Clinical Parasitology

Lecture | Week 12 | Semifinal

HEMOFLAGELLATES EPIMASTIGOTES
Morphologic Forms → Slightly wider than that of the
promastigote
AMASTIGOTE → Large single nucleus is located
at the posterior end of the
→ Roundish and oval that measures 5X3 um in organism.
size → Kinetoplast is located anterior
Contains: to the nucleus.
→ a single, large nucleus that is off-center, → Undulating membrane,
sometimes present more toward the edge of measuring half the body length,
the organism forms into a free flagellum at
→ basal body structure known as the anterior end
blepharoblast which is a dotlike structure
and is attached to an axoneme. The
axoneme extends to the edge of the
organism.
→ and a single, small parabasal body that is
located adjacent to the blepharoblast
→ Kinetoplast is an umbrella term that is used
to refer to the blepharoblast and small
parabasal body.

TRYPOMASTIGOTE
→ Typically measures 12 to 35 um
long by 2 to 4 um wide
Contains:
→ May often assume the shape of
the letters C, S, or U in stained
blood films
→ Kinetoplast is located posteriorly
from which emerges a full body
length undulating membrane
PROMASTIGOTE → The single large nucleus is
located anterior to the
→ Measures 9 to 15 um in length kinetoplast
Contains: → An anterior free flagellum may
→ The large single nucleus is located in or or may not be present
near the center of the long slender body
→ Kinetoplast is located in the anterior end
of the organism

→ Measures approximately 9 to

General Morphology and Life Cycle Notes

Amastigote and are the two forms

trypomastigote routinely found in
15 um in length. human specimens
Contains: Amastigote are found primarily in
tissue and muscle, and

By: HORLADOR, CJ 1
Clinical Parasitology
Lecture | Week 12 | Semifinal
CNS within
macrophages, where
they multiply
Trypomastigote reproduce and are
visible in the peripheral
blood.
Promastigote stage may be seen only if
blood sample is
collected immediately
after transmission into a
healthy individual or
when the appropriate
sample is cultured
Laboratory Diagnosis & Clinical Symptoms
Specimens of choice: blood, lymph node and ulcer
aspirations, tissue biopsies, bone marrow, and
cerebrospinal fluid.
Laboratory Diagnosis: Serologic and molecular tests
are also available for confirming the presence of these
organisms
Symptoms:
→ small red papule at the infection site
→ with intense itching
→ secondary bacterial infections
→ fever, and diarrhea
→ to kidney involvement
→ mental retardation
→ a comatose state and death
→ In some cases, the initial skin lesions
spontaneously heal, others remain dormant
for months or even years
Baghdad boils common name for an
infection with
Leishmania tropica; it is
a cutaneous form of
Leishmaniasis
presenting with
puscontaining ulcers
Bay sore a common name for a
cutaneous form of
infection caused by
Leishmania mexicana
Chiclero ulcer – leishmaniasis caused
cutaneous by L. mexicana;
commonly found in
Belize, Guatemala, and
the Yucatan peninsula
in areas where chicle
sap is harvested for
making chewing gum
Oriental sore a common reference for
the cutaneous
leishmaniasis caused
by the infecting agents
comprising the
Leishmania tropic
complex
Dum dum fever a common name for
visceral leishmaniasis
caused by Leishmania
donovani
Kala-azar another name for the
most severe form of
visceral leishmaniasis
caused by members of
the Leishmania
donovani complex
Yuta reference to
mucocutaneous
leishmaniasis in the
Peruvian Andes
Espundia another name for an
infection resulting from
Leishmania braziliensis,
the principal cause of
mucocutaneous disease
in Central and South
America, particularly
Brazil
Forest yaws another name for the
infection with
Leishmania guyanensis,
the principal cause of
mucocutaneous
leishmaniasis in the
Guianas, parts of Brazil
and Venezuela, also
known as pian bois
LEISHMANIASIS
Leishmania braziliensis complex
Leishmania donovani
Leishmania mexicana
Leishmania tropica complexes
By: HORLADOR, CJ 2
Clinical Parasitology
Lecture | Week 12 | Semifinal
→ Increased travel and exposure to different
environments has resulted in the
transmission of the various
→ parasitemias, a general term for parasitic
infection of the blood, into new
environments, finding new host organisms
and new vectors
LEISHMANIA BRAZILIENSIS COMPLEX
Comprised of Leishmania braziliensis,
Leishmania panamensis, Leishmania
peruviana, and Leishmania guyanensis
→ Found in Mexico, Argentina,
Panama, Colombia, and the
Peruvian Andes, Guiana, Brazil,
Bolivia, Paraguay, Ecuador, and
Venezuela
→ This leishmanial complex and the
diseases for which its organisms are
the causative agent may also be
referred to as New World because of
their geographic location in what is
commonly considered the New
World
Leishmania spp. Life Cycle
1. Sandflies of the genera Lutzomyia and
Psychodopygus are responsible for
transmitting the promastigotes of L.
