12B - Modul 1-1

FACULTY OF MEDICINE Makassar, 12th November 2021
INDONESIAN MUSLIM UNIVERSITY

TROPICAL BLOCK

TUTORIAL REPORT
MODULE 1
Tutor :
dr. Nurul Fadilah Ali Polanunu, M.Biomed

Compiled by :
Group 12B
Maghfirah Tara Zakiyyah 11020190232

Puput S 11020190246
Syu’a Almadina 11020190234
Farah Zhafirah Sudirman 11020190243
Nadhifah Wasila Khairun 11020190236
Wira Pratiwi Oktaviani 11020190248
Andi Nirwana Widya Ningsih 11020190238
Andi Batari Ramadhina S 11020190250
Adinda Pradana Putri 11020190240
Nur Afdhaliyah 11020190251
Ahmad Fajar Fitra Akbar 11020190242
FAKULTAS KEDOKTERAN
UNIVERSITAS MUSLIM INDONESIA
MAKASSAR
2021
FOREWORD
In the name of Allah SWT, the Most Gracious, the Most Merciful, we offer praise
and gratitude to Him, who has bestowed His grace, guidance, and inayah to us, so
that we can complete the Program Based Learning Report Module I " Fever "
Scenario 6.
We have compiled this report to the maximum extent and the preparation of this
report would not have gone smoothly without the help of various parties, therefore on
this occasion we would like to thank:
Doctors who always provide advice and guidance during the discussion, our
supervisor, dr. Nurul Fadilah Ali Polanunu, M.Biomed for the guidance given to us.
Literature sources used as references in our enrichment.
Despite all that, we are fully aware that there are still shortcomings both in terms
of sentence structure and grammar. Therefore, we welcome all suggestions and
criticisms from readers so that we can improve this report.
Finally, we hope that this Module I “Fever” Scenario 6 Based Learning Program
Report can provide benefits to many people.
Makassar, 12 November 2021
Group 8B
SCENARIO 6
A 35-year-old man came to the public health center with a chief complaint of fever
since 10 days ago. Complaints accompanied by nausea, vomiting, calf pain and
urinating which colour like tea. On examination of vital signs, blood pressure 100/60
mmHg, pulse 100 beats per minute, and axillary temperature 38˚C. On physical
examination, jaundice and sclera injection were found. There was a history of the
patient's house experiencing flooding one week earlier
DIFFICULT WORD
 Jaundice
Jaundice also known as hyperbilirubinemia is defined as a yellow
discoloration of the body tissue resulting from the accumulation Of excess
bilirubin
Reference : Joseph, Abel, Samant Hrisnikesh.2021. Jaundice.ncbi
 Scleral injection
The main sign of inflammation in the eye. Most cases are mild condisitions
and can recover completely. Red eye is divided into 2 types, namely ciliary
injection and conjunctival injection.
Reference : Akbar, Muhammad, dkk. 2019 . Conjunctival Laceration of The
Tarsalis Palpebra Inferior Et Cousing By A Fishing Hook. Jurnal Medical
Proffesion. 1 (2) Juni 2019.
KEY SENTENCES
1. A 35-year-old man
2. Fever since 10 days ago
3. Complaints accompanied by nausea, vomiting, calf pain and urinating which
colour like tea.
4. Blood pressure 100/60 mmHg
5. Pulse 100 beats per minute
6. Axillary temperature 38˚C
7. On physical examination, jaundice and sclera injection were found
8. There was a history of the patient's house experiencing flooding one week
earlier
QUESTIONS
1. Explain the definition, classification, etiology of fever !

2. Explain what tropical desease that can cause fever and their etiology !
3. Explain the pathomecanism of the main complaint ( fever ) based on the
scenario !
4. Explain the diagnostic step of the scenario !
5. What are the differential diagnosis related to the scenario !
6. What prevention can be given to the patient ?
7. What are the complications that can occur regarding the scenario?
8. Perspective islam based on scenario
ANSWERS
1. Explain the definition, classification, etiology of fever !

The Definition
The International Union of Physiological Sciences Commission for Thermal

Physiology defines fever/febrile as a state of elevated core temperature, which
is often (but not necessarily) part of the defense response of a multicellular
organism (host) against invading microorganisms or inanimate objects that are
pathogenic or foreign to the host. . El-Rahdi and colleagues define fever
(pyrexia) in terms of pathophysiological and clinical. Pathophysiologically,
fever is an increase in the thermoregulatory set point of the hypothalamic
center mediated by interleukin 1 (IL-1). While clinically, fever is an increase
in body temperature of 1oC or greater above the average value of normal
temperature at the place of recording. In response to this change in set point,
there is an active process to reach the new set point. This is achieved
physiologically by minimizing heat release and producing heat.
Normal body temperature varies according to the circardian temperature

rhythm (diurnal variation). The lowest temperature is reached in the morning
at 04.00 – 06.00 and the highest in the early evening at 16.00 – 18.00. The
fever curve usually also follows this diurnal pattern.1,2 Body temperature is
also influenced by individual and environmental factors, including age, sex,
physical activity and ambient air temperature. It is therefore clear that there is
no single value for normal body temperature. The results of body temperature
measurements vary depending on the place of measurement.
Table 1. Normal temperature in different places

Range; average
Measurement Fever
Type of thermometer normal
place o
(oC)
temperature ( C)
Axilla Mercury, electronics 34,7 – 37,3; 36,4 37,4
Sublingual Mercury, electronics 35,5 – 37,5; 36,6 37,6
Rectal Mercury, electronics 36,6 – 37,9; 37 38
Ears Infrared emission 35,7 – 37,5; 36,6 37,6
Normal rectal temperature is 0,27o – 0,38oC (0,5 – 0,7oF) higher than oral
temperature. The axillary temperature is approximately 0,55oC (1oF) lower
than the oral temperature. For practical clinical purposes, a patient is
considered to have a fever if the rectal temperature reaches 38oC, the oral
temperature is 37.6oC, the axillary temperature is 37.4oC, or the tympanic
membrane temperature is 37, 6 oC.1 Hyperpyrexia is a term used for fever
when the body temperature exceeds 41.1 oC (106 oF).
The Classification
The classification of fever is as follows:
a. Septic Fever
Body temperature gradually rises to very high levels at night and drops
back to above normal levels in the morning. Often accompanied by
complaints of chills and sweating. When the high fever drops to a
normal level, it is called hectic fever.
b. Remittent Fever
Body temperature can drop every day but never reaches normal body
temperature. The possible causes of temperature recorded can be as
high as two degrees and not as large as the temperature difference
noted for septic fever.
c. Intermitten Fever
Body temperature drops to normal levels for several hours of the day.
If a fever like this occurs every two days it is called tersiana and if it
occurs two days free of fever between two attacks of fever it is called
quartana.
d. Continous Fever
Temperature variations throughout the day do not differ by more than
one degree. At the level of fever that is continuously very high is
called hyperpyrexia.Fever pattern in typhoid fever (shows relative
bradycardia).
e. Periodic Fever
Periodic fever is characterized by recurrent episodes of fever at regular
or irregular intervals. Each episode is followed by one to several days,
weeks or months of normal temperature. Examples that can be seen
are malaria (the term tertiana is used when fever occurs every 3rd day,
quartana when fever occurs every 4th day)and brucellosis. Malaria
fever pattern.
Table 2. Fever patterns found in pediatric disease
Fever Pattern Disease

Continuous Typhoid fever, malignant falciparum malaria
remittance Most viral and bacterial diseases
intermittent Malaria, lymphoma, endocarditis
Hectic or septic Kawasaki disease, pyogenic infection
Quotidian Malaria due to P. vivax
Double quotidian Kala azar, gonococcal arthritis, juvenile rheumatoid arthritis,
some drug fevers (eg carbamazepine)
Relapse or Malaria tertiana or quartana, brucellosis
periodic
Recurrent fever Familial Mediterranean fever
The Etiology
Fever is often caused by infection. Causes of fever other than infection

can also be caused by toxemia, malignancy or reactions to drug use, as well as
disturbances in the central temperature regulation center (eg cerebral
hemorrhage, coma). Basically, to achieve an accurate diagnosis of the cause
of fever, it is necessary to include: accuracy in taking the patient's medical
history, carrying out a physical examination, observing the course of the
disease and evaluating laboratory examinations, as well as other supports in a
precise and holistic manner.
Fever occurs when heat generation exceeds output. Fever can be associated
with infection, collagen disease, malignancy, metabolic disease or other
diseases. Fever can be caused by abnormalities in the brain itself or toxic
substances that affect the temperature regulation center, bacterial diseases,
brain tumors or dehydration
Fever is often caused by; upper respiratory tract infection, otitis media,
sinusitis, bronchiolitis, pneumonia, pharyngitis, dental abscess, gingival
vostomatitis, gastroenteritis, urinary tract infection, pyelonephritis,
meningitis, bacteremia, immune reaction, neoplasm, osteomyelitis.
Basically, to achieve an accurate diagnosis of the cause of fever, it is

necessary to include: thorough taking of patient's disease history, carrying out
a physical examination, observing the course of the disease and evaluating
laboratory tests and other supports in a precise and holistic manner. Some
special things to pay attention to in fever are the way the fever arises, the
duration of the fever, the height of the fever and the complaints and symptoms
that accompany the fever.
Reference :
 Pratiwi, N. R. R. (2018). Penerapan Kompres Hangat pada Anak

