Study Guide Infection Tayang 27 Nov 2013

Study Guide 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, nternal Medicine, etc have been integrated and incorporated into
several bloc!s" #ne of these bloc!s is nfections and nfectious Diseases" n this bloc! $ill
be e%plained in general about pathogenesis, pathophysiology, sign, symptoms, clinical
features, diagnosis, and management of certain infectious diseases commonly occur in
community"
&his guide boo! aims to give general information for medical students about infections
and infectious diseases and important for facilitators and resource person $hile facilitate or
guiding the students in learning process" &his study guide consists of general information on
learning time table, bloc! team members, facilitators, and the core curriculum including
learning outcomes, learning situations, learning tas!s and self-evaluation items"
&he bloc! nfection and nfectious Diseases has the e'uivalent of (si%) credits" As a
bloc! of si% credits, the learning processes $ill be carried out for *+ days starts from ,-
th
of
.ovember ,+/* as sho$n in the &ime &able" &he final e%amination $ill be conducted on /*
th
of 0unuari ,+/1" During the *+ days of learning activities, the students $ill discuss several
topics in varied forms of learning situations such as independent learning, small group
discussion, lecture, and s!ill lab"
More than half of the learning material must be learned independently and in small
group discussions" A lecture is given only to emphasi2e crucial things or objectives of
material and to prepare the students before discussion" For small group discussion, the
students $ill be given learning tas!s to solve and discuss" After discussion, students also
have to evaluate their learning progress independently (self evaluation)"
From this bloc!, $e hope every medical student have !no$ledge and s!ill to diagnose
and manage infections and certain infectious diseases commonly occur in community, as a
frontline in community health"
3ince the integrated curriculum of the Faculty of Medicine Udayana University is still in
progress, this 3tudy 4uide $ill also, naturally, have some revisions in the future" &herefore,
$e !indly invite readers to give any comments or suggestions for its improvement and
development"
Planners
Faculty of Medicine U.UD,M5U 1
CURRICULUM OF THE BLOCK
AIMS
&o comprehend the biology of the infectious diseases
&o apply and interpret common laboratory diagnosis of infectious diseases
&o diagnose and manage common infectious diseases
&o carry out basic immuni2ation in children and adults
LEARNING OUTCOMES
6omprehend the practical and clinical implications of the biology of infection
Apply the general principles of approach to patients $ith infectious diseases
Apply and interpret common laboratory diagnosis of common infectious
diseases
Apply the basic principles of immuni2ation in children and adults
Diagnose and manage common bacterial infections (common 4ram positive
and negative, spirochetal)
Diagnose and manage common parasitic infections (common nematode,
trematode, cestode, and proto2oal infections)
Diagnose and manage common fungal infections
6linically diagnose and manage common viral infections (caused by common
respiratory virus, herpesvirus, arbovirus)
6linically diagnose and manage puerperial nfection
CURRICULUM CONTENT
/" &he biology of infection7 bacterial, viral, fungal and parasitic"
a" Principles of bacterial infections such as Staphylococci, Streptococci,
Neisseria, Salmonella, Vibrio, anaerobic bacteria8 Leptospira, Mycobacteria,
4ram positive bacilli)
b" Principles of viral infections such as respiratory virus (influen2a virus,
mumps, measles), retrovirus (9:), herpesvirus (93: /, 93: ,, :;:,
arbovirus (dengue virus, 0apanese B encephalitis virus)"
c" Principles of fungal infections such as Candida, Pneumocytis jiroveci,
Histoplasma, Cryptococcus
d" Principles of parasitic infections such as Plasmodium, Tooplasma !ondii,
"ntamoeba histolytica and soil transmitted helminthes"
," 4eneral approach to the patients $ith infection such as7
a" 6linical manifestations (local and systemic infections)
b" <aboratory e%amination to support diagnosis of infections i"e" Microbiological
e%amination, Parasites e%amination, 6linical pathology e%amination,
Pathology e%amination and maging e%amination
*" Management patients $ith infection such as7
a" 6ommon bacterial infections such as bacterial meningitis, typhoid fever,
diarrhea, endocarditis, diphtheria, tetanus, food poisoning, genital
gonorrhoeae, non gonococcal urethritis, etc"
b" 6ommon parasitic infections such as malaria, amoebiasis, to%oplasmosis"
c" 6ommon fungal infection such as dermatophytosis, systemic candidiasis,
histoplasmosis, cryptococcosis, pneumocytis jiroveci pneumonia"
d" 6ommon viral infections such as mumps, measles, influen2a (especially
9=./), 3A>3, varicella, herpes labialis, herpes genitalis, dengue fever,
0apanese B encephalitis, and 9:"
1" mmuni2ation in children and adults, and general advice to international traveler
=" Puerperial nfection
3&A.DA> ?#MP5&5.3 D#?&5>
PLANNERS TEAM
No Name Departement Phone
/
Prof" Dr" dr" &uti Par$ati Merati, 3pPD,
?P& (6oordinator)
nternal Medicine
+@/,*@+AA,A
,
Dr" dr" Bagus ?omang 3atriyasa,
M">epro (3ecretary)
Pharmacology
+@-----B++A1
+*A/--@B*=BB
*
Dr" dr" De$a Made 3u!rama, M"3i,
3pM?
Microbiology +@/**@,B/BA=
1
Prof" Dr" dr" >a!a 3ude$i, 3p"3 (?) .eurology +@/A-/+,11
=
dr" 4? Darmada, 3p??
Dermatology and
:enereology
+@/**@+11B,/
A
dr" "B" .gurah, M"For Pharmacology +@/,*A@-,@@
-
dr" Agus 3omia, 3p"PD nternal Medicine +@/,*B@B*=*
@
dr" Made 3udarmaja, M"?es Parasitology +@/,*B=*B1=
LECTURER
NO NAME DEPT PHONE
/" Prof" Dr" dr" &uti Par$ati Merati, 3pPD,
?P&
nternal Medicine
+@/,*@+AA,A
,"
Prof"Dr" dr" >a!a 3ude$i, 3p"3 (?) .eurology
+@/A-/+,11
*"
Prof"Dr"dr" "B" >ai, 3pP (?) Pulmonology
+@/,*@+1=-B
1"
dr" Agus 3omia, 3pPD nternal Medicine
+@/,*B@B*=*
="
dr" A"A"4"P" Ciraguna, 3p??
Dermatology D
:enereology
+@/**@A1=,@@
A"
Prof"dr" M" 3$asti!a Adiguna, 3p?? (?)
Dermatology D
:enereology
+@/,*@,@=1@
-"
dr" 4A" 3umedha Pindha, 3p?? (?)
Dermatology D
:enereology
+@/==-*=B--
@" dr" D$i <ingga, 3pA (?)Edr C"
4usta$an,M"3c", 3p"A
6hild 9ealth
+@/,=A@1A=AE
+@/,*@1@,1/
B" dr" 4?" Darmada, 3p??E dr" Darmaputra,
3p"??
Dermatology D
:enereology
+@/**@+11B,/
/+"
dr" .i Made Aditarini 3p" M? Microbiology
+@/**@A-=*11
//"
dr" <uh Ari$ati Parasitology
+@/,*AA,*//
/,"
dr" .yoman Mahartini, 3pP? 6linical Pathology
+@/**-/A==--
/*"
dr" "B" .gurah, M" For Pharmacology +@/,*A@-,@@
/1"
Dr" dr" Bagus ?omang 3atriyasa, M">epro Pharmacology +@-----B++A1
/="
dr" ?ade! 3$asti!a, M"?es Parasitology +@/,1A1B++,
/A" Prof" dr"De$a Putu Cidjana, DAPD5,
3p"Par?"
Parasitology +@//*@+1=++
/-"
Prof" dr" 4M" Aman, 3pF? Pharmacology +@/**@--+A=+
/@"
dr" 3ri Budayanti, 3p"M? Microbiology +@=@*-//*B@
/B"
dr"De$a Ayu A" 3ri <a!smi,M"3c Parasitology +@/*B,+/-/+-
,+"
dr" Made 3usila Utama, 3p"PD nternal Medicine +@/,*@/=+,=
,/"
dr"Made Agus 9endrayana, M"?ed Microbiology +@/,*B,/=B+
,,"
dr"<ely >ahayu, 3p"&9&-?< 5.& +@//*@+B@@,
,*"
dr" A" Ci$ie! ndrayani, M"?es Pharmacology +@@@A@==+,-
,1"
dr" ?" 0anuartha, M"?es Microbiology +@/,*@*/-/+
,="
dr" Made 0a$i, M"?es Pharmacology +@/-B-@-B-,
,A"
dr" .yoman Bayu Mahendra,3p"#4
#bstetrics D
4ynecology
+@/**B==+1,*
,-"
"B" .yoman Putra D$ija, 3"3i, M"Biotech Microbiology +@/-B-1-=+,
,@"
dr"Putu Ayu Asri Damayanti,M"?es Parasitology +@=**@=A=-@*
,B"
dr"Made 3udarmaja,M"?es Parasitology +@/,*B=*B1=
FACILITATORS
(REGULAR CLASS)
NO NAME GROUP DEPT PHONE ENUE
/ dr" 4usti .yoman 3ri Cirya$an,
M">epro
/
9istology +@/,*B,=/+1
,
nd
floor7
>","+/
, dr" 4ede Budhi 3etia$an,
3p"B(?)#n!
,
3urgery +@/,*B,*B=A
,
nd
floor7
>","+,
*
dr" Made Bagiada, 3p"PD
*
nterna +@/,*A+-@-1
,
nd
floor7
>","+*
1
dr" Made Muliarta, M"?es"
1
Fisiology +*A/@+@-=B,
,
nd
floor7
>","+1
=
dr" Made #!a .egara, 3"?ed
=
Andrology +@/,*B-B*B-
,
nd
floor7
>","+=
A
dr" ?etut Agus 3omia, 3p"PD-?P&
A
nterna +@/,*B@B*=*
,
nd
floor7
>","+A
-
dr" Made 3udarmaja, M"?es
-
Parasitology +@/,*B=*B1=
,
nd
floor7
>","+-
@
dr" Made 3udipta, 3p"&9&-?<
@
5.& +@/,*@*-+A*
,
nd
floor7
>","+@
B
dr" Made 3u!a Adnyana, 3p, BP
B
3urgery +@/,*A,@@B-=
,
nd
floor7
>",",/
/+
dr" 4usti Ayu 3ri Darmayani, 3p" #4
/+
DM5 +@/**@A111//
,
nd
floor7
>",",,
(ENGLISH CLASS)
NO NAME GROUP DEPT PHONE ENUE
/ dr" 4ede .gurah 9arry Cijaya
3urya, 3p #4
/
#bgyn +@//*@AB*=
,
nd
floor7
>","+/
,
dr" 4st".gr"?etut Budiarsa , 3p"3
,
.eurology
+@//*BBA-*
,
nd
floor7
>","+,
* dr" 4usti Ayu Agung 5lis ndira ,
3p"??
*
Dermatology
+@/**@-/@*@1
,
nd
floor7
>","+*
1 dr" Agus >oy >usly 9ariantana
9amid, 3p"BP
1
3urgery +@/,*=//A-*
,
nd
floor7
>","+1
= dr" 4usti Ayu Putu 5!a Prati$i,
M"?es",3p"A
=
Pediatric +@/,*B,+-=+
,
nd
floor7
>","+=
A
dr" .yoman Arcana , 3p"Bio!
A
Biochemistry
+@//*B-BA+
,
nd
floor7
>","+A
- dr" 4usti Ayu 3ri Mahendra De$i,
3p"PA(?)
-
6linical Anatomy +@/**@-*A1@/
,
nd
floor7
>","+-
@
dr" 4usti ?etut Darmada, 3p"??(?)
@
Dermatology
+@/**@+11B,/
,
nd
floor7
>","+@
B dr" 4usti Made 4de 3urya 6handra
&rapi!a, M"3c
B
Pharmacology
+@/,*A,,*A/
,
nd
floor7
>",",/
/+ dr" 4usti .gurah Mahaalit Ariba$a,
3p"An"
/+
Anesthesi
+@/,*BA@//
,
nd
floor7
>",",,
TIME!TABLE (B"o#$ In%e#t&on an' &n%e#t&o() D&))*)
DA+, DATE
T&me
Top&#
Learn&n-
)&t(at&on
P"a#e PIC
Re-("ar
C"a))
En-"&)h
C"a))
./
0e'ne)'a1
No2* .3
th
/4
+@"++-+@"*+ +B"++-+B"*+ Le#t(re /
Intro'(#t&on to the
5"o#$ (A-ent 6Ho)t
En2&ronment6 an'
&n%e#t&on
man&%e)tat&on)
ntroduction to
the Bloc!
6lass room Prof" Dr" dr" &uti
Par$ati Merati,
3pPD, ?P&
+@"*+-+B"++ +B"*+-/+"++ Le#t(re .
5a#ter&a"
#"a))&%&#at&on
dr" ?" 0anuarta,
M"?es
+B"++-/+"*+ /,"++-/*"*+ ndividual
learning
- -
/+"*+-/,"++ /*"*+-/="++ 3mall group
discussion
Disc" >oom Facilitator
/,"*+-/1"++ /+"++-//"*+ 3tudent
Project
Prof" Dr" dr" &uti
Par$ati Merati,
3pPD, ?P& dr" ?"
0anuarta, M"?es
/1"++-/="++ /="++-/A"++ Plenary
3ession
Par$ati Merati,
3pPD, ?P& dr" ?"
0anuarta, M"?es
.
Th(r)'a1
No2* .7
th
/4
+@"++-+B"++ +B"++-/+"++ Le#t(re 4
Me#han&)m o%
5a#ter&a"
Patho-ene)&)
Le#t(re 6lass room dr" Agus
9endrayana, M"?ed
+B"++-/+"*+ /,"++-/*"*+ ndividual
learning
/+"*+-/,"++ /*"*+-/="++ 3mall 4roup
Discussion
/,"*+-/1"++ /+"++-//"*+ 3tudent
Project
6lass
>oom
dr" Agus
9endrayana, M"?ed
/1"++-/="++ /="++-/A"++ Plenary 6lass
>oom
dr" Agus
9endrayana, M"?ed
4
Fr&'a1
No2* .8
th
/4
+@"++-+@"*+ +B"++-+B*"+ Le#t(re 9
&ra" #"a))&%&#at&on
Le#t(re 6lass
>oom
Dr" dr" 3ri
Budayanti, 3p"M?
+@"*+-+B"++ +B"*+-/+"++ Le#t(re :
Me#han&)m o% &ra"
Le#t(re 6lass room Dr"dr" 3ri Budayanti,
3p"M?
DA+, DATE
T&me
Top&#
Learn&n-
)&t(at&on
P"a#e PIC
Re-("ar
C"a))
En-"&)h
C"a))
Patho-ene)&)
+B"++-/+"*+ /,"++-/*"*+ ndividual
<earning
/+"*+-/,"++ /*"*+-/="++ 3mall group
discussion
Disc" >oom
/,"*+-/1"++ /+"++-//"*+ 3tudent
Project
Dr" dr" 3ri
Budayanti, 3p"M?
/1"++-/="++ /="++-/A"++ Plenary 6lass room Dr" dr" 3ri
Budayanti, 3p"M?
