganisms must multiply to cause infection. After multiplication
begins, one of three things can happen:
1. Microorganisms continue to multiply and overwhelm the body’s defenses.
2. A state of balance is achieved, causing chronic infection.
3. The body—with or without medical treatment—destroys and eliminates the invading
microorganism.
Defenses Against Infection
Host defenses that protect against infection :
– Natural barriers (eg, skin, mucous membranes)
– Nonspecific immune responses (eg, phagocytic cells [neutrophils,
macrophages] and their products)
– Specific immune responses (eg, antibodies, lymphocytes)
Nonspecific Immune Responses
• Cytokines (including IL-1, IL-6, tumor necrosis factor-alpha, and interferon-gamma)
are produced principally by macrophages and activated lymphocytes and mediate
an acute-phase response that develops regardless of the inciting microorganism.
• The response involves fever and increased production of neutrophils by the bone
marrow. Endothelial cells also produce large amounts of IL-8, which attracts
neutrophils.
• The inflammatory response directs immune system components to injury or infection
sites and is manifested by increased blood supply and vascular permeability, which
allows chemotactic peptides, neutrophils, and mononuclear cells to leave the
intravascular compartment.
Specific Immune Responses
• After infection, the host can produce a variety of antibodies (complex glycoproteins
known as immunoglobulins) that bind to specific microbial antigenic targets.
Udayana University Faculty of Medicine, DME, 2016
44
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
Antibodies can help eradicate the infecting organism by attracting the host’s WBCs
and activating the complement system.
• The complement system destroys cell walls of infecting organisms, usually through
the classical pathway. Complement can also be activated on the surface of some
microorganisms via the alternative pathway.
• Antibodies can also promote the deposition of substances known as opsonins (eg,
the complement protein C3b) on the surface of microorganisms, which helps
promote phagocytosis. Opsonization is important for eradication of encapsulated
organisms such as pneumococci and meningococci.
Interaction between host and the microbes are depend on factors from the host, the
microbes and environment
Host Genetic Factors
• For many pathogens, the host's genetic make-up influences the host's susceptibility
and the resulting morbidity and mortality. For example, patients who have
deficiencies of the terminal complement components (C5 through C8, perhaps C9)
have an increased susceptibility to infections caused by neisserial species.
Factors Facilitating Microbial Invasion
Microbial invasion can be facilitated by the
following:
• Virulence factors
• Microbial adherence, biofilm
• Resistance to antimicrobials
• Defects in host defense mechanisms
Defects in Host Defense Mechanisms
Two types of immune deficiency states affect the host’s ability to fight infection:
• Primary immune deficiency : are genetic in origin; > 100 primary immune deficiency
states have been described. Most primary immune deficiencies are recognized
during infancy; however, up to 40% are recognized during adolescence or
adulthood.
• Secondary (acquired) immune deficiency : are caused by another disease (eg,
cancer, HIV infection, chronic disease) or by exposure to a chemical or drug that is
toxic to the immune system.
Defects in immune responses may involve
• Cellular immunity
• Humoral immunity
• Phagocytic system
• Complement system
Mechanism
• Cellular deficiencies are typically T-cell or combined immune defects. T cells
contribute to the killing of intracellular organisms; thus, patients with T-cell defects
can present with opportunistic infections such as Pneumocystis jirovecii or
cryptococcal infections. Chronicity of these infections can lead to failure to thrive,
chronic diarrhea, and persistent oral candidiasis.
• Humoral deficiencies are typically caused by the failure of B cells to make
functioning immunoglobulins. Patients with this type of defect usually have infections
involving encapsulated organisms (eg, H. influenzae, streptococci). Patients can
present with poor growth, diarrhea, and recurrent sinopulmonary infections.
Udayana University Faculty of Medicine, DME, 2016
45
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
•
A defect in the phagocytic system affects the immediate immune response to
bacterial infection and can result in development of recurrent abscesses or severe
pneumonias.
• Primary complement system defects are particularly rare. Patients with this type
of defect may present with recurrent infections with pyogenic bacteria (eg,
encapsulated bacteria, Neisseria sp) and have an increased risk of autoimmune
disorders (eg, SLE).
Clinical manifestation
• Most infections increase the pulse rate and body temperature, but others (eg,
typhoid fever, tularemia, brucellosis, dengue) may not elevate the pulse rate
commensurate with the degree of fever.
•
Hypotension can result from hypovolemia, septic shock, or toxic shock.
Hyperventilation and respiratory alkalosis are common.
• Alterations in sensorium (encephalopathy) may occur in severe infection regardless
of whether CNS infection is present. Encephalopathy is most common and serious in
the elderly and may cause anxiety, confusion, delirium, stupor, seizures, and coma.
• Infectious diseases commonly increase the numbers of mature and immature
circulating neutrophils. Mechanisms include demargination and release of immature
granulocytes from bone marrow, IL-1- and IL-6-mediated release of neutrophils from
bone marrow, and colony-stimulating factors elaborated by macrophages,
lymphocytes, and other tissues. Exaggeration of these phenomena (eg, in trauma,
inflammation, and similar stresses) can result in release of excessive numbers of
immature leukocytes into the circulation (leukemoid reaction), with leukocyte counts
up to 25 to 30 × 109/L.
• Conversely, some infections (eg, typhoid fever, brucellosis) commonly cause
leukopenia. In overwhelming, severe infections, profound leukopenia is often a poor
prognostic sign.
• Characteristic morphologic changes in the neutrophils of septic patients include
Döhle bodies, toxic granulations, and vacuolization.
• Anemia can develop despite adequate tissue iron stores. If anemia is chronic,
plasma iron and total iron-binding capacity may be decreased. Serious infection may
cause thrombocytopenia and disseminated intravascular coagulation (DIC).
Learning Tasks:
A 40 years-old female admitted to hospital with decreased of consciousness. She suffering
from high fever since a week ago, and she also did not eat and drink much as for her
weaknesses. She had headache, sometimes vomits and feel abdominal discomfort.
1. What is the working diagnosis of the patient?
2. What kind of examination do you need to do for this patient?
3. Please explain if there is a possibility of a defective imune response in this patient?
Self Assessment:
1. Describe the host response to infection in this patient.
2. Based on the pathogenesis, please describe the management of the patient.
Udayana University Faculty of Medicine, DME, 2016
46
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
LECTURE 34, 35, 36
DENGUE FEVER, DENGUE HEMORRHAGIC FEVER, DENGUE SHOCK
SYNDROME
dr. Dewi Dian Sukmawati, SpPD
ABSTRACT
Dengue is mosquito borne viral infection, which causing acute fever and
occasionally develops into potential lethal complication. Dengue virus is transmitted by
female mosquitoes mainly of the species Aedes aegypti and, to a lesser extent, Ae.
albopictus. This mosquito also transmits Chikungunya, Yellow Fever and Zika infection.
About half of world’ population were at risk, Dengue is widespread throughout the tropics,
with local variations in risk influenced by rainfall, temperature and unplanned rapid
urbanization.
There are 4 distinct, but closely related, serotypes of the virus that can cause
dengue (DEN-1, DEN-2, DEN-3 and DEN-4). Recovery from infection by one provides
lifelong immunity against the particular serotype with partial and temporary cross-immunity
to the other serotypes after recovery. Subsequent infections by other serotypes increase the
risk of developing severe dengue.
Dengue should be suspected when a high fever is present, accompanied by 2 of the
following symptoms: severe headache, pain behind the eyes, muscle and joint pains,
nausea, vomiting, swollen glands or rash. Symptoms usually last for 2–7 days, after an
incubation period of 4 – 5 days (range 3 – 14 days) after the bite from an infected mosquito.
Severe dengue is a potentially deadly complication due to plasma leakage, fluid
accumulation, respiratory distress, severe bleeding, or organ impairment. Warning signs
occur 3–7 days after the first symptoms in conjunction with a decrease in temperature and
include: severe abdominal pain, persistent vomiting, and rapid breathing, bleeding gums,
fatigue, restlessness and blood in vomit. The next 24–48 hours of the critical stage can be
lethal; proper medical care is needed to avoid complications and risk of death.
For the purpose of clinical management, WHO classifies dengue illness as (i)
dengue with or without warning signs for progression towards severe dengue and (ii) severe
dengue. Warning signs of severe dengue include abdominal pain or tenderness, persistent
vomiting, clinical fluid accumulation, mucosal bleeding, lethargy or restlessness, liver
enlargement of >2 cm, or an increase in Hematocrit concurrent with a rapid decrease in
platelet count. Criteria for severe dengue include any sign of severe plasma leakage leading
to shock or fluid accumulation with respiratory distress, severe bleeding, or severe organ
impairment.
There is no specific treatment for dengue, maintenance of the patient’s body fluid
volume is critical in management of severe dengue. Vaccine for prevention is now
commercially available, Dengvaxia (CYD – TDV) for use in individual age 9 – 45 years living
in area with high burden of disease.
LEARNING TASK
Case 1:
IMD, 16 year old male student come to a private clinic with acute onset of high fever. The
fever starts abruptly one day before accompanied by nausea and retro orbital pain.
Udayana University Faculty of Medicine, DME, 2016
47
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
Questions:
1. What other information needed in anamnesis of this patient? What data should be
obtained during physical examination?
2. The evaluation shows vital sign was stabile without any sign of bleeding, the patient
able to drink plenty and eat normally. What is the diagnosis of this patient? How
about further plan for this case, including planning for diagnostic, treatment,
monitoring and patient and family’s education?
3. The next day, he showed his laboratory evaluation. WBC: 1.03 x 103/uL. Hb. 17
g/dL. HCT 54 %. Plt. 98 x 103/uL. What is the diagnosis of this patient? How about
further plan for this case, including planning for diagnostic, treatment, monitoring and
patient and family’s education?