braziliensis complex into unsuspecting
humans via blood meal, resulting in a skin
bite.
2. The promastigotes quickly invade the
reticuloendothelial cells and transform into
amastigotes, which actively reproduce
causing tissue damage.
3. The skin and mucous membrane areas of
the body are primarily affected
4. The diagnostic stage in humans is the
amastigote while it serves as the infective
stage for the sandflies.
5. On ingestion, during blood meal of an
infected human, the amastigote transform
back into promastigotes in the fly midgut and
multiply and the resulting developed forms
eventually migrate into the salivary gland of
the fly, where they are ready to be
transferred to a new human during a blood
meal
Clinical Symptoms
Mucocutaneous Leishmaniasis
→ Symptoms typically occur within a few weeks
to months after transmission into a
previously uninfected human
Diseases and Conditions associated with
Leishmaniasis
→ Large ulcers in the oral or nasal mucosa
areas (mucocutaneous) develop in some
patients after the initial invasion of the
reticuloendothelial cells. There may be large
cutaneous lesions, mucosal lesions, or
combination of both.
→ A cutaneous lesion may heal on its own.
→ Untreated mucosal lesions result in the
eventual destruction of the nasal septum.
The lips, nose and other surrounding soft
parts may also be affected.
→ Edema and secondary bacterial infections,
combined with numerous mucosal lesions,
may cause disfigurement of the patient’s
face.
→ Death is attributed to secondary bacterial
infection
Laboratory Diagnosis
Specimen of choice: Biopsy of the Infected
Ulcer
Giemsa-stained preparations should reveal the
typical amastigotes
Other diagnostic methods:
→ culturing the infected material which
often demonstrates the promastigotes;
and serologic testing
Research methods:
→ Schizodeme analysis – restriction
analysis of the kinetoplast DNA
→ Zymodeme analysis – nuclear DNA
hybridization, and isoenzyme patterns
analysis
Treatment, Prevention and Control
Antileishmanial agent with antimony compounds is
the most widely used treatment for mucocutaneous
leishmaniasis.
→ However, L.braziliensis has shown
increased resistance to pentavalent
antimonials such as sodium stibogluconate
(Pentosan). Even with drug resistance and
the adverse effects, these classes of drugs
are still considered the most effective
treatment for the L.braziliensis complex.
Alternative treatment:
→ liposomal amphotericin B (Ambisome) and
oral antifungal drugs such as fluconazole
(Diflucan), ketoconazole (Nizoral) and
itraconazole (Sporonox)
Prevention and control:
→ public awareness, exercising personal
protection(e.g., protective clothing,
repellants, screening) against contact with
sandflies
→ Prompt treatment and eradication of infected
ulcers and control of sandfly population and
reservoir host (dogs and forest rodents).
By: HORLADOR, CJ 3
Clinical Parasitology
Lecture | Week 12 | Semifinal

LEISHMANIA DONOVANI COMPLEX → Weight loss and emaciation tend to occur

Comprised of Leishmania donovani, following invasion of the liver and spleen.
