nd invade the genital ridges in the sixth week of development. here they form primitive sex cords. in the absence of tdf, medullary cords disappear and get replaced by a vascular stroma (ovarian medulla). cortical cords develop and surround one or more primitive germ cells. the germ cells subsequently develop into oogonia, while the surrounding epithelial cells form the follicular cells. this differentiates undifferentiated gonads into ovaries. stroma of ovary develops from basal mesenchyme. granulosa and theca cells develop from celomic epithelium. development of genital ducts development of genital duct system and the external genitalia occurs under the influence of hormones circulating in the fetus. sertoli cells in the fetal testes produce a nonsteroidal substance known as müllerian inhibiting substance (mis) that causes regression of müllerian ducts. androgen from the fetal testes causes masculinization of external genitalia. in the absence of mis, müllerian ducts develop and mesonephric duct system regresses. in the absence of androgen, external genitalia differentiate into female phenotype. the müllerian duct develops between the fifth and sixth weeks lateral to intermediate cell mass and wolffian duct. the müllerian duct has the following three parts: •cranial vertical portion that opens into celomic cavity. later it differentiates into fallopian tubes. •horizontal part crosses the mesonephric duct. •caudal vertical part that fuses with its partner from opposite side. this fused part later differ entiates into uterus, cervix, and upper one-third of the vagina. the dorsal celomic epithelium (which forms müllerian duct) remains open at its site of origin and ultimately forms the fimbriated ends of the fallopian tubes. at their point of origin, each of the müllerian ducts forms a solid bud. each bud penetrates the mesenchyme lateral and parallel to the wolffian duct. as the solid buds elongate, a lumen appears in the cranial part, beginning at each celomic opening. the caudal end of each müllerian duct crosses the way

1. HCM 124: MEDICAL PARASITOLOGY AND
ENTOMOLOGY
JACKSON C. KORIR (PhD)
0721- 413 606
jcheruiyot@mmust.ac.ke
Masinde Muliro University
of Science and Technology
(MMUST)
University of Choice

2. BLOOD & TISSUE FLAGELLATES/
HAEMOFLAGELLATES

3. Blood & Tissue Protozoa
The Hemoflagellates:
 The family Trypanosomatidae contains only
two genera that parasitize humans.
 Genus Trypanosoma contains members that
may be found either in the circulating blood or
intracellularly (in cardiac muscle). African -
blood; American - blood & cardiac muscle.
 Genus Leishmania are always intracellular,
principally in cells of the reticuloendothelial

4. Haemoflagellates
 Originally parasites of insects; these now serve as
intermediate hosts.
 American trypanosomiasis - transmitted by reduviid
bugs.
 African trypanosomiasis - transmitted by Glossina
spp. tsetse flies.
 "Old World” leishmaniasis - transmitted
Phlebotomus spp. sandflies.
 American leishmaniasis - transmitted by
Lutzomyia spp. sandflies.

5. Morphologic forms
 There are 4 morphologic forms seen in
hemoflagellates:
1) Amastigote
2) Promastigote
3) Epimastigote
4) Trypomastigote
-they can exist in two or more of the 4 morphologic
forms  depending on the species.

6. Morphologic forms

7. Kingdom: Protisata
Phylum: Sarcomastigophora
Class: Zoomastigophora
Order: Kimetoplastida
Family: Trypanosomatidae
Genus: Leishmania
Species: donovani , tropica, mexicana, braziliensis
Leishmania

8. Leismania sp.
Can cause:
1) Cutaneous leishmaniasis: a localized
infection of the capillaries of the skin.
2) Mucocutaneous leishmaniasis: cause
lesions of the skin and mucous membranes,
specifically of the oral and nasal mucosa.
3) Visceral/systemic leismaniasis: more
generalized symptoms leading to
enlargement of the internal organs,
especially the liver, lymph nodes and
spleen.

9.  Indistinguishable in appearance.
 Differentiated based on:
- Geographic distribution.
- Pathogenesis.
- Kinetoplast DNA (kDNA) analysis
- DNA hibridization
- Serologic testing.

10. Geographical distribution

11. Leishmania sp.
Divided into 4 groups:
1) Leishmania tropica complex – Old World
Cutaneous Leismaniasis.
2) Leishmania mexicana complex – New World
Cutaneous Leishmaniasis.
3) Leishmania braziliensis complex –
Mucocutaneous Laishmaniasis.
4) Leishmania donovani complex – Visceral
leishmaniasis.