Case 2:
25 year old woman, working as a private secretary, come to the clinic with 4 days of fever.
Since morning she also had her menstrual bleeding which comes 2 weeks early. The initial
evaluation revealed moderately ill, fully alert. Blood pressure 90/76 mmHg. Pulse rate 124
x/minutes. Respiratory rate: 22 x/minutes. Temperature axillae: 36.7˚C. Hepatomegaly 3 cm
below costal arch, tender on palpation, the acrals were cold. She has her laboratory
evaluation: WBC: 3.02 x 103/uL; Hb. 16 g/dL. HCT: 51.2 %. Plt.32 x 103/uL
1. What is the diagnosis of this patient? How about further plan for this case, including
planning for diagnostic, treatment, monitoring and patient and family’s education?
2. Is there any indication for platelet transfusion in this case? Why?
3. The patient was then hospitalized, by the third day of her hospital stay, she complain
about shortness of breath and cough if she change position from supine to sitting.
The physical evaluation revealed dullness on lower part of right hemithorax with
decreased breath sounds. What kind of complication can be expected in severe
dengue cases? How can we establish the diagnosis?
Self assessment
1. How can we differentiate between dengue fever and dengue hemorrhagic fever?
Make a comparison chart on this issue!
2. Both DHF grade 3 and 4 are included as DSS. How can we differentiate between the
two of them?
3. What is NS1 dengue antigen? When is the best way to use it?
4. How about dengue serology? When IgM anti-Dengue become positive? When the Ig
G anti-dengue become positive? Make the chart on the possible result and its
interpretation!
REFERENCES:
1. World Health Organization. Dengue Guidelines for Diagnosis, Treatment, Prevention
and Control. Geneva, Switzerland: 2009. Available at http://www.who.int/tdr/
publications/documents/dengue-diagnosis.pdf
2. Messina JP, et al. Global spread of dengue virus types: mapping the 70 year history.
Trends Microbiol. 2014;22(3):138–146.
3. Guzman MG, et al. Dengue. Lancet. 2015;385(9966):453–465.
4. Comprehensive guidelines for prevention and control of dengue and dengue
hemorrhagic fever. WHO SEARO 2011
5. Handbook for clinical management of dengue. WHO 2012
Udayana University Faculty of Medicine, DME, 2016
48
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
LECTURE 37
INFECTION IN PREGNANCY (TORCH)
Dr. dr. IB Fajar Manuaba, SpOG
Abstract
Infections have historically been a major cause of maternal and fetal morbidity and mortality
worldwide, and they remain so in the 21st century. The unique maternal-fetal vascular
connection in some cases serves to protect the fetus from infectious agents, whereas in
other instances it provides a conduit for their transmission to the fetus. TORCH infections
include infections associated with Toxoplasma, Other organisms (Parvovirus, human
immunodeficiency virus, Epstein-Barr virus, herpesviruses 6 and 8, varicella, syphilis,
enteroviruses), Rubella, Cytomegalovirus (CMV), and Hepatitis. Despite the recent
emphasis in the screening, antibiotic prophylaxis, and management of early-onset many
neonates and children yearly experience the consequences of classic perinatal infections
Introduction
Infections have historically been a major cause of maternal and fetal morbidity and mortality
worldwide, and they remain so in the 21st century. The unique maternal-fetal vascular
connection in some cases serves to protect the fetus from infectious agents, whereas in
other instances it provides a conduit for their transmission to the fetus. Maternal serological
status, gestational age at the time infection is acquired, the mode of acquisition, and the
immunological status of both the mother and her fetus all influence disease outcome.
TORCH is an acronym for a group of congenitally acquired infections that may cause
significant morbidity and mortality in neonates. TORCH infections include infections
associated with Toxoplasma, Other organisms (Parvovirus, human immunodeficiency virus,
Epstein-Barr virus, herpesviruses 6 and 8, varicella, syphilis, enteroviruses), Rubella,
Cytomegalovirus (CMV), and Hepatitis. Despite the recent emphasis in the screening,
antibiotic prophylaxis, and management of early-onset many neonates and children yearly
experience the consequences of classic perinatal infections.
Toxoplasmosis
The obligate intracellular parasite Toxoplasma gondii has a life cycle with two distinct
stages. The feline stage takes place in the cat—the definitive host—and its prey.
Unsporulated oocysts are secreted in feces. In the non-feline stage, tissue cysts containing
bradyzoites or oocysts are ingested by the intermediate host, including humans. Human
infection is acquired by eating raw or undercooked meat infected with tissue cysts or by
contact with oocysts from cat feces in contaminated litter, soil, or water. Prior infection is
confirmed by serological testing, and its prevalence depends on geographic locale and
parasite genotype.
Most acute maternal infections are subclinical and are detected only by prenatal or newborn
serological screening. In some cases, maternal symptoms may include fatigue, fever,
headache, muscle pain, and sometimes a maculopapular rash and posterior cervical
lymphadenopathy. The incidence and severity of fetal toxoplasmosis infection depend on
gestational age at the time of maternal infection. Risks for fetal infection increase with
Udayana University Faculty of Medicine, DME, 2016
49
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
pregnancy duration A metaanalysis estimated the risk to be 15 percent at 13 weeks, 44
percent at 26 weeks, and 71 percent at 36 weeks. Conversely, the severity of fetal infection
is much greater in early pregnancy, and these fetuses are much more likely to have clinical
findings of infection.
Pregnant women suspected of having toxoplasmosis should be tested. The parasite is
rarely detected in tissue or body fluids. Anti-toxoplasma IgG develops within 2 to 3 weeks
after infection, peaks at 1 to 2 months, and usually persists for life—sometimes in high
titers. Although IgM antibodies appear by 10 days after infection and usually become
negative within 3 to 4 months, they may remain detectable for years. Thus, IgM antibodies
should not be used alone to diagnose acute toxoplasmosis. IgA and IgE antibodies are also
useful in diagnosing acute infection. Toxoplasma IgG avidity increases with time. Thus, if a
high-avidity IgG result is found, infection in the preceding 3 to 5 months is excluded. Multiple
commercial avidity tests are now available that provide a 100-percent positive predictive
value of high avidity confirming latent infection.
No randomized clinical trials have been performed to assess the benefit and efficacy of
treatment to decrease the risk for congenital infection. A systematic review of data from
1.438 treated pregnancies found weak evidence for early treatment to reduce congenital
toxoplasmosis risks. Treatment has been associated with a reduction in rates of serious
neurological sequelae and neonatal demise.
Prenatal treatment is based on two regimens—spiramycin alone or a pyrimethamine–
sulfonamide combination with folinic acid. These two regimens have also been used
consecutively. Little evidence supports the use of a specific regimen. That said, most
experts will use spiramycin in women with acute infection early in pregnancy.
Pyrimethamine–sulfadiazine with folinic acid is selected for maternal infection after 18
weeks or if fetal infection is suspected.
Parvovirus
Human parvovirus B19 causes erythema infectiosum, or fifth disease. The B19 virus is a
small, single-stranded DNA virus that replicates in rapidly proliferating cells such as
erythroblast precursors. This can lead to anemia, which is its primary fetal effect. Only
individuals with the erythrocyte globoside membrane P antigen are susceptible. In women
with severe hemolytic anemia—for example, sickle-cell disease—parvovirus infection may
cause an aplastic crisis.
In 20 to 30 percent of adults, infection is asymptomatic. Fever, headache, and flu-like
symptoms may begin in the last few days of the viremic phase. Several days later, a bright
red rash with erythroderma affects the face and gives a slappedcheekappearance. The rash
becomes lacelike and spreads to the trunk and extremities. Adults often have milder rashes
and develop symmetrical polyarthralgia that may persist several weeks.
There is vertical transmission to the fetus in up to a third of maternal parvovirus infections
Fetal infection has been associated with abortion, nonimmune hydrops, and stillbirth. In a
review of 1089 cases of maternal B19 infection from nine studies, Crane (2002) reported an
overall fetal loss rate of 10 percent. It was 15 percent for infections before 20 weeks but was
only 2.3 percent after 20 weeks.
Udayana University Faculty of Medicine, DME, 2016
50
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
Depending on gestational age, fetal transfusion for hydrops may improve outcome in some
cases. Mortality rates as high as 30 percent have been reported in hydropic fetuses without
transfusions. With transfusion, 94 percent of hydrops cases resolve within 6 to 12 weeks,
and the overall mortality rate is < 10 percent. Most fetuses require only one transfusion
because hemopoiesis resumes as infection resolves.
There is currently no approved vaccine for human parvovirus B19, and there is no evidence
that antiviral treatment prevents maternal or fetal infection. Decisions to avoid higher-risk
work settings are complex and require assessment of exposure risks. Pregnant women
should be counseled that risks for infection approximate 5 percent for casual, infrequent
contact; 20 percent for intense, prolonged work exposure such as for teachers; and 50
percent for close, frequent interaction such as in the home. Workers at day-care centers
and schools need not avoid infected children because infectivity is greatest before clinical
illness. Finally, infected children do not require isolation.
Rubella—German Measles
This RNA togavirus typically causes infections of minor importance in the absence of
pregnancy. Rubella infection in the first trimester, however, poses significant risk for
abortion and severe congenital malformations. Transmission occurs via nasopharyngeal
secretions, and the transmission rate is 80 percent to susceptible individuals. The peak
incidence is late winter and spring.