Leishmania infantum, Leishmania chagasi → Advanced stages of disease result in kidney
→ Organisms of the complex and their diseases damage and granulomatous areas of skin. A
may be referred to as Old or New World, characteristic darkening of the skin may
depending on the geographic location of the be noted. This symptom is referred to by the
species of Leishmania involved. common disease name, kala-azar, meaning
→ L.donovani is capable of being transmitted black fever.
person to person via blood transfusions. → Chronic cases usually leads to death in 1 or
→ High levels of galactosyl-alpha(1-3) 2 years.
galactose antibodies in patients successfully Laboratory Diagnosis
treated with visceral leishmaniasis may
Montenegro skin test – Used for screening
indicate parasite remnants.
large populations at risk for infections caused
by Leishmania spp. Its reliability in detecting
Life cycle exposure to the organisms causing
Life cycle of the members of L.donovani complex is leishmaniasisis related to the patient’s
identical to that of L.braziliensis with two exceptions: disease status
→ Not a good method for diagnosing
→ First, the specific sandfly species responsible active disease
for L.donovani transmission vary with each → Skin reactions to MST ≥ 5 mm are
subspecies. considered positive and < 5 mm are
→ Second, L.donovani primarily affects the considered negative. Patients with
visceral tissue of the infected human negative MST and diagnostic
Subspe Geographic Vector Reserv confirmation by other tests are more
cies Distribution oir prone to relapse. MST is a marker
Host of cellular immune response.
L.donova Central Lutzomyi Dogs, → Giemsa-stained slides of blood,
ni America,esp.M a sandfly cats, bone marrow, lymph node aspirates
chagasi exico, West foxes and biopsies of the infected areas
Indies, South are better choices for demonstrating
America the diagnostic amastigote forms.
L.donova Parts of Africa, Phleboto India: → Giemsa-stained buffy coat films
ni India, Thailand, mus none prepared from venous blood is a
donovani China, Burma sandfly China: safer, less invasive procedure.
dogs → Culture of blood, bone marrow and
L.donova Mediterranean Phlebot Dogs, other tissues may show the
ni Europe, Near mus foxes, promastigote forms
infantum East, Africa, sandfly jackals, → Serologic methods: IFA, ELISA,
Romania, porcupi Direct Agglutination Test (DAT)
Hungary, nes Research methods: Shizodeme
Siberia,
Southern Life Cycle
Siberia and
→ Their life cycle is similar to that
region of
of the Leishmania braziliensis
former Soviet
complex.
Union
analysis, zymodeme analysis, and
nuclear DNA hybridization
Clinical Symptoms
Treatment, Prevention and Control
Visceral Leishmaniasis
→ Drug of choice: Liposomal
→ Also known as kala-azar or dum dum fever
amphotericin B (Ambisome)
→ Patients often present with nondescript → Sodium stibogluconate
abdominal illness and hepatosplenomegaly. (Pentosam) is also an effective
→ Early stages may resemble malaria or treatment, however resistance
typhoid fever with the development of fever has been demonstrated by
and chills.
organisms in India and the
→ Onset of symptoms is gradual and follows an
Mediterranean
incubation period ranging from 2 weeks to
→ Gamma interferon combined
18 months.
pentavalent antimony has
→ Diarrhea and anemia may be present

By: HORLADOR, CJ 4
Clinical Parasitology
Lecture | Week 12 | Semifinal
accomplished successful
treatments
→ Infected patients with AIDS
respond to allopurinol.
→ Prevention includes protection
against sandflies by repellants,
protective clothing and
screening are essential
measures to avoid infection.
→ Prompt treatment of infected
persons, control of sandfly
population and reservoir hosts.
LEISHMANIA MEXICANA COMPLEX
Comprised of Leishamania mexicana,
Leishamania pifanoi, Leishmania
amazonensis, Leishmania
venezuelensis, & Leishmania
garnhami.