12. Stage of life
 Only have 2 stages of life:
1) Amastigote
2) Promastigote

13. Amastigote
 Size: 5 by 3µm
 Shape: oval to round
 Nucleus: One,
eccentric.
 Kinetoplast: Present,
Consisting of dot-like
blepharoplast, with
small axoneme and
prabasal body.
 Flagellum: absent

14. Promastigote
 Size: 9-15µm
 Shape: long and
slender.
 Nucleus: one,
central.
 Kinetoplast: Anterior
end of the organism,
no undulating
membrane.
 Flagellum: Single,
anterior free
flagellum.

15. Leishmaniasis is transmitted by
the bite of female phlebotomine
sandflies. 1.The sandflies inject
the infective stage,
promastigotes, during blood
meals . Promastigotes that
reach the puncture wound are
phagocytized by macrophages2
and transform into amastigotes 3
. Amastigotes multiply in infected
cells and affect different tissues,
depending in part on the
Leishmania species 3. This
originates the clinical
manifestations of leishmaniasis
4. Sandflies become infected
during blood meals on an
infected host when they ingest
macrophages infected with
amastigotes (5,6). In the
sandfly's midgut, the parasites
differentiate into promastigotes 7
, which multiply and migrate to
the proboscis 8 .

16. Leishmania tropica complex – Old
World Cutaneous Leismaniasis.
 L. tropica - mediterranean region, middle East,
Armenia, Caspian region, Afghanistan, India and
Kenya (particularly in urban areas)
 L. aethiopica – Highlands of Ethiopia, Kenya and
Southern Yemen.
 L. major – Desert regions of Turkmenistan,
Uzbekistan and Kazakhstan, Northern Africa and
the Sahara, Iran, Syria, Israel and Jordan.

17. Pathology
 Cause a chronic disease: cutaneous leishmanisis.
 Also known as Oriental sore, Delhi boil and dry or
urban cutaneous leishmaniasis.
 Characterized by: production of dry, raised,
ulcerated lesions at bite sites.
 Vectored by: tiny sandflies of the genera
Phlebotomus.

18. L. tropica

19. Vector: Phlebotomus sandfly

21. Transmission & Pathogenesis
 Incubation period vary from several weeks to as
three years.
 First sign of cutaneous leishmaniasis= the
development of a small red papule at the initial
site of the insect bite.
 A local granulomatous response leads to the
formation of a crateriform lesion  2cm or more.
 L. tropica n L. aethiopica produce dry lesions.
 L. major  produce moist lesions with a serous
exudate.
 Lesions can heal spontaneously but may leave
serious scars.

22.  Contact spread of infection also possible.
 Patient may produce multiple sores by scrathing and
autoinoculating normal skin.
 Diffuse cutaneous leishmaniasis (DCL):
-occur in anergic patient (who is unable to amount an
adequate immune response).
-characterized by the presence of multiple nodular
lesions, particularly on the face and limbs.
-loaded with parasites and do not heal spontaneously.

23. DCL

25. Laboratory Diagnosis
 Montenegro (leishmanin) skin test
-delayed hypersensitivity reaction provoked by
a suspension of killed leishmanial
promastigotes administered intradermally.
-local inflammatory reaction appears at the site
of injection within 48-72 hours.
 Microscopy examination
 Isoenzyme studies
 Molecular diagnostic technique- PCR
 Serologic test – ex: indirect fluorescent
antibody assay.

26. Treatment
 Sodium stibogluconate (antimony sodium
gluconate: Pentostom).
 Meglumine antimonate
 Glucantime
 Ampotericin B
 Ketoconazole

27. Prevention
 Use of bed netting
 Insect repellent and residental spraying
 Rodent control in reducing transmission.
 Individuals with active lesions  promptly treated,
wound covered  to prevent autoinfection and
further insect transmission to other individuals.

28. Leishmania mexicana complex –
New World Cutaneous Leishmaniasis
 L. mexicana – Belize, Guatemala, and the Yucatan
peninsula.
 L. pifanoi – Amazon river basin and parts of Brazil
and Venezuela.
 L. amazonensis – Amazon basin of Brazil.
 L. venezuelensis – forests areas of Venezuela.
 L. garnhami – Venezuelan Andes.