Maternal rubella infection is usually a mild, febrile illness with a generalized maculopapular
rash beginning on the face and spreading to the trunk and extremities. Other symptoms
may include arthralgias or arthritis, head and neck lymphadenopathy,and conjunctivitis. The
incubation period is 12 to 23 days. Viremia usually precedes clinical signs by about a week,
and adults are infectious during viremia and through 5 to 7 days of the rash. Up to half of
maternal infections are subclinical despite viremia that may cause devastating fetal
infection.
Rubella may be isolated from the urine, blood, nasopharynx, and cerebrospinal fluid for up
to 2 weeks after rash onset. The diagnosis is usually made, however, with serological
analysis. Specific IgM antibody can be detected using enzyme-linked immunoassay from 4
to 5 days after onset of clinical disease, but it can persist for up to 6 weeks after appearance
of the rash. Importantly, rubella reinfection can give rise to transient low levels of IgM.
Serum IgG antibody titers peak 1 to 2 weeks after rash onset. This rapid antibody response
may complicate serodiagnosis unless samples are initially collected within a few days after
the onset of the rash. If, for example, the first specimen was obtained 10 days after the
rash, detection of IgG antibodies would fail to differentiate between very recent disease and
preexisting immunity to rubella. IgG avidity testing is performed concomitant with the
serological tests above. High-avidity IgG antibodies indicate an infection at least 2 months in
the past.
Rubella is one of the most complete teratogens, and sequelae of fetal infection are worst
during organogenesis. Pregnant women with rubella infection and a rash during the first 12
weeks of gestation have a fetus with congenital infection in up to 90 percent of cases
Udayana University Faculty of Medicine, DME, 2016
51
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
At 13 to 14 weeks’ gestation, this incidence was 54 percent, and by the end of the second
trimester, it was 25 percent. Defects are rare after 20 weeks.
There is no specific treatment for rubella. Droplet precautions for 7 days after the onset of
the rash are recommended. Primary prevention relies on comprehensive vaccination
programs. To eradicate rubella and prevent congenital rubella syndrome completely, a
comprehensive approach is recommended for immunizing the adult population. MMR
vaccine should be offered to nonpregnant women of childbearing age who do not have
evidence of immunity whenever they make contact with the health-care system. Vaccination
of all susceptible hospital personnel who might be exposed to patients with rubella or who
might have contact with pregnant women is important. Rubella vaccination should be
avoided 1 month before or during pregnancy because the vaccine contains attenuated live
virus. Although there is a small overall theoretical risk of up to 2.6 percent, there is no
observed evidence that the vaccine induces malformations. MMR vaccination is not an
indication for pregnancy termination. Prenatal serological screening for rubella is indicated
for all pregnant women. Women found to be nonimmune should be offered the MMR
vaccine postpartum.
Cytomegalovirus
This ubiquitous DNA herpes virus eventually infects most humans. Cytomegalovirus (CMV)
is the most common perinatal infection in the developed world. Specifically, some evidence
of fetal infection is found in 0.2 to 2.5 percent of all neonates. The virus is secreted into all
body fluids, and person-to-person contact with viral-laden saliva, semen, urine, blood, and
nasopharyngeal and cervical secretions can transmit infection. The fetus may become
infected by transplacental viremia, or the neonate is infected at delivery or during breast
feeding.
Primary maternal CMV infection is transmitted to the fetus in approximately 40 percent of
cases and can cause severe morbidity. In contrast, recurrent maternal infection infects the
fetus in only 0.15 to 1 percent of cases. A review of nine studies of CMV vertical
transmission rates reported first-trimester transmission in 36 percent, second-trimester in 40
percent, and third-trimester in 65 percent. Naturally acquired immunity during pregnancy
results in a 70-percent risk reduction of congenital CMV infection in future pregnancies.
However, as noted earlier, maternal immunity does not prevent recurrences, and maternal
antibodies do not prevent fetal infection. Also, some seropositive women can be reinfected
with a different viral strain that can cause fetal infection and symptomatic congenital
disease.
Routine prenatal CMV serological screening is currently not recommended. Pregnant
women should be tested for CMV if they present with a mononucleosis-like illness or if
congenital infection is suspected based on abnormal sonographic findings. Primary infection
is diagnosed using CMV-specific IgG testing of paired acute and convalescent sera. CMV
IgM does not accurately reflect timing of seroconversion because IgM antibody levels may
be elevated for more than a year. Moreover, CMV IgM may be found with reactivation
disease or reinfection with a new strain. Thus, specific CMV IgG avidity testing is valuable in
confirming primary CMV infection. High anti-CMV IgG avidity indicates primary maternal
infection > 6 months before testing. Finally, viral culture may be useful, although a minimum
of 21 days is required before culture findings are considered negative.
Udayana University Faculty of Medicine, DME, 2016
52
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
Several fetal abnormalities associated with CMV infection may be seen with sonography,
computed tomography, or magnetic resonance imaging. In some cases, they are found at
the time of routine prenatal sonographic screening, but in others they are part of a specific
evaluation in women with CMV infection. Findings include microcephaly, ventriculomegaly,
and cerebral calcifications; ascites, hepatomegaly, splenomegaly, and hyperechoic bowel;
hydrops; and oligohydramnios.
The management of the immunocompetent pregnant woman with primary or recurrent CMV
is limited to symptomatic treatment. If recent primary CMV infection is confirmed, amnionic
fluid analysis should be offered. Counseling regarding fetal outcome depends on the
gestation age during which primary infection is documented. Even with the high infection
rate with primary infection in the first half of pregnancy, most fetuses develop normally.
There is no CMV vaccine. Prevention of congenital infection relies on avoiding maternal
primary infection, especially in early pregnancy. Basic measures such as good hygiene and
hand washing have been promoted, particularly for women with toddlers in day-care
settings. Although there may be sexual transmission from infected partners, there are no
data on the efficacy of preventive strategies.
Hepatitis B
Chronic hepatitis B virus (HBV) infection is estimated to affect >350 million people
worldwide and represents a significant cause of morbidity and mortality related to cirrhosis
and hepatocellular carcinoma. Mother-to-child transmission (MTCT) of HBV remains an
important source of incident cases of HBV. Current barriers to eradication of incident HBV
infections via MTCT include underutilization of immunoprophylaxis with hepatitis B
vaccination and hepatitis B immune globulin in certain endemic regions as well as failure of
immunoprophylaxis.
Hepatitis B perinatal transmission remains a common mode of viral transmission, especially
in highly endemic areas globally.The availability over the past decade of effective oral
agents that suppress viral replication has allowed the consideration of thirdtrimester
treatment to reduce the risk of this transmission. This is important, particularly in pregnant
women with very high viral levels (>108 copies/mL or 2 × 107 IU/mL), in whom the risk is
highest, but transmission can occur even at levels >200 000 IU/mL. Treatment decisions
necessitate careful discussion of risks and benefits as emerging data suggest some
possible effect on bone mineral concentration in tenofovir-exposed pregnant women, which
must be balanced by a nearly 10% risk of chronic infection with an incurable virus. Pregnant
women with HBV must be monitored for clinical flares, with or without medications, and
breastfeeding should be allowed as well.
In the absence of HBV immunoprophylaxis, 10 to 20 percent of women positive for HBsAg
transmit viral infection to their infant. This rate increases to almost 90 percent if the mother
is HBsAg and HBeAg positive. Immunoprophylaxis and hepatitis B vaccine given to infants
born to HBV-infected mothers has decreased transmission dramatically and prevented
approximately 90 percent of infections.
Hepatitis C
Udayana University Faculty of Medicine, DME, 2016
53
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
Hepatitis C virus (HCV) is a well known cause of chronic liver disease in adults, but the
burden of HCV in pregnant women and children is underappreciated. The leading route of
HCV acquisition in children is vertical transmission.
Women with chronic HCV infection often have uneventful pregnancies without worsening of
liver disease or other maternal or infant adverse effects; some women mayeven have
improvement. For example, in a series of 266 pregnant women infected with HCV, elevated
serum alanine aminotransferase (ALT) levels were detected in 56% of women at the
beginning of pregnancy but only 7% during the third trimester. However, 55% of women
returned to elevated ALT levels by 6 months postpartum. Such changes may be due to the
significant changes in the maternal immune system during pregnancy.
Infants born to women infected with HCV were more likely to be low birth weight, small for
gestational age, and require neonatal intensive care and assisted ventilation. In the same
cohort, women infected with HCV had an increased risk for gestational diabetes but only
when combined with excessive gestational weight gain.
There is currently no licensed vaccine for HCV prevention. The chronic HCV infection
treatment has traditionally included alpha interferon (standard and pegylated), alone or in
combination with ribavirin. This regimen is contraindicated in pregnancy because of the
teratogenic potential of ribavirin in animals.
Learning task
1. What is IgG avidity ? Who important this result for the treatment scenario ?
2. Describe about indication, side effect, effective dose, contra indication of spiramycin
?
3. How to protect pregnant women from Parvovirus infection ?
4. Describe about MMR vaccination ?
5. How to protect pregnant women from Cytomegalovirus infection ?
Self assement
1. Explain how to manage pregnant women with human immunodeficiency virus ?
2. Explain how to manage pregnant women with Epstein-Barr virus ?
3. Explain how to manage pregnant women with herpesviruses 6 and 8 ?
4. Explain how to manage pregnant women with varicella ?
5. Explain how to manage pregnant women with syphilis ?
6. Explain how to manage pregnant women with enteroviruses ?
LECTURE 38
MALARIA
dr. Susila Utama, SpPD-KPTI
Abstract
Malaria is caused by infection of red blood cells with protozoan parasites of the
genus Plasmodium inoculated into the human host by a feeding female anopheline
Udayana University Faculty of Medicine, DME, 2016
54
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
mosquito. The five human Plasmodium species transmitted from person to person are
P. falciparum, P. vivax, P. Ovale (two species), P. Malariae and P. Knowlesi. The first
symptoms of malaria are nonspecific and similar to those of a minor systemic viral illness.