→ Associated with New World
cutaneous leishmaniasis,
chiclero ulcer, bay sore
→ The diseases and their
causative agents maybe
referred to as New World
because of the geographic
location of its members
Clinical Symptoms
New World Cutaneous Leishmaniasis
→ Characterized by a single pus-containing
ulcer, which is generally self-healing
→ Approximately 40% of infections affect the
ear and can cause serious damage to the
surrounding cartilage.
→ Small red papule initially develops at the bite
site that is 2 cm or larger in diameter and
may cause pruritis.
→ Spontaneous healing of ulcers do not occur
on some occasions due to anergic, inability
of an individual to mount an adequate
immune response, and hypersensitivity
immunologic responses.
→ Diffuse cutaneous leishmaniasis (DCL) is
rare in the New World.
→ In DCL caused by L.pifanoi, the initial lesions
appears, ulcerates and disappears and, after
months to years, appears in local and distant
areas from the bite site with lepramatous –
appearing lesions.
→ Infections with L.amazonensis have been
known to progress to incurable DCL form
Treatment, Prevention and Control
→ Pentavalent antimonials, such as sodium
stibogluconate are considered the drug of
choice
→ Antimony combined with pentoxifylline taken
orally three times a day for 30 days has
shown superior effect than antimony alone.
→ Amphotericin B and Ambisome
→ Prevention and control measures are the
same with L.braziliensis complex and
L.donovani complexes
Associated with diseases and condition
namely, Old World Cutaneous
Leishmania tropica complex
Leishmaniasis, Oriental sores, Delhi
boils, Baghdad boils, dry or urban
cutaneous leishmaniasis.
→ Comprised of Leishmania tropica,
Leishmania aethiopica, and Leishmania
major
→ Soldiers during the Gulf war that were
stationed in Saudi Arabia had been infected.
→ Approximately, 16,000 cases of
leishmaniasis are reported every year in
Saudi Arabia.
Life Cycle
→ The life cycle of L.tropica complex
is like that of the L.braziliensis
complex except for the specific
sandfly specie as its vector and the
area of the body they affect.
→ All three of the subspecies are
transmitted by Phlebotomus
sandfly. L.tropica complex primarily
attacks the human lymphoid tissue
of the skin
By: HORLADOR, CJ 5
Clinical Parasitology
Lecture | Week 12 | Semifinal
Trypanosoma brucie gambiensi
Trypanosoma brucie rhodesiense
Trypanosoma cruzi
Trypanosoma rangeli
Trypanosomiasis
→ Due to anergic and hypersensitivity
immunologic responses, spontaneous
healing of the ulcers does not occur.
→ DCL occurs especially on the limbs and face
when an immune response fails to take
place.
→ Thick plaques of skin, along with multiple
lesions or nodules, usually results. Joint
pains(arthralgias) and muscle
pains(myalgias), headache, bleeding gums,
hair loss and intestinal disorders may occur
Laboratory Diagnosis
→ Microscopic examination of Giemsa-stained
slides of aspiration of fluid underneath the
ulcer bed for the typical amastigotes.
→ Culture of the ulcer tissue
→ Serologic tests such as IFA
Research methods:
→ include schizodeme analysis, zymodeme
analysis, and nuclear DNA hybridization
→ Skin test (Montenegro skin test) can be
used, however patients with active infection
tests negative.
Treatment, Prevention and Control
→ Effective treatment: sodium
stibogluconate (Pentosam)
→ Use of steroids, application of heat to the
infected lesions, meglumine antimonate
(Glucantime), pentamidine, and oral
ketoconazole. Paramomycin may be
given to aid in healing.
→ Vaccines have been developed but
clinical trials are still on going.
→ Prevention and control measures are the
same to the previously mentioned
methods
TRYPANOSOMIASIS
→ These diseases have been well documented
through the ages. Ancient papyri discussed
the disease from veterinary and human
perspective.
→ 1985 – David Bruce, Scottish pathologist,
identified Trypanosoma brucie as the
causative agent of the trypanosomal
diseases known as nagana (a form of
disease found in cattles) and sleeping
sickness. This is later known as
Trypanosoma brucie gambiensi.
→ 1909 – Carlos Chagas, a young medical
student, described Trypanosoma cruzi, the
causative agent of Chagas’ disease.
