PBL GROUP REPORT

"FEVER MODULE"
TROPICAL INFECTION BLOCK

Tutor : dr. Dzul Ikram

ARRANGED BY:
Group 14

Eka Dewi Mulyani 11020160003

M. Arif Munandar K 11020160030
Zulfikar Anand Pratama 11020160034
Suci Ramadhani 11020160083
Muh. Agung Gunadi 11020160096
Ratu Sri Bestari 11020160104
Rahmawaty Kurnia Putri 11020160111
Gita Ananda Pratiwi 11020160117
Hartina Burhan 11020160155
Firmawati AR 11020160171

MEDICAL FACULTY
UNIVERSITAS MUSLIM INDONESIA
MAKASSAR
2018
A. SCENARIO
A 6 years old famale came to the public health centre with a chief complaint of
fever lasting for 2 days ago followed by pain during swallowing, shortness of
breath and enlarged in the right neck. The patient felt weak and inert. Weight : 19
kg, height : 120 cm.

B. CLARIFICATION OF KEYWORDS
Keywords
1. A 6 years old female
2. Fever lasting for 2 days ago
3. Pain during swalllowing, shortness of breath and larged in the right neck
4. Weak and inert
5. Weight : 19 kg, height : 120 cm.

C. IDENTIFICATION OF PROBLEMS
Question
1. What is the definition and classification of fever ?
2. Explain the pathomechanism of fever, fatigue and inert !
3. Explain the pathomechanism of shortness of breath and pain during
swallowing !
4. Explain the pathomechanism of enlarged in the right neck !
5. Explain the kinds of tropical diseases with complains of fever !
6. How to diagnose based on scenario ?
7. How is the first management of the case in the scenario ?
8. Mention the differential diagnosis according to the scenario!
9. Islamic perspective according to the scenario!
D. ANSWER QUESTION
1. What is the definition and classification of fever ?
Answer :
Definition
The International Union of Physiological Sciences for Thermal
Physiology defines febrile as a state of increased core temperature, which is
often (but not supposed to) be part of the defense response of multicellular
(host) organisms against invasion of microorganisms or inanimate objects
that are pathogenic or considered alien by hosts . El-Rahdi and friends define
fever (pireksia) in terms of pathophysiological and clinical aspects.
Pathophysiologically, fever is an increase in thermoregulatory set point from
the hypothalamic center mediated by interleukin 1 (IL-1). While clinically a
fever is an increase in body temperature of 1 ° C or greater above the average
normal temperature at the place of recording. In response to changes in the set
point, an active process occurs to reach the new set point. This is achieved
physiologically by minimizing heat release and producing heat. Normal body
temperature varies according to the rhythm of the circardian temperature
(diurnal variation). The lowest temperature is reached in the morning at 04.00
- 06.00 and the highest at the beginning of the night at 16.00 - 18.00. The
fever curve usually follows this diurnal pattern. Body temperature is also
influenced by individual factors and the environment, including age, sex,
physical activity and ambient air temperature. Therefore it is clear that there
is no single value for normal body temperature. The results of measurements
of body temperature vary depending on the place of measurement (Table 1) .
Table 1. Normal temperature at different places
Normal
Measuring Fever
Type thermometer temperature
Place (oC)
average(oC)
Axillary Mercury, elektronics 34,7 – 37,3; 36,4 37,4
Sublingual Mercury, elektronics 35,5 – 37,5; 36,6 37,6
Rectal Mercury, elektroncs 36,6 – 37,9; 37 38
Ear Infrared Emission 35,7 – 37,5; 36,6 37,6
 Normal rectal temperature of 0.27o - 0.38oC (0.5o - 0.7oF) is higher than
oral temperature. The axillary temperature is approximately 0.55 oC (1oF)
lower than the oral temperature.5 For practical clinical purposes, the patient is
considered fever if the rectal temperature reaches 38oC, oral temperature
37.6oC, axillary temperature 37.4oC, or tympani membrane temperature
reaches 37, 6oC.1 Hyperpirexia is a term in fever used when the body
temperature exceeds 41.1oC (106oF) .
FEVER PATTERN
Thus changing patterns, or serial temperature measurements carried out
in different places. However, if the pattern of fever is recognizable, although
not pathognomonic for certain infections, this information can be a useful
diagnostic guide (Table 2) .1 The interpretation of a fever pattern is difficult
for various reasons, including children who have received antipyretics
Table 2. Fever patterns found in pediatric disease
Pattern of fever Disease
Continuation Typhoid fever, malignant falciparum malaria
Remitten Most viral and bacterial diseases
Intermittent Malaria, lymphoma, endocarditis
Hecticor septic Kawasaki Disease, pyogenic infection
Quotidian Malaria because of P.vivax
Double quotidian Kala azar, gonococcal arthritis, juvenile rheumathoid
arthritis, multiple drug fever (example carbamazepine)
Relapsing atau periodic Tertiana or quaternary Malaria, brucellosis
Fever recurrent Familial Mediterranean fever

Assessment of fever patterns includes the type of onset (slowly or

sudden), variation in degree of temperature over a 24-hour period and during
episodes of pain, fever cycle, and therapeutic response. An overview of the
classic fever pattern includes:
Continuous fever
Continuous fever (Figure 1.) or a sustained fever is characterized by an
increase in body temperature that persists with a maximum fluctuation of
0.4oC over a 24-hour period. Diurnal fluctuations in normal temperature
usually do not occur or are not significant.
Remiten Fever
Remittent fever is characterized by a decrease in temperature every day
but does not reach normal with fluctuations exceeding 0.5 ° C per 24 hours.
This pattern is the type of fever that is most often found in pediatric practice
and is not specific to certain diseases . Diurnal variations usually occur,
especially if fever is caused by an infection process.
Intermittent fever
In intermittent fever the temperature returns to normal every day,
generally in the morning, and peak during the day (Figure 3.). This pattern is
the second most common type of fever found in clinical practice.
Septic / Hectonic Fever
Septic or haemorrhagic fever occurs when remittent or intermittent
fever shows a difference between a peak and a very low temperature point.
Quotidian fever
The quotidian fever, caused by P. Vivax, is characterized by fever
paroxism that occurs every day.
Double Quotidian Fever
Double quotidian fever (Figure 4.) has two peaks in 12 hours (12 hour
cycle).
Undulant Fever
Undulant fever describes a slow and steady increase in temperature for
several days, then slowly drops to normal. Prolonged Fever Prolonged fever
describes a disease with a long fever that exceeds what is expected for the
disease, for example more than 10 days for upper respiratory tract infection.
Recurrent Fever
Recurrent fever is a fever that recurs with irregular intervals in a disease
involving the same organ (for example the urinary tract) or multiple organ
systems.
Biphasic fever
Biphasic fever shows one disease with two different episodes of fever
(camelback fever pattern, or saddleback fever). Poliomyelitis is a classic
example of this pattern of fever. Biphasic features are also typical for
leptospirosis, dengue fever, yellow fever, Colorado tick fever, spirillary rat-
bite fever (Spirillum minus), and African hemorrhagic fever (Marburg, Ebola,
and Lassa fever).
Relapsing Fever and Periodic Fever
 Periodic fever
Periodic fever is characterized by episodes of recurrent fever at
regular or irregular intervals. Each episode is followed by one to several
days, several weeks or several months of normal temperature. An example
that can be seen is malaria (the term tertiana is used if fever occurs every
3rd day, quartana if fever occurs every 4th day) (Figure 5.) and
brucellosis.
 Relapsing Fever
Relapsing fever is a term commonly used for recurrent fever caused
by a number of Borrelia species (Figure 6.) and is infectious (louse-borne
RF) or tick (tick-borne RF). This disease is characterized by sudden high
fever, which recurs suddenly takes place for 3-6 days, followed by a free
period of fever with almost the same duration. The maximum temperature
can reach 40.6 °C in tick-borne fever and 39.5 oC in louse-borne fever.
The accompanying symptoms include myalgia, headache, abdominal pain,
and changes in consciousness. Resolution of each fever episode can be
accompanied by Jarish-Herxheimer reaction (JHR) for several hours (6-8
hours), which generally follows antibiotic treatment. This reaction is
caused by the release of endotoxins when the organism is destroyed by
 antibiotics. JHR is very often found after treating syphilis patients. This
reaction is less common in cases of leptospirosis, Lyme disease, and
brucellosis. Symptoms vary from mild and fatigue fever to full-blown
anaphylactic reactions. Another example is rat-bite fever caused by minus
Spirillum and Streptobacillusmoniliformis. History of rat bite 1 - 10 weeks
before the onset of symptoms is a diagnostic indication. Pel-Ebstein fever ,
described by Pel and Ebstein in 1887, was originally thought to be typical
of Hodgkin's lymphoma (LH). Only a few patients with Hodgkin's disease
experience this pattern, but if present, it is suggestive for LH. The pattern
consists of recurrent episodes of fever lasting 3 - 10 days, followed by an
afebrile period of similar duration. The cause of this type of fever
may be associated with tissue destruction or associated with hemolytic
anemia.