29. Pathology
 Distribution extends from Southern Texas in the
United states, through Mexico, Central and South
America.
 L. mexicana causes chiclero ulcer or Bay sore.
 L. pifanoi causes DCL.
 L. amazonensis causes cutaneous and DCL.
 L. venezuelensis causes cutaneous leishmaniasis.
 L. garnhami causes Venezuelan Andean
cutaneous leishmaniasis.

30. Life cycle
 Transmitted by Lutzomiya sandfly
 Reservoir host: rodents, opossums, domestic
dog, cat etc.
 Life cycle same with L. mexicana complex.

31. Vector: Lutzomiya sandfly

32. Transmission & Pathogenesis
 L. mexicana - produces a lesion known as chiclero
ulcer or Bay sore – common among workers who
collect chicle gum from the Chicazapote trees in the
rain forest in Nicaragua, Guatemala, Belize and the
Yucatan peninsula of Mexico.
 Clinical manifestation: a single cutaneous papule,
nodule or ulcer located on the ear or face. Lesion
generally heal spontaneously but may cause
cartilage destruction and gross disfigurement.

33.  L. pifanoi and L. amazonensis – produce a single but
more likely to progress to the DCL – the majority
patient infected, clustered in the Amazon river Basin
of Brazil and Venezuela.
 Clinical presentation of DCL may be confused with
Leptomatous Leprosy.
 L. garnhami and L. venezuelensis – assosiated with
cutaneous leishmaniasis in rural parts of Venezuela
– infection with either organism present with a
solitary lesion that is usually self-limiting.

34. Leptomatous Leprosy
Picture: Mildly elevated indurating nodules are seen on the face
and extremities (gross findings).

36. Diagnosis
 Giemsa stained smears –amastigotes will be
seen.
 Cultivation – promastigotes forms can be
obtained.
 Immunological testing methods.

37. Treatment
 In most cases, the infections are self-limiting and
require no treatment.
 Treatment is paramount if:
-the lesion should endure or
-threaten cartilaginous structures; ear,nose.
 Therapeutic agents: same as the treatment of
Oriental sore.

38. Prevention
 Same as the prevention ways of Oriental sore.
 applied insect repellent to the skin and garments
along with aerial spraying.

39. Leishmania braziliensis complex –
Mucocutaneous Leishmaniasis
 L. braziliensis – Mexico to Argentina
 L. panamensis – Panama and Columbia
 L. peruviana – Peruvian Andes.
 L. guyanensis – Guiana and parts of Brazil and
Venezuela.

40. Epidemiology
 Cause infections throughout the Americas from
Mexico to Argentina.
 The distinguishing feature of these infectious is the
development of ulcers on or about the oral and nasal
mucosa
 L. braziliensis causes espundia.
 L. guyanensis causes pain bois.
 L. peruviana causes uta.
 All cause considerable morbidity and mortility in the
endemic areas.

41. espundia

42. Life cycle
 Same with L. mexicana complex
 Vector: Lutzomyia and Psychodopygus sandflies.

43. Pathogenesis
 The primary lesion-same manner as the
Oriental sore: macrophage ingest the
parasites  become heavy laden with
replicating amastigotes  tissue damage.
 Invade mucous membranes of the mouth and
nasopharynx.
 Spread by: direct extension of the primary
lesion or metastasis via the bloodstream or
lymphatics.
 Progression of disease may take years.

44.  Resulting disease: may produce ulcers that erode
soft tissues of the face and palate or form polyp-like
appendages in the nasal cavity.
 Patient commonly present with enlargement of the
regional lymph nodes and secondary bacterial
infections.
 Untreated  patients generally succumb to these
secondary infection or to starvation if destruction of
the oral cavity is extensive.

47. Diagnosis
 By demonstrating amastigotes of Leishmania in
Giemsa stained smears or biopsy material from
the edge of an active ulcer.
 Cultivation.
 Serologic test.
 Montenegro skin test.