Demam dengan Gangguan Pemenuhan Kebutuhan Nyaman di RSUD
Sleman. Eprints.Poltekkesjogja.Ac.Id, 8–30.
 El-Radhi AS, Carroll J, Klein N, Abbas A. Fever. Dalam: El-Radhi
SA, Carroll J, Klein N, penyunting. Clinical manual of fever in
children. Edisi ke-9. Berlin: Springer-Verlag; 2009.h.1-24.
2. What tropical desease that can cause fever and their etiology !
a. Typhoid fever
Typhoid fever is an acute infection of the digestive tract caused by the
bacterium Salmonella typhi. Salmonella is a gram-negative bacteria, not
encapsulated, has flagella and does not form spores, Transmission of disease
is through water and food, salmonella can survive for a long time in food. Can
cause the sufferer to have a fever for more than 7 days.
b. PES
Plague or another name for plague is a zoonotic disease caused by the
bacterium Yesrsinia pestis (Pasteurella pestis). Yersinia pestis is a gram-
negative, immobile, non-spore forming bacillus. The reservoir animals are
rodents (rodents), including rats, rabbits. While the vector that transmits the
disease is Culex iritans. Which will cause a fever for no apparent reason
(fever of unknown origin) and the fever can be high.
c. Leptospirosis
Leptospirosis is an acute infection caused by the Leptospira bacteria.
Leptospira bacteria are spiral-like threads with a length of 6-12 millimicrons.
This form causes leptospires to move very actively. These bacteria are
sensitive to acids. These bacteria can be spread through the urine or blood of
infected animals, such as rats, cattle, dogs, and pigs. In the first phase
(leptospiremia) is characterized by a sudden high fever.
d. diphtheria
The cause of this disease is the bacterium Corynebacterium diphtheria. This
disease has two forms, namely the first
1. Respiration type caused by strains of bacteria that produce toxins
(toxigenetic) which usually cause severe symptoms to death.
2. Cutanal type caused by toxigenetic or non-toxigenetic strains, generally
mild symptoms with atypical inflammation.
Transmission of this disease occurs through droplets when the sufferer
(career) coughs, sneezes, and talks. However, dust or vomit of the patient can
also be a medium of transmission. Can cause fever, although not high.
e. anthrax
Anthrax disease is a disease caused by Bacillus anthracis in livestock
(zoonotic) livestock and wild animals that can be transmitted to humans.
Bacillus anthracis is a gram-positive, immobile, encapsulated, and spore-
forming bacterium. These bacteria are rod-shaped, arranged in rows that form
formations such as bamboo segments or elongated bricks. Gastrointestinal
anthrax can cause symptoms, one of which is fever.
f. Dengue Hemorrhagic Fever (DHF)

Dengue hemorrhagic fever (DHF) is an infectious disease caused by the
dengue virus transmitted by infected Aedes aegypti and Aedes albopictus
mosquitoes which are the main vectors of dengue disease. Which, can give
symptoms in the form of fever for 2-7 days for no apparent reason.
g. Yellow fever
An acute systemic disease caused by a virus called a flavivirus. In severe
cases, viral infection causes a high fever, bleeding into the skin, and necrosis
(death) of cells in the kidneys and liver.
h. Hepatitis
Hepatitis is a disease caused by the hepatitis A virus (VHA). VHA can be
found in feces. Hepatitis is known as jaundice or liver because this virus
attacks the liver. The causes of hepatitis are viral infections, metabolic
disorders, alcohol consumption, autoimmune, complications due to other
diseases, frequent use of drugs etc. Can cause moderate fever in patients.
i. Rubeola
It is an acute, highly infectious disease caused by the measles virus from the
Paramyxovirus family, genus Morbillivirus. This virus is an RNA virus that is
known to have only 1 antigen. The structure of this virus is similar to the
viruses that cause epidemic parotitis and parainfluenza. This disease is
characterized by initial symptoms such as fever, cough, runny nose, and
conjunctivitis, which is then followed by rashes.
j. SARS
Severe acute respiratory syndrome (SARS) or severe acute respiratory
syndrome is a syndrome caused by a sudden viral infection of the lungs. At
first the virus that causes SARS was thought to be a Paramyxovirus. In its
development, WHO determined that the cause of SARS was Coronavirus.
Which can be detected by examination of antibody tests (IgG/IgM), molecular
examination (PCR), culture examination. SARS can cause sufferers to have a
sudden fever > 38 degrees Celsius.
k. Influenza
Influenza or commonly called the flu is a disease caused by the influenza
virus. Influenza virus is highly contagious and is transmitted by the sufferer
through the air. This virus attacks the respiratory tract so that the sufferer has
difficulty breathing. Symptoms that arise due to influenza are runny nose,
fever, dizziness, dry cough to cough with phlegm, itchy throat, stuffy nose,
runny nose, sneezing to red nose, body aches.
l. Varicella
Varicella is a disease caused by a virus, called varicella zoster virus (VZV),
herpesvirtus varicellae (HHV3) which is a member of the herpesvirus group.
Symptoms are fever, runny nose, weakness, fatigue, lethargy and then a red
rash appears on the body filled with fluid.
m. Ebola
Ebola is a disease caused by the Ebola virus. This disease is very terrible
because the patient's body will bleed all over the patient's body. Other
symptoms are fever, vomiting, diarrhea and body aches.
n. Mumps
Mumps is an infectious disease that often occurs in children and adolescents
between the ages of five to fifteen years, but rarely occurs in infants. Mumps
is caused by the mumps virus from the paramyxovirus group that attacks the
salivary glands in the mouth, primarily attacking the parotid glands located on
each side of the face below and in front of the ears. The incubation period is
about two weeks. Can cause symptoms such as fever in sufferers.
o. Polio
An acute disease that attacks the peripheral nervous system caused by the
polio virus. The poliovirus belongs to the enterovirus genus. There are 3
types, namely types 1, 2, and 3. Symptoms that can appear, one of which is a
mild fever.
p. Bird flu
The cause of bird flu is avian influenza (AI) virus from the family
Orthomyxoviridae. This strain A virus is distinguished according to the type
of hemagglutinin (H) and neuraminidase (N), so that this virus can be
classified according to its subtypes such as H1N1, H2N1, and so on. The
H5N1 subtype can be genetically mutated with other subtypes so that it can be
transmitted to humans or animals other than birds. Symptoms in some cases
(possible cases) can cause fever > 38 degrees Celsius accompanied by cough,
and sore throat.
q. Rabies
A disease that attacks the central nervous system. The cause of rabies is the
rabies virus, which belongs to the Rhabdovirus family. The shape of the virus
resembles a bullet, measuring 180 nm with a diameter of 75 nm. This virus is
composed of protein, fat, RNA, and carbohydrates. In humans, the symptoms
caused are soreness, heat, and itching around the wound which can be
followed by fever.
r. Malaria
Malaria is a disease that attacks red blood cells caused by the plasmodium
parasite, which is transmitted to humans through the bite of an infected female
Anopheles mosquito.
s. Trichinosis
Trichinosis is a disease caused by infection with nematode parasitic worms
that live in the intestines of pigs and other animals. Which gives the main
symptoms such as fever, diarrhea can be up to 14 weeks, malaise, etc.
t. Schistosomiasis
Schistosomiasis is an acute and chronic parasitic disease caused by trematode
worms of the genus Schistosoma. Which will cause the sufferer to complain
of the main complaints, namely fever, chills, and give the main signs of
katayama fever (fever plus eosinophilia).
Reference :
 Widoyono. 2011. Textbook of Tropical Diseases: Epidemiology,

Transmission, Prevention & Eradication. Edition 2. Jakarta : Erlangga.
 Brooks, GF, Butel, JS, Ornston, LN, Jawetz, E., Melnick, JL, Adelberg,
EA, Jawetz, Melnick & Adelberg's: Medical Microbiology, 20 edition,

Prentice-Hall International Inc.
 Prevention and control of schistosomiasis and soil-transmitted
helminthiasis. Geneva: WHO. 2020.
3. Explain the pathomecanism of the main complaint ( fever ) based on the

scenario !
The substance that causes fever is pyrogens. Pyrogens can come from
exogenous or endogenous. Exogenous pyrogens come from outside the body
while endogenous pyrogens come from within the body. Exogenous pyrogens,
which can be infectious or non-infectious, will stimulate macrophages,
monocytes, lymphocytes, and endothelial cells to release interleukin (IL)-1,
IL-6, Tumor Necrosing Factor (TNF)-α, and interferon (IFN). )-γ hereinafter
referred to as endogenous pyrogens/cytokines. This endogenous pyrogen,
after binding to its receptor in the hypothalamic preoptic area will stimulate
the hypothalamus to activate phospholipase-A2, which in turn releases
arachidonic acid from the phospholipid membrane, and then by the
cyclooxygenase-2 (COX-2) enzyme it will be converted into prostaglandin E2
(PGE2). . It is this prostaglandin stimulation, either directly or through the
release of cyclic AMP, that sets the thermostat to a higher body temperature.
This is the beginning of an integrated reaction of the autonomic nervous
system, endocrine system, and behavioral changes in the occurrence of fever
(increased temperature).
The heat centers in the hypothalamus and brainstem will then send
signals for increased heat production and conservation so that the body
temperature rises to a new set temperature level. This can be achieved by
vasoconstriction of the blood vessels of the skin, so that the blood that reaches
the surface of the body is reduced and the body heat that occurs in the core
will maintain the body's core temperature. Epinephrine released due to
sympathetic nerve stimulation will increase body metabolism and muscle
tone. There may be a process of shivering and/or individuals trying to wear
thick clothes and trying to fold certain body parts to reduce evaporation.
During fever, arginine vasopressin (AVP), alphamelanocyte-

stimulating hormone and corticotropin releasing factor are released by the
body. This substance can work as an endogenous / intrinsic antipyretic to
reduce fever reactions. This antipyretic effect will create a feedback circuit to
the hypothalamus. AVP or vasopressin, also known as antidiuretic hormone,
which is produced during fever causes water retention by the kidneys and this
may play a role in regulating body temperature during fever. Initially, what
was thought to be the trigger for the fever reaction was infection and the
products of infection. In subsequent developments, it turns out that several
endogenous molecules such as antigen-antibody complexes, complement,
lymphocyte products and inflammation bile acids can also stimulate the
release of cytokine pyrogens. The concept that cytokines can induce other
cytokines is also important to understand in order to explain the mechanism of
fever due to non-infectious diseases.
Reference :
 Price Sylvia A, Wilson Lorraine M. Patofisiologi: Konsep Klinis
Proses-Proses Penyakit. Jakarta: EGC; 2012.
4. Explain the diagnostic step of the scenario !
Anamnesis
1) Identity; name,address,date of birth,age: 35 year old, gender : male,
occupation, status.
2) Chief complaint: 10 days fever
3) Take a history of disease :
a. Onset and duration of fever: sudden onset, when?
b. Fever nature: intermittent, continuous, higher in the afternoon
4) Ask the accompanying symptoms:
a. Respiratory system disorders: cough, shortness of breath
b. Gastrointestinal disorders: nausea, vomiting, constipation, abdominal
pain, diarrhe
c. Urogenital disorders: urine color, oliguria, dysuria
d. Complaints: fever, the patient is accompanied by nausea and
vomiting, pain in the urine and calves like tea.
5) Travel history; history of contact with immigrants or travelers, period of 6
weeks prior to onset or date of complaint.
6) Exposure history; contact history with possible cases.
7) Family history
8) History of going to a dentist or other doctor
9) Drug history
10) Vaccination history; date and type of vaccination
So based on the history according to the scenario, it was found

that a 35-year-old man came with complaints of fever for 10 days,
accompanied by complaints of nausea and vomiting, urinary and calf
pain like tea. And one week earlier the patient's house was flooded.
Physical Examination
A. Inspection
 Assess the presence of anemia, jaundice, edema etc
 Check status: decreased consciousness, dry hair, dirty tongue
 Watch for bleeding manifestations
 Test tourniquet
 Pay attention to the presence or absence of skin efflorescence
 Based on scenario
On physical examination, positive jaundice and scleral injection were
found
B. Palpation : Check for reflex disturbances
C. Auscultation
Abdominal examination: hepatomegaly, splenomegaly
D. Vital signs: body temperature, respiration, pulse, blood pressure
Based on scenario
Examination of vital signs obtained BP 100/60 mmHg, pulse