They comprise headache, lassitude, fatigue, abdominal discomfort and muscle and joint
aches, usually followed by fever, chills, perspiration, anorexia, vomiting and worsening
malaise. Disease progression to severe malaria may take days but can occur within a few
hours. Severe malaria usually manifests with one or more of the following: coma (cerebral
malaria), metabolic acidosis, severe anaemia, hypoglycaemia, acute renal failure or acute
pulmonary oedema. If left untreated, severe malaria is fatal in the majority of cases. All
patients with suspected malaria should be treated on the basis of a confirmed diagnosis by
microscopy examination or RDT testing of a blood sample. Management of uncomplicated
malaria using ACT (Artemisinine Combination Therapy) for 3 days but severe malaria must
treated with anti malaria intravenous (artesunate).
Learning task
1. Explain clinical symptom and sign of malaria
2. Differentiate between uncomplicated malaria and severe malaria
3. Management uncomplicated malaria and severe malaria
Self assessment
Case:
1. Male, 23 years old come to internal medicine clinic with fever for 6 days. Fever was
intermittenly every 2 days, fever was followed by chills and sweathing. He has
history travel to Papua.
- How to make diagnosis in this case?
- How to manage this case?
2. Female, 34 years old come to emergency room with severe headache and fever for
4 days. Physical examination: icterus +, lien S2. Lab examination Hb 4 g/dL, bil total
4,3 mg/dL and plasmodium falciparum on smear.
- What is the assessment?
- How to manage this case?
LECTURE 39
LEPTOSPIROSIS
dr. Agus Somia, SpPD-KPTI
Abstract
Leptospirosis is a widespread zoonosis caused by pathogenic leptospira spp genus.
Transmission of disease to new hosts is facilatated by contact with contaminated urine or
water source, because leptospira can penetrate broken skin or muocsal surfaces of new
hosts. Infection of new host may be asymptomatic or may be causes acute severe
disease: the Weil’s disease ( acute renal failure, haemorrhagic diastesis and jaundice) or
severe pilmonary haemorrhagic syndrome. The severity of the disease in human depend on
leptospira species, the health and immune status of the patient. The mechanisms by which
leptospira cause disease are not well understood. There are factors that role in
pathogenesis including: toxin production, entry and invasion to the host, immune
Udayana University Faculty of Medicine, DME, 2016
55
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
mechanisms and surface lipoprotein leptospira. These mechanism cause pathological
alteration is caharacterizes by the development of vasculitis, endothelial damage, and
inflammatory infiltrates composed of monocytic cell, plasma cells, histiocytes, and
neutrophils.
These pathological alteration can cause multiple hemorrhages and
deterioration of organ functions are among the most striking clinical manifestation acute
severe leptospirosis
Antibiotic therapy of leptospirosis including: mild leptospirosis is treated with
doxycycline, ampicillin, or amoxicillin. For severe leptospirosis, intravenous penicillin G has
long been the drug of choice, although the third-generation cephalosporins cefotaxime and
ceftriaxone have become widely used. Alternative regimens are ampicillin, amoxicillin, or
erythromycin. Several other antibiotics may be useful—for example, macrolides,
fluoroquinolones, and carbapenems but clinical experience with these agents is more
limited.
Severe cases of leptospirosis can affect any organ system and can lead to
multiorgan failure. Supportive therapy and careful management of renal, hepatic,
hematologic, and central nervous system complications are important.
Keyword: Leptospirosis, pathogenesis, clinical manifestation
Reference:
1. Speelman P. Leptospirosis. In: Kasper DL., Braunwald E., Fauci AS., Hauser SL.,
Longo DL., Jameson JL. eds. Harrison’s Principles of Internal Medicine. 16th ed. Volume
1. Mc. Grow-Hill companies. 2005. p.988-91
2. Edwards CN. Leptospirosis. In: Cohen J., Powderly W.G., Berkley S.F., Holland S.M.,
Opal S.M., Callandra T. Infectious disease. Mosby. London. 2004. p. 1669-70.
Learning Task:
Case 1
A 21-year-old, previously healthy man, a farmer by profession, was brought to the
Emergency Room by relatives due to high fever, headache, nausea and vomiting, and
constant sleepiness. At admission, he was lethargic and clinically dehydrated. At physical
examination, conjunctival congestion and petechia in the soft palate region were observed.
Pupils were symmetric and reactive. Sclera: icteric. Axillary temperature was 38.8°C, blood
pressure was 130/90 mmHg and heart rate was 100 beats/min.
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
Self assessment:
1. Explain pathogenesis of:leptospirosis
2. Define clinical spectrum of leptospirosis
Udayana University Faculty of Medicine, DME, 2016
56
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
3. Define signs and symptoms of leptospirosis
4. Define management of leptospirosis
5. Describe about complication of leptospirosis
LECTURE 40
SKIN INFECTION
dr. Ratih Karna, SpKK
ABSTRACT
Skin Infection is a very common problem in health care setting. This condition can caused
by various agents, including bacteria, virus or fungal group. Skin infection is not always
caused by pathogenic agent, but also by normal flora of the skin such as Staphylococcus
aureus or Candida sp. Examples of skin infection cause by bacteria are furuncles and
erysipelas whereas infection cause by virus including Varicella, Herpes Zoster and Herpes
Simpleks. Skin infection occurred not merely by the role of infectious agents, but more
likely as an interaction of host, agent and enviromental role. Agent factors consist of the
pathogenic or virulence factors of the agent itself. Enviromental factor includes the
temperature, moisture, climate and enviromental hygiene and crowd. The most important
host factor is the function of the skin as protection barriers. Others includes immunological
status of the patient and also the presence of other systemic disease, Skin infections
caused by different agent group need to be properly diagnosed and treated with appropiate
treatment to avoid serious complications.
LEARNING TASK
1. A 50 years old women came to emergency room, complaint arose some blister of her left
chest since yesterday. It was painful that make her couldn’t sleep well. Since 1 week ago
she felt tired and felt burning sensation of that left chest. She went to cardiogist, the doctor
said she was fine.
a. What other anamnesis neded to ask to this patient
b. What are possible differential diagnosis of this patient
c. What is the laboratory examination need to confirm diagnosis
d. How is the management of the patient
e. What are the complication of this patient
SELF ASSESSMENT
1. Explain what we should ask in the anamnesis
2. Explain symptom, sign and what kind of examination do we need for the patient
LECTURE 41
CENTRAL NERVOUS SYSTEM INFECTION
Prof. Dr. dr. Raka Sudewi, SpS(K)
Udayana University Faculty of Medicine, DME, 2016
57
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
LECTURE 42
CHILD IMMUNIZATION
dr. W. Gustawan, SpA
ABSTRACT
Immunization or vaccination is the most effective health program and efficient than
other health program in the prevention of an infectious disease. Immunity of the body
against the disease is the main purpose of the vaccination.
Immunity can be given passive and active. Vaccination and immunization are the
example of artificial active immunity in which the vaccine stimulate the body's active to make
specific antibodies. The vaccine components consist of viruses and bacteria, both viruses
and bacteria attenuated or components of viruses and bacteria.
Some examples of vaccine are BCG, DPT, Hepatitis B, Hib, measles,
pneumococcus, and others. Immunization is based on the immunization schedule in
accordance with the age.
Learning Task
1. Please describe about the natural and artificial immunity?
2. Please describe about immunization and vaccination?
3. Please describe about the immunological aspects of the immunization process?
4. Please describe about the aim of immunization?
5. Please describe about Universal Child Immunization program?
6. Please describe about type of immunizations?
7. Please describe about immunization schedule?
8. Please describe about adverse events following immunization?
Self Assessment
A 2 months old boy came to the clinic to get immunization. The history of his immunization
were BCG, Hepatitis B and Polio. There is no fever, cough, and runny nose.
1. What immunization should be obtained by the child at this time?
2. What is the aim of giving each of these immunizations?
3. Please describe about how to give DPT immunization, vaccine doses, and the
adverse events following immunization?
4. Please describe about how to give Polio immunization, vaccine doses, and the
adverse events following immunization?
LECTURE 43
THYPOID FEVER
dr. Agus Somia, SpPD-KPTI
Abstract
Typhoid fever is an acute systemic infection which is caused by Salmonella typhi. S typhi is
a gram-negative bacilli , aerobic, and moving with flagellae. S. typhi enters the human body
Udayana University Faculty of Medicine, DME, 2016
58
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
form contaminated food, and then penetrate to gut mucosal membranes, continue to gut
lymph nodes . S.typhi become reproductive and then from thoracic ducts enters to the blood
stream, going to the reticuloendothelial system (first bacteremia), occurs in 24-72 hours
after S typhi’s entrance and rarely diagnosed diagnosed because it’s asymptomatic. First
bacteremia will soon be ended after this microorganism is not shattered because of
fagocytosis, due to protection from Vi cappsule. In this organ of reticuloendothelial system,
the microorganism continued to be reproductive. This process lasted in 7 until 10 days. And
then the microorganism continue to enter the blood stream and cause the secondary
bacteremia.
Clinical Findings During prodromal stage, there is increasing malaise, headache,
abdominal pain and constipation, while the fever ascends in astepwise. After 7-10 days, the
fever reaches a plateau and the patient is much more ill, appearing exhausted and often
prostrated. There may be marked abdominal distention, especially early, or “pea soup”
diarrhea; marked abdominal distention occurs as well. During the early prodrome, physical
sign are few. Later, typhoid tongue, splenomegaly, abdominal distention and tenderness,
relative bradicardia appear.