→ 1910 – Stephens and Fantham described
Trypanosoma brucie rhodesiensi
Trypanosomiasis: Sleeping Sickness
→ Infection occurs in two stages, an
initial haemolymphatic stage followed
by a meningoencephalitic stage after
the trypanosomes invade the central
nervous system (CNS).
1. First-stage symptoms may be
preceded by the development of a
trypanosomal chancre at the site of
inoculation within two days to two
weeks of being bitten by an infected
fly .
2. First-stage symptoms for both
types of sleeping sickness include
headache, malaise, weakness,
fatigue, pruritis, and arthralgia. First-
stage signs can include hepato-
splenomegaly, weight loss and
intermittent fevers lasting one day to
one week.
3. Lymphadenopathy, mainly
posterior cervical but in some cases
axillary, inguinal or epitrochlear, may
also occur. Posterior triangle cervical
lymphadenopathy, or “Winterbottom’s
sign” is commonly seen in T. b.
gambiense infections
4. T. b. gambiense infection
progresses to the second stage after
an average of 300–500 days,
whereas T. b. rhodesiense infection
progresses to the second stage after
an estimated 21–60 days
By: HORLADOR, CJ 6
Clinical Parasitology
Lecture | Week 12 | Semifinal
6. The sleep/wake cycle becomes
reversed, hence the common name
“African sleeping sickness”, with
daytime somnolence, nocturnal
insomnia, and sudden urges to sleep
Trypanosoma brucie gambiense
Associated with the diseases: West African
Sleeping Sickness, Gambian trypanosomiasis
→ Found in the tropical areas of western and
central Africa especially in shaded areas
along stream banks where the tsetse fly
vector breeds.
→ Glosina palpalis and Glosina tachinoides are
the two specie of tsetse flies responsible for
the transmission of T.b.gambiense
→ Less aggressive than that of its East African
Counterpart
→ Has shown to be acquired through blood
transfusion, organ transplantation, and
congenital transmission.
Life Cycle
1. Humans become infected with T.b.
gambiense following injection of
trypomastigotes by the tsetse fly during its
blood meal.
2. The entering trypomastigotes migrate
through the blood steam into the lymphatic
system, multiplying by binary fission.
3. Some of the trypomastigotes are destroyed
by the host’s immune system, but some
manage to escape and continue to
reproduce.
4. CNS invasion may occur.
5. The trypomastigotes are transmitted back to
the tsetse fly vector when it feeds on an
infected individual. Once ingested by the
tsetse fly, the trypomastigotes continue to
multiply and eventually migrate back to the
salivary gland, converting into epimastigotes
along the way.
6. In the salivary gland, the epimastigotes
transform back into trypomastigotes, thus
completing the cycle.
Clinical Symptoms
West African (Gambian) Sleeping Sickness
→ Symptoms begin to occur after an
asymptomatic incubation period of a
few days to several weeks.
→ First notable symptom is the
development of a painful chancre
(ulcer), surrounded by a white halo at
the bite site.
→ Fever, malaise, headache,
generalized weakness, and anorexia
are often experienced when the
trypomastigotes settle into the
lymphatic system.
→ Lymph node enlargement
(lymphadenopathy)
→ Winterbottom’s sign which refers to
the enlargement of the cervical lymph
nodes in reference to this
trypanosomal disease.
→ Other signs: erythematous rash,
pruritis, edema and Kerandel’s sign
(a delayed sensation to pain)
Laboratory Diagnosis
Specimens of choice: Blood, lymph node
aspirations and CSF
→ Giemsa-stained preparations reveal the
typical trypomastigotes.
Tests that can be performed on CSF:
→ microscopic examination of the
sediment for trypomastigotes, detection
of the presence of immunoglobulin M
(IgM), and detection of the presence of
proteins.
Infected patients:
→ typically have high levels of botj IgM and
proteins in their CSF. Presence
→ of IgM in serum and/or CSF is generally
considered diagnostic.