100x/minute and axillary temperature 38 degrees C.
Supporting investigation
1) outine blood
2) Serological test
3) Bacteriological
4) Stool examination
5) Radiology
 X-ray: Through X-ray examination, it can be seen whether there are
worms in the intestine. X-rays can also be done to see if there are
larvae in the lungs.
 Ultrasound: Can show if there are worms in the pancreas or liver.
 CT scan or MRI: These two examination methods are useful to see if
worms are blocking the ducts of the liver or pancreas.
Referensi:
 Vitayani,dkk.2015. Buku Panduan Kerja Clinical Skill Lab

Kedokteran tropis. Fakultas Kedokteran Universitas Hasanuddin
5. What are the differential diagnosis related to the scenario !
LEPTOSPIROSIS
Definition
Leptospirosis is a zoonotic disease caused by a spiral-shaped bacterial

infection of the genus Leptospira which is pathogenic, transmitted directly and
indirectly from animals to humans. Leptospira bacteria are spiral-shaped with
hook-like ends, measuring 5-15 micrometers long and 0.1-0.2 micrometers
wide, flexible, thin and flexible. The disease is most commonly transmitted
from animals to humans when people with open skin sores come into contact
with water or soil that has been contaminated with animal urine. Animals that
are the source of leptospirosis transmission are rats, pigs, cows, goats, sheep,
horses, dogs, cats, insects, birds, insectivores (porcupines, bats, squirrels),
while foxes can be carriers of leptospira.
Epidemiology
Leptospirosis occurs in various parts of the world but generally in

tropical and subtropical areas with high rainfall. Leptospirosis is an endemic
disease in a number of countries and even in the world. Generally human
cases of Leptospirosis are reported from India, Indonesia, Thailand and Sri
Lanka during the rainy season. Major outbreaks of Leptospirosis in the
Southeast Asian region have been reported in Jakarta (2003), Mumbai (2005)
and Sri Lanka (2008). Based on reports of recent years, the global incidence
of Leptospirosis cases is estimated from 0.1-1 per 100,000 per year in
temperate climates and 10-100 per 100,000 per year in the humid tropics. The
incidence of this disease can reach more than 100 per 100,000 per year in
outbreaks and exposure is high in risk groups.
In 2007 there was an increase in cases of Leptospirosis in humans,

reported as many as 667 cases and 93% confirmed laboratory results with an
8% mortality rate. In 2010 cases of Leptospirosis in Indonesia were reported
as many as 410 cases with 46 deaths (CFR 11.2%). The number of male
patients with leptospirosis is higher than female.
Etiology
Leptospirosis is caused by pathogenic organisms of the genus

Leptospira which are included in the order Spirochaeta in the
Trepanometaceae family. This bacterium is spiral-shaped with a tight twist
and the ends are shaped like hooks so that the bacteria are very active in both
rotating movements along their axis, back and forth, or curved. The size of
these bacteria is 0.1 mm x 0.6 mm to 0.1 mm x 20 mm. Leptospira can be
stained with carbolfuchsin stain. However, these bacteria can only be seen
with a dark field microscope. These bacteria are obligate aerobes with optimal
growth at a temperature of 280C-300C and a pH of 7.2 to 8.0.
The genus Leptospira is divided into two serovarians, namely L.

interrogate which is pathogenic (i.e. has the potential to cause disease in
animals and humans) and L. biflexa which is non-pathogenic/saprophytic (i.e.
free-living and generally considered not to cause disease). Pathogenic
leptospires are maintained in nature in the renal tubules and genital tracts of
certain animals.
Various animal species, especially mammals, can act as a source of

human infection, including:
1. Small mammal species, such as wild rats (including mice, porcupine
squirrels)
2. Domestic animals (cows, pigs, dogs, sheep, goats, horses, buffalo)
3. Fur-producing animals (silver fox) in captivity
4. Reptiles and amphibians may also carry leptospires
Clinical Manifestations
According to Widoyono (2008), clinical symptoms of leptospirosis in

humans can be divided into three stages, namely:
a. First Stage (leptospiremia)

1. Fever, chills
2. Headache
3. Red spots on the skin
4. Malaise and vomiting
Conjunctivitis and redness of the eyes
Pain in the muscles, especially the calf and back muscles.
5. These symptoms will appear between 4-9 days
b. Second Stage
1. At this stage, antibodies are usually formed in the patient's body
2. The symptoms that appear at this stage are more varied than in the
first stage, including jaundice (yellowness)
3. If the fever and other symptoms reappear, meningitis is likely
4. Usually this phase lasts for 4-30 days.
c. Third Stage
According to some clinicians, this disease can also show clinical
symptoms in the third stage (convalescent phase). Complications
Leptospirosis can cause the following symptoms:
1. In the kidneys, renal failure that can cause death

2. In the eyes, closed conjunctiva represents a septicemic phase which
is closely related to photobia and hemorrhagic conjunctiva.
3. In the liver, jaundice (yellowing) that occurs on the fourth and sixth
day with an enlarged liver and soft consistency
4. In the heart, arrhythmias, dilatation of the heart and heart failure that
can cause sudden death
5. In the lungs, hemorrhagic pneumonitis with coughing up blood, chest
pain, respiratory distress and cyanosis
6. Bleeding due to vascular damage from the respiratory tract, digestive
tract, kidneys and genital tract
Infection in pregnancy causes abortion, stillbirth, premature birth and
birth defects.
Supporting investigation
Diagnosis can be made by microscopic examination, as well as by

leptospira culture. The clinical sample that should be collected for
examination depends on the phase of the infection. Specimens came from
blood and cerebrospinal fluid (first week of illness) and urine (after the first
week to day 40). The specimens were grown on Fletcher's media or EMJH
media in combination with neomycin or 5-fluorouracil. On this medium,
growth will be seen within a few days to 4 weeks. The presence of leptospires
in this medium can be seen using a dark field microscope or using a
fluorescent microscope (fluorerescent antibody stain). Immunoserological
testing is also important for the diagnosis of leptospirosis. In general, new
antibodies are found after the 7th or 10th day. The titer will increase and will
peak at the 3rd or 4th week of illness. The immunoserological tests commonly
used are: Microscopic Agglutination Test, Enzymelinked immunosorbent
assay (ELISA), polymerase chain reaction (PCR) and dipstick assays, as well
as Leptospira-specific antigen, namely lipoprotein rLipl32 which can be the
gold standard for diagnosis.
The most useful and most frequently collected samples are:
1. Blood with heparin for culture in the first 10 days.

2. Blood or frozen serum for serological examination is taken in
the septicemic phase. The diagnosis is based on a 4-fold antibody
seroconversion between acute and convalescent. A negative serological
result in the early stages of the disease does not exclude the diagnosis of
leptospirosis.
3. Urine for culture is taken in the immune phase.
4. Post mortem samples. It is important to collect specimens from
as many organs as possible for serology. Post mortem samples should be
collected aseptically and inoculated into the culture medium as soon as
possible after death. Samples should be stored and transported at 4°C. In
addition, crust staining, immunostaining, and immunohisto-chemistry
may be helpful.
5. CSF and dialysate for culture were taken in the septicemic
phase. In the case of an-icteric leptospirosis, normal leukocyte counts
with neutrophilia, increased erythrocyte sedimentation rate (ESR) and
protein in the CSF can be found.
Management
a) Medicine
Severe cases of leptospirosis should be given high doses of IV
penicillin (IV benzylpenicillin 30 mg/kg, maximum 1.2 g, 6 hours for
5-7 days). Milder cases may be treated with oral antibiotics such as
amoxicillin, ampicillin, doxycycline (2 mg/kg, maximum 100 mg,
every 12 hours for 5-7 days), or erythromycin.
b) Supportive therapy and dialysis

Severe cases require hospitalization with aggressive supportive
care and close monitoring of fluid and electrolyte balance. Peritoneal
dialysis or hemodialysis is indicated in renal failure. Good supportive
care and dialysis have reduced the mortality of this disease in recent
years. If prothrombin is disturbed, vitamin K can be given.
Complications
Aseptic meningitis is the most common complication, but encephalitis,

myelitis, radiculitis, peripheral neuritis (unusual) in the second week may
occur due to a hypersensitivity reaction. Severe complications in patients with
severe leptospirosis can be in the form of shock, massive bleeding and ARDS
which is the main cause of death for severe leptospirosis. Shock occurs due to
changes in body homeostasis that play a role in the onset of tissue damage.
Renal failure, liver damage, pulmonary hemorrhage, vasculitis and cardiac
disorders in the form of myocarditis, pericarditis and arrhythmias are rarely
found although they are common causes of death. Although rare, uveitis can
be found after 2 years of symptoms of leptospira.
Prognosis
Mortality in severe leptospirosis is about 10%, death is most often due

to kidney failure, massive bleeding or ARDS. Liver and kidney function will
return to normal, despite severe dysfunction, even in patients on dialysis.
About a third of cases with aseptic meningitis may experience periodic
headaches. Some patients with a history of leptospirosis uveitis experience
loss of visual acuity and blurred vision.
Perevention
According to Rusmini (2011) in general, the prevention of leptospirosis

that can be done is as follows:
1. Familiarize yourself with Clean and Healthy Life Behavior (PHBS)