9
Mon'a1
De)* .
th
/4
+@"++-+@"*+ +B"++-+B*"+ Le#t(re ;
Man&%e)tat&on o% 2&r()
an' 5a#ter&a" &n%e#t&on
Le#t(re 6lass
>oom
dr"Agus somia,
3p"PD
+@"*+-+B"++ +B"*+-/+"++ Le#t(re 3
Ba)&# #on#ept o%
Para)&t&# In%e#t&on)
Le#t(re 6lass room Prof" dr" D"P"
Cidjana, DAPD5,
3p"Par"?
+B"++-/+"*+ /,"++-/*"*+ ndividual
<earning
/+"*+-/,"++ /*"*+-/="++ 3mall group
discussion
Disc" >oom
/,"*+-/1"++ /+"++-//"*+ 3tudent
Project
dr"Agus
somia3p"PD
Prof" dr" D"P"
Cidjana, DAPD5,
3p"Par"?
/1"++-/="++ /="++-/A"++ Plenary 6lass room dr"Agus
somia3p"PD
Prof" dr" D"P"
Cidjana, DAPD5,
3p"Par"?
:
T(e)'a1
De)*4
r'
/4
+@"++-+B"++ +B"++-/+"++ Le#t(re 7
Treatment o% &ra"
In%e#t&on (PK,PD)
<ecture 6lass room Prof" 4M Aman,
3p"F?
+B"++-/+"*+ /,"++-/*"*+ ndividual
learning
-
/+"*+-/,"++ /*"*+-/="++ 3mall group
discussion
/,"*+-/1"++ /+"++-//"*+ 3tudent
Project
Prof" 4M Aman,
3p"F?
/1"++-/="++ /="++-/A"++ Plenary
3ession
6lass room Prof" 4M Aman,
3p"F?
;
0e'ne)'a1
De)*9
th
/4
+@"++-+B"++ +B"++-/+"++ Le#t(re 8
Treatment o%
M&#ro5a#ter&a"
In%e#t&on) I (T1pe o%
ant&m&#ro5a#ter&a")
(PK,PD)
<ecture 6lass room
Dr"dr" B"?"
3atriyasa,M">epro
+B"++-/+"*+ /,"++-/*"*+ ndividual
learning
-
/+"*+-/,"++ /*"*+-/="++ 3mall group
discussion
Disc" >oom
/,"*+-/1"++ /+"++-//"*+ 3tudent
Project
6lass room Dr"dr" B"?"
3atriyasa,M">epro
/1"++-/="++ /="++-/A"++ Plenary 6lass room Dr"dr" B"?"
DA+, DATE
T&me
Top&#
Learn&n-
)&t(at&on
P"a#e PIC
Re-("ar
C"a))
En-"&)h
C"a))
3ession 3atriyasa,M">epro
3
Th()'a1
De)*:
th
/4
+@"++-+@"*+ +B"++-/+"++ Le#t(re /<
Treatment o%
M&#ro5a#ter&a"
In%e#t&on) II
(Re)&)tan#e6 rat&ona"
treatment6 an' 'r(-
#om5&nat&on)
<ecture dr" Made 0a$i,
M"?es
+@"*+-+B"++ /,"++-/*"*+ Le#t(re //
Ant&m&#ro5&a"
)()#ept&5"1
ndividual
learning
dr" .i Made adi
&arini, 3p"M?
+B"++-/+"*+ /*"*+-/="++ 3mall group
discussion
/+"*+-/,"++ /+"++-//"*+ 3tudent
Project
6lass room dr" .i Made adi
&arini, 3p"M? dr"
Made 0a$i, M"?es
/,"*+-/1"++ /="++-/A"++ Plenary
3ession
6lass room Dr" Made 0a$i,
M"?es
7
Fr&'a1
De)*;
th
/4
+@"++-+@"*+ +B"++-+B*"+ Le#t(re /.=
Re)pon' Ho)t a-a&n)t
para)&t&# an' #"&n&#a"
man&%e)tat&on
Le#t(re 6lass room dr" Made 3usila
Utama,3p"PD
+@"*+-+B"++ +B"*+-/+"++ Le#t(re /4
Treatment o%
para)&t&# &n%e#t&on
(PK,PD)
Le#t(re 6lass room dr" A" Ci$ie!
ndrayani, M"?es
+B"++-/+"*+ /,"++-/*"*+ ndividual
learning
/+"*+-/,"++ /*"*+-/="++ 3mall group
discussion
/,"*+-/1"++ /+"++-//"*+ 3tudent
Project
6lass room dr" Made 3usila
Utama,3p"PD
dr" A" Ci$ie!
ndrayani, M"?es
/1"++-/="++ /="++-/A"++ Plenary
3ession
Utama,3p"PD
dr" A" Ci$ie!
ndrayani, M"?es
8
Mon'a1
De)*8
th
/4
+@"++-+@"*+ +B"++-+B*"+ Le#t(re /9=
The Ro"e o% Imm(n&t1
to &n%e#t&on (Ba)&#)
Le#t(re 6lass room Dr"dr" De$a Made
3u!rama, M"3i,
3p"M?
+@"*+-+B"++ +B"*+-/+"++ Le#t(re /:= In%e#t&on
o% M1#o5a#ter&(m
(TBC)
Le#t(re 6lass room Prof Dr"dr" B
>ai,3p"P
+B"++-/+"*+ /,"++-/*"*+ ndividual
learning
/+"*+-/,"++ /*"*+-/="++ 3mall group
discussion
Disc" >oom
/,"*+-/1"++ /+"++-//"*+ 3tudent
Project
6lass room Dr"dr" De$a Made
3u!rama, M"3i,
3p"M?
Prof Dr"dr" B
>ai,3p"P
DA+, DATE
T&me
Top&#
Learn&n-
)&t(at&on
P"a#e PIC
Re-("ar
C"a))
En-"&)h
C"a))
/1"++-/="++ /="++-/A"++ Plenary
3ession
6lass room Dr"dr" De$a Made
3u!rama, M"3i,
3p"M?
Prof Dr"dr" B
>ai,3p"P
/<
T(e)'a1
De)*/<
th
/4
+@"++-+@"*+ +B"++-+B*"+ Le#t(re /;= In%e#t&on
o% M1#o5a#ter&(m
(Lepro)1)
Le#t(re 6lass room dr" Dharma putra,
3p"??
+@"*+-+B"++ +B"*+-/+"++ Le#t(re /3=
Ant&m1#o5a#ter&a"
Dr(-) ( ant& TBC6 Ant&
"epra) (PD,PK)
Le#t(re 6lass room dr" B .gurah, M"For
+B"++-/+"*+ /,"++-/*"*+ ndividual
<earning
/+"*+-/,"++ /*"*+-/="++ 3mall group
discussion
/,"*+-/1"++ /+"++-//"*+ 3tudent
Project
6lass room dr" Dharma putra,
3p"??
dr" B .gurah, M"For
/1"++-/="++ /="++-/A"++ Plenary 6lass room dr" Dharma putra,
3p"??
dr" B .gurah, M"For
//
0e'ne)'a1
De)*//
th
/4
+@"++-+@"*+ +B"++-+B*"+ Le#t(re /7=
Contro" o%
m&#roor-an&)m
(&n%e#t&on #ontro")
Le#t(re 6lass room dr" . D$i
Fatma$ati, 3p"M?,
Ph"D
+@"*+-+B"++ +B"*+-/+"++ Le#t(re /8=
Imm(n&>at&on &n #h&"'
Le#t(re 6lass room dr" D$i <ingga,
sp"AE dr" C"
4usta$an,3p"A
+B"++-/+"*+ /,"++-/*"*+ Le#t(re .< = &n%e#t&on)
&n (pper re)p&rator1
tra#t (%ar&n-&t)6
ton)&""&t&)6 "ar&n-&t)6
ot&t&)6 ma)to'&t&)6
rh&n&t&)6 )&n()&t&)6
%(r(n$e"&t&))
<ecture Dr <ely
/+"*+-/,"++ /*"*+-/="++ 3mall group
discussion
/,"*+-/1"++ /+"++-//"*+ 3tudent
Project
6lass room dr" . D$i
Fatma$ati, 3p"M?,
Ph"D
dr" D$i <ingga,
sp"AE dr" C"
4usta$an,3p"A
/1"++-/="++ /="++-/A"++ Plenary 6lass room dr" . D$i
Fatma$ati, 3p"M?,
Ph"D
dr" D$i <ingga,
sp"AE dr" C"
4usta$an,3p"A
DA+, DATE
T&me
Top&#
Learn&n-
)&t(at&on
P"a#e PIC
Re-("ar
C"a))
En-"&)h
C"a))
/.
Th()'a1
De)*/.
th
/4
+@"++-+@"*+ +B"++-+B*"+ Le#t(re .<
Ant&)ept&# an'
'&)&n%e#tant
<ecture 6lass room Dr"dr"B"?"
3atriyasa,M">epro
+@"*+-+B"++ +B"*+-/+"++ Le#t(re ./
Un&2er)a" Pre#a(t&on
<ecture 6lass room dr Agus
3omia,3p"PD
+B"++-/+"*+ /,"++-/*"*+ ndividual
learning
- -
/+"*+-/,"++ /*"*+-/="++ 3mall group
discussion
/,"*+-/1"++ /+"++-//"*+ 3tudent
Project
6lass room Dr"dr"B"?"
3atriyasa,M"repro
dr Agus
3omia,3p"PD
/1"++-/="++ /="++-/A"++ Plenary 6lass room Dr"dr"B"?"
3atriyasa,M"repro
dr Agus
3omia,3p"PD
/4
Fr&'a1
De)*/4
th
/4
+@"++-+B"++ +B"++-/+"++ Le#t(re ..
Proto>oa In%e#t&on I
(Ma"ar&a6 Amoe5&a)&)6
Le&)man&a)&)6Tr&pano
)om&a)&)6To?op"a)mo
)&)6 Tr&#homon&a)&))
<ecture 6lass room dr"De$a Ayu A" 3ri
<a!smi,M"3c,
M"?es
dr" Putu Astri
Damayanti,M"?es
+B"++-/+"*+ /,"++-/*"*+ ndividual
learning
/+"*+-/,"++ /*"*+-/="++ 3mall group
discussion
/,"*+-/1"++ /+"++-//"*+ 3tudent
Project
dr"De$a Ayu A" 3ri
<a!smi,M"3c,
M"?es
dr" Putu Astri
Damayanti,M"?es
/1"++-/="++ /="++-/A"++ Plenary dr"De$a Ayu A" 3ri
<a!smi,M"3c,
M"?es
dr" Putu Astri
Damayanti,M"?es
/.*<<!/4*4< M&''"e 5"o#$ meet&n-
/9
Mon'a1
De)*/;
th
/4
+@"++-+@"*+ +B"++-+B*"+ Le#t(re .4
Proto>oa In%e#t&on II
(Mana-ement o%
proto>oa In%e#t&on))
<ecture 6lass room dr Fuli 4ayatri,
3p"PD
+@"*+-+B"++ +B"*+-/+"++ Le#t(re .9
In%e#t&on o%
Entero5a#ter
<ecture 6lass room dr Agus
3omia,3p"PD
DA+, DATE
T&me
Top&#
Learn&n-
)&t(at&on
P"a#e PIC
Re-("ar
C"a))
En-"&)h
C"a))
(Th1po&'6 C*
5ot("&n(m)
+B"++-/+"*+ /,"++-/*"*+ ndividual
learning
/+"*+-/,"++ /*"*+-/="++ 3mall group
discussion
/,"*+-/1"++ /+"++-//"*+ 3tudent
Project
6lass room dr Fuli 4ayatri,
3p"PD
dr Agus
3omia,3p"PD
/1"++-/="++ /="++-/A"++ Plenary 6lass room dr Fuli 4ayatri,
3p"PD
dr Agus
3omia,3p"PD
/:
T(e)'a1
De)*/3
th
/4
+@"++-+@"*+ +B"++-+B*"+ Le#t(re .:
Sep)&) an'
Ba#terem&a
<ecture 6lass room dr" Made 3usila
utama, 3p"PD
+@"*+-+B"++ +B"*+-/+"++ Le#t(re .;
C(taneo() &ra"
In%e#t&on (ar&#e""a6
@o)ter6 Herpe))
<ecture 6lass room dr"4A 3umedha
Pindha, 3p"??Edr"
5lis ndira,3p"??
+B"++-/+"*+ /,"++-/*"*+ ndividual
learning
/+"*+-/,"++ /*"*+-/="++ 3mall group
discussion
/,"*+-/1"++ /+"++-//"*+ 3tudent
Project
utama, 3p"PD
dr"4A 3umedha
Pindha, 3p"??Edr"
5lis ndira,3p"??
/1"++-/="++ /="++-/A"++ Plenary 6lass room dr" Made 3usila
utama, 3p"PD
dr"4A 3umedha
Pindha, 3p"??Edr"
5lis ndira,3p"??
/;
0e'ne)'a1
De)*/7
th
/4
+@"++-+@"*+ +B"++-+B*"+ Le#t(re .3
Retro2&ra" In%e#t&on
(HI)
<ecture 6lass room Prof" Dr" dr" &uti
Par$ati Merati,
3pPD, ?P&
+@"*+-+B"++ +B"*+-/+"++ Le#t(re .7
In%"(en>a
<ecture 6lass room Prof" Dr" dr" &uti
Par$ati Merati,
3pPD, ?P&
+B"++-/+"*+ /,"++-/*"*+ ndividual
learning
/+"*+-/,"++ /*"*+-/="++ 3mall group
discussion
DA+, DATE
T&me
Top&#
Learn&n-
)&t(at&on
P"a#e PIC
Re-("ar
C"a))
En-"&)h
C"a))
/,"*+-/1"++ /+"++-//"*+ 3tudent
Project
Par$ati Merati,
3pPD, ?P&
/1"++-/="++ /="++-/A"++ Plenary 6lass room Prof" Dr" dr" &uti
Par$ati Merati,
3pPD, ?P&
/3
Th(r)'a1
De#*/8
th
/4
+@"++-+@"*+ +B"++-+B*"+ Le#t(re .8
In%e#t&on &n #h&"'ren
(DBD6 D&%ter&6 )ep)&)6
Campa$)
<ecture 6lass room dr" D$i <ingga,
sp"AE dr" C"
4usta$an,3p"A
+@"*+-+B"++ +B"*+-/+"++ Le#t(re 4<
&n%e#t&on) &n (pper
re)p&rator1 tra#t
(%ar&n-&t)6 ton)&""&t&)6
"ar&n-&t)6 ot&t&)6
ma)to'&t&)6 rh&n&t&)6
)&n()&t&)6 %(r(n$e"&t&))
<ecture 6lass room dr" <ely, 3p"&9&
+B"++-/+"*+ /,"++-/*"*+ ndividual
learning
/+"*+-/,"++ /*"*+-/="++ 3mall group
discussion
Disc" >oom
Facilitator
/,"*+-/1"++ /+"++-//"*+ 3tudent
Project
6lass room dr" D$i <ingga,
sp"AE dr" C"
4usta$an,3p"A
dr" <ely, 3p"&9&
/1"++-/="++ /="++-/A"++ Plenary 6lass room dr" D$i <ingga,
sp"AE dr" C"
4usta$an,3p"A
dr" <ely, 3p"&9&
/7
Fr&'a1
De)*.<
th
/4
+@"++-+B"++ +B"++-/+"++ Le#t(re 4/
@oono)&) In%e#t&on
(Ra5&e)6
Lepto)p&ro)&))
<ecture 6lass room Prof"Dr" dr" >a!a
3ude$i, 3p"3 (?)
Dr" dr" 3ri
Budayanti, 3p"M?