Treatment, Prevention and Control
Melarsoprol, suramin, pentamidine
and eflornithine are used for treatment of
T.b.gambiense infections.
Treatment of choice depends on the
situation and is dictated by a number of
factors including patient’s age, stage of
disease, and whether the patient is pregnant
at the time.
→ Caution must be used when selecting
the specific treatment and appropriate
dosage due to high toxicity levels of
these medications.
→ Prevention and control measures
include the control of tsetse fly
population by destroying their breeding
areas via chemical treatment and
clearing of bush. Proper protective
clothing, repellents, as well as prompt
treatment of infected individual, will
reduce the risk of future T.b.gambiense
infection.
TRYPANOSOMA BRUCIE
RHODESIENSE
Commonly associated with East African
Sleeping Sickness, and Rhodesian
trypanosomiasis.
→ Found in eastern and central Africa
especially in the brush areas. Cattle
and sheep, as well as wild game
animals, are known as reservoir
hosts.
By: HORLADOR, CJ 7
Clinical Parasitology
Lecture | Week 12 | Semifinal
→ More aggressive than that of the
West African Sleeping Sickness.
East African(Rhodesian) Sleeping
Commonly associated with Chaga’s disease and
American trypanosomiasis
Sickness
→ Following a short incubation period,
patients suffering from acute East
African sleeping sickness
experience fever, myalgia and
rigors.
→ Winterbottom’s sign may or may not
be present and Lymphadenopathy
is absent.
→ Rapid weight loss is common, and
CNS becomes involved early in the
disease course.
→ Mental disturbance, lethargy, and
anorexia may be present.
→ A rapid and fulminating disease
results, with large number of
trypanosomes circulating in the
blood.
→ Death is caused by subsequent
kidney damage(glomerulonephritis)
and myocarditis(inflammation of the
heart) which usually occurs 9 to 12
months in untreated persons.
Laboratory Diagnosis
Specimen of choice are blood slides stained with
Giemsa and microscopic examination of CSF
sediments which demonstrates the typical T.b
rhodesiense typomastigotes.
→ Protein and IgM studies may be performed.
Presence of IgM is diagnostic for
T.b.rhodesiense.
→ Serologic tests
Treatment and Prevention and Control
→ Melarsoprol, suramin, pentamidine and
eflornithine are used for treatment of
T.b.rhodesiense infections, identical to
T.b.gambiense.
→ Extreme early treatment is crucial to halt
further transmission of the disease due to its
rapid course.
→ Additional prevention and control measures
include prompt medical treatment of infected
domestic animals, as well as protective
clothing, screening and repellents.
Clinical Symptoms
→ Clearing of brush areas and control of tsetse
fly population may reduce the risk of future
disease transmission
Trypanosoma cruzi
→ Found in the southern portions of the United
States, Mexico, and Central and South
America.
→ The disease course for this illness often
present itself with cardiac and
gastrointestinal distress.
→ Apart from humans, a number of mammals
serve as reservoir hosts for T. cruzi, e.g.,
armadillos, opossums, raccoons, woodrats,
some other rodents, and domestic dogs.
Common triatomine vector species for
trypanosomiasis belong to the genera
Triatoma, Rhodnius, and Panstrongylus.
→ The reduviid bug species is also known as
the “kissing bug”, “conenose bug”, and
“triatomid bug
Life Cycle
1. Most frequently transferred to a human host
when a reduviid bug vector defecates
infective trypomastigotes near the site of its
blood meal. The presence of the bite
produces an itching sensation in the host. As
the host scratches the bite area, the
trypomastigotes conveniently gain entry into
the host by literally being rubbed into the bite
wound.
2. Following entry into the host, the
trypomastigotes invade surrounding cells,
where they transform into amastigotes. The
amastigotes proceed to multiply, and destroy
host cells, and convert back into
trypomastigotes. The resulting
trypomastigotes migrate through the blood,
penetrate additional cells in the body, and
transform back into amastigotes, and their
replication and destruction cycle repeats.
Heart muscle,liver and brain may become
infected.