Laboratory findings: Typhoid fever is best diagnosed by blood culture, which is positive in
the first week of illness in 80% patients who have no taken antimicrobial. Culture of bone
marrow occasionally are positive when blood cultures are not. The other laboratory test
including: PCR, specific serologic test: widal
Management: Fluids and electrolytes should be monitored and replaced. Oral nutrition with
a soft digestible diet is preferable in the absence of abdominal distension or ileus. No
specific limitations on activity are indicated for patients with typhoid fever. As with most
systemic diseases, rest is helpful, but mobility should be maintained if tolerable. The patient
should be encouraged to stay home from work until recovery. Several antibiotics including:
ampicillin, azithromycin. Chlorampenicol, third generation cephalosporins, and quinolon are
effective for treatment.
Learning Task:
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.
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
Self assessment:
1. Explain pathogenesis of Typhoid fever
2. Define signs and symptoms of Typhoid fever
3. Define management of Typhoid fever
4. Describe about complication of Typhoid fever
Udayana University Faculty of Medicine, DME, 2016
59
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
LECTURE 44
ACUTE GASTROENTERITIS
dr. Yuli Gayatri, SpPD
Abstract
Acute gastroenteritis is define as the inflammation of the mucus membranes of the
gastrointestinal tract and is characterized by diarrhea and/or vomiting. It causes significant
mortality in developing countries and significant economic burden to developed countries.
Worldwide, gastroenteritis affects 3-5 billion children each year, and accounts for 1.5 to 2.5
million deaths per year or 12% of all deaths among children less than 5 years of age.
Viruses are responsible for approximately 70% of episodes of acute gastroenteritis and
rotavirus is the one of the best studies of these viruses. In developing countries, enteric
bacteria and parasites are more prevalent than viruses and typically peak during the
summer months. The most common bacterial causes are Salmonella species,
Campylobacter sp, Shigella sp and Yersinia sp. Vibrio cholera remains a major cause of
gastroenteritis especially after a disaster where sanitation is compromised. Giardia lamblia,
Cryptosporidium sp and Entamoeba histolytica are common protozoal infection. The initial
clinical evaluation of the patient should focus on assessing the severity of the illness and the
need for rehydration and identifying likely causes on the basis of history and clinical
findings. Correcting fluid and electrolyte disturbance take patients who are dehydrated of
febrile or have blood or pus in their stool. Oral rehydration therapy is as effective as
intravenous therapy in treating mild to moderate dehydration in acute gastroenteritis and is
strongly recommended as the first line therapy. Antimicrobial therapy are reliably helpful
only for patients with bloody diarrhea (most likely shigellosis), suspected cholera with
severe dehydration and serious non-intestinal infections ( e.g., pneumonia). Antimicrobial
are to be considered the drugs of choice for empirical treatment of traveler’s diarrhea and
community-acquired secretory diarrhea when the pathogen is known. Anti-emetics are not
routinely recommended in treating acute gastroenteritis, but often used because vomiting is
unpleasant and a distressing symptom which can increase the likelihood or dehydration,
electrolyte imbalance, pulmonary aspiration and most importantly the need for intravenous
hydration or hospitalization. Prevention including; water, sanitation, hygiene, safe food and
immunization can substantially reduce the incidence and severity of the disease.
Learning task:
A 61-years-old woman with diarrhea 6-8 times per day, for 1 day prior to admission,
consistency watery and sometime semisolid, without blood or mucus. He complained with
sudden onset of vomiting (more than 10 times/day), abdominal pain, nausea, headache,
muscle-ache, fever and chills. She is a foreign traveler. Based on an initial examination,
patient was conscious, dry mouth, Blood pressure 90/60 mmHg, body temperature was 38,5
˚C, increasing bowel sound and acral clamy.
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
6. Define management of this case
Udayana University Faculty of Medicine, DME, 2016
60
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
7. Define complication and prognosis
8. Define prevention based on individual, family, and community
Self assessment:
1. Describe how do people get acute gastroenteritis
2. Describe symptoms of acute gastroenteritis
3. Describe people at risk for acute gastroenteritis
4. Describe diagnosis of acute gastroenteritis
5. Define management of acute gastroenteritis
6. Define prevention of acute gastroenteritis
LECTURE 45
URINARY TRACT INFECTION
Dr. dr. Wayan Sudhana, SpPD-KGH
LECTURE 46
LOWER RESPIRATORY TRACT INFECTION
dr. Made Bagiada, SpPD-KPTI
LECTURE 47
TOXOPLASMOSIS
dr. Yuli Gayatri, SpPD
Abstract
Toxoplasmosis is a parasitic infection due to Toxoplasma gondii ( T gondii) an
obligate intracellular protozoan parasite. This parasite was identified in 1908 by Nicolle and
Manceaux, in North African rodent. Its intermediate hosts could be humans or other warm
blooded animals. The infections are reported in approximately half of the world’s population,
but most are asymptomatic. The high rates of latent Toxoplasma infection (41.9-72%) were
reported in South America and in approximately half of the studies (≥40%) from the Asia
continent. Of estimated 750 deaths caused by toxoplasmosis in the United States each
year.
The contamination of the parasite is generally occurred via consumption of infected
food or water or, raw/undercooked contaminated meat; by ingesting oocysts via soil (for
example, by way of gardening, handling/eating unwashed vegetables). Infection with T
gondii could be transmitted vertically from mother to child, even if a minority of infected
individuals worldwide acquires the parasite congenitally. There are four groups of
individuals in whom, the diagnosis of toxoplasmosis is most critical: pregnant woman who
acquire their infection during gestation, fetuses and newborns who are congenitally infected,
immunocompromised patient and those with chorioretinitis. Co-infection with other
pathogens in humans infected with HIV -1 may enhance the progression of the disease to
AIDS. In concurrence with HIV infection, cerebral toxoplasmosis occurs primarily due to
Udayana University Faculty of Medicine, DME, 2016
61
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
reactivation of latent Toxoplasma infection and is one of the most frequent opportunistic
infections, particularly in patients with full-blown AIDS. Cerebral Toxoplasmosis is the most
common clinical presentation of toxoplasmosis and is one of the most frequent causes of
focal intra-cerebral lesions that complicates AIDS. Cerebral toxoplasmosis is undoubtedly a
serious life-threatening disease but it is treatable when there is a timely diagnosis and
prompt treatment, and there are no other concurrent co-infections.
Diagnosis of toxoplasmosis in humans is elaborated using various techniques such
as detection of anti-Toxoplasma antibodies, mouse inoculation, histological revelation of
tachyzoit in tissue sections or smears of body fluid, but the detection of Toxoplasma gondii
DNA by molecular methods has revolutionized prenatal diagnosis of congenital
toxoplasmosis including the usefulness of molecular methods. Cerebral toxoplasmosis in
HIV/AIDS patients usually presents with focal findings, occurs with CD4 < 200, Ig G
Toxoplasma antibody (+). Brain scans called CTs or MRIs demonstrate multiple contrastenhancing ring-like lesions.
There are few options other than anti- Toxoplasma regimens used as the first choice
initial therapy; 6 weeks with sulfadiazine (1.0-1.5g per oral (PO) every 6 hours with
pyrimethamine (100-200mg PO loading dose, then 50 mg PO daily) and folinic acid (10-20
mg PO daily) that can reduced the hemato-toxicities related to pyrimethamine. The other
regimens is trimethoprim-sulphamethoxazole (Co-trimoxazole 5/25 mg/kg PO or
intravenous (iv) every 12 hours for 4-6 weeks. Several alternative therapies, principally used
in patients who are intolerant to this combination, have been reported to be effective,
including clindamycin and pyrimethamine or sulfadiazine, clarithromycin
and
pyrimethamine, or azithromycin and pyrimethamine.
Learning task:
Case 1:
A 41-years-old man with los of consciousness for 5 days prior to admission. He complained
with high grade fever since 1 month, headaches, lost of appetite and chronic diarrhea. Lost
of body weight about 20 kg in 1 month. He sought treatment from local district hospital
doctor, in 2 days admission, such as; dexametasone 10 mg iv every 12 hours,
cotrimoxazole 1x 960 mgper oral (PO), paracetamol 3x500 mg PO, ranitidin 1x50 mg iv,
antasida 3xCI. He was referred to Sanglah Hospital for intensive treatment, with diagnosis:
lost of consciousness probable due to SOL cerebri. Based on an initial examination, patient
was unconscious, look pale and severe ill, body temperature was 38,5 ˚C, with oral plaque.
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 or radiology examination to diagnose e.q. serology
test, imaging, tissue biopsy 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 how do people get Toxoplasmosis
2. Describe symptoms of Toxoplasmosis
Udayana University Faculty of Medicine, DME, 2016
62
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
3.
4.
5.
6.
7.
8.
Describe people at risk for toxoplasmosis
Describe the life-cycle of toxoplasma gondii
Describe pathogenesis of toxoplasmosis
Describe diagnosis of toxoplasmosis
Define management of toxoplasmosis
Define prevention of toxoplasmosis
LECTURE 48
FILARIASIS
dr. Dewi Dian Sukmawati, SpPD
ABSTRACT
Filariasis is a disease group affecting human and animal, caused by filariae, a
nematode (round worm) parasite from Filariidae order. The transmission of filariasis from
infected individual to uninfected individual via mosquito bite. Mosquitoes of the
genera Aedes, Anopheles, Culex, or Mansonia are the intermediate hosts and vectors of all
species that cause lymphatic filariasis. There were hundreds filarial species and fortunately
only eight use humans as their definitive host. In Indonesia, there were 241 districs from 26
provinces with endemic filariasis; with national eradication program, the government
targeted by the year 2020, Indonesia will be free from elephantiasis. The WHO has
identified lymphatic filariasis as the second leading cause of permanent and long term
disabilities after leprosy. In lymphatic filariasis, repeated episode of lymphedema and
inflammation lead to lymphatic damage, chronic edema and elephantiasis of the leg, arms,
scrotum, vulva and breast.