2. Wash hands with soap before eating and drinking.
3. Use clean water for bathing and washing.
4. Vegetables and fruit should be washed with clean water.
5. Store food properly and correctly to avoid the reach of rats (closed
tightly, put in the cupboard).
6. Use footwear, especially when activities outside the home.
7. Avoid contact with sewer water or standing water, both in the home
environment and at work.
8. Avoid contact with flood waters.
9. Bathing and washing hands, feet and body parts with soap after work,
especially when in fields/gardens/trash cans/soil/sewers and other
polluted places.
10. Protecting body parts with personal protective equipment (PPE) when
working in a place where there is a risk of contamination.
11. Cover the wound on the skin with a waterproof wound dressing.
12. Avoid the presence of mice in the house or workplace.
13. Avoid pollution and improve rat control.
14. Set a mousetrap.
15. Bury or burn rat carcasses in a safe place.
16. Immediately check with the available health facilities if you experience
symptoms
sick.
Reference :
 Setadi, B., Setiawan, A., Effendi, D. & Hadinegoro, SRS Practical

Instructions for Leptospirosis. Sari Pediatr. 3, 163–167 (2001).
 Rampang, NH Leptospirosis Novie H. Rampengan. J. Biomedicine 8,
143–150 (2016).
 Sitohang, RV, Burni, E., Gasem, MH & Muhadir, A. Instructions for
Leptospirosis Control Techniques. Ministry. health. RI 126 (2017).
MALARIA
Definition
Malaria is an infectious disease caused by the Plasmodium parasite that lives
and reproduces in human blood cells. This disease is naturally transmitted
through the bite of the female Anopheles mosquito.
Based on the severity, malaria is divided into severe malaria and mild malaria
(i.e. with or without complications).
1) Severe malaria (complications)

Defined as symptoms or signs of vital organ dysfunction in patients
with documented Plasmodium falciparum parasitemia. Patients must
have 1 of the following criteria to be categorized as severe according
to WHO:
a. Hypotension
- Adults: systolic blood pressure less than 80 mm Hg
- Children: systolic blood pressure less than 50 mm Hg
b. General weakness or prostration
c. Impaired consciousness or coma
d. Recurrent generalized seizures
e. Acute respiratory distress syndrome with pulmonary edema
f. Jaundice plus evidence of other organ dysfunction
g. Abnormal bleeding
h. Hemoglobinuria
i. Acute kidney injury (creatinine level higher than 3 mg/dL)
j. Metabolic acidosis (plasma bicarbonate level less than 15
mmol/L)
k. Serum lactate level higher than 5 mmol/L
l. Hypoglycemia (glucose level less than 40 mg/dL)
m. Severe normocytic anemia
- Adults: hemoglobin less than 7 g/dL
- Children: hemoglobin less than 5 g/dL
n. CDC criteria include a parasite density of 5% or greater
2) Mild malaria
Malaria without vital organ dysfunction
Epidemiology
Malaria is found in almost all parts of the world, especially in

countries with tropical and subtropical climates such as the continents of
Africa and Southeast Asia. In 2019, there were an estimated 229 million cases
of malaria worldwide. The estimated number of malaria deaths reached
409,000 in 2019. Children under 5 years of age are the group most vulnerable
to malaria, they account for 67% (274,000) of all malaria deaths worldwide.
In 2019, the African region was home to 94% of malaria cases and deaths.
The Ministry of Health noted that the total number of malaria cases in
Indonesia in 2019 was 250,644. Around 86% occurred in Papua (216,380
cases). Then, followed by East Nusa Tenggara with 12,909 cases and West
Papua with 7,079 cases. Meanwhile, there are 300 regencies/cities (58%) that
have reached elimination. This means that around 208.1 million Indonesians
(77.7%) live in malaria-free areas.
Etiology
Malaria is a systemic febrile disease caused by infection with one of 5

species of Plasmodium (Plasmodium falciparum, Plasmodium vivax,
Plasmodium malariae, Plasmodium ovale, or Plasmodium knowlesi) which is
transmitted through the bite of the female Anopheles mosquito, can also be
caused by congenital infection.
Based on the causative species (each species name can also function as
an adjective; for example, malaria vivax is Plasmodium vivax malaria)
1) Plasmodium falciparum malaria

 Geographical areas affected: Haiti, Dominican Republic, parts of the
Middle East, sub-Saharan Africa, Afghanistan and the Indian
subcontinent, South America, Southeast Asia, Oceania and Papua
New Guinea
 Including mild malaria and severe malaria
 The course of the disease does not recur
2) Plasmodium vivax malaria

 Geographical areas affected: Mexico, Central America, Middle East,
North Africa, Afghanistan and the Indian subcontinent, South
America, Southeast Asia, Oceania and Papua New Guinea
 Usually malaria is not severe
 Recurrence
3) Plasmodium malariae malaria

 Geographical areas affected: rare, but present in most malaria-
affected areas, especially Central and West Africa
 The course of the disease that does not recur, but can become a
chronic low-grade infection
4) Plasmodium ovale malaria

 Geographical areas affected: mainly Africa, which accounts for a
minority of cases; sometimes seen in some parts of Asia
 The course of relapsing disease
5) Plasmodium knowlesi malaria

 Geographical areas affected: where humans live in close contact
with apes, particularly in Borneo and peninsular Malaysia; several
cases have been reported elsewhere in Southeast Asia
 The species primarily infects nonhuman primates, but infections in
humans are now being reported
 Could be severe malaria
Risk Factors
1. Age
a. In travelers, occurs at all ages
b. In endemic areas, long-term residents develop partial immunity with
age, so most clinical disease occurs in children
c. Children are more susceptible to severe malaria
2. Genetics
Certain genetic conditions are protective (increases survival advantage)
a. Sickle cell trait (hemoglobin S heterozygous)

b. G6PD . deficiency
c. Thalassemia
d. HLA-Bw53
e. Southeast Asia Ovalocytosis
f. Absence of Duffy factor (glycophorin A)
3. Other exposures
a. Blood transfusion
b. Organ transplant
c. Contaminated needle
Pathophysiology
Symptoms of malaria occur when the erythrocytes burst containing the
parasite. Fever begins to arise with the outbreak of blood schizonts that
secrete various antigens. This antigen will stimulate macrophages, monocytes
or lymphocytes that secrete various cytokines, including Tumor Necrosis
Factor (TNF). TNF will be carried by the bloodstream to the hypothalamus,
which is the center for regulating body temperature. As a result of fever there
is peripheral vasodilation which may be caused by vasoactive substances
produced by the parasite. 5,6 The spleen is a reticuloendothelial organ. The
enlargement of the spleen is caused by an increase in the number of
erythrocytes infected with parasites, the activation of the reticuloendothelial
system to phagocytose erythrocytes infected with parasites and the remaining
erythrocytes due to hemolysis. Anemia is mainly caused by the rupture of
erythrocytes and phagocytosis by the reticuloendotetial system. The severity
of hemolysis depends on the type of plasmodium and the immune status of the
host. Anemia is also caused by autoimmune hemolysis, sequestration by the
spleen in infected and normal erythrocytes and impaired erythropoiesis.
Hyperglycemia and hyperbilirubinemia are common. Hemoglobinuria and
Hemoglobinemia are found when hemolysis is severe. Pathological
abnormalities of capillary blood vessels in tropical malaria, due to the fact that
infected red blood cells become stiff and sticky, their passage in the capillaries
is disrupted so that they stick to the capillary endothelium due to protrusion of
the erythrocyte membrane. After the accumulation of cells and cell debris
material, capillary flow is inhibited and tissue hypoxia occurs.
(Figure 1. Plasmodium life cycle. Source: Shia medical journal Kuala Volume
11 Number 2)
Clinical Symptoms
The most common early symptoms

The life cycle of Plasmodium occurs every 24 hours (Plasmodium knowlesi);
every 48 hours (Plasmodium vivax, Plasmodium ovale, and Plasmodium
falciparum); or every 72 hours (Plasmodium malariae), causing symptoms
that may be erratic or cyclic:
 Fever
 Diaphoresis
 Chills
 Fatigue
 Nauseous
 Gag
Other Symptoms
 Headache
 Myalgia (especially back pain)
 Arthralgia
 Stomach ache
 Diarrhea
Additional symptoms associated with severe malaria
Systemic symptoms
 Weakness
 Respiratory disorders
 Urine is red or black
 Bloody diarrhea
Cerebral symptoms (cerebral malaria)
 Confusion
 Sleepy
 Seizures
Symptoms suggestive of pulmonary edema and shock
 Cardiogenic
 Dyspnea
 Dizzy
 Chest pain
Symptoms can progress rapidly from mild to severe in disease caused by

Plasmodium falciparum or Plasmodium knowlesi.
Diagnosis
History
 Determine geographic area of exposure and history of previous

antimalarial treatment or prophylaxis
 Symptoms are usually milder in long-term residents in endemic areas due
to partial immunity
 Symptoms usually appear within 30 days of a visit to an endemic country,
but may occur months to (rarely) years later.
 Plasmodium vivax and Plasmodium ovale can cause late recurrence of
symptoms (up to 4 years after initial infection)
 With acute infection, the symptoms may be indistinguishable from other
febrile illnesses. Once infection is established, symptoms may occur
episodic, coinciding with synchronous rupture of blood schizonts (infected
hepatocytes).
Main Diagnostic
 High index of suspicion based on travel history, symptoms, and physical
examination
 Immediate initial diagnosis through Giemsa-stained peripheral blood
smear microscopy or rapid diagnostic tests
 Immediately after initial diagnosis, seek laboratory confirmation of the
species with experienced microscopy or molecular testing and
quantification of parasite density
 Fever, chills and diaphoresis may be present; absence of fever on any
given day does not rule out malaria
Physical Examination
 Fever (touch or measurement with a thermometer)
 Paleness of the palpebral conjunctiva or palms.
 Enlarged spleen (splenomegaly).
 Enlarged liver (hepatomegaly).
In suspected severe malaria, one or more of the following clinical signs
can be found; Axillary temperature >40 C.
 Systolic blood pressure 35 x per minute in adults or 40 x per minute in
toddlers, children under 1 year > 50 x per minute.
 Decreased level of consciousness
 Bleeding manifestations (petechiae, purpura, hematoma).
 Signs of dehydration (sunken eyes, reduced skin turgor and elasticity, dry
lips, less urine production).
 Signs of severe anemia (pale conjunctiva, pale palms, pale tongue).
 Visible yellow / icteric eyes.
 There are crackles in both lungs.
 Enlargement of the spleen and/or liver.
 Renal failure is characterized by oliguria to anuria.
 Neurological symptoms (neck stiffness, reflex pathology).
Children
 Coma usually resolves within 1 or 2 days in hospitalized patients
 Seizures are common (30% of patients)
 Decortication/decerebrate posture with opisthotonic stiffness is common
Mature
 Coma can last 2 to 4 days despite treatment
 Seizures are less common (12% of patients)
 Posture is rare
Increased blood pressure with decreased heart rate and/or papilledema

indicates increased intracranial pressure
Laboratory Examination
 Microscopic tests
Examination of thick and thin blood preparations (SD) is the gold

standard examination and it is to determine:
a. The presence or absence of malaria parasites (positive or negative).