3. T.cruzi trypomastigotes are transmitted back
into the reduviid bug when it feeds, via a
blood meal, on an infected human. On
ingestion, it transforms into epimastigote in
the midgut. Multiplication of the
epimastigotes produces thousands of
additional parasites that convert back into
trypomastigotes when they reach the
hindgut. Then passed into the feces,and the
cycle begins again.
4. Additional routes of transferring T.cruzi
include blood transfusions, sexual
intercourse, transplacental transmission, and
By: HORLADOR, CJ 8
Clinical Parasitology
Lecture | Week 12 | Semifinal
entry through the mucous membranes when
the bug bite is near the eye or mouth.
Clinical Symptoms
Chaga’s disease
→ May be asymptomatic, chronic or acute in
nature
→ Most common initial symptom is Chagoma,
an erythematous nodule, that develops at the
site of infection and is produced by the
proliferation of the T.cruzi organism. This is
frequently located on the face and may last 2
to 3 months before subsiding.
→ Edema as well as a rash around the eyes
and face may subsequently occur.
→ Romaña’s sign – happens when patients
contract T.cruzi through the ocular mucosa
and develop a characteristic conjunctivitis
and unilateral edema of the eyelids
→ Chronic Chaga’s disease may occur after the
initial diagnosis of an acute disease or years
to decades after being asymptomatic.
Multiple destruction of tissues which
presents as myocarditis,
hepatosplenomegaly, enlargement of the
colon, and esophagus sometimes referred to
as megacolon and megaesophagus,
respectively. CNS involvement,
cardiomegaly and electrocardiographic
changes maybe seen.
→ Patients suffering from the acute Chaga’s
disease typically experience fever, chills,
fatigue, myalgia and malaise.
An attack of the acute infection may
result in one of the following scenarios: 1.
recovery;
2. transition to the chronic stage of disease;
or
3. death, which usually occurs a few weeks
after the attack.
→ Chaga’s disease is most commonly seen in
children younger than 5 years. These
patients characteristically present with
symptoms of CNS involvement and
experience the most severe form of the
disease
Laboratory Diagnosis
Giemsa-stained blood slides are the
specimens of choice for the detection of
T.cruzi trypomastigotes.
→ Lymph node biopsy Giemsa-stained slides,
and blood culture may reveal the typical
amastigote.
→ Serologic tests include Complement fixation,
DAT, and indirect immunofluorescence, PCR
and ELISA are available for diagnostic
purposes. ELISA is presently used in blood
donor screening to help ensure the safety of
transfusable blood and transplantable organ.
→ Xenodiagnosis is a traditional method of
diagnosing T.cruzi.
→ PCR method may replace xenodiagnoses in
patients with chronic disease and that it can
be used in the screening of blood bank
donors
Treatment, Prevention and Control
Treatment of choice is nifurtimox (Lampit).
→ Other medications include benznidazole,
allopurinol, and the antifungal agent
ketoconazole.
→ Prevention and control measures
include the eradication of reduviid bug
nests and the construction of homes
without open design. DDT has proved to
be useful, not only to control the reduviid
population but also to decrease the
incidence of malaria when used in
buginfested homes.
→ Educational programs designed to
inform people of,especially in endemic
areas, of the disease, its transmission,
and possible reservoir hosts
TRYPANOSOMA RANGELI
→ Found in many geographic regions as
T.cruzi
→ No common names known for disease
caused by this organism. Infections are
generally asymptomatic and tend to show
no pathologic changes or signs of
disease.
→ Its life cycle is the same as that of T.
cruzi. The reduviid bug, Rhodinus
prolixus, which transmit parasitic disease
via saliva and is attracted to the open
house design, is responsible for T.rangeli
transmission.
→ It has numerous reservoir hosts such as
monkeys, dogs, cats, armadillos and
rodents
→ Giemsa-stained blood slides are the
specimen of choice for its detection. It can
also be diagnosed by xenodiagnoses,
serologic testing and PCR based
methods.
→ The drug of choice for its treatment
are nifurtimox and benzimidazole
By: HORLADOR, CJ 9