FEVER CLASSIFICATION
Fever classification is needed in carrying out a problem-based
approach. For diagnostic purposes, fever can be distinguished from acute,
subacute, or chronic, and with or without localizing signs. Table 3.Shows
three main groups of fever found in pediatric practice along with the
definition of the term used
Table 3. The three main groups of fever found in pediatric practice
Long fever in
Classification Common causes
general
Upper respiratory tract
Fever with localizing signs <1 week
infection
Viral infections, urinary tract
Fever without localizing <1 week
infections
Infection, juvenile idiopathic
Fever of unknown origin >1 week
arthritis

Fever with Localizing Signs

Fever that is most often found in pediatric practices falls into this
category. Fever usually shortens, either because it subsides spontaneously or
 because of specific treatments such as giving antibiotics. Diagnosis can be
made through history taking and physical examination and confirmed by a
simple examination such as chest x-ray examination
Fever without Localizing Signs
About 20% of all fever episodes show no localizing signs when they
occur. The most common cause is viral infection, especially during the first
few years of life. Such infections should be considered only after removing
urinary tract infections and bacteremia. Shows the most frequent causes of
this group.1 Fever without localizing signs generally has acute onset, lasts
less than 1 week, and is a diagnostic dilemma that is often faced by
pediatricians in treating children less than 36 months.

2. Explain the pathomechanism of fever, fatigue and inert !

Answer :
a. Fever
Fever occurs due to the release of pyrogen in the body. Pyrogen
substances themselves can be divided into two, namely exogenous and
endogenous. Exogenous pyrogens are pyrogens originating from outside
the body such as microorganisms and toxins. While endogenous
pyrogens are pyrogens originating in the body including interleukin-1
(IL-1), interleukin-6 (IL-6), and tumor necrosing factor-alpha (TNF-A).
The main sources of endogenous pyrogens are monocytes, lymphocytes
and neutrophils. All of the above substances cause mononuclear
phagocytic cells (monocytes, tissue macrophages or copper cells) to
make 10 cytokines that act as endogenous pyrogens, a small protein
similar to interleukin, which is a mediator important inter-cell immune
processes. These cytokines are produced systemically or locally and
successfully enter the circulation. Interleukin-1, interleukin-6, tumor
necrosis factor α and interferon α, interferon β and interferon γ are
cytokines that play a role in the process of fever. These cytokines are also
produced by cells in the Central Nervous System (CNS) and then work in
the preoptic area of the anterior hypothalamus. Cytokines will trigger the
release of arachidonic acid from the phospholipid membrane with the
help of phospholipase A2 enzyme. Arachidonic acid is then converted to
prostaglandin because of the role of the cyclooxygenase enzyme (COX,
also called PGH synthase) and causes fever at the level of the
thermoregulation center in the hypothalamus. The cyclooxygenase
enzyme is in two forms (isoforms), namely cyclooxygenase-1 (COX-1)
and cyclooxygenase-2 (COX-2). Both isoforms have different
distributions on the network and also have different regulatory functions.
COX-1 is a constitutive enzyme that catalyzes the formation of
regulatory prostanoids in various tissues, especially in the membranes of
the gastrointestinal, renal, platelet and vascular epithelial tracts. While
COX-2 is not constitutive but can be induced, among others, if there are
inflammatory stimuli, mitogenesis or oncogenesis. After these stimuli,
prostanoids are formed which are pain and inflammation mediators. This
finding leads to, 11 that COX-1 catalyzes the formation of prostaglandins
responsible for carrying out physiological regulatory functions, whereas
COX-2 catalyzes the formation of the causing prostaglandin.
Frostaglandin E2 (PGE2) is one type of prostaglandin that causes fever.
The anterior hypothalamus contains many thermosensitive neurons. This
area is also rich in serotonin and norepineprin which acts as an
intermediary for fever, endogenous pyrogens increase the concentration
of these mediators. Furthermore, these two monoamines will increase
cyclic adenosine monophosphate (cAMP) and prostaglandin in the
central nervous system so that the temperature of the thermostat increases
and the body becomes hot to adjust to the temperature of the thermostat.
 Buku Ajar IlmuPenyakitDalam.Jilid I. Edisi 6. 2014.Interna Publishing.

b. Weak and Jaded

Anemia is caused by decreased hemoglobin levels in erythrocytes.
Decreased hemoglobin levels are caused by many things, for example,
severe bleeding, deficiency of nutrients (iron, folic acid & vitamin B12),
production of blood cells in the declining bone marrow, destruction
premature blood cells with large amounts, and so on. With the above
causes, the hemoglobin level in our body drops from its normal level.
Hemoglobin is a carrier of oxygen for all body tissues, with hemoglobin
levels falling, oxygen levels drop indirectly. The decreased oxygen level
causes, cell metabolism to decrease, with the decrease in cell metabolism,
the energy produced is also small, so that the person will be easily weak
because of lack of energy. When aerobic metabolic processes are not
optimal, anaerobic metabolism takes place. On anaerobic metabolism, the
energy produced is small and produces lactic acid which causes muscle
fatigue.
 Reduced hemoglobin will cause decreased levels of oxygen in the
blood because the function of hemoglobin is to bind oxygen in the blood.
This will cause a decrease in tissue oxygenation. To adjust this condition
the body will vasoconstrict blood vessels to maximize oxygen delivery to
vital organs. For pale conditions like this will cause pallor.

3. Explain the pathomechanism of shortness of breath and pain during

swallowing !
Answer :
At first, bacteria enter the body through the upper respiratory tract, but
can also enter through the skin, genital tract or eyes. Sensitivity to respiratory
epithelial cells can be greatly reduced by blocking the production of two
small piles or by using antibodies directed at them.
Microorganisms enter through the nose, then develop in upper airway
mucosal epithelial cells, especially in the tonsils, sometimes found in the skin
and conjunctiva or genitalia. This basil then produces exotoxins, which are
released by the endosome, causing a local inflammatory reaction, then tissue
damage and necrosis occur. Toxins consist of two forming protein fragments.
Fargmen B bind to receptors on the surface of vulnerable host cells and their
proteoliic properties cut off the membrane lipid layer, thus helping fragment
A enter into the host cell. Furthermore there will be inflammation and
destruction of epithelial cells which will be followed by necrosis. In the area
 of necrosis, fibin is formed, which is then infiltrated by white blood cells,
resulting in patchy exudates which can be peeled off.
In more advanced conditions the toxin will be produced more so that the
area of cirrhosis becomes wider and deeper so that necrotic tissue is formed,
fibrin, epithelial cells, leukocyte cells, erythrocyte cells that are gray to black.
This membrane is difficult to peel, if forced to cause bleeding. Furthermore,
the membrane will spread to the bronchial, causing respiratory tract
obstruction and dyspnoea.