b. Plasmodium species and stages (Pf, PV, Pm, Po, and trophozoites,
schizonts, gametocytes).
c. Parasite density:
Semi quantitative
 (-) : SD negative (no parasites found in 100 LPB)
 (+) : SD positive 1 (found 1-10 parasites in 100 LPB). O
 (++): SD positive 2 (found 11-100 parasites in 100 LPB).
 (+++): SD positive 3 (found 1-100 parasites in 1 LPB).
 (++++): SD positive 4 (found 11-100 parasites in 1 LPB).
d. Morphological Examination
e. Plasmodium knowlesi is similar to P. malariae. P, malariae is
characterized by compact parasites (all stages) and does not alter
host erythrocytes or cause enlargement. Trophozoites extending
across the erythrocyte, the so-called “band form”, are sometimes
seen. Schizonts will typically have 8-10 merozoites which are
often arranged in a rosette pattern with a clump of pigment in the
center.
If the result is negative for malaria parasites, repeat the test every 12 to 24
hours for a total of 3 sets of smears before determining the result as
definitively negative.
1. Plasmodium falciparum
 Ring trophozoites are characterized by a smooth, thin ring with
little cytoplasm opposite the nucleus
 Often greater than 5% infestation with parasitic erythrocytes of all
ages
 Double chromatin dots are present in the ring, and the ring is
attached peripherally to the inside of the erythrocyte membrane
 Several parasitic erythrocytes (more than 1 parasite in one
erythrocyte) can be seen
 Schizonts and trophozoites are usually absent
 Banana-shaped gametocytes may be present; the presence of this
and several ring shapes in a single red blood cell are unique
identifying features
2. Plasmodium vivax
 Thicker ring across the nucleus (seal shaped)
 Fewer erythrocytes affected
 Large ameboid trophozoites that impair erythrocyte morphology
are seen
 Macrocytes (reticulocyte equivalents) are more frequently affected,
and all phases of the parasite life cycle are present in circulating
erythrocytes.
 Schüffner dots (pink dots in the cytoplasm of erythrocytes) are
visible
3. Plasmodium malariae
 Band shape is present in older erythrocytes, and is a distinguishing
feature
 Low-grade parasitemia (rarely 1% of erythrocytes are parasitized)
 There is a rosette-shaped schizont
4. Plasmodium ovale
 Affects early erythrocytes (reticulocyte equivalent) with frayed
edges
 Schüffner dots may be visible
 Rapid test
1 FDA-approved antigen detection rapid diagnostic test in the United

States (BinaxNOW) for hospitals, commercial, and reference
laboratories
a. Requires a blood sample to be applied to a test card and left for 15

minutes
b. The band pattern in the test window indicates the presence of
Plasmodium species; Plasmodium falciparum can be identified, but
other malaria species cannot be trusted
c. Unclear reliability for detecting Plasmodium malariae and
Plasmodium ovale
d. The test may not be sensitive enough to detect low levels of
parasitaemia
e. Confirm all results with a microscope
Governance
Target :
- Relieves symptoms
- Eliminates parasitemia and prevents recurrent disease
Select treatment according to Plasmodium species, geographic likelihood

of drug resistance, previous use of antimalarial drugs (eg, prophylaxis), and
severity of infection. If species cannot be identified immediately, treat with
regimen for Plasmodium falciparum, based on geographic probability of
resistance to antimalarial agents.
 Drug therapy
1. Chloroquine
 Chloroquine Phosphate Oral Tablets; Infants, Children and
Adolescents: 16.6 mg (10 mg base)/kg/dose [Max: 1,000
mg/dose (600 mg base/dose)] PO once, then 8.3 mg (5 mg
basis)/kg /dose [Max : 500 mg/dose (300 mg base/dose)] PO in
6 to 8 hours, then 8.3 mg (5 mg base)/kg/dose [Max: 500
mg/dose (300 mg base/ dose)] PO once daily for 2 days.
 Chloroquine Phosphate Oral Tablets; Adult: 16.6 mg (10 mg
base)/kg/dose [Max: 1,000 mg/dose (600 mg base/dose)] PO
once, then 8.3 mg (5 mg base)/kg/dose [Max: 500 mg/dose (300
mg base/dose)] PO over 6 to 8 hours, then 8.3 mg (5 mg
base)/kg/dose [Max: 500 mg/dose (300 mg base/dose)] PO once
a day for 2 days.
2. Hydroxycycloroquine
 Hydroxychloroquine Sulfate Oral Tablets; Children and
Adolescents weighing 31 kg or more: 13 mg (10 mg
base)/kg/dose [Max: 800 mg (620 mg base)/dose] PO, then 6.5
mg (5 mg base)/ kg/dose [Max: 400 mg (310 mg base)/dose] PO
at 6, 24, and 48 hours after initial dose for a total dose of 32.5
mg (25 mg base)/kg [Max: 2,000 mg (1,550 mg) language)].
 Hydroxychloroquine Sulfate Oral Tablets; Adult: 800 mg (620
mg base) PO, then 400 mg (310 mg base)/dose PO at 6, 24, and
48 hours after the initial dose for a total dose of 2,000 mg
(1,550 mg base).
3. Quinine sulfate
For the treatment of uncomplicated malaria due to Plasmodium
falciparum or Plasmodium vivax
 Quinine Sulfate Oral Capsules; Children and Adolescents 1 to
15 years†: 10 mg/kg/dose (Max: 648 mg/dose) PO every 8
hours for 3 days, in general, or 7 days for Southeast Asia.
 Quinine Sulfate Oral Capsules; Adolescents 16 to 17 years: 648
mg PO every 8 hours for 3 days, generally, or 7 days for
Southeast Asia.
 Quinine Sulfate Oral Capsules; Adult: 648 mg PO every 8 hours
for 3 days, generally, or 7 days for Southeast Asia.
For the treatment of severe malaria before the availability of IV

artesunate
 Quinine Sulfate Oral Capsules; Children and Adolescents: 10

mg/kg/dose (Max: 648 mg/dose) PO every 8 hours.
Discontinue when IV artesunate therapy is started.
 Quinine Sulfate Oral Capsules; Adult: 648 mg PO every 8
hours. Discontinue when IV artesunate therapy is started
4. Tetracycline
 Tetracycline Hydrochloride oral capsule; Children 1 to 7 years
of age: 25 mg/kg/day PO divided 4 times daily (Max: 250
mg/dose) for 7 days.
 Tetracycline Hydrochloride oral capsule; Children and
Adolescents 8 to 17 years: 25 mg/kg/day PO divided 4 times
daily (Max: 250 mg/dose) for 7 days.
 Tetracycline Hydrochloride oral capsule; Adult: 250 mg PO 4
times daily for 7 days.
5. Doxycycline
 Oral

falciparum or Plasmodium vivax
 Doxycycline calcium oral suspension; Children 1 to 7 years:
2.2 mg/kg/dose (Max: 100 mg/dose) PO twice daily for 7
days.
 Doxycycline Monohydrate Oral capsules; Children and
Adolescents 8 to 17 years: 2.2 mg/kg/dose (Max: 100
mg/dose) PO twice daily for 7 days.
 Doxycycline Monohydrate Oral capsules; Adult: 100 mg PO
twice daily for 7 days.
For the treatment of severe malaria after completion of IV

artesunate therapy
 Doxycycline Monohydrate Oral capsules; Children and
mg/dose) PO twice daily for 7 days.
 Doxycycline Monohydrate Oral capsules; Adult: 100 mg PO
twice daily for 7 days.
 Intravenous

artesunate therapy
 Doxycycline Hyclate Solution for injection; Children and

mg/dose) IV every 12 hours. Switch to oral therapy as soon
as possible for a total treatment duration of 7 days.
 Doxycycline Hyclate Solution for injection; Adult: 100 mg
IV every 12 hours. Switch to oral therapy as soon as
possible for a total treatment duration of 7 days.
6. Clindamycin
 Oral
falciparum
 Clindamycin Palmitate Hydrochloride Oral solution;
Infants, Children and Adolescents: 20 mg/kg/day PO
divided 3 times daily for 7 days.
 Clindamycin Hydrochloride Oral Capsules; Adult: 20
mg/kg/day PO divided 3 times daily for 7 days.
artesunate therapy
 Clindamycin Hydrochloride Oral Capsules; Infants and
Children under 8 years: 20 mg/kg/day PO divided 3 times
daily for 7 days.
 Clindamycin Hydrochloride Oral Capsules; Adolescent
Pregnant Women: 20 mg/kg/day PO divided 3 times daily
for 7 days
 Clindamycin Hydrochloride Oral Capsules; Pregnant
Women Adults: 20 mg/kg/day PO divided 3 times daily for
7 days.
 Intravenous

artesunate therapy
 Clindamycin Solution for injection; Infants and Children

under 8 years: 10 mg/kg IV initially, then 5 mg/kg/dose IV
every 8 hours. Switch to oral therapy as soon as possible for
a total treatment duration of 7 days.
 Clindamycin Solution for injection; Adolescent Pregnant
Women: 10 mg/kg IV initial dose, then 5 mg/kg/dose IV
 Clindamycin Solution for injection; Pregnant Women
Adults: 10 mg/kg IV initial dose, then 5 mg/kg/dose IV
7. Primaquine
 Must check for G6PD deficiency before prescribing
 Not prescribed for pregnant patients
 Primaquine Phosphate Oral tablets; Infants†, Children and
Adolescents†: 0.5 mg base/kg/dose (Max: 30 mg base/dose) PO
once daily for 14 days.
 Primaquine Phosphate Oral tablets; Adult: 52.6 mg (30 mg
base) PO once daily for 14 days.
 Primaquine Phosphate Oral tablets; Adults with threshold G6PD
deficiency: 78.9 mg (45 mg base) PO once weekly for 8 weeks.
8. Taphenoquine
 Should check for G6PD deficiency before prescribing.
Tafenoquine is contraindicated in patients with G6PD
deficiency or unknown G6PD status because of the risk of
hemolytic anemia.
 Should not be used in children under 16 years of age or in those
with a history of psychotic disorders
 Not recommended during breastfeeding or pregnancy
 Taphenoquine tablets Oral; Adolescents 16 years and older: 300
mg PO as a single dose on the first or second day of appropriate
antimalarial therapy.
 Taphenoquine tablets Oral; Adult: 300 mg PO as a single dose
on the first or second day of appropriate antimalarial therapy.
9. Mefloquine (recommended use only when other options are not

available because of the risk of severe neuropsychiatric side effects at
treatment doses)
For the treatment of uncomplicated malaria due to Plasmodium vivax
 Mefloquine Hydrochloride Oral Tablet; Infants†, Children and
Adolescents†: 15 mg/kg/dose (Max: 750 mg/dose) PO as initial
dose then 10 mg/kg/dose (Max: 500 mg/dose) PO at 6 to 12 hours
after dose beginning.
 Mefloquine Hydrochloride Oral Tablet; Adult: 1,250 mg PO as a
single dose, or alternately, 750 mg PO as initial dose then 500 mg
PO 6 to 12 hours after the initial dose.
For the treatment of uncomplicated malaria due to mefloquine-

susceptible Plasmodium falciparum strains
 Mefloquine Hydrochloride Oral Tablet; Infants 1 to 5 months†:

15 mg/kg/dose PO as initial dose then 10 mg/kg/dose PO at 6
to 12 hours after initial dose.
 Mefloquine Hydrochloride Oral Tablet; Infants, Children and
Adolescents 6 months to 17 years: 20 to 25 mg/kg/dose (Max:
1,250 mg) PO as a single dose, or alternately, 15 mg/kg/dose
(Max: 750 mg/dose) PO as initial dose then 10 mg/kg/dose
(Max: 500 mg/dose) PO at 6 to 12 hours after initial dose.
 Mefloquine Hydrochloride Oral Tablet; Adult: 1,250 mg PO as
a single dose, or alternately, 750 mg PO as initial dose then
500 mg PO 6 to 12 hours after the initial dose.
For the treatment of severe malaria, before IV artesunate was available

Adolescents: 15 mg/kg/dose (Max: 750 mg/dose) PO as initial
after initial dose. Discontinue once IV artesunate therapy is started.
 Mefloquine Hydrochloride Oral Tablet; Adult: 750 mg PO as
initial dose then 500 mg PO 6 to 12 hours after initial dose.
Discontinue once IV artesunate therapy is started.
For the treatment of severe malaria, after IV artesunate is completed

Adolescents: 15 mg/kg/dose (Max: 750 mg/dose) PO as initial
after initial dose.
 Mefloquine Hydrochloride Oral Tablet; Adult: 750 mg PO as
initial dose then 500 mg PO 6 to 12 hours after initial dose.
10. Atovaquone-proguanil
 Atovaquone, Proguanil Hydrochloride Oral Tablet; Infants and
Children weighing 5 to 8 kg: 2 pediatric strength tablets (62.5 mg
atovaquone; 25 mg proguanil per tablet) PO once daily for 3
consecutive days.
Children weighing 9 to 10 kg: 3 pediatric strength tablets (62.5 mg
consecutive days.
Children weighing 11 to 20 kg: 1 adult-strength tablet (250 mg
consecutive days.
 Atovaquone, Proguanil Hydrochloride Oral Tablet; Children
weighing 21 to 30 kg: 2 adult-strength tablets (250 mg atovaquone;
100 mg proguanil per tablet) PO once daily for 3 consecutive days.
 Atovaquone, Proguanil Hydrochloride Oral Tablet; Children and
Adolescents weighing 31 to 40 kg: 3 adult-strength tablets (250 mg
consecutive days.
 Atovaquone, Proguanil Hydrochloride Oral Tablet; Children and
Adolescents weighing more than 40 kg: 4 adult-strength tablets
(250 mg atovaquone; 100 mg proguanil per tablet) PO once daily
for 3 consecutive days.
 Atovaquone, Proguanil Hydrochloride Oral Tablet; Adults: 4 adult
strength tablets (250 mg atovaquone; 100 mg proguanil per tablet)
PO once daily for 3 consecutive days.
11. Artemeter-lumefantrine
 Use is contraindicated with concomitant use of strong CYP3A4
inducers (eg, carbamazepine, phenytoin, rifampin, St. John's wort).
Concomitant use of strong CYP3A4 inducers can lead to a marked
decrease in artemether; lumefantrine concentrations and loss of
anti-malarial efficacy.
 Artemether, Lumefantrine Oral tablet; Infants and Children 2
months or older and weighing 5 to 14 kg: 1 tablet (20 mg
artemether; 120 mg lumefantrine per tablet) PO as initial dose and 1
tablet PO at 8 hours after initial dose, then 1 tablet PO twice a day
(morning and evening) for 2 days.
 Artemether, Lumefantrine Oral tablet; Infants and Children 2
months or older weighing 15 to 24 kg: 2 tablets (20 mg artemether;
120 mg lumefantrine per tablet) PO as initial dose and 2 tablets PO
at 8 hours after initial dose, then 2 tablets PO twice daily ( morning
and evening) for 2 days.
 Artemether, Lumefantrine Oral tablet; Children and Adolescents
weighing 25 to 34 kg: 3 tablets (20 mg artemether; 120 mg
lumefantrine per tablet) PO as initial dose and 3 tablets PO at 8
hours after initial dose, then 3 tablets PO twice daily (morning). and
afternoon) for 2 days.
 Artemether, Lumefantrine Oral tablet; Children and Adolescents
weighing 35 kg or more: 4 tablets (20 mg artemether; 120 mg
lumefantrine per tablet) PO as initial dose and 4 tablets PO at 8
hours after initial dose, then 4 tablets PO twice daily (morning and
evening). afternoon) for 2 days.
 Artemether, Lumefantrine Oral tablet; Adult: 4 tablets (20 mg
artemether; 120 mg lumefantrine per tablet) PO as initial dose and 4
tablets PO at 8 hours after initial dose, then 4 tablets PO twice daily
(morning and evening) for 2 days
12. Artesunate
 Treat all patients with severe malaria, regardless of the infecting
species, with IV art artesunate
 Artesunate for injection was approved by the FDA in 2020 for the
treatment of severe malaria; Quinidine IV has been discontinued
and is no longer available
 Artesunate solution for injection; Infants and Children weighing
less than 20 kg: 2,4 or 3 mg/kg/dose IV given at 0, 12, and 24
hours, and thereafter, once daily until switch to oral therapy. If
unable to tolerate oral therapy, continue for a total of 7 days or
switch to IV doxycycline (8 years or older) or clindamycin for 7
days.
 Artesunate solution for injection; Children and Adolescents
weighing 20 kg or more: 2.4 mg/kg/dose IV given at 0, 12, and 24
hours, and thereafter, once daily until switch to oral therapy. If
unable to tolerate oral therapy, continue for a total of 7 days or
switch to IV doxycycline (8 years or older) or clindamycin for 7
days.
 Artesunate solution for injection; Adult: 2.4 mg/kg/dose IV given
at 0, 12, and 24 hours, and thereafter, once daily until switch to
oral therapy. If unable to tolerate oral therapy, continue for a total
of 7 days or switch to IV doxycycline or clindamycin for 7 days.
 The CDC recommends checking parasite density after 24 hours of
therapy. If, after the third IV dose of artesunate, the patient's
parasite density is greater than 1% (assessed on a blood smear
taken 4 hours after the last artesunate dose), continue IV treatment
with artesunate using the recommended daily dose for a maximum
of 7 days. Doses given at 0, 12, and 24 hours count as 1 day, which
means up to 6 additional days. If the parasite density is 1% or less
and the patient can tolerate oral treatment, a complete treatment
with a follow-up regimen should be given.
Complications
Malaria caused by Plasmodium falciparum and Plasmodium knowlesi is often

severe (complications), causing the following:
 Cerebral malaria
 Pulmonary edema
 Acute respiratory distress syndrome
 Heart attack
 Kidney failure
 Spleen rupture
 Disseminated intravascular coagulation
 Hemolysis
 Pregnancy complications
 Death due to multiorgan failure
Prognosis
Prognosis depends on the treatment given. In tropical malaria (caused by

Plasmodium falciparum) there can be a dangerous complication called black
water fever (haemoglobinuric feber) with acute renal failure.
References :
 WHO: World Malaria Report 2019. WHO; 2019