+B"++-/+"*+ /,"++-/*"*+ ndividual
learning
/+"*+-/,"++ /*"*+-/="++ 3mall group
discussion
/,"*+-/1"++ /+"++-//"*+ 3tudent
Project
6lass room Prof"Dr" dr" >a!a
3ude$i, 3p"3 (?)
Dr" dr" 3ri
Budayanti, 3p"M?
/1"++-/="++ /="++-/A"++ Plenary 6lass room Prof"Dr" dr" >a!a
3ude$i, 3p"3 (?)
Dr" dr" 3ri
Budayanti, 3p"M?
/8
Mon'a1
De)*.4
th
/4
+@"++-+*+"++ +B"++-+B"*+ Le#t(re 4.
Pr&n#&p"e) o% F(n-a"
In%e#t&on (Morpho"o-1
o% F(n-a")
<ecture 6lass room dr" <uh Ari$ati
+@"*++-+B"++ +B"*+-/+"++ Le#t(re 44=
)(per%&#&a" %(n-a"
In%e#t&on) (T&nea6
<ecture 6lass room Prof" M" 3$asti!a
Adiguna
DA+, DATE
T&me
Top&#
Learn&n-
)&t(at&on
P"a#e PIC
Re-("ar
C"a))
En-"&)h
C"a))
T&nea 2er)&$o"or6
$a'&'&a)&)
m($o$(taneo())
+B"++-/+"*+ /,"++-/*"*+ ndividual
learning
/+"*+-/,"++ /*"*+-/="++ 3mall group
discussion
Disc" >oom
/,"*+-/1"++ /+"++-//"*+ 3tudent
Project
6lass room dr" <uh Ari$ati
Prof" M" 3$asti!a
Adiguna
/1"++-/="++ /="++-/A"++ Plenary 6lass room dr" <uh Ari$ati
Prof" M" 3$asti!a
Adiguna
.<
T(e)'a1
De)*.9
th
/4
+@"++-+@"*+ +B"++-+B"*+ Le#t(re 49
Deep F(n-a" In%e#t&on
Le#t(re 6lass room Prof"Dr"dr &uti
Par$ati,3p"PD
+@"*+-+B"++ +B"*+-/+"++ Le#t(re 4:
Treatment o% F(n-a"
In%e#t&on (PD,PK)
<ecture 6lass room dr" B".gurah,
M"ForEdr" $i$ie!
ndrayani, M"?es
+B"++-/+"*+ /,"++-/*"*+ ndividual
learning
/+"*+-/,"++ /*"*+-/="++ 3mall group
discussion
/,"*+-/1"++ /+"++-//"*+ 3tudent
Project
6lass room Prof"Dr"dr &uti
Par$ati,3p"PD
dr" B".gurah,
M"ForEdr" $i$ie!
ndrayani, M"?es
/1"++-/="++ /="++-/A"++ Plenary 6lass room Prof"Dr"dr &uti
Par$ati,3p"PD
dr" B".gurah,
M"ForEdr" $i$ie!
ndrayani, M"?es
./
Fr&'a1
De)*.3
th
/4
+@"++-+@"*+ +B"++-+B"*+ Le#t(re 4;
He"m&nthe) In%e#t&on
Le#t(re 6lass room Dr" dr" Made
3udarmaja, M"?es
+@"*+-+B"++ +B"*+-/+,++ Le#t(re 43
In%e#t&on o%
Nemato'a6 Ce)to'a
an' Tremato'a
<ecture 6lass room dr" ?ade!
3$asti!a,M"?es
+B"++-/+"*+ /,"++-/*"*+ ndividual
learning
/+"*+-/,"++ /*"*+-/="++ 3mall group
discussion
/,"*+-/1"++ /+"++-//"*+ 3tudent
Project
6lass room dr" Made
3udarmaja, M"?es
dr" ?ade!
3$asti!a,M"?es
/1"++-/="++ /="++-/A"++ Plenary 6lass room dr" Made
3udarmaja,
M"?esE3taff
..
+@"++-+@"*+ +B"++-+B"*+ Le#t(re 47
F&"ar&a)&)
Le#t(re 6lass room dr" ?" Agus 3omia,
3p"PD
+@"*+-+B"++ +B"*+-/+"++ Le#t(re 48 <ecture 6lass room dr" Made 3usila
DA+, DATE
T&me
Top&#
Learn&n-
)&t(at&on
P"a#e PIC
Re-("ar
C"a))
En-"&)h
C"a))
Mon'a1
De)*4<
th
/4
Den-(e &ra" In%e#t&on Utama, 3p,PD
+B"++-/+"*+ /,"++-/*"*+ ndividual
learning
/+"*+-/,"++ /*"*+-/="++ 3mall group
discussion
/,"*+-/1"++ /+"++-//"*+ 3tudent
Project
6lass room dr" ?" Agus 3omia,
3p"PD
dr" Made 3usila
Utama, 3p,PD
/1"++-/="++ /="++-/A"++ Plenary 6lass room dr" ?" Agus 3omia,
3p"PD
dr" Made 3usila
Utama, 3p,PD
.4
T(e)'a1
De)*4/
th
/4
+@"++-+B"++ +B"++-/+"++ Le#t(re 9<
Treatment o%
(PK,PD)
<ecture 6lass room Dr"dr"
B"?"3atriyasa,M">
repro
+B"++-/+"*+ /,"++-/*"*+ ndividual
learning
6lass room
/+"*+-/,"++ /*"*+-/="++ 3mall group
discussion
Facilitator
/,"*+-/1"++ /+"++-//"*+ 3tudent
Project
6lass room Dr"dr"
B"?"3atriyasa,M">
repro
/1"++-/="++ /="++-/A"++ Plenary
3ession
6lass room Dr"dr"
B"?"3atriyasa,M">
repro
.9
0e'ne)'a1
Aan*/
)t
/9
+@"++-+B"++ +B"++-/+"++ Le#t(re 9/
O2er2&eB o% P(erpera"
In%e#t&on
<ecture 6lass room dr" .ym Bayu
Mahendra,3p"#4
+B"++-/+"*+ /,"++-/*"*+ ndividual
learning
/+"*+-/,"++ /*"*+-/="++ 3mall group
discussion
/,"*+-/1"++ /+"++-//"*+ 3tudent
Project
6lass room dr" .ym Bayu
Mahendra,3p"#4
/1"++-/="++ /="++-/A"++ Plenary
3ession
6lass room dr" .ym Bayu
Mahendra,3p"#4
.:
Th()'a1
Aan*.
n'
/9
+@"++-+B"++ +B"++-/+"++ Le#t(re 9.
O2er2&eB o% Se?(a""1
Tran)m&tte' In%e#t&on
<ecture 6lass room Dr" dr" A"A"4"P"
Ciraguna, 3p"??
(?), F.3D:
+B"++-/+"*+ /,"++-/*"*+ ndividual
learning
/+"*+-/,"++ /*"*+-/="++ 3mall group
discussion
Disc" >oom Facilitaor
DA+, DATE
T&me
Top&#
Learn&n-
)&t(at&on
P"a#e PIC
Re-("ar
C"a))
En-"&)h
C"a))
/,"*+-/1"++ /+"++-//"*+ 3tudent
Project
6lass room dr" A"A"4"P"
Ciraguna, 3p"??
/1"++-/="++ /="++-/A"++ Plenary
3ession
6lass room dr" A"A"4"P"
Ciraguna, 3p"??
.;
Fr&'a1
Aan*4
r'
/9
+@"++-/="++ +B"++-/A"++ Pra#t&#e / =
La5orator1 '&a-no)&)
o% M&#ro5&a" &n%e#t&on
<aboratory "B" .yoman Putra
D$ija, 3"3i,
M"Biotech
.3
Mon'a1
Aan*;
th
/9
+@"++-/="++ +B"++-/A"++ Pra#t&#e . =
La5orator1 '&a-no)&)
o% M&#ro5&a" &n%e#t&on
<aboratory "B" .yoman Putra
D$ija, 3"3i,
M"Biotech
.7
T(e)'a1
Aan*3
th
/9
+@"++-/="++ +B"++-/A"++ Pra#t&#e 4 =
La5orator1 D&a-no)&)
o% C"&n&#a" Patho"o-1
<aboratory Dr .yoman
Mahartini 3pP?
.8
0e'ne)'a1
Aan*7
th
/9
+@"++-/="++ +B"++-/A"++ Pra#t&#e 9 =
La5orator1
E?am&nat&on o%
para)&t&# &n%e#t&o()
dr" ?ade!
3$asti!a, M"?es
4<
Th()'a1
Aan*8
th
/9
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La5orator1
E?am&nat&on o%
para)&t&# &n%e#t&o() ()
dr" ?ade!
3$asti!a, M"?es
4/
Fr&'a1
Aan*/<
th
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S&"ent Da1
4.
Mon'a1
Aan*/4
th
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ECAMINATION BLOCK TEAM
MEETING OF STUDENT REPRESENTATIES
n the middle of bloc! period, a meeting is designed among the student representatives of
every small group discussion, facilitators and source person of the bloc!" &he meeting
discuss about the ongoing teaching and learning process, 'uality of facilitator and lectures
as a feedbac! to improve the ne%t process"
MEETING OF THE FACILITATORS
All facilitators are invited to discuss all bloc! activities $ith bloc! contributors / $ee! after
meeting of student representatives"
ASSESSMENT METHOD

/" Assessment $ill be held on ,=
th
day of the bloc! period" &he time provision is /++
minutes" &he number of M6G is /++ $ith passing point -+"
," Assessment in this bloc! consists of7
34D 7 =H
3tudent Project (Paper) 7 /+H
Final e%am 7 @=H
STUDENT PROAECT
&&<5
(3ubjectEtopic7 choose from competency list)
.ame7
.M7
Faculty of Medicine, Udayana University
,+//
/" ntroduction (Pendahuluan)
," 6ontent (si sesuai dengan judul paper)
*" 3ummary (>ing!asan)
1" >eferences (Daftar pusta!a)7 :an6ouver style
=" Pages7 A-/+, 3pasi7 /"=, &ime .e$ >oman7/,
St('ent ProDe#t
.o &opic ?ompetensi
/ 3taphylococcus bacteremia
/" 3taphylococcus7 microbiologis aspect
," 6linical spectrum of staphylococcus
infection
*" 9o$ are staphylococcus infection
diagnosed
1" 6omplication of staph infection
=" &reatment and prevention of staph
infection
,
, 3inusitis
/" etiopathogenesis of sinus infection
," clinical symptoms and sign of sinus
infection
*" management of sinus infection
1" complication of sinus infection
,
* #titis Media
/" #titis media acute7 etiopathogenesis
," #titis media acute7 management
*" #titis media purulenta
1" #titis media !hronic suppurative
=" 6omplication of acute titis media
,
1 Mastoiditis
/" etiologi
," pathogenesis
*" diagnosis
1" management
=" complication
,
= Peritonsilar abses
/" etiopathogenesis
," clinical manifestation
*" diagnosis
1" management
,
A >heumatic fever
/" etiologi
," pathogenesis
*" diagnosis
1" management
=" complication
,
- >heumatic disease ,
/" etiopathogenesis
*" management
1" complication
@ Meningitis Purulenta
/" ethiopathogenesis
*" diagnosis
1" management
=" complication
/
B Meningitis serosa
ethiopathogenesis
clinical manifestation
diagnosis
management
complication
,
/+ Pla'ue (Pes)
5tiologi
&ransmisi
Management
6omplication
,
// Actinomycosis
Diagnosis (microbiology)
6linical manifestation
Management
/
/, 6hromoblastomycosis
Management
/
/* Maduromycosis
Management
/
/1 Fever
- Patogenesis of fever
- Metabolic respon of fever
- 9o$ to measure body temperature and
fever pattern
- Algorithm management of acute fever
illness
- Management of fever
/= 6M:
- 6M:7 virology
- 6linical spectrum of 6M:
- 6M: in immunocompetent
- 6M: infection in immunocompromi2ed
- Management of 6M:
*A
/A Malaria
- etiopatogenesis of severe malaria
- clinical spectrum of severe malaria
- malaria cerebral
1
- clinical approach management of severe
malaria
- malaria in pregnant
/- Dengue infection
- 9o$ to !no$ $arning simptom and sign
- severe dengue
- management of severe dengue
- management
1
/@ &yphoid fever
- typhoid to%ic
- &yphoid fever7 intestinal complication
-
1
/B 9:EAD3
- stigma of 9:EAD3
- :6&
- P6&
- 63& (care support treatment)
- A>:
*A
,+ nfluen2a
- seasonal influen2a
- s$ine influen2a
- Avian influen2a
- Management
- Prevention
1
,/ Acute 4astroenteritis
- $atery diarrhea7
- inflammatory diarrhea
- ho$ to assement of severity of
dehydration
- ho$ to do rehydration
- ho$ to do rectal s$ab
1
,, Fa$s (pate!)
- etiopatogenesis
- clinical picture
- laboratory confirmation
- Management
- Prevention
1
,* >abies
- etiopatogenesis of rabies
- clinical picture of rabies
- laboratory confirmation of rabies
- ho$ to manage dog bite
- ho$ to giving vaccination (M and
subcutans)
1
,1 6andidiasis
- clinical spectrum of candida infection
- <aboratory confirmation
- Management
,= <eptospirosis
- etiopatogenesis
- clinical picture
- laboratory confirmation
*B
- Management
- Prevention
,A 5merging and reemerging disease7 legionalle
Diagnosis microbiology
Management
,- 5merging and reemerging disease7 5nterovirus
-/ (9FMD)
Management
,@ 5merging and reemerging disease7 6oronavirus
(3A>3)
Management
,B 5merging and reemerging disease7 Bunyaviruses
(9antavirus)
Management
*+ nfe!si noso!omial
Definition
Manifestation
Management
Prevention
*/ Antibiotic resisten
Mechanism of resistence
>ationale of using antibiotica
Prevention
*, 9o$ to using prudent antibiotic
Profile of antibiotic
LEARNING PROGRAM
LECTURE /
Introduction to the block (Agent ,Host Environment, and infection
manifestation)
O"eh=
Pro%* Dr* 'r* T(t& ParBat& Merat&6 SpPD6 KPTI
================================================
Le#t(re .=
Bacterial classification
O"eh=
'r* K*Aan(artha P* P&nat&h6 M$e)
/" Describe relationship bet$een microbes and human in health and disease
," 5%plain normal human flora and opportunistic infections
*" Describe the establishment of microbial infection
1" 5%plain the difference bet$een 4ram-positive and 4ram-negative bacterial cell $all I
=" 6lassify the spherical bacteria (cocci) into 4ram-positive and negative group" <ist
their virulence factors and related diseases caused by them I
A" 6lassify the rod bacteria (bacilli) into 4ram-positive and negative group" <ist their
virulence factors and related diseases caused by them I
-" <ist the important enteric bacteria (5nterobacteriaceae), their virulence factors and
related diseases I
@" 6lassify the anaerobic bacteria according to their capabilities to form spores" <ist
their virulence factors and related diseases caused by them I
B" 5%plain the spesific characteristic of Mycobacteria cell-$all and the implication to
their natural resistance I
/+" 5%plain the virulence factors and pathogenesis of infection caused by Mycobacteria I
Le#t(re 4=
PATHOE!E"I" O# BA$TE%IA& I!#E$TIO!