4. Explain the pathomechanism of enlarged in the right neck !

Answer :
The combination of cervical lymphadenopathy and neck mucosal edema
raises a "bull neck" appearance for many infected patients. For this reason,
the mechanism of lymphadenopathy and mucosal edema are as follows :
a. Lymphadenopathy
The lymphatic system is the center of effective functioning of the
immune system. Macrophages and other antigen-presenting cells migrate
to the lymph nodes to present antigens found to T and B cells. When T and
B cells recognize antigens, they proliferate in the lymph nodes to produce
an effective immune response. Lymphadenopathy (local / systemic) is a
consequence of this proliferation.
When direct invasion occurs, solitary lymph nodes become infected
with bacteria or other types of antigens. The effects of this immune
response are lymph node structure hyperplasia, T and B cell proliferation,
and other immune cell infiltrations to overcome infection. These things
cause inflammation and swelling of the lymph nodes.
In the event of a systemic infection, reactive hyperplasia can occur.
An antigen (intracellular or extracellular) stimulus is carried to the lymph
nodes and presented to T and B cells, lymphocytes, and other cells in the
lymph nodes, causing their proliferation.
b. Edema mucosa cervical
major vascular changes in the inflammatory process is the increase of
blood flow caused by the dilation of blood vessels and increased vascular
permeability, both of these are designed to bring a virgin cell and protein
to the site of infection. In the early stages, harmful stimuli such as
microbes are faced by macrophages and other cells in the connective
tissue, then a vascular reaction is triggered triggered by this interaction and
will dominate the initial phase.
i. Changes in vascular cavity and blood flow
● After brief vasoconstriction (lasting only a few seconds) arteriolar
vasodilation occurs, which results in an increase in local blood flow
so that at the end of the capillary area is full of blood. This vascular
expansion will cause erythema and heat, which is a typical sign of
acute inflammation.
● Small blood vessels become more permeable, and protein-rich fluids
will flow out into extravascular tissue. This results in an increase in
the concentration of red blood cells in the blood flowing, thereby
increasing blood viscosity and slowing blood flow. This is called
stasis.
● After the onset of stasis, leukocytes (especially neutrophils) begin to
cluster on the vascular surface of the vascular endothelium
(margination), which is the first step in leukocyte release into the
interstitial tissue through the vascular endothelium.
ii. Increased vascular permeability
Increased permeability results in a flow of protein-rich fluids and
blood cells to extravascular tissue, resulting in increased osmotic
pressure of interstitial fluid and causing more water to flow out of the
blood into the tissues. The result of this protein-rich fluid accumulation
is called exudate. Accumulation of extravascular fluid causes tissue
edema.
 Contraction of endothelial cells causes the formation of interstices
between cells in small blood vessels is the most common cause of
increased vascular permeability. Endothelial cell contractions occur
immediately after binding with histamine, bradykinin, leukotrienes, and
many other mediators for specific receptors.

5. Explain the kinds of tropical diseases with complains of fever !

Answer :
a. Dengue hemorrhagic fever
Dengue / DF fever and dengue haemorrhagic fever / DHF are
infectious diseases caused by dengue virus with manifestations of fever,
muscle aches and / joint pain accompanied by leukopenia, rash,
lymphadenopathy, thromboitopenia and hemorrhagic diathesis.
Etiology
Dengue hemorrhagic fever is caused by the dengue virus, which
belongs to the genus flavivirus, family of flaviviridae. The flavivirus is a
30 nm diameter virus consisting of a single chain ribonucleic acid with a
molecular weight of 4x106
There are 4 viral serotypes, namely DEN-1, DEN-2, DEN-3, and
DEN-4, all of which can cause dengue fever or dengue hemorrhagic fever.
The four serotypes found with DEN-3 are the most serotypes. There is a
cross reaction between dengue dengue serotype and other flaviviruses such
as yellow fever, Japanese encehphalitis and west nile virus.
In the laboratory dengue virus can replicate in mammals such as rats,
rabbits, dogs, bats and primates. The epidemiology survey in livestock has
antibodies to dengue virus in horses, cattle and pigs. Research on
arthropods shows that dengue virus can replicate in the mosquitoes of the
genes aedes (stegome) and toxorhynchites.
Clinical features
The clinical manifestations of dengue virus infection can be
symptomatic, or it can be an unusual fever, dengue fever, dengue
 hemorrhagic fever or a syndrome of dengue shock (SSD).
In general, patients experience a fever phase for 2-7 days, followed by a
critical phase for 2-3 days. During this phase the patient has no fever, but
has the risk of shock if he does not receive adequate treatment.
b. Malaria
Malaria is a parasitic infectious disease caused by plasmodium which
attacks erythrocytes and is characterized by the discovery of asexual forms
in the blood. Malaria infection presents with symptoms such as fever,
chills, anemia and splenomegaly. Can occur without complications or
experience systemic complications known as severe malaria. A type of
parasitic infection that resembles malaria is a pigose infection that causes
porkosis.
Etiology
The cause of malaria infection is plasmodium, which in addition to
infecting humans also infects animals such as birds, reptiles and humans.
Including the plasmodium genus from the family plasmodidae.
Plasmodium in humans infects erythrocytes and undergoes asexual culture
in liver tissue and erythrocytes. Asexual breeding occurs in the body of the
mosquito, the female anophles. Overall there are more than 100
plasmodium which infects animals (82 in birds and reptiles and 22 in
primates).
Clinical symptoms
The clinical manifestation of malaria depends on the immune
immunity of the patient's immunity, the high transmission of malaria
infection. The severity of the infection is influenced by the type of
plasmodium (p. Falciparum often provides complications), the area of
origin of infection (pattern of resistance to treatment), age (old age and
baby is often heavier) there are allegations of genetic constitution, health
and nutrition, comoprofilactics and treatment previous.
c. Yellow fever
 Yellow fever is an acute infectious disease caused by the yellow fever
virus, the word "yellow" is taken from some of the conditions of patients
who become jaundiced. This disease was first known when an outbreak
occurred in 1648 in an area called the new world.
The yellow virus is believed to have originated from Africa and spread to
the new world via merchant ships transporting slaves. The vector of this
disease is the aedes aegypti mosquito.
Etiology
Yellow viruses include the flavivirus genus, family of flaviviridae.
This virus is a single strand RNA virus and positive sense. Virion is
spherical in shape and has envelopes, measuring between 35-45 nm, and
the genome consists of 10,862 nucleotides. This two layer lipid (lipid
bilayer envelope) wrapper contains matrix protein (M) and wrapping
protein (E). It also has three structures C, M, and E as well as several NS
non-structural proteins.
This virus can be inactivated with chloroform, ether and ultraviolet
light while at a temperature of 40C it lasts one month in dry conditions it
can last for years. There are differences in genotypes between isolates
obtained from Africa and South America. There are two genotypes
circulating in Africa and one or two in South America.
Clinical features
Classic yellow fever is a biphasic disease with 3 stages, namely
infection, remission and intoxination. The clinical picture can be
subclinical infection, influenza-like infection or in 15-25% of cases
fulminant can occur and cause death within a few days.
After an incubation period of 3-6 days a sudden onset of fever and chills
are followed by headache, back pain, myalgia, nausea, and vomiting. You
can also see red faces and red conyungtiva with relative phaget and
bradycardia.
After 3-4 days, symptoms of fever disappear for several hours to one
or two days and only recur in patients who develop fulminant intoxination.
 Type of fever is biphasic. The first fever phase is associated with the acute
phase of the disease and is accompanied by relative bradycardia.
Furthermore, the fever decreases associated with the remission phase and
increases again and the aggravating phase in the intoxination phase.
The disease develops into multisystem dengue fever characterized by the
body becoming yellow, renal dysfunction and bleeding manifestas can
cause hypotension and even fatal shock. Mucosal bleeding, bleeding in
syringe scars, gastrointestinal bleeding can be severe as a result of
synthesis of clotting factors by decreased liver cells, platelet dysfunction
and disseminated intravascular coagulation (KID)
d. Avian influenza
Avian influenza is an infectious disease caused by the usual influenza
type A virus regarding poultry. Influenza viruses themselves include
poultry. Influenza viruses themselves are included in the family of
orthomyxoviruses which consists of 3 types, namely A, B, and C.
Influenza types B and C can cause disease in humans with symptoms that
are mild and not fatal so it is not too a problem. Influenza type A viruses
are divided into many subtypes based on markers in the form of protein
protrusions on the surface of viral cells. There are 2 proteins that mark
influenza A viruses, namely the hemagglutinin protein represented by H
and the neuraminidase protein represented by N. There are 15 kinds of
proins H, H1-H15. While N consists of 9 types. N1-N9. The combination
of these two proteins can produce many variants of the subtype of
influenza type A virus
All subtypes of influenza A virus can infect birds that are natural
hosts, so that influenza type A is also called bird influenza or avian
influenza. On the other hand not all influenza type A virus subtypes attack
humans. Typical subtypes also found in humans are from groups H1, H2,
H3 and N1 and N2 and are referred to as human influenza. The cause of
this influenza avian influenza or avian influenza is the H5N1 subtype
influenza A virus which is briefly called H5N1. Henceforth the intended
 avian influenza virus is this A (H5N1) virus. This avian influenza virus is
classified as a highly pathogenic avian influenza (HPAI).