48. Treatment
 Sodium antimony (Pentostom).
 Cycloguanil pamoate (Camolar).
 Amphotericin B (Fungizone).
 Meglumine antimonate
 Glucantime
 Ketoconazole

49. Prevention
 Personal protective measures such as :protecting
clothing, insect repellents and etc.
 Vector control
 Reservoir host control
 Public health educational programs.
 Prompt treatment of infected individuals  to
break the cycle of disease transmission.

50. Leishmania donovani complex –
Visceral leishmaniasis
 L. donovani – India, Pakistan, Thailand, parts of
Africa and the Peoples Republic of China.
 L. infantum – Mediterranean area, Europe, Africa,
the Near East, and parts of the former Soviet Union.
 L. chagasi – Central and South America.

52. Morphology
 Visceral leishmanisis also known as Kala Azar
or dum-dum fever.
 The most severe of the Leishmaniasis.
 Generally a disease of juveniles and young
adults.
 Natural reservoir: rodents and dog.
 In India, man appears to be the only mamalian
reservoir.
 L. donovani complex –parasitize the
reticuloendothelial cells, viscerotropic, infected
macrophages remaining fixed or disseminate
throughout the body.

53.  In the Mediterranean are, Europe, Africa, Soviet
union – Phlebotomus sandfly remains the vector.
Natural reservoir: domesticated dogs, canines and
porcupines.
 In the New World (Central and South America) –
Lutzomiya sandfly remains the vector. Natural
reservoir: Foxes, domestic dogs and cats.

54. Life cycle
 Same with L. mexicana complex.
 The infected mononuclear phagocytes do not
remain confined to the skin or mucous
membranes.
 Parasitized macrophages are carried by the
bloodstream to lymphoid tissue throughout the
body especially to the spleen, liver and bone
marrow.
 Amastigotes multiply in great numbers in this
tissues.
 Vectors: Phlebotomus sandfly and Lutzomiya
sandfly .

55. Transmission & pathogenesis
 Transmitted by sandflies.
 Incubation period: 3 weeks to 2 years.
 The infected macrophages migrate by lymphatic and
hematogenous  spread to distant lymphoid tissues
throughout the body.
 Transmission via blood transfusion is also possible.

56.  Early symptoms: prodome of headache, malaise,
fever, possible weight loss and abdominal pain.
 Fever may occur in periodic intervals mimicking
tertian or quartan malaria.
 Another symptoms: diarrhea, consistent with
typhoid fever, enlargement of liver and spleen
(hepatosplendomegaly) and lymph nodes
(lymphadenopathy), and increase in serum
globulin levels.
 Microscopically, parasitized macrophages may
be found in the tissue of the spleen, liver, heart,
kidneys, lymph nodes, intestines and bone
marrow.

57.  Rapid proliferation of reticuloendothelial cells within
the involved organs lead to organ hypertrophy.
 Parasitized macrophages may crowd out other
hematopoietic cells leading to various degrees of
anemia and leukopenia.
 The infiltration of the intestinal mucosa may result in
ulceration and yield malabsorption, and wasting.

58.  As the patient become more emaciated, the
abdominal distention from the hepatosplenomegaly
becomes more pronounced.
 A characteristic hyperpigmentation of the forehead
and hands, known in India as Kala Azar, may also be
observed.
 The prognosis for untreated cases is poor.
 Mortality rate can be as high as 95%.
 In chronic cases, death usually occurs from medical
complications or bacterial infections within 2 years of
diagnosis.

59.  With treatment, the prognosis is usually much better.
 Recovering leads to a lasting immunity.
 In some patients, a condition called post- kala azar
dermal leishmaniasis, or dermal leishmoid, may
develop following the treatment with antimony
compounds.
 The clinical presentation of this condition is marked
by the appearance of either erythematous or
hypopigmented lesions anywhere on the body.

60.  A butterfly rash is a characteristic of systemic lupus
erythemous. – may develop on the malar portion of
the face.
 The dermal lesions, whether a papule or patch, may
progress to nodules and resemble lepromatous
leprosy.
 These lesions do contain viable parasites and can
serve as a reservoir of infection.

63. Diagnosis
 Tissues Biopsy
 Direct examination of stained smears.
 Cultivation.
 Serologic test.
 Direct agglutination test (DAT).
 Complement fixation test (CF).
 Indirect fluorescence technique.
 Molecular diagnostic technique.
 Montenegro skin test (not reactive in people
with active disease).