'ade Agus Hendra(ana
ABSTRACT
&he pathogenesis of bacterial infection includes initiation of the infectious process
and the mechanisms that lead to the development of signs and symptoms of disease"
6haracteristics of bacteria that are pathogens include transmissibility, adherence to host
cells, invasion of host cells and tissues, to%igenicity, and ability to evade the hostJs immune
system" Many infections caused by bacteria that are commonly considered to be pathogens
are inapparent or asymptomatic" Disease occurs if the bacteria or immunologic reactions to
their presence cause sufficient harm to the person"
Bacteria (and other microorganisms) adapt to the environment, including animals
and humans, $here they normally reside and subsist" n doing so, the bacteria ensure their
survival and enhance the possibility of transmission" By producing asymptomatic infection or
mild disease, rather than death of the host, microorganisms that normally live in people
enhance the possibility of transmission from one person to another"
3ome bacteria that commonly cause disease in humans e%ist primarily in animals
and incidentally infect humans" #ther bacteria produce infection of humans that is
inadvertent, a mista!e in the normal life cycle of the organismK the organisms have not
adapted to humans, and the disease they produce may be severe"
&he clinical manifestations of diseases (eg, diarrhea, cough, genital discharge)
produced by microorganisms often promote transmission of the agents"
Many bacteria are transmitted from one person to another on hands" A person $ith S
aureus carriage in the anterior nares may rub his nose, pic! up the staphylococci on the
hands, and spread the bacteria to other parts of the body or to another person, $here
infection results" Many opportunistic pathogens that cause nosocomial infections are
transmitted from one patient to another on the hands of hospital personnel"
&he most fre'uent portals of entry of pathogenic bacteria into the body are the sites
$here mucous membranes meet $ith the s!in7 respiratory (upper and lo$er air$ays),
gastrointestinal (primarily mouth), genital, and urinary tracts" Abnormal areas of mucous
membranes and s!in (eg, cuts, burns, and other injuries) are also fre'uent sites of entry"
.ormal s!in and mucous membranes provide the primary defense against infection" &o
cause disease, pathogens must overcome these barriers"
#nce in the body, bacteria must attach or adhere to host cells, usually epithelial cells" After
the bacteria have established a primary site of infection, they multiply and spread directly
through tissues or via the lymphatic system to the bloodstream" &his infection (bacteremia)
can be transient or persistent" Bacteremia allo$s bacteria to spread $idely in the body and
permits them to reach tissues particularly suitable for their multiplication and cause the
diseases"
Learn&n- Ta)$
Ca)e =
A *= years old female, a secretary at private company come to general practician
complained that she has unreasonable pain $hen urinate since = days" 3he feels pain too
at lo$er abdominal" &he urine color is dar! yello$ and little bit cloudy" #ther physical
e%amination results are normal" &he practician as! for laboratory e%amination for urine
analysis and urine culture" After fe$ days, the urine analysis sho$n that she has urinary
tract infection" &he urine culture sho$n colonies of "scherichia coli bacteria and significant
as agent of infection"
E(e)t&on) =
/" n this case, "scherichia coli as a pathogen bacteria" Chen is "scherichia coli called
as coloni2ation bacteriaL
," 5%plain the differentiation bet$een true pathogen and opportunistic pathogenI
*" 5%plain the pathogenesis ho$ "scherichia coli can infect the urinary tract (from
transmission until infection and cause the disease) I
1" Chat are "scherichia coli#s virulence factors that can cause urinary tract infectionL
=" 5%plain the microbial virulence factors that you !no$I
A" 5%plain the differentiation bet$een e%oto%ins and endoto%in I
-" Describe ho$ several pathogens are able to survive inside the macrophages I
@" 5%plain the routes of transmission that you !no$ and give e%amples of each I
Se"% A))e))ment
/" 5%plain the meaning of this term above 7
A" 6ontamination
B" 6oloni2ation
6" nvasion
D" nfection
5" Pathogen
F" 6arrier
4" .onpathogenic
9" #pportunistic pathogen7
" Pathogenicity7
0" &o%igenicity7
?" :irulence7
<" 3ymbiosis
M" 6ommensalism
." Parasitism
#" ;oonoses
," 4ive e%amples of attachment mechanism I
Re%% =
0a$et2, Melnic!, Adelberg" ,+/+" 6hapter B" Pathogenesis of Bacterial nfection in Medical
Microbiology, ,=th 5dition by :ishal " &he Mc4ra$-9ill 6ompanies" <ange Microbiology"
&ecture )
*iral classification
Oleh+
dr, "ri Buda(anti, "-,'.
////////////////////////////////////////////////////////
&ecture 0
'echanism of *iral Pathogenesis
Oleh+
dr, "ri Buda(anti, "-,'.
=======================================
&ecture 1
'anifestation of virus and bacterial infection
dr.Agus somia, Sp.PD
========================================================
&ecture 2
Basic conce-t of Parasitic Infections
#leh7
Prof" dr" D"P" Cidjana, DAPD5, 3p"Par"?
MMMMMMMMMMMMMMMMMMMMMMMMMMMMMMMMMMMMMMMMMMMMMMMMMMMMMMMMMMMMMMM
&ecture 3
Treatment of *iral Infection (P.4P5)
Prof. dr. IGM Aman, Sp.FK
Most of antiviral agents e%erts their actions on viral replication, at the stage of nucleic acid
synthesis ot the stage of late protein synthesis and processing" Most of antiviral agents
active against herpes viruses and against the 9uman mmunodeficiency :irus (9:) are
antimetabolites, so that it must first undergo conversion to active forms, usually triphosphate
derivatives" #ne of the most important recent trends in viral chemotherapy has been
combination therapy, $here treatment $ith combination result in greater effectiveness and
prevent or delay the emergence of resistance, especially in the treatment of 9: disease"
3uch combination usually include t$o .ucleoside >everse &ranscriptase nhibitor (.>&s)
plus Protease inhibitor" n some combination regimens, a non nucleoside reverse
transcriptase inhibitor (..>&) has been used place of Protease inhibitor" 9ighly active
antiretroviral therapy (9AA>&) is recommended for AD3 patients"
Learn&n- Ta)$
A male patient, *+ year old, is 9:-positive, has a 6D1 count *++Eul and a viral >.A load
=++ copiesEml" &he physician give him antiviral drug" &$o $ee!s later he complained
anore%ia, nausea, vomiting, and abdominal pain" 9is abdomen $as tender in the epigastric
area" Finally the physician diagnose him as acute pancreatitis"
/" <ist drugs that have cross resistance $ith acyclovir, and e%plain the reason $hy
cross resistance happenedL (?at2ung p"@,1)
," <ist and describe the drugs preserved for acyclovir resistant strain" (?at2ung p"@,1)
*" n the treatment of 9: disease, the combination of antiviral is needed" 5%plain the
adventages of drug combination" n the case $hatNs li!ely antiviral drug given by the
doctor"
1" 9o$ do you manage this patientL
3elf assessment7
/" A patient suffering from herpes simple%, treated $ith acyclovir" But 93: is resistant
to acyclovir" &he alternative drug can choose7
/" 4anciclovir
," :alaciclovir
*" Famciclovir
1" 6idofovir
," As antiviral, the clinical use of acyclovir are as follo$7
/" :aricella
," >etinitis by 6M: (cytomegalovirus)
*" 9erpes 2oster
1" >eccurent herpes labialis
*" &he antiviral that are good for treating hepatitis patient are7
/" <amivudin
," >ibavirin
*" nterferon
1" 3tavudin
1" For treated AD3 patient a combination of antiviral are needed" &he combination that
are effective for this patient are7
/" ndinavir O Didanosine O <amivudin
," Acyclovir O Amantadine O ;idovudine
*" ;idovudine O Didanosine O .evirapine
1" 4anciclovir O 3orivudine O 6idofovir
&ecture 6
Treatment of 'icrobacterial Infections I (T(-e of antimicrobacterial)
(P.4P5)
Oleh+
Dr"dr" B"?" 3atriyasa,M">epro
A5)tra#t
Many of microorganism are classified as either 4ram-positive or 4ram-negative" Both of
them could be differentiated by several respect, not least in the structure of the cell $all,
$hich has implications for the action of antibiotics" &he cell $all of 4ram-positive organisms
is a relatively simple structure and it consist of =+H peptidoglycan" &he cell $all of 4ram-
negative organisms is much comple%, so more difficult in penetrating by some antibiotics"
Antibiotic for $hich penetration is a problem include ben2ylpenicillin, methicillin, macrolides,
vancomycin, bacitracin, and novobiocin" &here are many mechanisms of action of
antibiotics or antimicrobial drugs in !illing or inhibited the bacterial gro$th such as7 inhibit
cell $all synthesis, inhibit protein synthesis, as a antimetabolites, and inhibit microbial
nucleic acid metabolism" &he emergence of microbial resistance pose a constant challenge
to the use of antimicrobial drugs" Mechanism of underlying microbial resistance to the cell
$all synthesis inhibitors include the production of antibiotic-inactivating en2ymes, change in
the structure of target receptors, increased efflu% via drugs transporters, and decreases in
the permeability of microbes cellular membranes to antibiotics" 3trategies designed to
combat microbial resistance include the use of adjunctive agents that can protect against
antibiotic inactivation, the use of antibiotic combination and avoid the misuse of antibiotic"
Learn&n- Ta)$
A-*A-year old $oman recently treated for leu!emia is admitted to the hospital $ith malaise,
chills, and high fever" Bram stain of blood reveals the presence of 4ram negative bacilli"
&he initial diagnosis is bacteremia" &he records of the patient reveal that she had a severe
urticarial rash after oral penicillin :"
a" f you a medical doctor $hat antibiotic $ould you choose for this $omanL
b" 5%plain the mechanism of action and adverse reaction of the drugs that you choosed
c" n your opinion is there appropriate if that pasien treated by 6hloramphenicolL 5%plain
your ans$er"
3elf assessment7
/" Chich one of the follo$ing item is beta lactamase inhibitors7
a" Mafenide
b" Penicillin :
c" 6lavulanic acid
d" Amo%ycillin
e" #flo%acin
," 6iproflo%acin and the other fluoro'uinolone mechanism of action is by7
a" nhibiting the synthesis of bacterial protein
b" nhibiting an en2yme deo%yribonucleic acid (D.A) gyrase
c" nterfering cell $all synthesis
d" nhibiting the production of mycolic acid
e" nhibiting en2yme dehydrofolate reductase
*" &he follo$ing antibiotics inhibit bacterial protein synthesis and are considered as
bacteriostatic7
a" A2ithromycin
a. #flo%acin
b. 6hlarithromycin
c. 6iproflo%acin
1" &he follo$ing drugs are used for topical application7
a. Mafenide
b. 3ulfasala2ine
c. 3ilversulfadia2ine
d. Penicillin
=" Chich ones are the contraindication of tetracycline7
a. Producing a yello$ discoloration of teeth
b. 4ro$th retardation in relation to infant s!eletal development
c. Depression of bone gro$th
d. 6rystalluria
A" &hese statements are true about chloramphenicol7
a. t is a potent inhibitor of microbial protein synthesis
b. t binds reversibly to the p1=+ as sub unit of bacterial ribosomal
c. t inhibits the peptidyl transferase step of protein synthesis
d. t is a bacteriostatic broad spectrum antibiotic
-" Antibiotic that has ototo%ic and nephroto%ic effect is7
a" 5rythromycin
b" 3treptomycin
c" 6hloramphenicol
d" Amo%ycillin
e" 6lindamycin
&e%tboo!
3ource 7
/" ?at2ung, B"4" ,++/" Basic and 6linical Pharmacology" 5ight 5dition" <ange Medical
Boo!sEMc4ra$ P9ill"
," ?at2ung and &revorNs" Pharmacology 5%amination and Board >evie$" 3i%th
5dition"<ange Medical Boo!sEMc4ra$-9ill"
&ecture 78
Treatment of 'icrobacterial Infections II (%esistance, rational treatment,
and drug combination)
Oleh+ Dr. Made Jawi, M.Kes
========================================================
&ecture 77
Antimicrobial susce-tibl(
!e"# dr. $i Made Adi %arini, Sp.MK
========================================================
&ecture 79+
%es-ond Host against -arasitic and clinical manifestation
dr. I Made Susi!a &'ama,Sp.PD
=================================================
&ecture 7:
Treatment of -arasitic infection (P.4P5)
dr, A, ;i<iek Indra(ani, ',.es
Abstract
Malaria is the most important proto2oal disease in tropical medicine" t is responsible
for , million deaths per year and much morbidity in the ,++ million people $orld$ide $ho
are infected" Malaria is caused by four species of plasmodial parasites that are transmitted
by female anophelene mos'uitoes" Anti malarial drugs are usually classified in terms of their
action against different stages of the parasite" &hey are used to prevent transmission or
cure malaria" &he aim of prophylactic use is to prevent the occurrence of infection in a
previously healthy individual $ho is at potential e%posure ris!" 3uppressive prophyla%is
involves the use of blood schi2onticides to prevent acute attac!sK causal prophyla%is
involves the use of tissue schi2onticides or drugs against the sporo2oite to prevent the
parasite established in the liver" Anti malarial drugs can be used curatively (therapeutically)
against an established infection" 3uppressive treatment aims to control acute attac!s,
usually $ith blood schi2onticidesK radical treatment aims to !ill dormant liver forms, usually
$ith a hypno2onticide, to prevent relapsing malaria" 3everal classes of antimalarial drugs
such as chloro'uine, amodia'uine, 'uinine, 'uinidine, meflo'uine, prima'uine, fansidar,
proguanil, artemisin, and atova'uone-proguanil" &he effectiveness of anti malarial agents
varies bet$een parasite species " n addition, drug resistance is an important therapeutics
problem, most notably $ith P falciparum$
Amoebic dysentery is caused by infection $ith "ntamoeba histolytica, $hich is
ingested in a cystic form" Dysentery results from invasion of the parasite in the intestinal
$all" #ccasionally, the organism insists in the liver, forming abscesses" 5" 9istolytica can
cause asymptomatic intestinal infection, mild to moderate colitis, severe intestinal infection,
ameboma, liver abscess and other e%tra intestinal infections" &he choice of drugs for
amoebiasis depends on the clinical presentation" Drugs of choice for asymptomatic
intestinal infection are luminal agent such as dilo%anide furoate, iodo'uinol and
paromomycinK for mild to moderate intestinal infection are metronida2ole plus luminal agentK
for severe intestinal infection and hepatic abscess are metronida2ole plus luminal agent "
&o%oplasmosis is an infection caused by to%oplasma gondii parasite" Most people
have no symptoms because their immune system !eeps the parasite from causing illness"
9o$ever, in people $ho have a $ea! immune system, to%oplasmosis can cause serious
medical problems, such as damage the eyes and brain" &he immune system can become
$ea! for a number of reasons"&he drug of choice for to%oplasmosis are pyrimethamine plus
clindamycin plus folinic acid
<earning &as!