Clinical manifestations
The incubation period for avian influenza is very short, which is 3
days, with a range of 2-4. The general manifestations of influenza clinics
are similar to ILI (influenza like illness), which are coughs, colds, fever.
Fever is usually quite high at> 38C. Other symptoms include cephalgia,
sore throat, myalgia and malaise. Gastrointestinal complaints include
diarrhea and other complaints in the form of conjunctivitis. Chest X-ray
abnormalities can be bilateral infiltrates with diffuse, multilocal, or diffuse
infiltrates. Or in the form of lobar collapse.
e. Severe acute respiratory syndrome (SARS)
Severe acure respiratory syndrome (SARS) is a respiratory tract
infection caused by a corona virus with a severe set of clinical symptoms.
Sars has the potential to spread very quickly, which has big implications
for health workers
Etiology
causes of sars in the form of infections that have been successfully
identified in the form of viral infections belonging to the genus
Coronavirus (CoV). Usually not stable in the environment. But this virus
can last for days at room temperature. This virus is also able to maintain its
viability well if it is still inside the stool.
The coronavirus genus comes from Order nodovirales, a group of
viruses that have capsule sheaths and a single chain RNA genome, based
on genetic studies and antigenicity, CoV is divided into 3 major groups
namely 1) group 1 human CoV 229E and porcine transsmissible viral
gastroenteritis. 2) group 2, human CoV OC34, bonive corona virus, viral
viral mice. 3) group 3, infectious bronchitis virus
Clinical manifestations
 SARS has an incubation period of 1-14 days with an average time of
around 4 days. Symptoms of predromal SARS begin with symptoms of
non-specific systemic infections such as fever, myalgia, chills and feeling
you are stiff in the body, non-productive cough, headache and dizziness.
With fever with a body temperature> 38 C included in the definition of the
initial case definition. Nevertheless not all SARS patients show symptoms
of fever. For example in elderly patients, fever may be a symptom that is
not prominent. Rigid and stiff in the body. High fever that goes up and
down is often associated with a feeling of shivering and stiffness in the
body. In addition, patients also often feel very well accompanied by
muscle aches that are felt throughout the body. In some cases, the fever
disappears on days 4-7, but this does not indicate an improvement in the
symptoms. Re-increase body temperature and worsen symptoms of the
disease often appear in second week.
f. Typhoid fever
Typhoid fever is still an endemic disease in Indonesia. This disease is
an infectious disease listed in Law No. 1962 concerning the outbreak. This
group of infectious diseases is a disease that is easily transmitted and can
attack many people so that it can cause an outbreak.
Clinical features
The period of shoot typhoid fever lasts between 10-14 days. In the
first week the clinical symptoms of this disease were found to have
complaints and symptoms similar to those of acute infectious diseases in
general, namely fever, headache, dizziness, nausea, vomiting, diarrhea,
unpleasant stomach, cough and epistaxis. The nature of the fever increases
slowly, especially in the afternoon to night, bradycardia, webbed tongue
(dirty in the middle, edge and end are red).
g. Leptospirosis
Leptospirosis is a zoonotic disease caused by micro organism
leptospia interograns regardless of the specific form of serotypes. This
disease is known by various names such as mud fever, slime fever, swamp
 fever, autumnal fever, infectious jaundice, field fever, cane fever etc.
Leptospirosis often escapes diagnosis because clinical symptoms are not
specific, and diagnostic confirmation is difficult without laboratory testing.
Etiology
Leptospirosis is caused by the genus leptospira, family
treponematacceae, a sphirochaeta microorganism. The characteristics of
this organism are convoluted, thin, flexible with a length of 5-14 um with a
very fine spiral, a width of 0.1-0.2 um. In simple terms the genus
Leptospira consists of two species: L interrogans that are pathogenic and L
biflexa which is non-pathogenic / saprophytic.
Clinical features
Often: fever, chills, meningismus, anorexia, myalgia, konyungtiva,
nausea vomiting, abdominal pain, jaundice, skin rash.
Rarely: pneumonitis, hemaptoe, delirium, bleeding, diarrhea, edema,
atralgia, kidney failure, ascites, myocarditis.
h. HIV / AIDS
AIDS can be interpreted as a collection or symptom of a disease
caused by a decrease in immunity due to the HIV virus which belongs to
the retroviridae family. AIDS is the final stage of HIV infection.
Epidemiology
Transmission of HIV / AIDS occurs due to body fluids containing the
HIV virus, namely through sexual relations, both homosexual, and
heterosexual, syringes in the use of narcotics, transfusion of blood
components and from HIV-infected mothers to babies born. Therefore
high risk groups for HIV / AIDS, for example the use of narcotics,
commercial sex workers and their customers and prisoners.
Clinical symptoms
Symptoms that occur are fever, painful swallowing, swollen lymph
nodes, rashes, diarrhea, or coughing.
i. Rabies
 Rabies is an acute infectious disease of the central nervous system in
humans and mammals which is fatal. This disease is caused by the rabies
virus which belongs to the genus Lyssa-virus, family of Rhabdoviridae and
infects humans through infected secretions in animal bites.

Etiology
The rabia virus is a prototype of the genus Lyssa-virus from the family
Rhabdoviridae. From the genus Lyssa-virus there are 11 types of viruses
that are antigenically similar to the rabies virus and those that infect
humans are the rabies virus, duvenhagemokola and europian bat lyssa-
virus. The rabies virus belongs to the RNA group. The bullet-shaped virus
is 180 x 75 nm in size. The viral envelope consists of lipids, matrix
proteins and glocoprotein. Inactive rabies virus in heating, at 56 C the half-
life is less than 1 minute and in humid conditions 37C can last several
hours. The virus will also die with detergent, soap, 45% ethanol, a iodine
solution. The rabies virus has 6 genotypes, rabies genotype 1, mokola
genotype 3, duvenhage genotype 4, and european bat lyssa virus genotype
5&6
Clinical symptoms
Pain in bite wounds, fever, malaise, anorexia, nausea, vomiting,
headache, lethargy, anxiety, depression
j. Diphtheria
Diphtheria is an acute infectious disease that occurs locally in the
respiratory mucosa or skin caused by gram-positive bacilli, which is
followed by common symptoms caused by exotoxins produced by this
bacillus.
Etiology
The cause of diphtheria is corynebacterium dyptheriae. Also called
klebs-loeffler. This includes gram-positive basil, pleomorphic, arranged in
pairs, immovable, does not form spores, aerobics and can produce
exotoxins.
 Clinical symptoms
Not high fever, sore throat, feeling bad, nausea, vomiting, lethargy,
headache, rhinorea, blood-mixed mucus