64. Treatment
 Pantavalent antimony sodium gluconate
(Pentostom).
 Pentamidine isothionate (Lomidine)
 Amphotericin B
 Allopurinol + Pentostom
 Gamma interferon + Pentostom.

65. Prevention
 Same with the others leishmania sp.

69. Trypanosomiasis

70. Etiologic agents
 Trypanosoma brucei complex – African
trypanosomiasis (sleeping sickness)
 Trypanosoma cruzi – American trypanosomiasis
(Chagas’ disease)

71. Important features
 These species may have amastigote, promastigote,
epimastigote, and trypomastigote stages in their life
cycle.
 Human trypanosomes of the African form, has only
epimastigote and trypomastigote stages
 Typical trypanosome structure is an elongated spindle-
shaped body that more or less tapers at both ends, a
centrally situated nucleus, a kinetoplast posterior to
nucleus, an undulating membrane arising from the
kinetoplast and proceeding forward along the margin
of the cell membrane and a single free flagellum at
the anterior end.

72. Human African trypanosomiasis (HAT)
 Also called sleeping sickness, is an illness endemic to
sub-Saharan Africa.
 Caused by the Trypanosoma brucei, which exists in 2
morphologically identical subspecies:
 Trypanosoma brucei rhodesiense (East African or Rhodesian
African trypanosomiasis)
 Trypanosoma brucei gambiense (West African or Gambian
African trypanosomiasis).
 Both of these parasites are transmitted to human hosts
by bites of infected tsetse flies
- (Glossina palpalis transmits T brucei gambiense
- Glossina morsitans transmits T brucei rhodesiense)

73. Causes
 A bite from an infected tsetse fly causes African
trypanosomiasis .
 Blood transfusions are a rare cause of parasitic
transmission.
 In rare cases, accidental transmission in the laboratory
has been implicated.
 The reservoirs of infection for these vectors are
exclusively human in West African trypanosomiasis.
However, East African trypanosomiasis is a zoonotic
infection with animal vectors.

74. Dr. JC Korir 2015

75. Dr. JC Korir 2015

76. Dr. JC Korir 2015

77. Pathophysiology
 The parasites escape the initial host defense mechanisms
by extensive antigenic variation of parasite surface
glycoproteins known as major variant surface glycoprotein
(VSG).
 This evasion of the humoral immune responses contributes
to parasite virulence.
 During the parasitemia, most pathologic changes occur in
the hematologic, lymphatic, cardiac, and central nervous
systems. This may be the result of immune-mediated
reactions against antigens on red blood cells, cardiac
tissue, and brain tissue, resulting in hemolysis, anemia,
pancarditis, and meningoencephalitis

78.  A hypersensitivity reaction causes skin problems,
including persistent urticaria, pruritus, and facial edema.
 Increased lymphocyte levels in the spleen and lymph
nodes infested with the parasite leads to fibrosis but
rarely hepatosplenomegaly.
 Monocytes, macrophages, and plasma cells infiltrate
blood vessels, causing endarteritis and increased vascular
permeability

79.  The gastrointestinal system is also affected. Kupffer cell
hyperplasia occurs in the liver, along with portal
infiltration and fatty degeneration.
 Hepatomegaly is rare. More commonly in East African
trypanosomiasis, a pancarditis affecting all heart tissue
layers develops secondary to extensive cellular infiltration
and fibrosis.
 The typical somnolence (sleeping sickness) usually
progresses to coma as a result of demyelinating
encephalitis.

80. Epidemiology
 Sleeping sickness threatens millions of people in 36 countries.
In 1986, it was estimated that some 70 million people lived in
areas where disease transmission could take place.
 In 1998, almost 40 000 cases were reported, but estimates
were that 300 000 cases were undiagnosed and therefore
untreated.
 By 2005, surveillance was reinforced and the number of new
cases reported on the continent was reduced; between 1998
and 2004 the number of both forms of the disease fell from
37 991 to 17 616. The estimated number of actual cases was
between 50 000 and 70 000.

81. Dr. JC Korir 2015

82. Current situation in endemic countries
 In the last 10 years, over 70% of reported cases
occurred in the Democratic Republic of Congo (DRC).
 In 2008 and 2009 only the DRC and Central African
Republic declared over 1000 new cases per year.
 Angola, Chad, Sudan and Uganda declared between
100 and 1000 new cases per year.