/" Ms" De$i, a ,= year old student, presents $ith a four day history of high fever (1+
6), general malaise , feeling intensely cold and sha!ing follo$ed by profuse
s$eating" 9e returned from <ombo! island * $ee!s ago" 3he ta!es drugs for
malaria" &oday she feel di22iness, nausea, diarrhea, tinnitus, blurred vision ,
flushed, s$eaty s!in and impaired hearing"
#uestions 7
/" Chich of the follo$ing antimalarial drugs causes a dose dependent to%icity L
," Describe the pharmacodynamic and pharmaco!inetic properties of the major
antimalarial drugs (chloro'uine, meflo'uine, 'uinine, prima'uine, and the
antifolate agents)I
&he five star hotel usually has screening their food handler s every si% months" Mr" Andi
had positive cysts amoebiasis $ithout dysentery symptom"
#uestions
/" Chich of the follo$ing anti amoebiasis drugs can use to treat Mr" Andi L
," Describe the pharmacodynamic and pharmaco!inetic properties of the major
amebicides (dilo%anide, emetine, iodo'uinol, and metronida2ole) I
Mrs >atna, a ,@ years old, come to hospital policlinic $ith chief complaints had abortus for *
times" 3he usually eat stea! or satay and has many cat in her house" Doctor suspect she
had infected by to%oplasma gondii"
#uestions
/" dentify the drugs useful for prophyla%is and treatment to%oplasmosis and !no$
their to%ic effects I
3elf Passesment 'uestions
/" Chich of the follo$ing antimalarial drugs should be used for prophyla%is for travel to
the 5ast of <ombo! island L
A" 6hloro'uine
B" Prima'uine
6" Meflo'uine
D" 9ydro%ychloro'uine
5" Pyrimethamine
," Chich of the follo$ing drugs has a major side effect of hemolysis in persons $ith
4APD deficiencyL
A" 6hloro'uine
B" Prima'uine
6" Meflo'uine
D" Pyrimethamine
5" Do%cycline
*" Chich of the follo$ing drugs is recommended as a single agent for oral treatment of
uncomplicated malaria due to chloro'uine-resistent P falciparum strains L
A" Do%ycline
B" odo'uinol
6" Prima'uine
D" Proguanil
5" Guinine
1" Chich of the follo$ing drigs is effective against 5" histolytica and other proto2oa that
live under anaerobic conditionsL
A" Metronida2ole
B" Pentamidine isethionate
6" Guinine
D" 5flornithine
5" 6hloro'uine
=" Chich one of the follo$ing statements about amebicides is least accurateL
A" Dilo%anide furoate is a luminal amebicide
B" 5metine is contraindicated in pregnancy and in patients $ith cardiac disease
6" Metronida2ole has little activity in the gut lumen
D" Paromomycin is effective in e%traintestinal amebiasis
5" 3ystemic use of iodo'uinol may cause thyroid enlargement and peripheral
neuropathy
&e%tboo!
3ource 7
*" ?at2ung, B"4" ,++/" Basic and 6linical Pharmacology" 5ight 5dition" <ange Medical
Boo!sEMc4ra$ P9ill"
1" ?at2ung and &revorNs" Pharmacology 5%amination and Board >evie$" 3i%th
5dition"<ange Medical Boo!sEMc4ra$-9ill"
&ecture 7)+
The %ole of Immunit( to infection (Basic)
Oleh+
5r,dr, 5e<a 'ade "ukrama, ',"i, "-,'.
/////////////////////////////////////////////////
&ecture 70+
Infection of '(cobacterium (TB$)
Prof 5r,dr, IB %ai,"-,P
////////////////////////////////////////////////////////
&ecture 71+
Infection of '(cobacterium (&e-ros()
5r, 5harma -utra, "-,..
Morbus 9ansen is an infectious disease primary affected the periphery nerve and
secondary affected s!in and the other organ caused by Mycobacterium leprae" >eadley and
0opping classification is &uberculoid-&uberculoid (&&), Borderline&uberculoid (B&),
Borderline-Borderline (BB), Borderlline-<epromatous (B<), and <epromatous-<epromatous
(<<)"
&he 1 cardinal sign of <eprosy are7 /" Macula hypopigmented or erythematous s!in,
," Anaesthesi, *" 5nlargement of periphery nerve, 1" Acid Fast Bacilli (AFB) found from slit
s!in smear" Diagnosis of leprosy is based on finding t$o from three cardinal sign of leprosy
or if only cardinal sign number 1"
&here are t$o !ind regimen therapy for leprosy i"e" the therapy for paucy bacillary
leprosy (&&, B& $ith AFB (-) are rimfapicin A++ mg a month and dafsonAH (DD3) /++ mg a
day continuous for si% month and for multi bacillary leprosy are rifampicin A++ mg a month,
clofacimin (lamprene) *++ mg a month continuous $ith lamprene =+ mg a day and dafson
(DD3) /++ mg a day continuous therapy for /, months"
?epusta!aan
/" Andre$s Diseases of the s!in" .ine 5d
," <eprosy" &hird edition" Antony Bryceson

ntoroduction of <eprosy
/" 5%plain the etiology of leprosy ( My cobacterium leprae)
," 5%plain the test for detection of M leprae 7 ;eihl-.eilsen staining test,
histopathological e%amination, lepromin test, 4una$an test and anaesthetic test in
supporting the diagnosis of leprosy
*" 5%plain the classification of leprosy
1" 5%plain the clinical sign and symptom of leprosy
=" 5%plain the complications of leprosy
A" 5%plain the management of leprosy and the complications
Ka)()
3eorang $anita, *= tahun mengeluh ada berca! merah pada punggung !iri dan !anan
dengan batas tida! tegas, selain itu juga dijumpai berca! merah di $ajah dan dada yg
tersebar simetris, !ecil-!ecil" Berca! merah tersebut tida! gatal" 3elain itu dijumpai
penebalan pada cuping telinga !anan dan !iri serta alis mata ronto!"
Pertanyaan 7
a" Apa yang perlu ditanya!an lagi pada penderita tersebutL
b" Pemeri!saan apa saja yang diperlu!an L
c" Apa diferensial diagnosis 3audara L
d" Apa diagnosa 3audara L
Bagaimana penatala!sanaannya L
&ecture 72+
Antim(cobacterial 5rugs ( anti TB$, Anti le-ra) (P.4P5)
dr, IB !gurah, ',#or
&he chemotherapy of infection caused by Mycobacterium tuberculosis is complicated
because7 limited information about the mechanism of drugs action, the development of
resistance, the intracellular site of mycobacterial, the chronic mycobacterial disease and
many drug drug to%icities, and patient compliance" 6hemotherapy of tuberculosis al$ays
the use of drug combinations to delay of resistance and increased antituberculosis efficacy"
&he 1 cardinal sign of <eprosy are7 /" Macula hypopigmented or erythematous s!in, ,"
Anaesthesi, *" 5nlargement of periphery nerve, 1" Acid Fast Bacilli (AFB) found from slit
s!in smear" Diagnosis of leprosy is based on finding t$o from three cardinal sign of leprosy
or if only cardinal sign number 1"
&here are t$o !ind regimen therapy for leprosy i"e" the therapy for paucy bacillary
leprosy (&&, B& $ith AFB (-) are rimfapicin A++ mg a month and dafsonAH (DD3) /++ mg a
day continuous for si% month and for multi bacillary leprosy are rifampicin A++ mg a month,
clofacimin (lamprene) *++ mg a month continuous $ith lamprene =+ mg a day and dafson
(DD3) /++ mg a day continuous therapy for /, months"
6ase /7
A 1+-year old man got cough since one month, lost of appetite and s$eating every night"
After e%amination the physician diagnosed the patient as tuberculosis"
/" Describe the combination therapy for tuberculosis $hich used best
," 5%plain the mechanism of action of each drugs
*" &he therapy of tuberculosis need long time" 5%plain $hat is the reason"
1" 5%plain the interaction of isonia2id $ith phenytoin
=" Descrie the to%ic effect of drugs for tuberculosis
A" <ist all drugs for leprosy
-" Describe the mechanism of action dapsose for leprosy
@" Describe $hy you use combination dapsone $ith rifampin and clofa2imine for
leprosy
B" Describe the to%ic effects of dapsone and treatment for erythema nodosum
/+" Describe the pharmacological aspects of rifampin for leprosy
//" Describe the pharmacological aspects of clofa2imine for leprosy
3elf assessment7
/" 6ompare the fate of isonia2id in slo$ asetilator patient and rapid asetilator patient"
," sonia2id for tuberculosis is usully combined $ith vitamin BA" Describe the reason
*" Chy do you choose pyra2inamide as primary drug for tuberculosis"
Le#t(re /7=
Control o% m&#roor-an&)m (&n%e#t&on #ontro")
'r* N& Ma'e A'&tar&n& Sp* MK
ABSTRACT
Microorganism li!e viruses, bacteria, fungi and proto2oans reproduce directly $ithin
the host" &hey are usually small and have a short generation time" >ecovery from infection
usually gives immunity against re-infectionK in the case of viral infections this may be
lifelong" Ce !no$, the source of infection can be from community and hospital, $hile the
transmission of infection varies to depending from microorganism" &he principle prevention
of infection must to !no$ the !ind of microorganism, transmission method and population of
infection" Among various major factors contributing to the emergence of infectious diseases,
the important ones are human demographics and behavior, industry and technology,
economic development and land use, globali2ation and international travel, microbial
adaptation and change, brea!do$n of public health measures, and economic disparity of
have and have-nots
#ne of the great achievements of applied medical research has been its success in
controlling so many infectious diseasesK smallpo% has been eradicated and other infections
are no$ controlled effectively in many parts of the $orld" &his control has been
accomplished in three main $ays by the use of chemotherapy, immuni2ation and improving
the environment (e"g" better sanitation, nutrition)
n general, chemotherapy is used to control infectious diseases in individuals,
$hereas immuni2ation and environmental improvements are used for control in populations"
Understanding the $ays in $hich these diseases arise, spread and can be controlled
re'uires detailed epidemiologic studies to provide an accurate basis for assessment of ris!s
and for planning intervention" &hese studies are based on !no$ledge of the infectious
agents and their patterns of association $ith their hosts, but re'uire the collection and
analysis of data, in conjunction $ith the use of mathematical models, to produce useful
pictures of disease transmission and control" Chere the causal lin!s bet$een a clinical
condition and an infectious agent or its mode of transmission are un!no$n, epidemiologic
investigations can establish this lin! and thus determine appropriate control strategies"
Learn&n- Ta)$
/" Describe ris! factors are influence to community infection and hospital infection
," Describe ho$ infections flo$ through a host population "
*" Describe some strategies for control of infectious diseases"
1" Describe some factors are influence to spread of infection"
=" Describe some factors are influence the success of vaccination"
Se"% A))e)ment
/" 6omparison of chemotherapy and vaccination
," 5%plain the meaning of this term above 7
a" 3usceptible host
b" ncubation period
c" <atent period
d" 4eneration time
*" Mention some factors are important at vaccination gift
Re%eren#e =
Mims" Medical Microbiologi, 1
th
5dition, Mosby 5lsevier" ,++@" p"11=-1=- D p" ==/-=A@
(ec'ure )*#
Immuni=ation in child
dr" D$i <ingga, sp"AE dr" C" 4usta$an,3p"A
Abstract
mmuni2ation is the process of artificially inducing immunity or providing protection from
disease" Active immuni2ation is the process of stimulating the body to produce antibody and
other immune responses through administration of a vaccine or to%oid" Passive
immuni2ation, the provision of temporary immunity by administration of preformed
antibodies derived from humans or animals" Biologic agents used to induce active
immuni2ation include vaccines and to%oids" A vaccine is defined as a suspension of live
(usually attenuated) or inactivated microorganisms, or fractions there of, $hich is
administered to induce immunity and prevent infectious disease or its se'uelae" &here are
some diseases that can prevent $ith immuni2ation" Polio, diphtheria, tetanus, pertusis,
tuberculosis, measles, hepatitis B, hepatitis A, influen2a, meningitis caused by hemophilus
influen2a type B" All vaccines may cause side effects, and immuni2ation safety is a real
concern" Unli!e most other medical interventions, vaccines are given to healthy people, and
people are far less $illing to tolerate vaccinesJ adverse effects than adverse effects of other
treatments" As the success of immuni2ation programs increases and the incidence of
disease decreases, public attention shifts a$ay from the ris!s of disease to the ris! of
vaccination,

and it becomes challenging for health authorities to preserve public support for
vaccination programs"
<earning tas!
&he baby, boy, = months old accompanied by his mother come to clinic to get immuni2ation"
9is mother told to doctor that her baby had fever after the first DP& immuni2ation" 9er baby
had fever until *@
+
6" 9e has no sei2ure, no high crying but his mother $orried about that
e%perience"
/" Chat is the e%planation that you must tell to his motherL
," 9o$ about the ne%t immuni2ation scheduleL
*" Chat is contraindication for ne%t immuni2ationL
&ecture 98
Antise-tic and disinfectant
5r,dr,B,., "atri(asa,',%e-ro
Abstract+
Disinfectants are chemical agent that inhibit or !ill microorganism in an inanimate
environment" Antiseptics are disinfecting agent $ith sufficiently lo$ to%icity for host cells that
they can be used directly on s!in, mucous membranes or $ound" Antiseptics and
disinfectants are e%tensively used in hospitals and other health care settings for a variety of
topical and hard-surface applications" A $ide variety of active chemical agents (biocides)
are found in these products, many of $hich have been used for hundreds of years, including
alcohols, phenols, iodine, and chlorine"
A $ide variety of active chemical agents (or QbiocidesR) are found in these products, many of
$hich have been used for hundreds of years for antisepsis, disinfection" Despite this, less is
!no$n about the mode of action of these active agents than about antibiotics" n general,
biocides have a broader spectrum of activity than antibiotics, and, $hile antibiotics tend to
have specific intracellular targets, biocides may have multiple targets" &he $idespread use
of antiseptic and disinfectant products has prompted some speculation on the development
of microbial resistance, in particular cross-resistance to antibiotics" &he process of
disinfectants prevent infection by reducing the number of potentially infective organism
either by !illing, removing, or diluting them"
Antiseptics are disinfecting agents $ith sufficiency lo$ to%icity for host cells that can used
directly in s!in, mucous membrane, or $ound" Disinfectants are strong chemical agents that
inhibit or !ill microorganisms in an inanimate environment" Disinfectant and antiseptics do
not have selective to%icity, and their clinical use are therefore limited" Most antiseptics delay
$ound healing" User of antiseptics and disinfectants need to consider their short-term and
long-term to%icity since they may general biocidal activity and may accumulate in the
environment or the body of the patients"
Learn&n- Ta)$
/" <ist the Disinfectants and antiseptics (?at2ung D &revorNs, ?at2ung, B4)
," 5%plain the mechanism of action disinfectants and antiseptics (?at2ung D &revorNs,
?at2ung, B4)
*" Describe the clinical use of disinfectants and antiseptics for nosocomial infection
1" Describe the side effect of disinfectants and antiseptics (?at2ung D &revorNs,
?at2ung, B4)
Se"% a))e))ment
/" Chich one the follo$ing antiseptics promote $ound healingL
A" odine
B" Alcohol
6" 9e%achlorophene
D" 6hlorhe%idine
5" .one of the above
," " Chich one the follo$ing antiseptics and disinfectant derivates of o%idi2ing AgentL
A" odine
B" Alcohol
6" 9e%achlorophene
D" 6hlorhe%idine
5" 9ydrogen pero%ide
*" Alcohols are not used as sterilants because they are" 5S65P&7
A" &hey are sporicidal
B" Do not penetrate protein-containing organic material
6" May not be active against hydrophilic viruses
D" <ac! residual action
+. &hey evaporate completely
," Mechanism of action of povidone-iodine is to
A" nhibitor of arabinosyl tranferase
B nhibitor of thymidilate syntetase
6 nhibitor of protein !inase
D Denature of protein
5" Denature of lipid
Le#t(re ./
Un&2er)a" Pre#a(t&on
dr Agus 3omia,3p"PD
<earning tas!