Based on the predilection of filarial infestation within human body, filariasis divided
into three groups: (1) Lymphatic filariasis, caused by Wucheria brancrofti, Brugia malayi and
Brugia timori. These worms occupy the lymphatic system including lymph nodes, in chronic
case may lead to syndrome of elephantiasis. (2) Subcutaneous filariasis, caused by Loa loa
(eye worm), Mansonella streptocerca, Onchocerca volvulus. These worms occupy
subcutaneous layer of the skin at the fat layer. (3) Serous cavity filariasis caused by
Mansonella perstans, Mansonella ozzardi. They occupy the serous cavity of abdomen.
Diagnosis of filariasis by detection of microfilaria through examination of blood
(microfilariae of all species that can cause lymphatic filariasis, Loaiasis (Loa loa),
Mansonella ozzardi, Mansonella perstans), urine (chyluria in lymphatic filariasis, in
concentrated urine evaluation may revealed microfilaria), skin ( Onchocerca volvulus and M
streptocerca infections are diagnosed when microfilariae are detected in multiple skin-snip
specimens from different sites located on both sides of the body), eye (microfilariae of O
volvulus may be detected in the cornea or anterior chamber of the eye using slit-lamp
examination). Imaging study and histology evaluation may be used to demonstrate and
monitor lymphatic obstruction.
Management of filariasis including antihelmintics (Diethylcarbamazine, ivermectin,
suramin, mebendazole, albendazole, flubendazole), surgerical excision can be considered
in lymphatic filariasis with large hydrocele and scrotal elephantiasis.
LEARNING TASKS
Udayana University Faculty of Medicine, DME, 2016
63
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
Case 1
A 32-year-old Indian man presented with tender swelling of the right scrotum after a fall. He
was a migrant worker from India who had come to Bali to work as a yoga teacher. Although
there was history of a fall, he denied injury to the groin. Clinical examination revealed
enlarged lymphnodes inguinal, tender and swollen right scrotum. Eosinophylia was found
on complete blood count. Ultrasound of the scrotum was performed and revealed multiple
oval cystic structures with multiple internal septa in the paratesticular region, adjacent to the
body and tail of the epididymis. Within one of the cysts, numerous short linear echogenic
linear structures were seen moving vigorously. A small right hydrocele was also present.
Question Case 1
1. What is the clinical diagnosis of this case?
2. What about the management of the patient? (including planning for diagnostic,
treatment, monitoring and education)
3. Describe the prevention strategy that available for this case!
Case 2
A 42 year old female patient came to outpatient clinic due recurrent fever which lasted 3 -5
days and recurrent for the last 3 weeks. She started to feel painful swelling from her left
axillae since the other day. From physical examination revealed lymphadenitis axillae with
redness, warm and tender on palpation in surrounding area.
Question case 2
1. What is the clinical diagnosis of this case?
2. What evaluation needed for diagnostic work up?
3. How do you manage this case?
4. How about the prognosis?
SELF ASSESSMENT
1. Define the filarial life cycle!
2. Describe the process on obtaining the microfilaria identification from blood sample!
3. Differentiate between acute and chronic stage of filariasis (comparison table
including duration of infection, clinical manifestation, diagnostic approach, treatment
and prognosis)
4. Differentiate between mass treatment and selective treatment for filariasis
(indication, duration, type of medication)
REFERENCES
1. Knopp S, Steinmann P, Hatz C, Keiser J, Utzinger J. Nematode infections:
filariases. Infect Dis Clin North Am. 2012 Jun. 26(2):359-81
2. Kazura J. Guerrant R, Walker DH, Weller PF, eds. Tropical Infectious Diseases:
Principles, Pathogens and Practice. Philadelphia, PA: Churchill Livingstone; 1999.
Vol 2: 852.
3. Strengthening the assessment of lymphatic filariasis transmission and documenting
the achievement of elimination. WHO Geneva 2014
4. Lymphatic filariasis: A handbook of practical entomology for national lymphatic
filariasis elimination programmes. WHO Department of control of neglected tropical
diseases 2013
Udayana University Faculty of Medicine, DME, 2016
64
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
LECTURE 49
HIV INFECTION
Prof. Dr. dr. Tuti Parwati Merati, SpPD, KPTI
Abstract
Retroviruses are enveloped viruses, with an RNA genome. The name is derived from the
fact that the virus particle contains an RNA-dependent DNA Polymerase (Reverse
transcriptase). This enzyme converts the RNA genome into DNA, which then integrates into
the host chromosomal DNA. The reverse transcriptase is highly error prone and rapid
genetic variation is a feature of this group.
The most common retrovirus in human is HIV (human immunodeficiency virus). Since
1981, the first cases presented with immune deficiency syndrome were detected in the
United State of America. Several years after that, in 1984 it was known that the syndrome
was caused by HIV infection. HIV targeted cells who carry CD4 receptor molecule as the
main receptor, though other co-receptor is also needed for HIV to infect the cells, such as
CCR5 and CXCR4. Transmissions: Commonly through sexual transmission, Blood
transfusion, Mother to infant and rarely accidental occupational exposure
Primary HIV infection may present with the clinical picture of a febrile illness approximately
2–4 weeks after exposure. The symptoms may include skin rash, myalgia, fatigue, sore
throat, diarrhoea, lymphadenopathy, hepatosplenomegaly and, rarely, neurological
symptoms. While this seroconversion illness may occur in up to 70–80% of individuals, it is
often not viewed as serious or related to HIV infection, due in part to its self-limited course.
Primary HIV infection seldom results in presentation to health care settings.
In line with the course of time of infection, when the immune system becomes progressively
damaged by HIV, reflected by an increased of HIV viral load and a steady decline of the
CD4 lymphocyte count to 200 – 350 cells/μL, the patient may develop symptoms that are
commonly associated with HIV disease. These include persistent fever, night sweats,
significant weight loss, oral thrush, herpes zoster and chronic diarrhoea. A range of
opportunistic infection will occur. Thrombocytopenia and lymphopenia may be present on
blood testing. It should be noted that any organ system can become involved in
opportunistic infections and the clinical presentation of acquired immunodeficiency
syndrome (AIDS) is therefore highly variable. Please see WHO Classification for disease
staging and also CDC classification of HIV infection based on laboratory examination and
the list of diseases referred as AIDS defining illnesses (ADI). So, infection with HIV will
covered a very wide range, from asymptomatic to severe clinical manifestation of
opportunistic infection.
Diagnosis of HIV infection can be made if there are risk factors of HIV infection, clinical
manifestation of disease mentioned above, especially in late stage will presented with AIDS
defining illness and laboratory test positive for HIV-antibody or any other test confirming
HIV infection, such as P24 Ag test and HIV viral load test.
Treatment to HIV/AIDS, include treatment to the specific manifestation of opportunistic
infection, antiretroviral treatment, supportive treatment, symptomatic drugs, supportive
counseling, psychological treatment and counseling to increased adherence.
Learning task:
A young man aged 35 years-old came to the hospital with difficulty in swallowing, dry mouth
and fever. He also had diarrhea since a couple months ago, loose 7 kg of his body weight,
Udayana University Faculty of Medicine, DME, 2016
65
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
and feel unwell to work. Because he cannot eat, he become very week and also had a dry
cough which made him mostly have to stay in bed.
1. What syndrome do this young man suffering from?
2. On history taking, what information do you want to know from the patient to lead you
to a possible working diagnosis? Please explain.
3. What is the diagnosis of this patient?
4. How do you manage this patient?
Self assessments:
1. Describe the pathogenesis of immune deficiency in HIV infection.
2. The clinical manifestation of HIV infection is very wide spectrum, from very mild and
asymptomatic to a severe- life threatening diseases. How can we make diagnosis of
the infection or diseases?
LECTURE 50
AVIAN INFLUENZA, SARS
dr. Agus Somia, SpPD-KPTI
Abstract
Bird flu (avian influenza, AI) is an infection caused by the influenza A virus subtype
H5N1, which generally attack birds (birds and chickens). Type A influenza viruses are
members of the Orthomyxoviridae family. On the surface of the virus type A, there are two
glycoproteins: hemagglutinin (H) and neuraminidase (N). Subtypes based on the nature of
H (H1 to H16) and N (N1 to N9). The avian influenza virus can survive in water up to 4 days
at a temperature of 22 0C and more than 30 days at a temperature of 00C. in poultry feces
and body sick poultry, the influenza virus can live long, but died on heating 60 0 C for 30
min, 56 0C for 3 hours and heating to 80 0 C for 1 minute. The virus will die with detergents,
disinfectants for example formalin, a liquid containing iodine or 70% alcohol.
Mode of transmission:
Transmission of the disease to humans can be through:
- Animals: direct contact with sick poultry or poultry products were sick.
- Environment: air or equipment contaminated with the virus both derived from poultry
feces or secretions are attacked AI
- Human: very limited and inefficient (found some cases in a group / cluster)
Period of communicability:
Period of transmission to humans is 1 day before, until 3-5 days after onset of symptoms. In
children, the infectious period can be up to 21 days.
High risk groups:
Group to watch and at high risk of AI infection are:
- farm workers / poultry processing (including veterinary / animal husbandry engineer)
- Laboratory workers who process the blood sample / patient secretions / poultry
infected
- The visitors livestock / poultry processing in one last week
had contact with poultry (chickens, ducks, birds) sick or died suddenly of unknown
causes and or pork as well as raw products in the past 7 days
Udayana University Faculty of Medicine, DME, 2016
66
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
- AI patients had contact with confirmation in the last 7 days.