6. How to diagnose based on scenario ?

Answer :
History
 Identity; name, address, date of birth, age, gender, ethnicity, race, country
of birth.
 Main complaint; onset, duration, location of infection, symptoms, signs.
 Complaining complaints
 Traveling history; history of contact with immigrants or travelers, a period
of 6 weeks before the on set or date of complaint.
 Exposure history; history of contact with possible cases.
 Family history
 History of treatment to a dentist or other doctor
 Medication history
 History of vaccination; date and type of vaccination, number of diphtheria
toxoid doses obtained, name of vaccine manufacturer. If not vaccinated,
ask the reason.
Physical Examination
 Inspection
 Palpasi
 Auscultation
 vital signs
Diphteriae Supportive Examination
a. Early rapid diagnosis can be made with Gram staining where rod-shaped
bacteria, Gram +, are not encapsulated, clustered, and do not move.
b. Bacterial culture, through the media of Tellurite or Loeffler, with
samples taken from pseudomembranes in the oropharynx of the nose,
cryptoid tonsils, or ulcerations, in the oral cavity. If possible, the swab is
taken from the bottom of the pseudomembrane, or a little
pseudomembrane must be removed. A sterilecotton-tipped applicatoris
used to wipe the tonsils of the pharynx. In the Loeffler medium, C.
diphteriae grows rapidly to form small, granular colonies, black in color
and circled in brown gray.
c. Examination of toxin production, by :
 Elekimmunodiffusion test. Bacterial toxin production can be detected
in 18-48 hours with the formation of precipitin band toxin-antitoxin in
order
 Polymerase Chain Reaction Test (PCR), to detect generegulation in
the production of toxins (dtxR) and diphtheria toxin (tox) genes.
 Rapid Enzyme Immunoassay (Rapid EIA)
 Shick test. Diphtheriatoxin in small amounts is injected intradermally.
After 48 and 96 hours, a reading is carried out. Non specific skin
reactions generally peak after 48 hours. At 96 hours, anery thematous
reaction with some necrosis that can occurindicates that there is
enough anti toxic immunity to neutralize the toxin.
d. Serological tests. Calculation of patient's antibody serum can help the
possibility of a diagnosis of diphtheria. If the antibody level is <0.01 IU /
ml, immunity may not be present. Butif > 0.01 IU / ml is considered
protective and diphtheria is not a patient's disease. Diphtheria antibody
levels between 0.01 IU / ml to 0.09 IU / ml indicate the presence of
immunity.
e. Complete Blood Test and Urinalysis. In patients with diphtheria, there is
usually an increase in leukocytes and proteinuria (1+ to 2+). Leukopenia
can be caused by the presence of sepsis from other infections.
f. Electrocardiography, to detect complications in the form of myocarditis.
7. How is the first management of the case in the scenario ?
Answer :
1) By using broad spectrum antibiotics, antipyretics, and mouthwash
containing disinfectants.
2) Isolation of Patients
Diphtheria sufferers must be isolated and can only be discharged after the
examination of the preparation immediately shows that there is no longer
Corynebacterium diphtheriae.
3) Immunization
Prevention is done by giving DPT immunization (diphtheria, pertussis,
and tetanus) to infants, and DT vaccine (diphtheria, tetanus) to children
of primary school age.
4) Search and then treat the career of diphtheria
Done with the Schick test, that is, if the test results are negative (maybe a
career patient has received immunization), then the throat must be
removed. If it turns out that Corynebacterium diphtheriae is found, the
patient must be treated and if necessary tonsillectomy.
5) Treatment
The goal of treating diphtheria sufferers is to inactivate toxins that have
not been bound as soon as possible, prevent and attempt to minimize
complications, eliminate C. diptheriae to prevent transmission and treat
diphtheria complication and complication.
 General Treatment
Patients were isolated until the acute period was exceeded and the
culture of the smear was negative 2 times in a row. In general, patients
remain isolated for 2-3 weeks. Rest bed rest for approximately 2-3
weeks, giving fluids and adequate diet. Especially for laryngeal
diphtheria, it is maintained that the breath remains free and is
maintained by humidity using a humidifier.
 Special Medicine
Antitoxin: Anti Diptheria Serum (ADS)
 Antitoxin must be given immediately after a diagnosis of diphtheria is
made. By giving antitoxin on the first day, the mortality rate in
patients is less than 1%. But with a delay of more than 6 days, this
death rate can increase to 30%. Before ADS administration, a skin test
or eye test must be done first.
Antibiotics
Antibiotics are given not as a substitute for antitoxin, but to kill
bacteria and stop the production of toxins. Treatment for diphtheria is
used chromromycin, penicillin, aqueous pensilin G crystals, or
procaine penicillin.
Corticosteroids
Corticosteroid administration is recommended in symptomatic
diphtheria cases.
 Treatment of complications
Treatment is primarily intended to keep hemodynamics good.
Complications caused by toxins are generally reversible. If there is
anxiety, irritability and progressive respiratory problems are indicative
of tracheostomy.
 Treatment Contact
Children who are in contact with patients should be isolated until the
following actions are carried out, namely nose and throat culture and
clinical symptoms are followed every day until the shoot period is
exceeded, serological examination and daily observation. Children
who have received basic immunization are given booster diphtheria
toxoid.
 Career treatment
Careers are those who show no complaints, have a negative Schick
test but contain diphtheria bacilli in the nasopharynx. Treatment that
can be given is penicillin 100 mg / kg / day oral / injection, or
erythromycin 40 mg / kg / day for one week. Tonsillectomy /
adenoidectomy may be needed.
a. Management of acute tonsillitis
 Antibiotics for penicillin or sulfanamid for 5 days and mouthwash or
suction drugs with disinfectants, if allergic to erythromycin or
clindomycin
 Adequate antibiotics to prevent secondary infections, corticosteroids
to reduce edema of the larynx and symptomatic drugs.
 Patients are isolated due to infectious, bed rest, to avoid complications
of the bag for 2-3 weeks or until the results of the throat stroke are 3x
negative.
 Giving antipyretics.
b. Management of chronic tonsillitis
 Local therapy for oral hygiene with mouthwash / suction.
 Radical therapy with tonsillectomy if medical therapy or conservative
therapy is unsuccessful.

The American Academy of Otolaryngology - Head and Neck Surgery in

Clinical Indicate Compendium in 1995 sets out indications for
tonsillectomy, namely:
 Attack on tonsillitis more than three times per year despite getting
adequate therapy
 Tonsil hypertrophy that causes tooth malocclusion and causes disruption
of orofacial growth
 Airway obstruction in the form of tonsillar hypertrophy with airway
obstruction, sleep apnea, swallowing disorders, and speech disorders.
 Chronic rhinitis and sinusitis, peritonsillitis, peritonsillary abscess, which
are not successful with treatment.
 Breath odor that is not successful with the treatment of recurrent
Tonsillitis caused by bacterial group A Sterptococcus β hemolyticus
 Tonsillar hypertrophy suspected of malignancy
  Otitis media effusion / supurate otitis media

8. Mention the differential diagnosis according to the scenario!

Answer :
a. DIPHTHERIA
Definition
Diphtheria is an acute infectious disease that occurs locally on the
mucosa or skin caused by Corynebacterium diphteriae which is
characterized by the formation of membrane-shaped exudates at the site of
infection and followed by general symptoms caused by exocytosine
produced by these bacteria.
Epidemiology
Race predilection for diphtheria has been reported, by sex. there was
no difference in the incidence of diphtheria in men and women. Diphtheria
is a disease in children, especially at the age of less than 12 years. babies
are susceptible to this disease at the age of 6-12 months
Currently the incidence of diphtheria also increases in adolescents and
ages 40 years or older. this is related to immunization status ie incomplete
immunization, never immunized, vaccine ineffective or not responding to
vaccination, and not receiving booster after previous vaccination.
Etiology
Corynebacterium diphteriae species are gram-positive stem bacteria
(aerobic bacilli), immovable, pleomorphic, non-encapsulated, do not form
spores, die at 60ºC heating, hold frozen and dry. With coloring, these
germs can be seen in the palisade arrangement, L or V shape, or are a
Chinese letter-like formation. Germs are not selective in their growth, their
isolation is facilitated by certain media (i.e. cystine tellurous blood agar)
which inhibits the growth of competing organisms, and if reduced by C.
diphteheriae will make the colonies black gray, or can also use loeffler
media namely medium containing serum which has been coagulated with
high concentration of phosphate, then metachromatic colored granules
occur with methylene blue, in this medium the colony will be cream
colored. In the human mucous membrane C. diphtheriae can live together
with saprophytic diphtheroid bacteria that have similar morphology, so to
distinguish it sometimes requires a special examination by means of
glycogen, starch, glucose, maltose or sucrose fermentation.