6ase /
A ,,-year-old male, $or! as an interns doctor in emergency care unit, had a patient $ith
suspected of 9: infection stage : and <ung &B and chronic diarrhea" &his doctor $ill do
the history-ta!ing, physical e%amination and giving first aid to the patient
<earning &as!7
/" Chat is the type of e%posure ris! that may happen to this doctorL
," Chat is specific precaution that this doctor have to do to prevent cross
transmissionL
*" Chat are the !ind of body protector that this doctor have to $ear L
1" f this doctor have to ta!e blood specimen $ith syringes needle to laboratory
e%amination, ho$ to recapping needles in order to prevent the infectionL
3elf assessment7
/" Describe about7
a" .osocomial infection
b" ?inds of nosocomial infection
c" 9o$ to do hygienic hand $ashing
d" 9o$ is the preparation and procedure of using sterile glovesL
e" 9o$ is the preparation and procedure unleashing sterile glovesL
," 5%plain pathogenesis of7
a" .osocomial blood stream infection
Le#t(re ..
Proto>oa In%e#t&on I (Ma"ar&a6 Amoe5&a)&)6
Le&)man&a)&)6Tr&pano)om&a)&)6To?op"a)mo)&)6 Tr&#homon&a)&))
O"eh=
'r*DeBa A1( A* Sr& La$)m&6M*S#6 M*Ke)
'r* P(t( A)tr& Dama1ant&6M*Ke)
ABSTRACT
Proto2oa are unicellular organisms that have tropho2oite form $ith one or more nuclei
containing nucleoli or !aryosome and bounded by a nuclear membrane and the usual
eu!aryotic cytoplasmic organelles including mitochondria ribosomes and endoplasmic
reticulum" &ropho2oite have a cell membrane but not cell $all" Most intestinal Proto2oa also
develop cyst that are more resistant than the fragile tropho2oite to drying, cold or other
environmental stresses"
Malaria and &o%oplasmosis $ell !no$n as parasitic disease and have great impact
due to their $orld$ide distribution" 9uman malarial parasite $ere first seen in /@@+ and
their development both in the anopheline mos'uito and in the human blood stream $as $ell
understood by /B++, ho$ever 3everal clinical syndromes !no$n to be caused by infection
of malaria parasites $ere first recogni2ed centuries before the discovery of their
pathogens"6onse'uently the diseases $ere referred to the type of febrile cycle" Guotidian,
tertian and 'uartan fevers denoted respectively ,1-,1@- and -, hour cycles of fever" &he
modern tendency is to refer the various types of malaria by the name of the agent"
&o%oplasma is caused by a coccidian parasite, Tooplasma !ondii" t has a
$orld$ide distribution and sho$s a broad host range from $arm blooded animals to birds
and reptiles" Man ac'uires the infection indirectly by ingesting oocysts from contaminated
environments, by consuming &o%oplasma cysts from tissues of other intermediate hosts
such as co$, goat, chic!en, duc!, rabbit, by blood transfusion or transplantation, or
directly by transplacental infection
9uman infection is generally asimptomatic and self limited e%cept in
immunocompromised host, infection can disseminated and fatal" &he prevalence of
antibody to to%oplasma in human and animal ranged from ,H to -=H in 3outheast Asian
6ountries"

6ats are the definitive host of T$ !ondiiK they are the only animals that pass
oocysts in their feces

"
LEARNING TASKS PROTO@OA INFECTION
/" Ca)e7
A *= year old man present to primary public health service $ith one $ee! history of
headache, fever, chills, s$eats and myalgia" Patient history reveals that he just returned
from Cest Papua after , months lived there" 9e too! chloro'uine malarial prophylactic
irregularly" Physical e%amination sho$ed raised body temperature (1+
+
6), a rapid pulse
rate, and generali2ed s$eating" 6omplete Blood 6ount $as ordered and demonstrated
intra erythrocyte organism"
a" Describe the laboratory e%aminations to define the diagnosis
b" Chen in blood smear demonstrate normal si2e erythrocyte containing crescent
shape gametocytes and multiple ring form $ithin the blood cell,
Chat is the most li!ely diagnosed in this patientL
$hat is et&o"o-1 of this cases and describe this para)&te "&%e #1#"e
c" Describe the pathogenesis of this disease
," Please compare the morphology characteristic of 1 type of plasmodium in human"
*" Describe briefly about chagasN disease"
1" Describe the life cycle of Trypanosoma cru%i and Leishmania donovani
:* Ca)e
A previously healthy ,@-year old man, $ho had recently returned from a trip to
<ombo!, $as seen by his family physician for crampy abdominal pain, malaise, slight
fever and bloody, mucoid diarrhea" <i'uid stool specimens $ere collected and
submitted for culture for enteric bacterial pathogens as $ell as parasites" 3tool cultures
$ere negative for bacterial pathogens, e%amination for ova and parasites $as positive
for motile tropho2oites in the saline $et amount, and ameboid tropho2oites $ith finely
granular cytoplasm and ingested red blood cells in the permanent trichrome stain"
a" Describe the life cycle of parasites above I
b" 5%plain the pathogenesis of parasite aboveI
c" Describe infective stages of parasite aboveI
A" Describe the life cycle of Trichomonas va!inalis
-" Describe infective stages of Trichomonas va!inalis
@" 5%plain $hat the differences of "ntamoeba histolytica and &iardia lamblia life cycleL
B" Describe the life cycle of Tooplasma !ondii
/+" 5%plain transmission of Tooplasma !ondii infection
//" 5%plain $hy to%oplasma infection became latencyL
Le#t(re .4
Proto>oa In%e#t&on II (Mana-ement o% proto>oa In%e#t&on))
'r +("& Ga1atr&6 Sp*PD
O5De#t&2e)
&o describe name the 1 important members of the 4enus Plasmodium
&o !no$n $hich from of Malaria is most dangerous and $hy"
&o describe disease that Malaria most commonly mimic
&o understand ho$ Malaria is diagnosed
&o describe the current recommendation for Malaria treatment and $hat factors
dictate the regimen of choice
>ecogni2ed $hen should chemoprofila%is be begun and ho$ long after completion
of a trip to an endemic area should preventive therapy be continued
&o describe clinical presentation of AmoebiasisE &o%oplasmosisE &richomoniasis
&o !no$ ho$ Amoebiasis E &o%oplasmosisE &richomoniasis
s diagnosedL
&o describe $hat are the treatment of choice of Amoebiasis &o%oplasmosisE
&richomoniasis

6ase /7
A ,/-years-old man complained $ith fever for A days prior to admission, relapsing chills,
muscle eches and lost of appetite" 9e too! several day trip to <ombo! island" &hey noted
some mos'uito bites and ate some fruits on the island" About * days into the illness 9e
became jaundice and began passing dar! urine" &hey sought treatment from local <ombo!
physician, $ho diagnosed hepatitis secondary to ingestion of to%ic food" &$o days later 9e
$as referred to 3anglah 9ospital for intensive treatment" Based on an initial e%amination,
patient $as conscious, loo! pale and icteric, body temperature $as *@,= T6"
<earning tas!7
/" Find !ey $ords related to this case
," Describe condition related to !ey $ords
*" Define organ system that involved in this condition and find probably cause of
the !ey $ords
1" Define differential diagnosis and other e%aminations to support the diagnosis
=" Describe !inds of laboratory e%amination to diagnose malaria e"'" blood
smear, thic! smear, rapid test, etc
A" Define management of this case
-" Define complication and prognosis
@" Define prevention based on individual, family, and community
3elf assessment7
/" Describe !inds of plasmodium
," Describe pathogenesis of malaria
*" Describe diagnosis of malaria
1" Describe pathogenesis of complication
=" Define management of uncomplicated malaria
A" Define management of malaria $ith severe complicatio
Le#t(re .9
In%e#t&on o% Entero5a#ter (Th1po&'6 C* 5ot("&n(m)
dr Agus 3omia,3p"PD
Ca)e /
A ,,-year-old male, $ith feeling generally un$ell $ith fever, headache, malaise and
diarrhea" the onset of fever since - days ago" 9is body temperature $as *B degree celcius,
blood pressure /,+E@+ mm9g, Pulse rate /++ beat per minute"
<earning &as!7
=" Define and describe others symptoms related to the patients that should be
as!ed to this patient
A" Describe physical e%amination to support diagnosis of this patient"
-" Chat is possibly diagnosis of this patientL
@" Describe differential diagnosis of this case
B" Describe laboratory and other e%amination to support the diagnosis
/+" Describe management of this patient
//" Describe ho$ to e%plain to this patient about prognosis of patientUs disease
Ca)e /=
A 1,-year-old man complained $ith diarrhea since last night" 9is diarrhea $as /+ times"
Diarrhea has accompanied $ith nausea, abdominal pain, and malaise" .o history of fever
and stomachache" 9e is a salesman" 9e too! medicine to retrieve his diarrhea, but it does
not $or!"
<earning tas!7
/" Define other sign and symptoms from this patient
," Describe physical e%amination must be done to this patient
*" Describe laboratory e%amination and other e%amination must be done to support
diagnosis
1" Describe management of this patient
=" Describe plan of therapy based on priority on this patient
3elf assessment7
*" 5%plain pathogenesis of7
a" Bacillare Dysentriae
b" &yphoid fever
c" 6holera
d" 6lostridium difficile associated diarrhea
1" Describe and interpret cerebrospinal fluid (63F) e%amination in bacterial meningitis,
viral meningitis, tuberculous meningitis, and streptococcal meningitis"
=" Define signs and symptoms of7
a" &yphoid fever
b" Bacillare dysentriae
c" 6holera
A" Differentiate clinical sign and symptoms of diarrhea caused by bacillare dysentriae,
cholera and 6lostridium associated diarrhea
-" Describe steps for ho$ $e doing rehydraton
@" Define management of these patients7
a" &yphoid fever
c" 6holera
B" Describe about complication of
a" &yphoid fever
c" 6holera
&ecture 90
"e-sis and Bacteremia
dr. Made Susi!a u'ama, Sp.PD
=================================================
&ecture 91
$utaneous *iral Infection (*aricella, >oster, Her-es)
Oleh+
'r*IGA S(me'ha P&n'ha6 Sp*KK,'r* E"&) In'&ra6Sp*KK
Learn&n- ta)$
An adult $oman, 1= years old came to clinic $ith chief complaints group of small blister in
right side of the bac! since * day ago then the lession spread to the right $aist and right
chest" &his complain is accompanied $ith burning sensation" #ne day before the blister
appeared patient had fever" 9istory of the same disease $as denied" 9istory of ta!ing
medicine before $as denied"
/" Chat should $e as!ed to the patient in the anamnesis L
," Describe the effloresensi in physical e%amination"
*" Chat are the differential diagnosis in this patient L
1" Chat <aboratory tests is needed to confirm diagnosis of this caseL
=" Chat is the diagnosis of this patient L
A" Mention about complication of this disease
-" Chat is the prognosis of the disease L
@" Chat is the treatment of this caseL
B" Chat advice $e can give to the patient L
3elf Assasement
/" Chat !ind of diseased that can caused by the herpes virus group and $hat is the nature
virus of this groupL
," Chat is the majority characteristic of these group of virusL
*" Chat is clinical manifestation of varicella L
1" 9o$ is pathogenesis of 9erpes ;oster infectionL
=" Mention about trigger factor the emergence of lesions in herpes simple%
A" Chat are the complication that occurs in 9erpes ;osterL
-" Mention about complication that could occur happens $hen pregnant $omen suffer from
varicella
@" Chat is the management of s!in diseases caused by virusesL
&ecture 92
%etroviral Infection (HI*)
Oleh+
Prof. Dr. dr. %u'i Parwa'i Mera'i, SpPD, KP%I
/////////////////////////////////////////////////
&ecture 93
Influen=a
Oleh+
Pro%* Dr* 'r* T(t& ParBat& Merat&6 SpPD6 KPTI
INFLUEN@A
A5)tra#t
nfluen2a virus infection, one of the most common infectious diseases, is a highly
contagious airborne disease that causes an acute febrile illness and results in variable
degrees of systemic symptoms, ranging from mild fatigue to respiratory failure and death"
&hese symptoms contribute to significant loss of $or!days, human suffering, mortality, and
significant morbidity" Accurately diagnosing influen2a A or B infection based solely on clinical
criteria is difficult because of the overlapping symptoms caused by the various viruses
associated $ith upper respiratory tract infection (U>&)" n addition, several serious viruses,
including adenoviruses, enteroviruses, and paramy%oviruses, may initially cause influen2a
li!e symptoms" &he early presentation of mild or moderate cases of flavivirus infections (eg,
dengue) may initially mimic influen2a" For e%ample, some cases of Cest .ile fever ac'uired
in .e$ For! in /BBB $ere clinically misdiagnosed as influen2a" Patients $ith influen2a
fre'uently present $ith various symptoms shared by many other viral infections" n the
northern and southern hemispheres, these symptoms are more common in the $inter
months"nfluen2a virus is a single-stranded >.A virus, divided into type A, B, and 6 $here
structurally and biologically similar but vary antigenically" t is family of #rthomy%oviridae"
&he most common prevailing influen2a A subtypes that infect humans are 9/./ and 9*.,"
5ach year, the trivalent vaccine used $orld$ide contains A strains from 9/./ and 9*.,,
along $ith an influen2a B strain" nfluen2a virus infection occurs after transfer of respiratory
secretions from an infected individual to a person $ho is immunologically susceptible" f not
neutrali2ed by secretory antibodies, the virus invades air$ay and respiratory tract cells"
#nce $ithin host cells, cellular dysfunction and degeneration occur, along $ith viral
replication and release of viral progeny" 3ystemic symptoms result from inflammatory
mediators, similar to other viruses" nfluen2a A is generally more pathogenic than influen2a
B" >ecently, mutation of influen2a A virus cause the emergence of ne$ strain of virus $hich
cause specific influen2a such as Birds flue (9=./) and 3$ine flue or .ovel 9/./"
Ca)e=
A man of 1+ year-old came to hospital complaining fever, headache, sore throat and
myalgia since 1 days " 9e just come from 9ong ?ong about a $ee! ago" 9e also had
cough, and feeling very $ea!"