Pathogenesis
The pathogenesis is determined by the virulence of the virus and the host immune
response. Factors affecting virulence include high haemaglutinin solution which is activated
by a variety of cellular protease which is a specific substitution in the polymerase basic
protein 2 (Glu627lys) which increasing replication. And a sbstitusi in nonstructural protein 1
(Asp92Glu) that confers increased resistance to constraints by interferon and TNF alpha in
vitro and extend replication in swine, increasing release of cytokines, especially TNF alpha
in macrophag human exposure to the virus.
Clinical spectrum
The incubation period: 3 days (average 1-7 days)
Clinical symptoms vary, not all existing symptoms, can vary from person to person, and
tends to quickly deteriorate and develop pneumonia or acute respiratory failure. Clinical
symptoms include: high fever (temperature ≥ 380C), cough, runny nose, sore throat,
headache, muscle pain, infection of the lining of the eyes, spasms, diarrhea or
gastrointestinal disturbances, fatigue.
Complication: acute respiratory failure
Laboratory:
confirmation test:
- Culture and identification of influenza A virus subtype H5N1
- RT-PCR testing for H5
Serology:
- Test immunofluorescence assay (IFA): antigen (positive) using a monoclonal
antibody influenza A subtype H5N1
- Neutralization test: there is an increase in specific antibody titers of influenza A
subtype H5N1 4 times, in paired serum neutralization test
Radiolography: chest x rays: ARDS
Diagnosis : Case definitions
suspected cases
- someone who has a fever / suhu ≥ 380C accompanied by one or more symptoms:
cough, sore throat, colds and shortness of breath, and followed by one or more of
the following circumstances:
had contact with poultry (chicken, duck, bird) illness or sudden death of
unknown cause and the raw products (meat, eggs, poultry manure, etc.) in
the last 7 days before onset of symptoms above
- live or have ever been in the area of poultry deaths have unusual (in large
quantities in a short time), in the last 7 days before onset of symptoms above
- had been in contact with patients confirmed AI cases in the last 7 days
before the onset of the above symptoms.
- had contact with the specimen in the last 7 days before onset of symptoms
above (working in the laboratory for AI)
- leukopenia
- found the H5 antibody titers against the examination HI test using horse
erythrocytes or ELISA test for without subtypes of influenza
- chest x rays found pneumonia picture that quickly deteriorate in the photo
series
OR
Udayana University Faculty of Medicine, DME, 2016
67
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
The presence of acute respiratory distress syndrome (ARDS) were not found
another cause with one more condition below:
 Leukopenia or relative limfositopeni obtained from counts with or
without thrombocytopenia (below normal values)
 chest film depicts atypical pneumonia or pulmonary infiltrates on both
sides of the widening in the photo series
The case probabel
criteria for suspected cases coupled with one or more of the following circumstances:
- found wearing titer antibodies against H5, a minimum of four times, with the
examination of HI test using horse erythrocytes or ELISA test
- Limited laboratory results positive for influenza H5 (H5 userspecific detection of
antibodies in a single serum) using test neutralisasi (sent to a reference laboratory)
The cases confirm
probabel suspected cases or with one or more of the following circumstances:
a. AI virus culture / H5N1 Positive
b. PCR AI / H5N1 Positive
c. In asssy immunofluorescence test (IFA) antigen (positive) by using monoclonal antibodies
AI / H5N1
d. The increase in antibody titer AI / H5N1 Positive konvalescen phase (paired sera) with
the neutralization test 4 times the value of the initial (acute phase)
Differential diagnosis:
- typhoid fever
- dengue fever
- pulmonary tuberculosis
- lung infections caused by bacteria or fungi.
Management:
- supportive therapy: oxygen, fluid therapy, nutrition
- Antiviral given as soon as possible (48 hours).
- Body weight > 40 Kg: Oseltamivir 2 X 75 mg per day for 5 days
References
1. Ministry of Health. Guidelines for Management of Avian Influenza in Health Care
Facilities. Jakarta. 2006
-
Learning Task:
Male 45 years, previously healthy, broilers collectors work, was escorted to the emergency
room, complaining of fever, cough, and shortness of breath since 3 days.. 1 month ago
history of some chickens on the farm, many died. on physical examination found awareness
of apathy, Blood pressure: 90/60, respiratory rate: 40 time per minute, pulse rate: 120 time
per minute, axillary temperature: 39oC. On thorax examination found: ronchy a both lung.
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 family this patient about prognosis of patient`s disease
8. Describe how to referral of this patient
Udayana University Faculty of Medicine, DME, 2016
68
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
Self assessment:
1. Explain pathogenesis of: avian influenza
2. Define clinical spectrum of avian influenza
3. Define signs and symptoms of avian influenza
4. Define management of avian influenza
5. Describe about complication of avian influenza
6. Define prognosis of avian influenza
LECTURE 51
SEVERE ACUTE RESPIRATORY SYNDROME (SARS)
dr. Agus Somia, SpPD-KPTI
Abstract
Severe acute respiratory syndrome (SARS) is a serious form of pneumonia. It is caused by
a virus that was first identified in 2003. Infection with the SARS virus causes acute
respiratory distress (severe breathing difficulty) and sometimes death.
Causes: SARS is caused by a member of the coronavirus family of viruses (the same family
that can cause the common cold). It is believed the 2003 epidemic started when the virus
spread from small mammals in China.
Transmission: When someone with SARS coughs or sneezes, infected droplets spray into
the air. The SARS virus may live on hands, tissues, and other surfaces for up to 6 hours in
these droplets and up to 3 hours after the droplets have dried. While the spread of droplets
through close contact caused most of the early SARS cases, SARS might also spread by
hands and other objects the droplets has touched. Airborne transmission is a real possibility
in some cases. Live virus has even been found in the stool of people with SARS, where it
has been shown to live for up to 4 days. The virus may be able to live for months or years
when the temperature is below freezing.
With other coronaviruses, becoming infected and then getting sick again (re-infection) is
common. This may also be the case with SARS.
Clinical manifestation: Symptoms usually occur about 2 to 10 days after coming in contact
with the virus. In some cases, SARS started sooner or later after first contact. People with
active symptoms of illness are contagious. But it is not known for how long a person may be
contagious before or after symptoms appear. The main symptoms are: cough,difficulty
breathing, fever greater than 100.4°F (38.0°C) and other breathing symptoms
Laboratory for identify the virus that causes SARS include: Antibody tests for SARS, direct
isolation of the SARS virus and rapid polymerase chain reaction (PCR) test for SARS virus
Radiolography: chest x rays found pneumonia and ARDS picture
Diagnosis: based on clinical manifestation and radiography finding
Management: supportive treatment, antiviral (ribavirin no strong evidence) and general
precaution for infection control
Learning Task
Case
Udayana University Faculty of Medicine, DME, 2016
69
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
Male 45 years, previously healthy, businessman , was escorted to the emergency room,
complaining of fever, runny nose, sneezing and cough since 7 days ago. He feel shortness
of breath getting worse since 3 days. He has history going to Hongkong 10 days ago and
transit at Singapore. On physical examination found awareness of apathy, Blood pressure:
90/60, respiratory rate: 40 time per minute, pulse rate: 120 time per minute, axillary
temperature: 38.7oC. On thorax examination found: ronchy a both lung.
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 family this patient about prognosis of patient`s disease
8. Describe how to referral of this patient
Self assessment:
1. Explain pathogenesis of SARS CoV infection.
2. Define clinical spectrum of SARS CoV infection.
3. Define signs and symptoms of SARS CoV infection.
4. Define management of SARS CoV infection.
5. Describe about complication of SARS CoV infection.
6. Define prognosis of SARS CoV infection.
LECTURE 52
PAROTITIS
dr. Dewi Dian Sukmawati, SpPD
ABSTRACT
The parotid glands are small exocrine glands that rarely function abnormally, mostly
they function perfectly normal throughout life. Dry mouth, drooling, swelling, and pain are
essentially the only symptoms caused by dysfunction of the salivary glands. Inflammatory
swelling of the glands may present a serious diagnostic challenge. Parotitis presents in
many forms and the symptoms vary from modest to prostrating. There are frequent
contradictions in the classification, etiology, and treatment of the disorders. A pure viral or
bacterial infection, an autoimmune inflammation, or a combination of these can be the
etiology.
In unilateral parotitis, consider a bacterial infection, local obstruction, or malignancy.
High fevers and a toxic appearance can develop in bacterial parotitis and should be
considered in the elderly, dehydrated, and malnourished patients. History and physical
should lead towards a cause. Biopsy may be necessary, especially if facial nerve paralysis
also present.
Parotitis epidemica (mumps)’s etiology in children usually due to viral infection from
a paramyxovirus. The mumps virus replicates in the upper respiratory tract and spreads
through direct contact with respiratory secretions or saliva or through fomites. The risk of
Udayana University Faculty of Medicine, DME, 2016
70
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
spreading the virus increases the longer and the closer the contact a person has with
someone who has mumps. Some complications of mumps are known to occur more
frequently among adults than children. Death from mumps is exceedingly rare. Mumps can
be prevented by administration of vaccine called MMR.
LEARNING TASKS
Case
A 25 year old pregnant woman came to outpatient clinic due to 3 days fever. In the last two
days she noticed pain, tenderness and swelling is first visible in front of the lower part of the
ear. It then extends downward and forward her cheek and jaw area. Three weeks before,
one of her niece which was 5 year old was suffered from the same condition. Some of the
children around the neighborhood within this past one month also ever suffered the same
complain
Question
1. What is likely the clinical diagnosis for this case?
2. How do you manage this case? (including diagnostic, treatment, monitoring and
education)
3. What condition can be present as a complication for this case?
Self assessment
1. What are the possible etiologies of parotitis?
2. How can we differentiate between viral, bacterial, autoimmune or malignancy
etiology?