83. Clinical Presentation
 History
 Stage 1 (early, or hemolymphatic, stage)
 Painless skin chancre that appears about 5-15 days after the
bite, resolving spontaneously after several weeks (seen less
commonly in T brucei gambiense infection)
 Intermittent fever (refractory to antimalarials), general malaise,
myalgia, arthralgias, and headache, usually 3 weeks after bite
 Generalized or regional lymphadenopathy (Posterior cervical
lymphadenopathy [Winterbottom sign] is characteristic of T
brucei gambiense African trypanosomiasis [sleeping sickness].)

84.  Facial edema (minority of patients).
 Transient urticarial, erythematous, or macular rashes
6-8 weeks after onset
 Trypanids (ill-defined, centrally pale, evanescent,
annular or blotchy edematous erythematous
macules on trunk)

85.  Stage 2 (late, or CNS, stage) Persistent
 headaches (refractory to analgesics)
 Daytime somnolence followed by nighttime insomnia
 Behavioral changes, mood swings, and, in some patients,
depression
 Loss of appetite, wasting syndrome, and weight loss
 Seizures in children (rarely in adults)
 Fevers, tachycardia, irregular rash, edema

86. Dr. JC Korir 2015

87. Dr. JC Korir 2015

88. Dr. JC Korir 2015

89. Dr. JC Korir 2015

90. Laboratory Studies
 General
 In African trypanosomiasis (sleeping sickness), the most
significant laboratory abnormalities include anemia,
hypergammaglobulinemia, low complement levels, elevated
erythrocyte sedimentation rate (ESR), thrombocytopenia, and
hypoalbuminemia, but not eosinophilia or abnormal liver
function.
 In West African trypanosomiasis, the total immunoglobulin M
(IgM) level is notably higher in blood and CSF (along with high
CSF protein).
 A definitive diagnosis of infection requires actual detection of
trypanosomes in blood, lymph nodes, CSF, skin chancre
aspirates, or bone marrow. However, symptomatic improvement
after empiric treatment is the usual confirmatory test in areas
where diagnostic studies are not readily available.

91.  Lymph node aspiration at a high dry magnification (X400)
is commonly used as a rapid test for trypanosomes. It
requires immediate search for parasites because they are
mobile for only 15-20 minutes. This test has more utility
in T brucei gambiense trypanosomiasis.

92. Blood smear
 A wet smear of unstained blood or Giemsa-stained thick
smear (more sensitive) is used to evaluate for mobile
trypanosomes, again for 15-20 minutes.
 Better assays are now available, including the hematocrit
centrifugation technique for buffy coat examination and
the miniature anion-exchange centrifugation technique
(mAECT), which filters out the red cells but not the
trypanosomes.

94.  Chancre aspirate can be used as a wet preparation,
especially in East African trypanosomiasis, but a blood
smear is more sensitive.
 Bone marrow aspiration results may be positive in some
patients.
CSF assay
 Lumbar puncture should be performed whenever
trypanosomiasis is suspected. CSF examination helps to
diagnose and stage the disease. However, a negative
result does not necessarily rule out the diagnosis.
 The double centrifugation technique is the most sensitive
method to detect the trypanosomes.

95. Imaging Studies
 CT scanning and MRI of the head: Both head CT
scanning and MRI reveal cerebral edema and white
matter enhancement, respectively, in patients with
late-stage African trypanosomiasis.
 EEG in neurologic involvement usually shows slow
wave oscillations (delta waves), a nonspecific finding

96. Other tests:
Serologic antibody detection
 The standard serologic assay to diagnose West African
trypanosomiasis is the card agglutination test for
trypanosomiasis (CATT).
 Antigen detection tests based on enzyme-linked
immunosorbent assay (ELISA) technology have been
developed. They have shown inconsistent results and are
not yet commercially available.
 Culture of CSF, blood, bone marrow aspirate, or tissue
specimens can be performed in liquid media.
 Other tests developed but not frequently used clinically
include antibody detection in the CSF and intrathecal
space (low sensitivity), polymerase chain reaction (PCR),
and serum proteomic tests.