&ecture 96
Infection in children (5B5, 5ifteri, se-sis, $am-ak)
'r* DB& L&n--a6 )p*A, 'r* 0* G()taBan6Sp*A
6ase /
A boy, A years A months has come to our clinic $ith s$elling and pain on the chee! under
right ear since , days ago" 9e has fever since 1 days ago" 9e hasnNt cory2a, cough and
cold" 9is appetite $as decrease" 9is friends on the school have the same complaint"
/" Chat is the close diagnosis of this caseL
," Chat is the differential diagnosisL
*" Chat is the laboratory support neededL
1" Chat is the therapyL
=" Chat are the complications of this caseL
6ase ,
A boy comes to my clinic $ith five days of fever as the chief complaint" 9e $as currently A
years and /+ months old and a first grade of elementary school student" Fever $as
spea!ing immediately and has resolved one day before the doctor visited" &his morning the
fever reappears, giving a pattern of saddle bac! fever, $hich is accompanied $ith
headache, muscular pain, articular and vertebra pain, retro orbital pain, nausea, vomiting
and s!in rashes" &he s!in rash appeared at the beginning of the disease, but subse'uently
vanished $ithout any mar!s" n physical e%amination, the child loo!ed compos mentis,
mildly ill $ith fever of *@"@
+
6" Dermatological e%amination reveals s!in rash, mainly on the
legs, foot soles and palms, the pharyn% $as slightly hyperemic and there is no palpable
enlarge lymph nodes on the nec!" Auscultator finding of the heart and lungs $ere $ithin
normal limits" Abdominal e%amination revealed epigastrial and right upper 'uadrant
tenderness on palpation" &here $as no liver enlargement" .o significant finding e%isted on
the e%tremities, e%cept for the positive tourni'uets test"
6ase *
A girl, , years, comes to clinic $ith fever and rash as the chief complaint" Fever $as appear
from = days ago and rash appear since yesterday, $hich is accompanied $ith headache,
cough, muscular pain, nausea, vomiting and red of her eyes" &he rash phase is
accompanied by high fever" &he macular rash begins on the head (above the hairline) and
spreads over of the body in ,1 hours in a descending fashion"
6ase 1
A boy, * years, comes to emergency department $ith unconsciousness since , hours ago"
&his complaint suddenly occurs $hen his mother tal! to him" 9e is no response to tal!, no
move, and his eye loo! opened" 9e had fever since = days ago and still high until no$" 9is
temperature $as unstable, it $as decrease after drin! parasetamol, and increase again fe$
hour after that" &he earliest symptoms are $ea!ness, nausea or abdominal pain, and
headache"
/" Chat is the differential diagnosisL
," Chat is the other data needed to complete this caseL
&ecture :8
>oonosis Infection (%abies, &e-tos-irosis, &isteriosis)
Pro%*Dr* 'r* Ra$a S('eB&6 Sp*S (K)
'r* Sr& B('a1ant&6 Sp*MK
nfections in central nervous system have certain uni'ue characteristics" First, they
occur $ithin an anatomic closed space" 3econdly, the natural history of illnesses due to
6.3 infection often differs stri!ingly from that of those due to infection at other sites, even
$hen caused by the same organism" &hirdly, many 6.3 infections cause high mortality the
patients survives, serious se'uelae after resolution of the acute infections"
&here are four cardinal manifestation of .3 infection are7 fever, headache, alteration
of mental status, and focal neurologic signs" 3ometimes, these signs can be found in
noninfectious 6.3 syndromes" &he time course of disease is especially important in the
evaluation of disease affecting the 6.3" &he date of onset, temporal relationship to
presdiposing factors, rate of progression, time to reach the pea! of severity, time needed to
respond to treatment, and rate of resolution are all highly informative"
nfections of 6.3 can be caused by bacteria (pyrogenic infections), fungal,
spirochetal, parasitic, and sarcoid" Pyrogenic infections of 6.3 such as bacterial meningitis,
septic thromboplebitis, brain abscess, epidural abscess, and subdural empyema" &he
granulomatous infections of 6.3 such as tuberculosis, syphilis, and other spirochetal
infections, and fungal infections"
6ase /
A ,- year-old man, Balinese, 9indu $ith unconciousness in emergency room 3anglah
9ospital" From his family told that it $as convulsion at least for * hours before arrived in
hospital" From physical e%amination, a%illary temperature *B,=
+
6"
<earning &as!7
/," Define and describe others symptoms related to the patients that should be
as!ed to his family
/*" Describe physical e%amination to support diagnosis of this patient"
/1" Chat is possibly diagnosis of this patientL
/=" Describe differential diagnosis of this case
/A" Describe laboratory and other e%amination to support the diagnosis
/-" Describe management of this patient
/@" Describe ho$ to e%plain to his family about prognosis of patientUs disease
3elf assessment7
/+" Describe about7
a" Meningitis
b" 5ncephalitis
c" Meningoencephalitis
d" Myelitis
e" 6erebral abscess
//" 5%plain pathogenesis of bacterial meningitis
/," Describe and interpret cerebrospinal fluid (63F) e%amination in bacterial meningitis,
viral meningitis, tuberculous meningitis, and streptococcal meningitis"
/*" Define signs and symptoms of7
a" Meningitis
b" 6erebral abscess
c" Acute Anterior Poliomyelitis
d" AD3 Dementia 6omple%
e" 6erebral cysticercosis
/1" Differentiate clinical sign and symptoms of bacterial meningitis, viral meningitis,
tuberculous meningitis, and streptococcal meningitis
/=" Define management of these patients7
a" 9erpes 3imple% 5ncephalitis
b" &uberculous meningitis
c" 6erebral abscess
/A" Define prognosis of7
a" Acute anterior poliomyelitis
b" &uberculous meningitis
c" 6erebral abscess
/-" Describe !inds or types of neurosyphilis
/@" Describe about tabes dorsalis
&ecture :7
Princi-les of #ungal Infection ('or-holog( of #ungal)
'r* L(h Ar&Bat&
A5)tra#t =
Fungi are eu!aryotic micro-organism, have a nucleus containing their D.A and a
>.A nucleolus, and cytoplasma" 3urrounding them is plasmalemma $hich containing
ergosterol and out side plasmalemma is a rigid cell $all" Fungi do not contain chlorophyl
and cannot synthesi2e macro molecules from carbon dio%ide and energy derived from light
rays, therefore all fungi lead a heterotrophic e%istence in nature as saprobes, commensals
or parasites"
Fungi can be divided into t$o basic morphologic form7 yeast and hyphae"
Feast are unicellular and reproduce ase%ually by budding and most fungi have branching,
threadli!e tubular filaments called hyphae" Dimorphic fungi e%ist in both form" All fungi
reproduce by ase%ual processes and most can reproduce by se%ual mechanism"
&he fungi contribute to food spoilage, destroy te%tile, etc" As saprobe, they share
$ith bacteria in the decay of comple% plant and animal remains in the soil" Fungi used in
production of antibiotics, products of fermentation such as beverages, soy sauce etc" Fungi
are free living and abundant in nature and a fe$ live in normal flora of humans" &housands
of species have been !no$n, but less than /++ are cause diseases in humans" &he effects
of fungi on humans are numerous such as mycoto%icosis, hypersensitivity and coloni2ation
of fungi $ith resultant diseases"
9umans have good barriers against fungal infection such as intact s!in, mucosal
surfaces, saliva, normal bacterial flora etc" 9ealthy, immunocompetent people have a high
innate resistant to fungi even though they are constantly e%posed to the propagules of fungi"
nfections and diseases occur $hen there are disruptions in the protection barrier of s!in
and mucus membrane or defect in immunity system" &he characteristic of fungal pathogens
categori2ed into groups according to tissue that they coloni2e7 superficial, cutaneous,
subcutaneous and systemic mycosis" Fungal infections that occur only because of
compromising situations are categori2ed as opportunistic mycosis"
Learn&n- ta)$=
/" Describe the structure of fungi
," 5%plain terms used in medical mycology 7 yeast, hyphae, mycelium and dimorphic
fungi"
*" Describe the mechanisms of fungal pathogenesis
1" Describe the effect (medical importance) of fungi on humans
=" Describe the laboratory diagnosis of fungal diseases
&ecture :9+
su-erficial fungal Infections (Tinea, Tinea versikolor, kadidiasis
mukokutaneous)
Pro%* M* SBa)t&$a A'&-(na
Male *= years old came to Dermatology 6linic $ith chief complain itching in the sites of
nec!, upper, lo$er e%tremitas, trun!, and inner surfaces of the thigh especially during the
hot climate" t began as a small erythematous and scaling or vesicular and crusted patch
that spreads peripherally and partly clear in the centre" &hese lesion may be slightly
elevated particularly at the border, $here they more inflamed and scaly"
/" Please e%plore another history to complete anamnesis
," Chat !ind of clinical e%amination $ill you doL
*" Chat !ind of laboratory e%amination $ill you do"
1" Chat $as the diagnosis of this patientL
=" Describe your planning therapy for this patient"
A" Describe your planning education for this patient"
3elf assessment7
/" Chat in the definition of dermatophytosis (tinea or ring $orm)
," Please, describe the fungi of dermatophytes
*" $hat is the differential diagnosis of dermatophytosis

Please describe the antifungal therapy
Le#t(re 44
Deep F(n-a" In%e#t&on
O"eh=
Pro%*Dr*'r T(t& ParBat&6Sp*PD
A5)tra#t
Fungal infections have become increasingly fre'uent especially in immune compromised
host such as AD3, cancer patients, organ transplantation , and also as a conse'uent of
the availability of advanced medical technology $hich allo$ to do more invasive
treatment using more invasive instruments" 3ystemic fungal infections (3F) or invasive
fungal infection are a significant cause of morbidity and mortality among immune
compromised patients, such as 9:-infected individuals, cancer patients, neonates and
patients in the intensive care unit"
&he infections considered as nosocomial infections in the hospital for patients $ho have ris!
factors such as immune compromised patients" &he aetiology are 7 Predominant fungi 7
6andida (6)7 such as 6" 'lbicans, 6" !labrata, 6" tropicalis and 6"parapsilopsis,
'sper!illus spp"and Cryptococcus spp", 5merging fungi 7 (usarium spp", and )hi%opus
spp" and 5ndemic fungi 7 Histoplasma capsulatum, *lastomyces dermatitidis and
Coccidioides immitis

6linical Diagnosis7 &here is no specific sign and symptoms of systemic fungal infection"
&hat is $hy suspected clinical diagnosis of systemic fungal infection is fre'uently late" ts
resemble bacterial infections, such as severe sepsis, septic shoc! and multi organ failure"
Alertness to this infection $ill comes late though sign and symptoms appear early" n many
cases the diagnosis $as done per e%lusionem" Diagnosis should be considered in patient
$ith ris! factors has the signs of systemic infection despite ade'uate antibiotics"
>is! Factors 7 Patients at the ntensive 6are Unit (6U), 6oloni2ation of s!in and mucous
membranes $ith Candida, Alteration of natural host barriers ($ounds, surgery), &he
coloni2ed 6andida might enter the blood stream $hen microbes balance disturbed by
antibiotics and the barrier altered, eg" nd$elling centralEperipheral catheter, .eutropenia
(hematology disorders), Malignancy, Post chemoEradiation therapy, #rgan &ransplant
patients, 9: infection"
Portal entry 7 4astro ntestinal tract, s!in, urogenital tract, 6atheter related
6ase study7
Female A= year-old consulted from a private hospital $ith chief complain 7 fever since =
days ago" #ther complain7 coughing -- days, has been treated $ith AB injection, improved ,
but $orsening in the last , days" 9istory of chronic diarrhoea, but not no$" <oss of appetite
and 3light odinophagia" Physical e%amination 7 decreased of consciousness, high fever
(*B,@ 6), BP7 /++EA+ mm 9g, Pulse /+@Emin, >> ,1Emin" 9eart 7 C.<, >onchi OEO
<earning &as!
Chat is DD of this patientsL
6hest S ray 7 infiltrates on both middle and lo$er lung, increased hilar mar!ing and
emphysematous lung" <ab" &est 7 6B6 7 9b -,, gEdl, P<& /1+, &<6 +,- % /+* Eml, CB6 1,=
% /+++Eml, #ther physical e%amination revealed 7 oral mucosa II , tounge 7 coated"
Chat lab test do you suggest L
Le#t(re 49
Treatment o% F(n-a" In%e#t&on (PK,PD)
'r*I B*N-(rah6 M*For,'r* B&B&e$ In'ra1an&6 M*Ke)
Abstract
6hemotherapy that are used as antifungal agents difficult to treat fungal infection
particularly in the immunocompromised or neutropenic patient" Drugs for systemic fungal
infections are amphotericin B, fluocytosine, and a2ole antifungal agents" 3ystemic drugs for
superficial fungal infections are griseofulvin, terbinafine, and a2oles" &opical drugs for
superficial fungal infections are nystatin, micona2ole, clotrima2ole, haloprogin, tolnafnate,
and undecylenic acid" #nly fe$ drugs are available for tretament of systemic fungal
infections" 5rgosterol is a sterol that is uni'ue to the fungal cell membrane" &he
predominant sterol of human cells is cholesterol"
A ,=-year old $oman $ith she feel itchy since , $ee!s ago and changes bro$n nail colour"
&he physician diagnosed as dermatophytes of the nail"
/" Chat !ind of antifungal the best to be used"
," 9o$ is the mechanism of action of the drugL
*" Describe the pharmaco!inetic of the drug
1" Chat $ill be happened if the drug is given concomitanly $ith coumarinL
3elf assessment7
/" <ist the systemic antifungals for systemic fungal infections and superficial fungal
infections
," <ist the topical drugs for superficial fungal infections
*" 5%plain the mechanism of action systemic antifungals and superficial antifungals
1" 5%plain the pharmaco!inetics of amphotericin B, fluocytosine, flucona2ole,
itracona2ole, !eto!ona2ole, griseofulvin, and terbinafine"
=" describe the clinical uses of systemic antifungals and superficialis antifungals"
A" Describe the to%ic effects of systemic antifungal and superficial antifungals"
Le#t(re 4:
'r* I Ma'e S('armaDa6 M*Ke)
n the .ational 3tandard of 6ompetency of Undergraduate Medical 5ducation, the core
content of curriculum related to helminthic infections has been identified" &his core must be
$ell mastered by the students" Although hundred or more species are identified as a
helminthes of medical importance, ho$ever, only a fe$ of those are considered as core"
&he core species are7 (/) Ascaris lumbricoides (,) &richiuris trichiura, (*) 9oo!$orm spp, (1)
3trongyloides stercoralisK (=) 5nterobius vermicularisK (A) 3pecies causing cutaneous larva
migrantK (-) Filaria sppK (@) 3chistosoma sppK and (@) &aenia spp" For those species, the
fourth level of studentNs competency has been formulated, in $hich students must be able to
perform clinical diagnosis based on physical e%amination and other additional e%aminations
(such as simple laboratory and S ray e%amination)" nstead of just ma!ing clinical diagnosis,