3. How about the vaccination strategy for mumps?
REFERENCES
1. McLean HQ, Fiebelkorn AP, Temte JL, et al. Prevention of measles, rubella,
congenital rubella syndrome, and mumps, 2013: summary recommendations of the
Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep. 2013
Jun 14. 62:1-34
2. Mumps; epidemic parotitis. In Oxford text book of medicine: Infection. Oxford
university press 2012
3. Kasper DL; Braunwald E; Fauci AS; Hauser SL; Longo DL; Jameson JL; Isselbacher
KJ; Eds. (2011). "194. Mumps".Harrison's Principles of Internal Medicine (18th ed.).
McGraw-Hill Professional
LECTURE 53
BACTEREMIA, SEPSIS
dr. Susila Utama, SpPD-KPTI
Abstract
Sepsis is defined as a known or suspected infection plus systemic manifestations of
infections (eg, traditional systemic inflammatory response syndrome criteria—tachy-cardia,
tachypnea, white blood count changes, and fever/hypothermia as well as other metabolic
perturbations or organ dysfunctions). Severe sepsis is defined as sepsis plus infectioninduced organ dysfunction or infection-induced acute tissue hypoperfusion. Bacteriemia is
Udayana University Faculty of Medicine, DME, 2016
71
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
the presence of viable bacteria in the blood. Early diagnosis, early antibiotic administration,
and adequate fluid resuscitation are key in decreasing sepsis morbidity and mortality.
Learning task
1. Explain definition of bacteriemia, sepsis, severe sepsis and septic shock
2. How to manage sepsis, severe sepsis and septic shock
Self assessment
Male, 69 years old was admitted in intensive care unit with severe pneumonia,
impending respiratory failure, blood pressure 80/60, pulse 124 irreguler per minute and
respiratory 29 perminute, temperature 35,2 o Celcius. Physical examination: rales on
paracardial of the right lung. Urine was 25 cc for 4 hours. Laboratory exam: WBC 23 and
metabolic acidosis on blood gas analysis
- What is the diagnosis of this case?
- How to manage this case?
LECTURE 54
RABIES
dr. Susila Utama, SpPD-KPTI
Abstract
Rabies, present on all continents and endemic in most African and Asian countries,
is a fatal zoonotic viral disease,transmitted to humans through contact (mainly bites and
scratches) with infected animals, both domestic and wild. Rabies is estimated to cause at
least 55 000 deaths per year worldwide, about 56%of which occur in Asia and 4 %in Africa,
particularly in rural areas on both continents.
The risk of infection depends on the severity of the wound, the site of the wound in
relation to its nerve supply and its distance from the brain, the amount and strain of virus
introduced. The initial symptoms of rabies resemble those of other systemic viral infections,
including fever, headache and generally feeling unwell. There may be discomfort or
paresthesia at the site of exposure (bite), followed by symptoms of cerebral dysfunction,
anxiety, confusion, agitation, progressing to delirium, abnormal behaviour, hallucinations,
and insomnia i.e. furious (or encephalitic) rabies. Fever is common and signs of autonomic
dysfunction, including hypersalivation, sweating, piloerection, and priapism (in males) may
be present. About 50% to 80% of patients develop hydrophobia, which is a characteristic
manifestation of rabies. Patients may initially experience pain in the throat or difficulty
swallowing. On attempting to swallow, they experience contractions of the diaphragm and
other inspiratory muscles, which last about 5 to 15 seconds. Subsequently, the sight, sound,
or even mention of water (or any liquids) may trigger the spasms. A draft of air on the skin
may have the same effect (ie, aerophobia). The disease may progress through paralysis,
coma, multiple organ failure, and eventually death. Viral encephalitis caused by other
viruses is generally associated with earlier impairment of consciousness compared with
rabies, with less prominent early evidence of brainstem involvement. Occasionally the
presentation is with sudden death. Neurological symptoms occur later in the disease
process. The acute period of disease typically ends after 2 to 10 days. Once clinical signs of
rabies appear, the disease is nearly always fatal, and treatment is typically supportive.
Udayana University Faculty of Medicine, DME, 2016
72
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
There is no specific treatment for rabies, which is a fatal disease. Prevention of rabies were
pre and post exposure prophylaxis, clean the wound was most important followed by
vaccine and immunoglobulin.
Learning task
1. Explain the symptom and sign of rabies
2. Explain rabies prevention by pre and pro exposure prophylaxis
Self assessment
Male, 13 years old was bite by dog 2 hours ago, so he come to polyclinic for rabies
vaccination. Please explain to the patient, what must we do? Is he need vaccination?
LECTURE 55
TETANUS
dr. Yuli Gayatri, SpPD
Abstract
Tetanus is a vaccine preventable disease that yearly cause a total of 309.000
deaths. The global incidence of tetanus has been estimated at approximately one million
cases annually mostly in underdeveloped countries. Mortality rates from tetanus very greatly
across the world, depending on access to the healthcare, and approach 100% in the
absence of medical treatment . Clostridium tetani is an anaerobic bacillus, whose spores
survive in soil and cause infection by contaminating wounds. Tetanus toxin, the product of
Clostridium tetani, is the cause of tetanus symptoms. Tetanus is taken up into terminals of
lower motor neuron and transported axonally to the spinal cord and /or brainstem. Here
toxin moves trans-synaptically into inhibitory nerve terminals, where vesicular release of
inhibitory neurotransmitter becomes blocked, leading to disinhibition of lower motor
neurons. Muscle rigidity and spasms ensue, often manifesting as trismus/lockjaw,
dysphagia, opistotonus, or rigidity and spams of respiratory, laryngeal and abdominal
muscles, which may cause respiratory failure. There is no diagnostic laboratory test for
tetanus; the diagnosis is entirely clinical. C tetani is recovered from wounds is only about
30% of cases and the organism is sometimes isolated from patients who do not have
tetanus. Serological results obtained before TIG is administered can support susceptibility if
they demonstrate very low or undetectable anti-tetanus antibody levels. Acute treatment of
tetanus is based on wound cleaning and antibiotic eradication of Clostridium tetani, e.g. with
intravenous metronidazole 500 mg three times daily or penicillin 100.000-200.000
IU/kg/day, treatment is continued for seven to ten days and the administration of tetanus
toxoid and/or tetanus immunoglobulin.
Learning Task:
1. Describe how do people get tetanus
2. Describe symptoms of tetanus
3. Describe people at risk for tetanus
4. Describe diagnosis of tetanus
5. Define management of tetanus
6. Define prevention of tetanus
Udayana University Faculty of Medicine, DME, 2016
73
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
~ CURRICULUM MAP ~
Smstr
Program or curriculum blocks
10
Senior Clerkship
9
Senior Clerkship
8
Senior clerksh
ip
7
Medical
Emergency
(3 weeks)
Special Topic:
-Travel medicine
(2 weeks)
Elective Study III
(6 weeks)
Clinic Orientation
(Clerkship)
(6 weeks)
6
BCS (1 weeks)
The Respiratory
System and
Disorders
(4 weeks)
The
Cardiovascular
System and
Disorders
(4 weeks)
The Urinary
System and
Disorders
(3 weeks)
The Reproductive
System and
Disorders
(3 weeks)
BCS (1 weeks)
Alimentary
& hepatobiliary 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)
BCS (1 weeks)
Musculoskeletal
system &
connective
tissue disorders
(4 weeks)
Neuroscience
and
neurological
disorders
(4 weeks)
Behavior Change
and disorders
(4 weeks)
BCS (1 weeks)
Hematologic
system & disorders & 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)
Medical
Professionalism
(2 weeks)
BCS(1 weeks)
Evidence-based
Medical Practice
(2 weeks)
BCS (1 weeks)
Health Systembased Practice
(3 weeks)
BCS(1 weeks)
Community-based
practice
(4 weeks)
-
BCS (1 weeks)
Studium
Generale and
Humaniora
(3 weeks)
Medical
communication
(3 weeks)
BCS (1 weeks)
The cell
as biochemical machinery
(3 weeks)
Growth
&
development
(4 weeks)
BCS (1 weeks)
BCS(1 weeks)
BCS: (1 weeks)
BCS (1 weeks)
Elective Study
II
(1 weeks)
5
4
3
2
1
BCS (1 weeks)
Special Topic :
- Palliative
medicine
-Compleme
ntary &
Alternative
Medicine
- Forensic
(3 weeks)
Elective
Study II
(1 weeks)
Special Topic
- Ergonomi
- Geriatri
(2 weeks)
Elective
Study I
(2 weeks)
The Visual
system &
disorders
(2 weeks)
Pendidikan Pancasila & Kewarganegaraan (3 weeks)
Udayana University Faculty of Medicine, DME, 2016
74
Study Guide Basic Microbiology, Parasitology, Infection and Infectious Diseases
REFERENCES
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, 244250.(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.160713.
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. 7 th ed.
1998.
15. Grainger RG and Allison DJ. Diagnostic Radiology. Churchill Livingstone. 2 nd 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. 9thed.
18. Bryceson A. Leprosy. 3rded.
19. King & Nicole. Sexually Transmitted Diseases. 2003
20. Holmes KK, Spiring PF, Mirdh P. Sexually Transmitted Diseases. 3rd ed. McGrawHill. 1999.
21. McMillan A, Young H, Ogilvie MM, Scott GR. Clinical Practice in Sexually
Transmissible Infection. Saunders. 2002.
22. Braunwald’s Heart Disease. Subacute bacterial endocarditis.
Udayana University Faculty of Medicine, DME, 2016
75