 Collins WE et al: Plasmodium malariae: parasite and disease. Clin
Microbiol Rev. 20(4):579-92, 2007
 Collins WE et al: Plasmodium ovale: parasite and disease. Clin
Microbiol ev. 18(3):570-81, 2005
 WHO: Management of Severe Malaria - A Practical Handbook. 3rd
ed. WHO; 2013
 CDC: Malaria: Treatment of Malaria: Guidelines for Clinicians
(United States). CDC website. Last Reviewed May 29, 2020.
Accessed July 29,
2020.https://www.cdc.gov/malaria/diagnosis_treatment/clinicians1.ht
ml
 Ministry of Health of the Republic of Indonesia. Malaria: The World's
Leading Cause of Death. 2021. https://www.malaria.id. accessed 14
November 2021 01:15
 Teuku Romi Imansyah Putra. Malaria and its problems. Shia medical
journal kuala Volume 11 Number 2 August 2011
TETANUS
Definition
Tetanus is an acute toxemia caused by a neurotoxin produced by
Clostridium tetani characterized by periodic and severe muscle spasms.
Tetanus is usually acute and causes spastic paralysis caused by tetanospasmin.
Tetanospasmin is a neurotoxin produced by Clostridium tetani. Tetanus can
also be defined as a state of acute hypertonia or muscle contractions that
causes pain (usually in the lower jaw and neck) and generalized muscle spasm
without other causes, and there is a history of previous injuries or accidents.
Epidemiology
Although tetanus affects people of all ages; however, the highest
prevalence is seen in newborns and young persons. The World Health
Organization (WHO) reports improvement in mortality rates from tetanus,
associated with aggressive vaccination campaigns in recent years. The WHO
estimates worldwide tetanus deaths in 1997 at around 275,000 with improved
rates in 2011 at 14,132 cases. However, of these cases, the prevalence of
tetanus is still disproportionately higher (some studies showing 135 times
higher) in low-resource settings than rates in developed countries, with
mortality rates of 20% to 45% with the infection. Mortality rates vary based
on the availability of resources, notably mechanical ventilation, invasive
blood pressure monitoring, and early treatment.
The incidence of neonatal tetanus is decreasing due to routine
vaccination worldwide, which is combined with other vaccines, pertussis, and
diphtheria (DPT). The occurrence of tetanus among neonates is mostly due to
incomplete vaccination of the infant. In 2013, approximately 84% of children
less than 12 months of age had coverage of tetanus worldwide.
In high-resource countries, such as the United States, cases of tetanus
occur in the unimmunized or in the elderly who have decreased immunity
over time. Intravenous drug users are also at risk owing to contaminated
needles or drugs.
Tetanus is a disease of the underdeveloped world. It is more
commonly found in areas where the soil is cultivated, in warm climates, and
among males. It is also more frequently seen in neonates and children in
countries where there is no immunization program in place.
Etiology
Tetanus is caused by an exotoxin (tetanospasmin) from the bacterium
Clostridium tetani. Clostridium tetani is an anaerobic Gram positive bacterium
found in soil and animal waste. These bacteria are rod-shaped and produce
spores, giving them a classic drumstick-like appearance, though not always
visible. These spores can last several months or even years. C. tetani is a
motile bacterium because it has flagella, which, according to the flagellar
antigen, are divided into 11 strains and produce the same neurotoxin. Spores
produced by these bacteria are resistant to many disinfectant agents, both
physical and chemical agents. Spores of C. tetani can survive boiling water for
several minutes (though destroyed by autoclaving at 121°C for 15-20
minutes). If these bacteria infect a person's wound or along with other objects,
these bacteria will enter the patient's body, then release a toxin called
tetanospasmin.
Spores or bacteria enter the body through open wounds. When
occupying a suitable place (anaerobic) the bacteria will grow and release the
tetanus toxin. In very low concentrations, this toxin can cause tetanus
(minimum lethal dose is 2.5 mg/kg).
Pathogenesis
Clostridium tetani in the form of spores enters the body through
wounds contaminated with dust, soil, animal feces, fertilizers. Ways of entry
of these spores through contaminated wounds include iron stab wounds,
burns, abrasions, otitis media, dental infections, chronic skin ulcers, abortions,
umbilical cords, sometimes the wounds are barely visible.
If conditions are favorable in which the wound site becomes
hypoaerobic to anaerobic accompanied by the presence of necrotic tissue,
dead leukocytes, foreign bodies, the spores turn into vegetative forms which
then develop. These germs are not invasive. When the bacterial cell wall
lyses, exotoxins are released, namely tetanospasmin and tetanolysin.
Tetanolysin, not associated with disease pathogenesis. Tetanospasmin,
commonly known as tetanus toxin, is the neurotoxin that causes the
manifestations of the disease.
Tetanospasmin enters the central nervous system through muscles
where there is an anaerobic environment that allows Clostridium tetani to live
and produce toxins. Then after entering the peripheral nervous system, the
toxin will be transported retrogradely to the presynaptic nerve, where the
toxin works. The toxin will inhibit the release of inhibitory neurotransmitters
and effectively block inhibition of interneuron signaling. But in particular the
toxin inhibits the release of Gamma Amino Butyric Acid (GABA) which
specifically inhibits motor neurons. This will result in unregulated activity of
the motor nervous system.
Tetanospasmin also affects the sympathetic nervous system in severe
cases, resulting in sympathetic overactivity in the form of labile hypertension,
tachycardia, excessive sweating and increased urinary excretion of
catecholamines. This can lead to cardiovascular complications.
Tetanospamine bound to the nervous tissue can no longer be neutralized by
the tetanus antitoxin.
Clinical Manifestation
The incubation period is 5-14 days, but can be shorter (1 day) or longer (3 or
several weeks).
Characteristics of tetanus:
• Seizures increase in severity during the first 3 days, and persist for 5 -7
days.
• After 10 days of seizures began to decrease in frequency
• After 2 weeks the seizures started to disappear.
• Usually preceded by muscle tension especially in the jaw from the neck.
Then there is difficulty opening the mouth (trismus, lockjaw) due to
spasm of the masseter muscle.
• Muscle spasms continue to stiff neck (opisthotonus, nuchal rigidity)
• Risus sardonicus due to spasm of the facial muscles with the appearance
of the eyebrows being pulled up, the corners of the mouth being pulled
out and down, the lips are strongly pressed.
• Typical general picture in the form of a rigid body with opisthotonos
• Existence, arms stiff with clenched fists, usually good consciousness.
• Due to very strong muscle contractions, asphyxia and cyanosis can
occur, urinary retention, and even vertebral column fractures (in
children).
There are three clinically recognized forms of tetanus, namely:

1. Localized tetanus (Local Tetanus)
In localized tetanus, persistent muscle contractions were found, in the
area where the wound occurred (agonists, antagonists, and fixators). This is
a sign of localized tetanus. These muscle contractions are usually mild, can
last for several months without progressing and usually disappear gradually.
Localized tetanus can progress to generalized tetanus, but in a mild form
and rarely causes death. It is also possible that localized tetanus is found as a
prodromal form of classic tetanus or is seen separately. This is especially
true after antitoxin prophylaxis.
2. Cephalic Tetanus
Cephalic tetanus is a rare form of tetanus. The incubation period ranges
from 1–2 days, originating from chronic otitis media (as reported in India),
injuries to the face and head, including the presence of foreign bodies in the
nasal cavity.
3. Generalized tetanus (generalized tetanus)
This form is the most widely known. Often causes unrecognized
complications, some localized tetanus because symptoms develop
insidiously. Trismus is the main symptom that is often found (50%), which
is caused by stiffness of the masseter muscles, together with stiffness of the
neck muscles which causes stiff neck and difficulty swallowing. Other
symptoms in the form of Risus Sardonicus (Sardonic grin) namely facial
muscle spasm, opisthotonus (back muscle stiffness), abdominal wall
spasms. Spasm of the larynx and respiratory muscles can cause airway
obstruction, cyanosis asphyxia. Dysuria and urinary retention may occur,
compression fractures and bleeding within the muscles may occur. The
increase in temperature is usually only slightly, but even so it can reach 40
C. If hyperthermia or hypothermia is found, blood pressure is unstable and
tachycardia is found, the patient usually dies. Diagnosis is made only based
on clinical symptoms.
4. Neonatal tetanus
Usually caused by infection with C. tetani, which entered through the
umbilical cord during the delivery process. Spores that enter are caused by
unsterilized delivery assistance, either by the use of equipment contaminated
with C. tetani spores, or the use of drugs for the umbilical cord that have
been contaminated. The habit of using unsterilized delivery aids and
traditional medicines is a major factor in the occurrence of neonatal tetanus.
Diagnosis
The diagnosis of tetanus is strong enough only on the basis of anamnesis
and physical examination. Examination of culture of C. tetani (+) in the
wound, is only a diagnostic support. The presence of trismus, dysphagia, or
risus sardonicus or painful muscle spasms and is usually preceded by a history
of trauma is sufficient to confirm the diagnosis.
Management
A. GENERAL
The purpose of this therapy is to eliminate tetany germs, neutralize the
circulation
toxins, prevent muscle spasms and provide respiratory support until
recovery.
1. Treat and clean the wound as well as possible, in the form of:
- Cleaning the wound, irrigation of the wound, debridement of the
wound (excision of necrotic tissue), removing foreign objects in the
wound and compressing with H202, in this case management, the
wound is carried out 1-2 hours after ATS and administration of
antibiotics. ATS is injected around the wound.
2. The patient is placed in an area that is minimal / minimal from various
stimuli.
4. Oxygen, artificial respiration and trachcostomy if necessary.
5. Regulate fluid and electrolyte balance.
B. PHARMACOLOGY
1) Toxin neutralization: TIG (tetanus immune globulin), 3000-10000 units
intramuscularly, divided into three equal doses and injected in three
different places. The sooner TIG treatment is given, the more effective it
is.
2) If TIG is not available, then ATS is given at a dose of 100,000-200,000
units: the first day 50,000 units intramuscularly and 50,000 units
intravenously. The second day 60,000 intramuscular units and the third
day 40,000 intramuscular units.
3) To treat muscle spasms and rigidity, diazepam is still effective, a dose of
0.1-0.3 mg/kgBW/time with an interval of 2-4 hours according to clinical
symptoms. If not controlled, other sedative drugs can be chosen, such as
phenobarbital 50-100 mg/kgBW at 2-4 hour intervals IM and
chlorpromazine 25-75 mg/kgBW/4 hours intramuscularly.
4) Treating the source of infection:
• Metronidazole is given intravenously with an initial dose of 15
mg/kgBW followed by a dose of 30 mg/kgBW/day every 6 hours for 7-
10 days if there is a mixed infection with beta-lactamase-producing
bacteria.
• The second line can be given penicillin procaine 50.000 U/kgBW/day
for 7-10 days.
• Penicillin allergy, given alternatives: erythromycin, clindamycin,
chloramphenicol, tetracycline. The dose of tetracycline is 30-40
mg/kg/day.
Complications
A dangerous complication of tetanus is obstruction of the airway so
that in severe tetanus, sometimes requiring ventilator assistance.
Approximately 78% of tetanus deaths are due to complications. Continuous
seizures can result in fractures of the spinal and long bones, as well as
rhabdomyolysis, which is often followed by acute renal failure.
Common nosocomial infections often occur due to prolonged
hospitalization. Secondary infections include sepsis from the catheter,
hospital-acquired pneumonia, and pressure ulcers. Pulmonary embolism is
very problematic in drug users and elderly patients. Aspiration pneumonia is a
common late complication of tetanus, found in 50%-70% of autopsy cases.27-
30 One complication that is difficult to treat is autonomic disturbance due to
uncontrolled release of catecholamines. These autonomic disorders include
hypertension and tachycardia which sometimes progress to hypotension and
bradycardia.
Preventions
A patient who is exposed to tetanus is not immune to repeated attacks,
meaning that he has the same chance of getting tetanus if an injury occurs as
other people who have never been immunized. No immunity is formed in the
patient after he has recovered because the toxin that enters the body is unable
to stimulate the formation of antitoxin (because tetanospasmin is very potent
and its toxicity can be very fast, even in minimal concentrations, which is not
in adequate concentrations to stimulate the formation of immunity).
References :
 Harrison, Tetanus in :Principles of Internal Medicine, volume 2, ed.

13th, McGrawHill. Inc, New York, 1994, .577-579.
 Ritarwan K. (2017). Tetanus. Department of Neurology, Faculty of
Medicine, University of North Sumatra / RSU H. Adam Malik
 Mubin H. Practical Guide to Medicine in Diagnosis and Therapy. 2th
edition. Medical Book Publisher: EGC
 Bae C, Bourget D. (2021). Tetanus. NCBI: StatPearls (Internet),
https://www.ncbi.nlm.nih.gov/books/NBK459217/
6. What prevention can be given to the patient ?