the students should also be able to manage all related problems completely and individually"
&he students must therefore be familiar $ith the life cycle, epidemiology, pathogenesis,
clinical manifestations, diagnosis as $ell as treatment procedures of all the above
mentioned helminthic infections, other$ise the four level of student competency can not be
achieved"
<earning &as!s
/" Differentiate the morphological characteristics of the class .ematode, 6estode and
&rematode
," Describe their life cycles and identify each of their infective stages
*" Define their epidemiological standpoints and list the factors that are closely related
to the transmission of the infections
1" dentify their stages of development $hich are useful from the vie$point of diagnosis
purpose and try to figure their morphological characteristics
=" Describe their pathogenesis and clinical manifestations
A" Manage appropriately the diagnosis, treatment, and prevention measures"
3elf evaluation
.i Made Artini, a previously healthy ,A year old female medical student of the Faculty of
Medicine University of Uadayana $as admitted to the emergency room of 3anglah 9ospital
due to sei2ure" 3he $as born in the :illage of ?ete$el, 3ub-district of 3u!a$ati, district of
4ianyar" and attended primary and secondary high school at the same village" 9er history
$as other$ise unremar!able, although she reported that she had been suffering from
severe headache for a couple of months" 9er neurological e%amination revealed no clear
abnormalities" 9o$ever, a computeri2ed tomography scan (6& scan) of the head sho$ed
multiple calcified lesions in both cerebral hemispheres"
Guestions
/" f it is a disease caused by parasitic infection, $hat parasite $ould you consider to
be responsible for the patientNs conditionL
," 9o$ does man ac'uire this infectionL
*" Chat are the factors that may predispose to this infectionL
1" 9o$ $ould you diagnose this patient properlyL
=" 9o$ $ould you treat this patient appropriatelyL
Le#t(re 43
F&"ar&a)&)
'r* K* A-() Som&a6 Sp*PD
<ymphatic filariasis is the commonest lymphatic system infection that is occurred in
community especially in eastern part of ndonesia" <ymphatic filariasis, onchocerciasis, and
loiasis are the three most important filarial infections of humans" <ymphatic filariasis is
caused by parasite transmitted by biting arthropods (mos'uitoes)" Almost B+H are caused
by +uchereria bancrofti, $hose only in human and most of the remainder are caused by
*ru!ia malayi" &he major vectors for +$ bancrofti are culicine mos'uitoes in most urban and
semiurban areas, anopheline mos'uitoes in the more rural areas of Africa and 'edes spp in
mnay of the endemic Pasific island"
A-*=-year-old $oman complaints her leg is s$elling" &he s$ollen is getting $orst
and pain since , $ee!s ago" 9alf of his s$ollen leg loo!s redness and felt pain" &he patient
lives in Bali and she comes from ?upang" 3he has been li!e this before and it is the *
rd
times" 3he gets fevers, fati'ue, and headache"
<earning tas!7
/" Define other things that should be found from history ta!ing of this
patient"
," Describe physical e%amination to diagnose this patient
*" Define other e%aminationE investigation to support the diagnosis
1" Define the invasive treatment should be done to this patient
=" Describe managementE treatment of this patient
3elf assessment7
6hoose >49& or C>#.4 of these statement
/" &he possibly diagnosis is limfangitis
," &he most possibly diagnosis is filariasis $ith inflammation
*" t needs cell blood count and thic! smear e%amination
1" <ymphograpy e%amination sho$ed obstruction, atresia, or dilatation can
helps to diagnose this disease
=" Diethylcarbama2ine ,-* mgE!g, * times a day is given for ,-* $ee!s"
Le#t(re 47
Den-(e &ra" In%e#t&on
'r* Ma'e S()&"a Utama6 Sp6PD
A5)tra#t
Dengue feverEdengue hemorrhagic fever caused by dengue viruses (type /,,,* and
1), transmission from human to human is by the mos'uito 'edes ae!ypti" 6linical spectrum
of dengue viral infections are $ide variation, from undifferentiated fever, dengue fever,
dengue hemorrhagic fever and dengue shoc! syndrome" &here is plasma lea!age in
dengue hemorrhagic fever, so differentiated $ith dengue fever"
Dengue fever should be treated supportively" Dengue hemorrhagic feverEdengue
shoc! syndrome is life threatening and re'uires immediate evaluation of vital sign,
hemoconcentration, dehydration, urine output, electrolit imbalance"
Re%eren#e
9alstead 3B" Dengue feverE Dengue 9aemorrhagic fever" Po$derly C4"(5d)" nfectious
disease" 3econd ed" ,++1" P" /A@/-1
Den-(e &n%e#t&on
6ase7
A Male, *1 years old, Balinese, came to the 3anglah 9ospital" &he chief of complain $as
fever since , days ago, he also complain about headache, joint pain, rash on the s!in" &he
neighbored $as admitted in the hospital $ith D9F
<earning tas!7
/" Chat the some specific factor in the history and e%amination suggest the need for
ma!ing diagnose
," $hat the laboratory e%amination the need for this patients
*" $hat the management for this patients
3elf assessments
/" describe the clinical spectrum of dengue infection
/" describe the pathogenesis of D9F
," describe the management approach for the dengue infections
>eferences
/" 9alstead 3B" Dengue feverE Dengue 9aemorrhagic fever" Po$derly C4"(5d)"
nfectious disease" 3econd ed" ,++1" P" /A@/-1
Le#t(re 48
Treatment o% He"m&nthe) In%e#t&on (PK,PD)
Dr"dr" B"?"3atriyasa,M">repro
Anthe"m&nt&#
9elminthic infections still as a problem on the $orld" &here are many of anthelminthic
drugs that can be used to eradicate the parasite in the intestinal tract or in the tissue of the
body" Most anthelminthics in use today are active against specific parasites, and some are
to%ic" &herefore parasites must be identified before treatment is started" n this topic $ill be
introduced the drugs for anthelmintic so after this program all of student be able to choose
anthelmintic drugs for the patients in rationally"
Anthe"m&nt&#
/" Discuss anthelmintic drugs that use to eradicate or reduce the number of helminthic
parasites in the intestinal tract or tissue of the body
," Discuss drugs of choice for the especially parasite and side effect of that drugs of
the body
*" Discuss the mechanism of action of anthelmintic drugs that you !no$
1" Discuss the principle of treatment of patient according to the parasite that $ill be
eradicated
3elf assessment7
/" Drug of choice for Ascaris lumbricoides is7
a" Pyrantel pamoate
b" Albenda2ole
c" Pipera2ine
d" <evamisole
e" Pra2i'uantel
," Drug of choice for cutaneus larva migran is7
a" Pyrantel pamoate
b" Albenda2ole
c" Pipera2ine
d" &hiabenda2ole
e" Pra2i'uantel
*" A patient suffered from taenia solium" Drug that can be used as drug of choice of this
$orm is7
a" Pyrantel pamoate
b" Albenda2ole
c" Pipera2ine
d" <evamisole
e" Pra2i'uantel
Le#t(re 9<
O2er2&eB o% P(erpera" In%e#t&on
dr" .yoman Bayu Mahendra,3p"#4
/" Abstract7
Puerperal nfection P is a general term used to describe any bacterial infection of
the genital tract after delivery along $ith preeclampsia and obstetrical
hemorrhage puerperal infection formed the lethal triad of causes of maternal
deaths because of effective antimicrobials, maternal deaths from infection have
become uncommon
," <earning tas!7
,"/" &o understand definition of puerperial infection"
,"," &o understand definition and management of puerperial fever
,"*" &o understand definition, predisposing factors, bacteriology and
management of uterine infection"
,"1" &o understand the complication of pelvic infection
,"=" &o understand the pathogenesis, clinical course and treatment of
infections of perineum, vagina and cervi%"
,"A" &o understand the to%ic shoc! syndrome
,"-" &o understand the prevention of puerperial infection
*" 6ase
A ,= year old $oman (4/P/) presents to your clinic eight days postpartum,
complaining of a temperature of at least *@"= degrees 6elsius over the past *
days, and a foul-smelling vaginal discharge" 3he is in other$ise good health,
and her baby, $ho $as born by emergency 6aesarian section in a rural clinic, is
doing $ell" Physical e%amination of your patient reveals an oral temperature of
*@"A degrees 6elsius, a clean and non-$eeping abdominal $ound, and pain of
palpation of her uterus"
Chat is the differential diagnosis of the site of infectionL Chat $as most li!ely
the source of this infectionL Chat features of your patientNs history and delivery
put her at higher ris! for puerperal infectionL
1" 3elf assessment7
/" 9o$ the student understand about definition, ris! factors, pathogenesis,
complication and management of puerperial infectionL
," 9o$ the student understand the definition of puerperial fever and the
deferential diagnosis of puerperial feverL
*" 9o$ the student understand the prevention of puerperial feverL
Le#t(re 9/
O2er2&eB o% Se?(a" Tran)m&tte' D&)ea)e)
dr" A"A"4"P" Ciraguna, 3p"??
6ase /7
A ,--year-old man had single painless ulcer on his glans penis * year ago" &his ulcers
disappear $ithout treatment" #ne year ago, he got married $ith a ,*-year-old $oman and
no$ his $ife is pregnant for 1 months" 9is $ife complain of having vaginal discharge $ith
itchy and odor" &his man no$ has rash on $hole body and mucopurulent urethral discharge,
they already $ent to a venereologist" &he result of laboratories e%aminations sho$s :D><
/7A1 and doctor referred this couple to go to the Department Dermato-:enereology 3anglah
9ospital"
<earning tas!E 'uestions7
/" Chat other history you need to find out from these patientsL
," Chat laboratories e%amination needs to be done for this coupleL
*" Chat is your diagnosis for this manL
1" Chat is your diagnosis for his $ifeL
=" Chat could possibly happen $ith her pregnancyL
A" Chat could possibly happen $ith their babyL
-" 9o$ $ould you treat this man, his $ife, and their baby based on their conditionsL
3elf assessment7
/" Describe the stages clinical manifestation of syphilis"
-. Describe the causes of genital ulceration"
*" Describe microorganism pathologic of urethral discharge"
1" Describe the ris! factors of se%ually transmitted infection patient
=" 9o$ to prevent management of 3&"
A" Describe microorganism pathologic of vaginal discharge and the clinical manifestation
-" 9o$ to treat clinical manifestation of vaginal discharge, the dose, and for ho$ long"

>5FF>5.653
/" 3picer C0" (,++)7 6linical Bacteriology, Mycology, and Parasitology, An llustrated
6olour &e%t" 6hurchill <ivingstone, /1-/B"
," 6linical Bacteriology, Mycology and Parasitology 7 An llustrated 6olour &e%t" C"
0ohn 3picer" 6hurchill-<ivingstone
*" Broo!s et al" pathogenesis and 6ontrol of :iral Diseases" n7 <ange Medical
Microbiology" ,*
rd
ed" Mc4ra$ 9ill" nternational 5d" ,++1" p" *B1 P 1/*"(Principles
of :iral nfection)
1" <evinson et al" <ange Medical Microbiology D immunology" 5%amination D Board
revie$" @
th
ed" Mc4ra$ 9ill" nternational 5d" ,++1" p" /@A P ,,+, ,=B-,AB, ,11-,=+"
(Principles of :iral nfection)
=" >oitt" ", Brostoff"0", Male" D" mmunology
A" Durac! D&, Chitley >0, and 3cheld CM" ntroduction7 Approach to the Patient $ith
6entral nervous 3ystem nfection" n 7 3cheld CM, Chitley >0, Durac! D&, (eds)"
nfections of &he 6entral .ervous 3ystem" >aven Press" .e$ For!" /BB/ p" /-1"
-" :ictor M and ropper A9" nfections of the .ervous 3ystem (Bacterial, Fungal,
spirochetal, Parasitic) and 3arcoid" n7 Adams and :ictorsN principles of the
.eurology" -
th
ed" Mc4ra$-9ill" .e$ For!E&oronto" P" -*1--@+"
@" #ttesen 5A" Filariasis"in Po$derly C4" (ed)" nfectious Diseases" ,
nd
ed" P"/A+--/*"
B" >ingsrud ?M, <inne 00" Urinalysis and Body Fluids A 6olorte%t and Atlas" /
st
ed"
Mosby" 3t" <ouisE &oronto" /BB=" p" B=-,+A"
/+" Burtis 6A" &iet2 Fundamentals of 6linical 6hemistry" 1
th
ed" CB 3aunders 6ompany"
PhiladelphiaE &o!yo" /BBA" p" ==@-=A/"
//" 3immons A" 3tatland B5" 9ematology A combined &heoritical and technical
Approach" ,
nd
ed" Buuter$orth-9einemann" BostonE 3ingapore" /BB-" p" /,B-/1,"
/," 3tites DP, &err A, Parslo$ &4" Medical mmunology" B
th
ed" Prentice-9all
nternational" /BB-" p" ,A1-,AB"
/*" ?asper D<, Fauci A3, <ongo D<, Braun$ald 5, et al" 9arrisonNs Principles of nternal
Medicine" /A
th
ed" :ol /" Mc4ra$-9ill" .e$ For!E &oronto" ,++=" p" B@/-//+*"
/1" 3utton D" >adiology and maging for Medical 3tudents" 6hurchill <ivingstone" -
th
ed"
/BB@"
/=" 4rainger >4 and Allison D0" Diagnostic >adiology" 6hurchill <ivingstone" ,
nd
ed"
/BB*"
/A" McAdam A0 and ?umar 3" nfectious Diseases in ?umar :, 6ontran >3 and >obbins
3<, >obbins Basic Pathology" P" *11-*B@"
/-" Andre$s" Diseases of &he 3!in" B
th
ed"
/@" Bryceson A" <eprosy" *
rd
ed"
/B" ?ing D .icole" 3e%ually &ransmitted Diseases" ,++*
,+" 9olmes ??, 3piring PF, Mirdh P" 3e%ually &ransmitted Diseases" *
rd
ed" Mc4ra$-
9ill" /BBB"
,/" McMillan A, Foung 9, #gilvie MM, 3cott 4>" 6linical Practice in 3e%ually
&ransmissible nfection" 3aunders" ,++,"
,," Braun$aldNs 9eart Disease" 3ubacute bacterial endocarditis"
~ CURRICULUM MAP ~
"mstr Program or curriculum blocks
78 Senior .!er/s"ip
6 Senior .!er/s"ip
3 Senior c!er/s"ip
2
Medica!
+mergenc0
12 wee/s3
4.S 1) wee/s3
Specia! %opic#
-%ra5e! medicine
1- wee/s3
+!ec'i5e S'ud0 III
16 wee/s3
.!inic rien'a'ion
1.!er/s"ip3
16 wee/s3
1
%"e 7espira'or0
S0s'em and
Disorders
1, wee/s3
4.S 1) wee/s3
%"e
.ardio5ascu!ar
S0s'em and
Disorders
1, wee/s3
4.S 1) wee/s3
%"e &rinar0
S0s'em and
Disorders
12 wee/s3
4.S 1) wee/s3
%"e 7eproduc'i5e
S0s'em and
Disorders
12 wee/s3
4.S 1) wee/s3
0
+!ec'i5e S'ud0
II
1) wee/s3
A!imen'ar0
8 "epa'o-
bi!iar0 s0s'ems
8 disorders
1, 9ee/s3
4.S 1) wee/s3
%"e +ndocrine
S0s'em,
Me'abo!ism and
Disorders
1, wee/s3
4.S 1) wee/s3
.!inica! $u'ri'ion
and Disorders
1- wee/s3
4.S 1) wee/s3
Specia! %opic #
- Pa!!ia'i5e
medicine
-.omp!eme
n'ar0 8
A!'erna'i5e
Medicine
- Forensic
12 wee/s3
+!ec'i5e
S'ud0 II
1) wee/s3
)
Muscu!os/e!e'a!
s0s'em 8
connec'i5e
'issue disorders
1, wee/s3
4.S 1) wee/s3
$euroscience
and
neuro!ogica!
disorders
1, wee/s3
4.S 1) wee/s3
4e"a5ior ."ange
and disorders
1, wee/s3
4.S1) wee/s3
%"e :isua!
s0s'em 8
disorders
1- wee/s3
4.S
1) wee/s3
: ;ema'o!ogic
s0s'em 8 disor-
ders 8 c!inica!
onco!og0
1, wee/s3
Immune
s0s'em 8
disorders
1- wee/s3
Infec'ion
8 infec'ious
diseases
1< wee/s3
%"e s/in 8 "earing
s0s'em
8 disorders
12 wee/s3
4.S 1) wee/s3 4.S1) wee/s3 4.S 1) wee/s3 4.S1) wee/s3
9
Medica!
Professiona!ism
1- wee/s3
4.S 1) wee/s3
+5idence-based
Medica! Prac'ice
1- wee/s3
;ea!'" S0s'em-
based Prac'ice
12 wee/s3
4.S 1) wee/s3
.ommuni'0-based
prac'ice
1, wee/s3
Specia! %opic
- +rgonomi
- Geria'ri
1- wee/s3
+!ec'i5e
S'ud0 I
1- wee/s3
7
S'udium
Genera!e and
;umaniora
12 wee/s3
Medica!
communica'ion
12 wee/s3
4.S 1) wee/s3
%"e ce!!
as bioc"e-
mica! mac"iner0
12 wee/s3
4.S1) wee/s3
Grow'"
8
de5e!opmen'
1, wee/s3
4.S# 1) wee/s3
Pendidi/an Pancasi!a 8 Kewarganegaraan 12 wee/s3

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