(Pict 1. Corynebacterium diphteriae)

In general, there are 3 main types of C. diphtheriae, namely the garvis,
intermedius and mystical types, but from the point of view of the actual
antigenity the basil is a heterogeneous species and has many serological
types. This might explain why in an ordinary patient it has colonization of
more than one type of C. diphtheriae. A distinctive feature of C.
diphtheriae is its ability to produce exotoxin both in-vivo and in-vitro, this
toxin can be demonstrated by in vivo toxin neutralization test on guinea
pigs (death test) or demonstrated in vitro by immunopresipitin agar
technique (Elek test) which is a reaction test observation polymerase. This
exotoxin is a protein with a molecular weight of 62,000 daltons, cannot
stand heat or light, has 2 fragments, namely fragment A (amino-terminal)
and fragment B (carboxy-terminal). The ability of a strain to form or
produce toxins is influenced by the presence of bacteriophages, toxins are
only commonly produced by C. diphtheriae which is infected by
bacteriophages containing toxigene.
Pathogenesis
Population density, poor hygiene and sanitation, mobilization,
incomplete immunization, poor health facilities and immunocompromised
patients, are risk factors for transmission of this disease. Humans are the
main host of this infection, but reported this disease can also attack
livestock. Infected patients and careers can transmit C. diphtheria directly
through respiratory droplets, and nasopharyngeal secretions. Indirectly
through dust, clothes, or contaminated objects. In diphtheria the skin is
spread through contact with exudates and respiratory secretions.
Bacteria usually enter the body through the upper respiratory tract, but
can also enter through the skin, genital tract or eyes. Cell surface C.
diphtheria has 3 different structures of the pilus: the main pilus shaft
(SpaA) and 2 small pili (SpaB, Spac). Sensitivity to respiratory epithelial
cells can be greatly reduced by blocking the production of two small piles
or by using antibodies directed at them.
C. Diphtheria in the nose or mouth, develops in upper airway mucosal
epithelial cells especially in the tonsils sometimes found in the skin and
conjunctiva or genitalia. This basil then produces exotoxins, which are
released by the endosome, causing a local inflammatory reaction, then
tissue damage and necrosis occur. Toxin consists of two forming protein
fragments. Fragment B binds to the surface receptors of susceptible host
cells, and its proteolytic properties cut off the lipid membrane layer, so
fragment A enters the host cell. Next will be inflammation and destruction
of epithelial cells which will be followed by necrosis. In the area of
necrosis, fibrin is formed, which is then infiltrated by white blood cells,
resulting in patchy exudates which can be peeled off.
In further circumstances more toxins are produced, so that the area of
necrosis becomes wider and deeper so that fibrous exudates (fake
membranes) are formed consisting of necrotic tissue, fibrin, epithelial
cells, leukocyte cells, erythrocyte cells that are gray to black. This
membrane is difficult to peel, if forced it will cause bleeding.
Clinical Manifestations
The onset of diphtheria symptoms generally has an incubation period
of 2-5 days (range 1-10 days). the initial symptoms are general and non-
specific, often resembling an upper respiratory viral infection. Depending
on various factors, the manifestation of this disease usually varies from
asymptomatic to a condition / disease that is hypertoxic and fatal. As a
primary factor, host immunity to diphtheria toxin, virulence and toxicity of
C. diphtheriae (the ability of bacteria to form toxins), and the location of
the disease anatomically. Other factors include age, concomitant systemic
disease and previous nasopharyngeal disease. Diphtheria has a shoot
period of 2 days. Patients generally come for treatment after several days
suffering from systemic complaints. Fever and other complaints and
symptoms depend on the localization of diphtheria. (3)

(Pict 2. Pseudomembran on Diphteriae)

Patients with diphtheria generally come with the following
complaints:
 Fever rarely exceeds 38.9ºC (50-80%)
 Malaise
 Sore throat (85-90%)
 Headache
 Respiratory lymphadenopathy and pseudomembrane formation (about
50%)
 Hoarseness
 Dysphagia (26-40%)
 Dispnea, stridor breathing, wheezing, coughing

Respiratory Diphtheria
In the classic description of 1400 cases of diphtheria from California
published in 1954, the focus of primary infections was tonsils or pharynx
at 94%, with the nose and larynx the next two most common places. After
around the incubation period of 2-4 days, local inflammatory signs and
symptoms occur. Fever is rarely higher than 39ºC.
Nasal Diphtheria
Nasal diphtheria initially resembles a common cold, with mild cold
symptoms without or accompanied by mild systemic symptoms. Anterior
nares infection (more often in infants) causes erosive, purulent,
serosanguinis rhinitis with membrane formation. The superficial ulceration
of the outer nares and inner lip is typical. On examination the white
membrane appears on the septal area of the rice. Toxin absorption is very
slow and systemic symptoms that arise are not real so the diagnosis is
made slowly. (4)
Pharyngeal diphtheria
In tonsillar and pharyngeal diphtheria, sore throat is a common initial
symptom, but only half sufferers suffer from dysphagia, hoarseness,
malaise or headache. Within 1-2 days, a membrane that is attached to the
white and gray color, a mild pharyngeal injection accompanied by
unilateral or bilateral tonsillar membrane formation, which extends
differently regarding uvula, soft palate, posterior oropharynx, hypopharynx
and glottic region. Soft tissue edema below and enlarged lymph nodes can
cause a "bull neck" picture. Furthermore, the symptoms depend on the
degree of toxicity and the extent of the membrane. In severe cases,
respiratory or circulatory failure can occur. There can be paralysis of the
soft palate both united and bilaterally, accompanied by difficulty in
swallowing and regurgitation. Stupor, coma, death can occur in 1 week to
10 days. In cases where healing occurs gradually and can be accompanied
by complications of myocarditis or neuritis. In mild cases the membrane
will be released in 7-10 days and usually complete healing. (6)
Laryngeal Diphtheria
Laryngeal diphtheria is usually an extension of pharyngeal diphtheria.
Patients with laryngeal diphtheria are very likely to suffocate due to soft
tissue edema and loose blockage of thick respiratory epithelium and
necrotic clots. In primary pharyngeal diphtheria the toxic symptoms are
less pronounced, because the laryngeal mucosa has a low absorption of
toxins compared to the pharyngeal mucosa so that the symptoms of upper
airway obstruction are more striking. The clinical symptoms of laryngeal
diphtheria are difficult to distinguish from other types of infectious croups,
such as wheezing, progressive stridor, hoarseness and dry cough. In severe
laryngeal obstruction there are suprasternal, intercostal and supraclavicular
retractions. If there is a release of the membrane that closes the airway, a
sudden death occurs. In severe cases, the membrane can extend to the
tracheobronchial branching. If laryngeal diphtheria occurs as an extension
of pharyngeal diphtheria, the symptoms that appear are a mixture of
symptoms of obstruction and toxemia.
Diphtheria Skin
Disease characterized by ulcers covered in gray membranes. ulcers are
often co-infected with Staphylococcus aureus and Streptococcus group A.
Contagious skin lesions, and bacteria from lesions can cause pharyngeal
infection and become a reservoir for infection.
Diagnosis
To make a diagnosis of C. diphtheriae infection, that is by isolating C.
diphtheriae either in culture media or identifying its toxin. Early rapid
diagnosis (presumtive diagnosis) can be done with Gram staining where
rod-shaped, gram-positive, non-capsulated, grouped and immobile bacteria
are found. Immunofluorescent or methylene blue staining can sometimes
be used for rapid diagnosis. Definitive diagnosis and identification of C.
diphtheriae bacillus by culture via tellurite or Loeffler media with samples
taken from pseudomembranes in the oropharynx of the nose, cryptic
tonsils, or ulcerations, in the oral cavity. Toxin examination aims to
determine the production of toxins by C. diphtheria.
Invitroly done by doing the Elek test plate and the inoculation
polymerase pig then detecting the line form on the filter paper which is
impregnated with antitoxin and then processed the agar culture from the
tested organism. A serum test for antibodies for diphtheria toxin can also
be done with a Shick test. Another examination using the Polymerase
Chain Reaction (PCR) method to detect the sequence of subunit DNA
encoding A tox + strain examination is fast and sensitive. On another
laboratory examination it is found in the blood edge of leukocytosis,
thrombocytopenia, and urinalysis can show temporary proteinuria. Levels
of cervical troponin I correlate, with myocarditis, ECG abnormalities if
there is a heart abnormality, radiological examination is found to be hyper
inflation.
Treatment
Treatment of diphtheria should begin immediately even though the
confirmation test has not been completed due to high mortality and
morbidity. Treatment consists of:
General care:
 Isolate all cases and do universal prevention of the risk of transmission
through droplets and limit the number of contacts.
 Minimum bed rest 2-3 weeks
 Soft or liquid food depends on the patient's condition, cleanliness of the
airway and mucus.
Regular ECG examination 2-3 times a week for 46 weeks to make a
diagnosis of myocarditis early. If myocarditis occurs, it must be totally
rested.
 If paralysis occurs, passive physiotherapy is carried out and active
physiotherapy is followed when the condition has improved. Paralysis of
the palate and pharynx can cause aspiration, so it is advisable to give liquid
food through the gastric tube. If laryngeal obstruction occurs as soon as
possible a tracheostomy is performed.
Special treatment aims:
a. Neutralizing the toxin produced by diphtheria bacilli
b. Kill diphtheria bacilli that produce toxins.
Anti-toxin is given as early as possible once the diagnosis is made,
there is no need to wait for the results of bacteriological examination.
Dosage depends on the type of diphtheria, not influenced by the age of the
patient, namely:
 Mild nasal / fausal diphtheria is given 20,000-40,000 U, iv within 60
minutes.
 Fausial diphtheria is being given 40,000-60,000 U iv
 High blood pressure (bullneck dyyephtheria) is given 80,000-120,000
iv
Antitoxin administration must be preceded by a sensitivity test,
because antitoxin is made from horse serum. If the test is positive
sensitivity, then desensitization is given at intervals of 20 minutes, with the
following dosage:
 0.1 ml of 1:20 solution, subcutaneously (in 0.9% NaCl liquid)
 0.1 ml of 1:10 solution, subcutaneously
 0.1 ml without dissolving, subcutaneously
 0.3 ml without being dissolved, intramuscularly
 0.5 ml without dissolving, intramuscularly
 0.1 ml without dissolving, intravenously
If there is no reaction the remaining IV is given slowly.
Giving Antibiotics
 Procurement Penicillin 1,200,000 units / day intramuscularly, 2 times a
day for 14 days
 Erythromycin: 2 grams per day orally with divided doses 4 times a day
 Other preparations that can be given are Amoxicillin, Rifampicin,
Clindamycin.