97. Dr. JC Korir 2015

98. Treatment & Management
 Pre-hospital care of African trypanosomiasis (sleeping
sickness) centers on management of the acute
symptoms of fever and malaise while closely
monitoring the patient’s neurologic status.
 In the emergency department, if CNS symptoms are
severe, then airway management to prevent
aspiration becomes important, along with an
immediate blood smear, CBC count, and lumbar
puncture for trypanosome detection.

99. Stage 2
(Neurologic [CNS]
Stage)
Stage 1
(Hemolymphatic
Stage)
Type of
Trypanosomiasis
Melarsoprol
Suramin
East African
trypanosomiasis
(caused by T brucei
rhodesiense)
Melarsoprol
or
Eflornithine
Pentamidine
isethionate
or
West African
trypanosomiasis
(caused by T brucei
gambiense)

101. American Trypanosomiasis
( Chagas Disease)

102.  Chagas disease, or American trypanosomiasis, is caused
by the parasite Trypanosoma cruzi.
 Infection is most commonly acquired through contact
with the feces of an infected triatomine bug (or "kissing
bug"), a blood-sucking insect that feeds on humans and
animals.
Infection can also occur from:
 mother-to-baby (congenital),
 contaminated blood products (transfusions),
 an organ transplanted from an infected donor,
 laboratory accident, or
 contaminated food or drink (rare)

103. Genera
• Triatoma
• Rhodnius
• Panstrongylus
Common Names
• triatomine bugs
• reduviid bugs
• assassin bugs
• kissing bugs
• conenose bugs

104. Epidemiology
 Chagas disease is endemic throughout much of
Mexico, Central America, and South America where an
estimated 8 to 11 million people are infected.
 The triatomine bug thrives under poor housing
conditions (for example, mud walls, thatched roofs),
so in endemic countries, people living in rural areas
are at greatest risk for acquiring infection

105. Dr. JC Korir 2015

106. Dr. JC Korir 2015

107. Types of Vector Transmission
Salivarian Stercorarian
 transmission via
mouth parts
 very efficient
 infection rate in
vector is low
 hind gut station
 acquired from feces
or eating vector
 inefficient
 infection rate in
vector is high
Dr. J.C. Korir 2015

108. Disease
 Chagas disease has an acute and a chronic phase.
If untreated, infection is lifelong.
 Acute Chagas disease occurs immediately after
infection, may last up to a few weeks or months, and
parasites may be found in the circulating blood.
Infection may be mild or asymptomatic.
 There may be fever or swelling around the site of
inoculation (where the parasite entered into the skin
or mucous membrane). Rarely, acute infection may
result in severe inflammation of the heart muscle or
the brain and lining around the brain.

109.  Following the acute phase, most infected people
enter into a prolonged asymptomatic form of disease
(called "chronic indeterminate") during which few or
no parasites are found in the blood.
 During this time, most people are unaware of their
infection. Many people may remain asymptomatic for
life and never develop Chagas-related symptoms.
However, an estimated 20 - 30% of infected people
will develop debilitating and sometimes life-
threatening medical problems over the course of
their lives.

110. Complications of chronic Chagas disease may
include:
 heart rhythm abnormalities that can cause sudden
death; a dilated heart that doesn’t pump blood well;
a dilated esophagus or colon, leading to difficulties
with eating or passing stool.
 In people who have suppressed immune systems
(for example, due to AIDS or chemotherapy),
Chagas disease can reactivate with parasites
found in the circulating blood. This occurrence can
potentially cause severe disease.

113. Laboratory Diagnosis
Demonstration of the causal agent is the diagnostic
procedure in acute Chagas disease. It almost
always yields positive results, and can be
achieved by:
 Microscopic examination: a) of fresh
anticoagulated blood, or its buffy coat, for motile
parasites; and b) of thin and thick blood smears
stained with Giemsa, for visualization of
parasites.
 Isolation of the agent: a) inoculation in culture
with specialized media (e.g. NNN, LIT); b)
inoculation into mice; and c) xenodiagnosis,
where uninfected triatomine bugs are fed on the
patient's blood, and their gut contents examined

114.  During the chronic phase of infection, parasitemia is
low; immunodiagnosis is a useful technique for
determining whether the patient is infected.
Antibody detection

116. The two drugs used to treat infection with Trypanosoma
cruzi are nifurtimox and benznidazole.