Prevention Based on WHO advice, efforts to prevent leptospirosis can
be carried out in three ways, namely in animals as a source of infection,
transmission routes and humans.
In animals as a source of infection, prevention is done by giving
vaccines to animals that have the potential to be infected with leptospirosis. In
addition, the cleanliness of the pet cage also needs to be considered to prevent
leptospirosis in animals.
In the transmission line, prevention that can be done is to cut off the
transmission line. The route of transmission is an environment that can be a
breeding ground for Leptospira bacteria. An environment with poor sanitation
conditions is a risk factor for leptospirosis. Activities that can be done to
prevent leptospirosis are to keep the environment around the place of
residence clean, so that it does not become a rat's nest, including water storage
areas, proper handling of waste so that it does not become a rat's nest.
In humans, prevention can be done by maintaining individual hygiene
after activities in locations that are at risk of exposure to leptospirosis
1) Health education to use personal protective equipment for workers who
work in an environment that is at risk of leptospirosis.
2) Maintain the cleanliness of the pet cage; cleaning the rat nest habitat;
eradication of rodents when conditions permit and the provision of
chlorine or sodium hypochlorite in the reservoir water to be used by the
community.
3) In addition, it is necessary to increase public awareness of the dangers of
this disease, especially for groups of people who have a high risk and also
health service providers.
References :
 Journal of Health Epidemiology and Communicable Disseases, 2019
7. What are the complications that can occur regarding the scenario?
There are several complications of leptospirosis, including acute

kidney failure (95% of cases), acute liver failure (72% of cases), acute
respiratory disorders (38% of cases), acute cardiovascular disorders (33% of
cases), and acute pancreatitis (25% of cases).
Complications that often occur in patients with leptospirosis are:
1. Acute kidney failure

Acute renal failure characterized by oliguria or polyuria can occur 4-10
days after symptoms of leptospirosis appear. The occurrence of acute renal
failure in patients with leptospirosis through 3 mechanisms:
a. Direct invasion/nephrotoxicity of leptospires
Leptospira invasion causes tubular and glomerular damage as a direct
effect of the migration of leptospires that spreads hematogen to the
peritubular capillaries and then to the interstitium, tubules, and tubular
lumen. Tissue damage is not clear whether it is only a migratory effect
or an endotoxin effect of leptospires.
b. Immunological reactions
Immunological reactions take place quickly, the presence of immune
complexes in the circulation and complement deposits and the
presence of electron density bodies in the glomerulus proves the
existence of an immune-complex glomerulonephritis process and
tubulointerstitial nephritis occurs.
c. Non-specific reaction to infection like other infections
→ renal ischemia
Hypovolemia and hypotension as a result of:
 Insufficient fluid intake
 Increased evaporation due to fever
 Release of kinins, histamine, serotonin, prostaglandins, all of
which will cause increased capillary permeability resulting in
albumin and intravascular fluid leakage.
 The release of cytokines due to endothelial damage causes
increased cellular and vascular permeability.
 Hypovolemia and hemoconcentration will stimulate RAA and
cause vasoconstriction.
 Hyperfibrinogenemia due to capillary endothelial damage
(DIC) causes blood viscosity to increase.
Renal ischemia, glomerulonephritis, tubulointerstitial nephritis,

and bacterial invasion cause necrosis → acute renal failure.
2. Acute liver failure

In the liver, there is focal centrilobular necrosis with Kupffer cell
proliferation with cholestasis. The occurrence of jaundice in leptospirosis
is caused by several things, including liver cell damage, impaired kidney
function which will reduce bilirubin excretion thereby increasing blood
bilirubin levels, bleeding in tissues and intravascular hemolysis will
increase bilirubin levels, the proliferation of Kupffer cells resulting in
intrahepatic cholestasis.
3. Respiratory disorders and pulmonary bleeding
The presence of pulmonary involvement is usually characterized by
various symptoms, including cough, dyspnea, and hemoptysis up to Adult
Respiratory Distress Syndrome (ARDS) and Severe Pulmonary
Haemorrhage Syndrome (SPHS). Lungs can bleed where the pathogenesis
is not known with certainty. Pulmonary bleeding occurs presumably due
to direct entry of endotoxin causing capillary damage and bleeding.
Bleeding occurs in the pleura, alveoli, tracheobronchial tree, abnormalities
in the form of pulmonary septal congestion, multifocal alveolar bleeding,
and mononuclear cell infiltration. Histological examination found
congestion in the pulmonary septum, edema and multifocal alveolar
bleeding, and fibrin sedation. Pulmonary bleeding can cause death in
patients with leptospirosis.
4. Cardiovascular Disorders
Cardiovascular complications in leptospirosis can include conduction
system disorders, myocarditis, pericarditis, endocarditis, and coronary
arteritis. Manifestations of this cardiovascular disorder vary from
asymptomatic to severe forms of fatal congestive heart failure. During the
septicemic phase, migration of bacteria, endotoxins, enzyme products, or
antigens occurs due to bacterial lysis, increasing endothelial permeability
and giving early manifestations of vascular disease.
5. Acute Pancreatitis
Acute pancreatitis is a rare complication in patients with severe
leptospirosis. Pancreatitis occurs due to necrosis of pancreatic cells due to
infection with leptospira bacteria (acute necrotizing pancreatitis). In
addition, the occurrence of acute pancreatitis in leptospirosis can be
caused by complications from a failure of other organs (multiple organ
failure), septic shock, and severe anemia (severe anemia).
References :
 Andani, L. (2014). Evaluation of the Use of Leptospirosis Diagnostic
Criteria (Who Searo 2009) in Leptospirosis Patients At Dr. Kariadi
Hospital Semarang. Faculty of Medicine, Diponegoro University.
8. Perspective islam based on scenario

Rasulullah shallallahu ‘alaihi wa sallam mengatakan,
‫ث ْال َح ِدي ِد‬

َ َ‫ َك َما ي ُْذ ِهبُ ْال ِكي ُر خَ ب‬،‫ فَإِنَّهَا تُ ْذ ِهبُ خَ طَايَا بَنِي آ َد َم‬،‫اَل تَ ُسبِّي ْال ُح َّمى‬
“Janganlah Engkau mencela demam. Karena demam itu bisa menghilangkan

kesalahan-kesalahan (dosa) manusia, sebagaimana kiir (alat yang dipakai
pandai besi) bisa menghilangkan karat besi.” (HR. Muslim no. 2575).
Oleh karena itu, tidak boleh bagi seorang mukmin mencaci maki penyakit
yang dideritanya, menggerutu, apalagi sampai berburuk sangka pada Allah
dengan musibah sakit yang dideritanya.
“ Bergembiralah wahai saudaraku, sesungguhnya Rasulullah shallallahu

‘alaihi wa sallam bersabda, “Sakit demam itu menjauhkan setiap orang
mukmin dari api Neraka” (HR. Al Bazzar )

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FACULTY OF MEDICINE Makassar, 12th November 2021

INDONESIAN MUSLIM UNIVERSITY

dr. Nurul Fadilah Ali Polanunu, M.Biomed

Maghfirah Tara Zakiyyah 11020190232

Makassar, 12 November 2021

1. Explain the definition, classification, etiology of fever !

1. Explain the definition, classification, etiology of fever !

The International Union of Physiological Sciences Commission for Thermal

Normal body temperature varies according to the circardian temperature

Table 1. Normal temperature in different places

The classification of fever is as follows:

Fever Pattern Disease

Fever is often caused by infection. Causes of fever other than infection

Basically, to achieve an accurate diagnosis of the cause of fever, it is

 Pratiwi, N. R. R. (2018). Penerapan Kompres Hangat pada Anak

f. Dengue Hemorrhagic Fever (DHF)

 Widoyono. 2011. Textbook of Tropical Diseases: Epidemiology,

EA, Jawetz, Melnick & Adelberg's: Medical Microbiology, 20 edition,

3. Explain the pathomecanism of the main complaint ( fever ) based on the

During fever, arginine vasopressin (AVP), alphamelanocyte-

4. Explain the diagnostic step of the scenario !

So based on the history according to the scenario, it was found

Examination of vital signs obtained BP 100/60 mmHg, pulse

 Vitayani,dkk.2015. Buku Panduan Kerja Clinical Skill Lab

Leptospirosis is a zoonotic disease caused by a spiral-shaped bacterial

Leptospirosis occurs in various parts of the world but generally in

In 2007 there was an increase in cases of Leptospirosis in humans,

Leptospirosis is caused by pathogenic organisms of the genus

The genus Leptospira is divided into two serovarians, namely L.

Various animal species, especially mammals, can act as a source of

2. Domestic animals (cows, pigs, dogs, sheep, goats, horses, buffalo)

3. Fur-producing animals (silver fox) in captivity

4. Reptiles and amphibians may also carry leptospires

According to Widoyono (2008), clinical symptoms of leptospirosis in

a. First Stage (leptospiremia)

1. In the kidneys, renal failure that can cause death

Diagnosis can be made by microscopic examination, as well as by

The most useful and most frequently collected samples are:

1. Blood with heparin for culture in the first 10 days.

b) Supportive therapy and dialysis

Aseptic meningitis is the most common complication, but encephalitis,

Mortality in severe leptospirosis is about 10%, death is most often due

According to Rusmini (2011) in general, the prevention of leptospirosis

1. Familiarize yourself with Clean and Healthy Life Behavior (PHBS)

 Setadi, B., Setiawan, A., Effendi, D. & Hadinegoro, SRS Practical

1) Severe malaria (complications)

Malaria is found in almost all parts of the world, especially in

Malaria is a systemic febrile disease caused by infection with one of 5

1) Plasmodium falciparum malaria

2) Plasmodium vivax malaria

3) Plasmodium malariae malaria

4) Plasmodium ovale malaria

5) Plasmodium knowlesi malaria

a. Sickle cell trait (hemoglobin S heterozygous)

The most common early symptoms

Additional symptoms associated with severe malaria

Cerebral symptoms (cerebral malaria)

Symptoms suggestive of pulmonary edema and shock

Symptoms can progress rapidly from mild to severe in disease caused by

 Determine geographic area of exposure and history of previous

Increased blood pressure with decreased heart rate and/or papilledema

Examination of thick and thin blood preparations (SD) is the gold