Prevention
Prevention in general by maintaining cleanliness and providing
knowledge about the dangers of diphtheria for children. In general, after a
child has diphtheria, the immunity to the disease is very low, so DPT
immunization and career treatment are needed. A child who has received
complete diphtheria immunization has antibodies to diphtheria toxin but
does not have antibodies to his organism. Such a situation allows a person
to become a person with diphtheria in his nasopharynx (career) or has mild
diphtheria.
The best prevention is vaccination in accordance with the
recommendations of the Pertussis Global Initiative. The forms of
diphtheria toxoid are four types:
 DTaP, for vaccination in children. Given at the age of 2 months, 4
months, 6 months, 15-18 months, and 4-6 years
 Tdap, for vaccinating adults
 DT, diphtheria and tetanus vaccines are given to adolescents, and in
adults it is given as a booster every 10 years or when exposure has
occurred
 Td, given to adolescents aged 11 or 12 years

Prognosis
Generally it depends on age, virulence of germs, location and spread
of membranes, immunization status, speed of treatment, accuracy of
diagnosis, and general care. In general the mortality rate of diphtheria
sufferers is 5-10%. in sepsis, the mortality rate is 30-40%. A high
mortality rate occurs at the age of less than 5 years and over 40 years
 The prognosis of diphtheria after ADS and antibiotics was found to be
better than before, such conditions have occurred in other countries. The
most common death in children less than 4 years is due to diphtheria
membranes. According to Krugman, sudden death in cases of diphtheria
can be caused due
a. Sudden airway obstruction caused by the release of diphtheria,
b. Presence of myocarditis and heart failure,
c. Paralysis of the diaphragm as a result of neuritis of the nephric nerve.
Children who have had myocarditis or neuritis as a complication of
diphtheria, generally will recover completely without sequelae;
nevertheless, permanent heart abnormalities have been reported. The cause
of the gravis strain is poor. Amegakariositic thrombocytopenia and
leukocytosis> 25,000 / poor prognosis. The highest mortality is
pharyngeal-laryngeal diphtheria (56.8%) following the nasopharyngeal
type (48.4%) and pharynx (10.5%).

b. TONSILO FARINGITIS
Definition
Pharyngitis is widely involved in tonsillitis, nasopharyngitis and
tonsillopharyngitis. Infection of the pharynx and surrounding areas which
is characterized by complaints of sore throat
Etiology
The virus is the most etiology of acute tonsillopharyngitis, especially
in children aged ≤ 3 years. Respiratory viruses such as adenovirus,
rhinovirus, and parainfluenza virus can be the cause. Group A beta
hemolytic streptococcus is the most common cause of tonsillopharyngitis
or acute tonsillopharyngitis. These bacteria cover 15-30% in children
while in adults only around 5-10% of cases. microorganisms such as
chlamydia and mycoplasma are reported to cause infection, but are very
rare.
 Chronic pharyngotonsillitis has a predisposing factor in the form of
chronic inflammation of the filter, such as chronic rhinitis, sinusitis,
chronic irritation by smoking, drinking alcohol, steam and dust inhalation,
several types of food, poor oral hygiene, weather effects, physical fatigue,
and treatment of previous acute tonsillitis inadequate
Pathogenesis
Nasopharynx and tonsils are places for these organisms, direct contact
with the nasopharyngeal mucosa and oropharynx that are infected or with
contaminated objects, and through food is a less influential mode of
transmission. The spread of group A beta hemolytic Streptococcus
requires vulnerable hosts and is facilitated by close contact.
Both bacteria and viruses can directly invade the pharyngeal mucosa
which then causes a local inflammatory response. Most inflammation
involves the nasopharynx, uvula, and mole palate. The course of the
disease is inoculation of infectious agents in the pharynx which causes
local inflammation which causes pharyngeal erythema, tonsils, or both.
Streptococcal infection is characterized by local invasion and release of
extracellular toxins and proteases. Transmission of the virus is more
common due to hand contact with nasal secretions or droplets than oral
contact. Symptoms will appear after a short incubation period of 24-72
hours.
Clinical Manifestations
Typical tonsillopharyngitis symptoms due to streptococcal bacteria
include sudden onset of sore throat, dysphagia, and fever. The sequence of
symptoms that are usually complained of by children over 2 years is
headache, abdominal pain, and vomiting. In addition it also found high
fever and sore throat. Symptoms such as rhinorrea, hoarseness, coughing,
conjunctivitis, and diarrhea are usually caused by a virus. Contact with
rhinitis patients can be found in history. On physical examination, not all
patients with acute tonsillopharyngitis streptococcus show signs of
streptococcal infection, namely erythema in the tonsils and pharynx
accompanied by enlarged tonsils. Streptococcal pharyngitis is very likely
if acute symptoms are present with nausea, pharyngeal hyperemia, fever,
sore throat, swollen tonsils with exudation, swollen and painful anterior
neck lymph nodes, swollen and red uvula, excoriation of the nose with
secondary impetigo, scarlatina rash, petekie palate mole.
The typical sign of tonsillopharyngitis is an asymmetrical membrane,
easy to bleed, and gray in the pharynx. Viral tonsillopharyngitis can be
found in the mole palate, and pharyngeal and exudate in the palate and
tonsils. Symptoms that arise can disappear within 24 hours lasting 4-10
days with a good prognosis
Diagnosis
Diagnosis is based on clinical symptoms, physical examination, and
laboratory tests. The gold standard for establishing a diagnosis of bacterial
or viral tonsillofaringitis is through examination of cultures from throat
swabs. At present there is a fast method of detecting group A
streptococcus antigens with high sensitivity and specificity.
Treatment
The purpose of giving this therapy is to reduce symptoms and prevent
complications of group A streptococcus pharyngitis is pharyngitis which
has strong indications and special rules for the use of antibiotics. Adequate
rest and administration of appropriate fluids are supportive therapies that
can be given. Giving mouthwash and medicine for suction in children is
large enough to reduce symptoms of sore throat. If there is excessive pain
or fever can be given paracetamol or ibuprofen. The chosen antibiotic in
the treatment of acute tonsillofaringitis group A is oral V suppression of
15-30 mg / kg / day divided by 3 doses for 10 days or single dose
benzathine penicillin G with a dose of 600,000 IU (BB <30 kg) and
1,200,000 IU ( BB> 30 kg). Amoxicillin can be used as a substitute for the
choice of penisislin in smaller children because in addition to the same
effect amoxicillin has a good taste. Amoxicillin at a dose of 50 mg / kg /
day divided by 2 for 6 days Besides erythromycin 40 mg / kg body weight
 / day, clindamycin 30 mg / kg body weight / day, cefadroxyl monohydrate
15 mg / kg body weight / day can be used for the treatment of
streptococcal tonsillopharyngitis in allergic patients against penicillin.
Complications
The incidence of complications in acute tonsillopharyngitis is very
rare. Compilation usually describes the expansion of streptococcal
infection from the nasopharynx. Some cases can progress to purulent
bacterial otitis media. In bacterial and viral tonsillofaringitis can be found
extensive complications of chronic ulcers. Complications of bacterial
tonsillopharyngitis occur due to direct or hematogenous expansion. As a
result of direct expansion can occur rhinosinusitis, otitis media,
mastoiditis, cervical adenitis, retropharyngeal or pharyngeal abscess, or
pneumonia.Hematogenous spread can result in meningitis, osteomyelitis,
or septic arthritis, while non-suppurative complications include rheumatic
fever and gromerulonephritis

c. MUMPS
Definition
Mumps is an acute systemic viral infection that mainly affects school-
age children and young adults with the main clinical infestation of
enlarged parotid glands. This infection is generally mild and can heal
itself, one third of infected people show no clinical symptoms. In adults
and old age clinical manifestations are usually more severe.
Epidemiology
Endemic mumps all over the world. In the United States mumps are
found throughout the year, but the peak incidence occurs between January
and May. From June 2009 to January 2010 there were reported mumps
outbreaks in New York and New Jersey which reached 1,521 cases, of
which 91% of patients were> 6 years old and 85% had received MMR
(measles, mumps, rubella) vaccine 2 doses. Mumps are rare in infants
under one year. There is no difference in the incidence of parotitis between
men and women. Humans are the only natural host of this virus and are
not known to be carrier conditions.

Virology
Mumps virus is a family of Paramyxoviridae. This family includes:
 Rubulavirus (mumps virus) is irregular spherical in shape with a
diameter of 90-300 nm.
 Paramyxovirus
 Morbilivirus
 neumavirus
The viral genome encodes 8 proteins. There are 13 genotypes (A to M)
known viruses, but only one mumps virus serotype is known. At a
temperature of 40C the virus can last several days, but at a temperature of
-650C the virus can live for months to years.
Pathogenesis
Virus transmission occurs through direct contact, droplet nuclei, vomit
that enters the nose or mouth. Mumps virus transmission is not as easy as
measles or varicella virus. The peak period of transmission occurs just
before or when parotitis arises. It is estimated that during the incubation
period, the virus proliferates in the upper airway epithelium and occurs
viremia, in the next stage localized to the glands and nerve tissue.
Pathology
On examination of parotid gland pathology infected with mumps
virus, interstitial edema and serofibrinous exudates were dominated by
mononucleus cells. Pathological features in the pancreas or affected testis
are similar to parotid, except interstitial bleeding and polymorphonucleus
cells are more common in the arthritis. Sometimes there is an area that has
an inflammation of the testes and in severe cases germinal epithelial
atrophy is accompanied by hygiene and fibrosis. In mumps encephalitis is
obtained perivenous demyelination, perivascular mononuclear cuffing, and
relatively good increase in microglia cells with neurons.
Clinical description
The incubation period of mumps is between 2-4 weeks, mostly 16-18
days. Prodromal symptoms include mild fever, anorexia, malaise,
headache. Within 1 day there is ear pain and pain in the unilateral parotid
gland. Within 2-3 days the parotid gland enlarges and reaches its
maximum size with severe pain. Generally, the other parotid dilates 1-2
days later. Parotid enlargement can cause trismus and difficulty
swallowing. After the parotid enlarges, the fever and pain are reduced and
the perotic gland returns to its normal size within 1 week.
Table. Main Clinical Manifestations of Mumps
Manisfestasi Frekuensi (%)
Glands
Parotis 60-70
submandibula/sublingual adenitis 10
Epidimo-orchitis 25 (pria setelah puber)
Oophoritis 5 (wanita setelah puber)
Pancreatitis 4
Neurology
Asymptomatic CSF pleocytosis 50
Aseptic meningitis 1-10
Encephalitis 0,02-0,3
Temporary deafness 4
The other/etc
ECG abnormalities 5-15
Mild kidney function disorders 30-60

Complication
Mumps virus infection in first trimester pregnant women can increase
the risk of fetal death in the womb and low birth weight (7.7%), but does
not cause fetal malformations. Some cases of diabetes at a young age are
also reported to be associated with mumps.
Diagnosis
Diagnosis of mumps is generally based on a typical clinical picture,
namely enlargement and pain in the parotid gland accompanied by
constitutional symptoms. On laboratory examination it is found normal
leukocyte count or leucopenia with relative leukocytosis. Generally
specific checks for typical mumps cases are not needed. Diagnosis of
defenitive ELISA or 4-fold increase in serum phase and convalescent
phase with CF, HAI, ELISA, neutralization tests confirm the diagnosis.
The RT-PCR method is the most sensitive and specific examination
technique.
Management
Therapy for parotitis is symptomatic and supportive. Analgesic-
antipyretic is given to reduce pain due to parotid swelling and reduce
fever. In patients with meningitis or pancreatitis with poor intake or
vomiting, intravenous fluids are needed. One study reported that
administration of interferon-alfa 2b in 4 patients with bilateral mumps
orchitis showed rapid improvement in symptoms and no testicular or
oligospermy atrophy during monitoring.
Prevention
To prevent transmission of the virus to others, patients with mumps
should be isolated for 5 days after the onset of parotitis, although this
effort is less effective because the virus can spread to other people a few
days before clinical symptoms appear.
Today active immunization is used with attenuated mumps viruses.
There are several strains of vaccines such as Jerryl-Lynn, Rubini, Urabe,
Leningrad, L-Zagreb. This vaccine is given subcutaneously and provides
95% protection. Vaccination is recommended for children aged 12-15
months and repeated at the age of 46 years together with the measles
vaccine (MMR). Side effects of MMR vaccine are rare. Like other live
virus vaccines, mumps vaccines should not be given to pregnant women,
patients with immunosuppressant therapy, high fever, malignancy,
congenital immunodeficiency or acquired. The MMR vaccines available in
Indonesia today are Trimovaxmerieux TM and MMR IITM.
9. Islamic perspective according to the scenario!
Answer :

"If you hear of an outbreak of disease in an area, do not enter the outbreak
area. And if the outbreak has occurred in an area while you are there, then
don't leave the area. " (HR. Bukhari)

In a other Hadith, the Prophet said, which means: Every disease has a cure. If
the drug is right about the target, then with God's permission the disease will
heal ". (HR. Muslim).
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