American

Trypanosomiasis
Causative agent: Trypanosoma
cruzi

Background information
Described

in 1909 by Carlos

Chagas
16- 18 million people estimated to be
infected
100 million people at risk of
becoming infected

Historical Background - 2

Carlos Chagas

Distribution of
Chagas,
Disease:Trypanosoma
cruzi

Geographical Distribution
Brazil,

chile, Argentina, Uruguay,

Paraguay, Bolivia, Peru,
Columbia, Guiana, Venezuela,
Panama, Costarica, Guatemala,
Mexico, Texas (U.S.A)

Morphology 1: Trypanosoma cruzi

The parasite exists in two forms: 1.

Trypomastigotes- Size: 20 m long and
assumes a C shape in blood
Nucleus
Kinetoplast
Flagellum

Morphology 2 - Trypomastigote

Morphology 3- 2. Amastigotes

Amastigotes in tissue

Morphology 4- Amastigote

Amastigote: 1.5 4 m in Diameter

Biology and Life Cycle

Location in Vertebrate host

Trypomastigotes In blood
Amastigotes Reticuloendothelial and other
tissues
Frequent locations in Man:
Reticuloendothelial cells of: Spleen, Liver,
Lymphnodes, Lymphatic tissues and
myocardium. Cells of striated muscles, bone
marrow, suprarenal glands , testes, ovaries ,
nervous system, histiocytes of cutenous
tissue, cells of the epidermis and the
intestinal mucous membrane.

Biology and Life cycle

Epidemiology -I
Chagas disease is a typical ZOONOTIC
disease
Transmission occurs when metacyclic
trypomastigotes are rubbed into the
puncture wound made by the insect/or
abrasion of the skin
Congenital transmission
Blood transfusion (contaminated blood
products)
Organ transplant from an infected donor

Epidemiology II Transmission

Laboratory accident
Contaminative
Eating infected bug
Children between a few months and two
years affected
Triatoma prefer to bite at junction of mucus
and cutaneous surface (painless bite
KISSING Bug
Incidence in vectors 40 -50% but current
control initiatives have reduced incidence to
low level. Bugs live in walls of mud and
thatch

Epidemiology -III

Reduviid Bugs

Pathogenesis, Pathology and

Symptomatology

Incubation period in man: About 7 to 14

days or 12 to 30 days
Acute Disease: Characterized by active
infection, inflammation and myocardial
damage.
At the site of Entry:
Metacyclics enter or are engulfed by
histiocytes
Invade adipose tissue and muscle cells
Multiplication as amastigote- Host cell
rupture on day 4 or 5
Polymorphonuclear cells, monocytes

Pathogenesis, Pathology and

Symptomatology - II
Result in local inflammatory reaction and
fibrotic encapsulation primary lesion
(CHAGOMA)
Reaction block lymphatic capillaries&produce
edema of the area (Romnas sign
characterized by swollen face, marked
edema of the eye leads of one or both
eyes)
Patient appears to be suffering from
myxedema, edema does not pit and the skin
is dry
Unilateral palpebral edema is most common

Symptomatology: Romanas sign

Symptomatology: Romanas sign

Pathogenesis, Pathology and

Symptomatology -III
Metastasis
Amastigotes metastasize to satellite lymphnodes
distributed in blood to: axillary and inguinal
lymphnodes, lungs, spleen, liver, Bone marrow
and mesenteric lymphnodes
Amastigotes multiply in: fixed histiocytes,
myocardium, neuroglia, microglia, pyramidal cells
of the brain cortex, adrenal cortex, thyroid gland
and intestinal mucosa
Trypomastigotes are released in blood when host
cell rupture. This is accompanied by fever &
characterize the acute phase

Pathogenesis, Pathology and

Symptomatology - IV
Heart is always invaded myocardial cells are
parasitized & destroyed This leads to
myocarditis in acute Chagas disease
Myocarditis manifest by tachycardia,
weakness, chest pain and
electrocardiographic changes
Acute stage resolve spontaneously in 3 to 4
months in the majority of cases. A fulminant
course end fatally in 3 to 4 weeks. Other acute
clinical symptoms include; malaise,
lymphadenopathy, hepatosplenomegaly,
vomiting and diarrhea

Destructive effects of
Amastigotes in Cardiac muscle

Amastigotes

Pathogenesis, Pathology and

Symptomatology -V
Chronic Chagas Disease
Predominant in adults
Symptoms are related to the damage sustained
during the acute phase and depend on the
localization of the intracellular parasites
Characterized by myocardial involvement or
mega syndromes, cardiomyopathy may be
present with arrhythmias, conduction defects,
cardiomegaly and congestive heart failure
Mega syndromes are a common feature of
chronic Chagas disease in certain geographical
locations

Pathogenesis, Pathology and

Symptomatology - VI
Strains: Geographical strains exist vary in
organs invaded
Neurotropic, Viscerotropic or
Cardiotropic
Neurotropic strains invade Neuroglia -encephalits, meningoencephalitis and
encephalomyelitis may occur and is fatal
in children
Viscerotropic Strains: Nerve cells in the
autonomic ganglia in the hollow viscera are
commonly destroyed.

Amastigotes of T. Cruzi in
Tissue

Amastigotes

Pathogenesis, Pathology and

Symptomatology - VII
This

results in disruption of neural

coordination for the initiation of
peristaltic waves in the viscusMEGA disease characteristic of
Chagas.
Conditions such as:
Megaesophagus, megacolony and
Megaureta occur
Cardiotropic forms 50% of patients
sudden death occur due to heart

Diagnosis
Clinical Diagnosis
History of living in bug infested house
Presence of Chagoma, Romanas sign
Cardiac or Gastrointestinal symptoms
Laboratory Diagnosis
Early stages: Trypomastigotes in blood
film

Amastigotes in muscle biopsies

Later stages: Parasites are usually low

Diagnosis - II
Methods:

(a) Xenodiagnosis use clean

laboratory reared bugs

(b) Serology IHA, IFAT,
ELISA
Differential

diagnosis: Kala- Azar

endemic in Latin America. Use cultures,
immunological tests or xenodiagnosis

Treatment
Symptom relief only
1. Nifurtimox- 5mg/kg/day in 4 divided
doses- increase by 2mg/kg/day every 2
weeks until a dosage of 15- 17 mg
/kg/day
2. Primaquine phosphate -26.3 mg ( 15mg
base/day) for 7 -10 days
3. Benzinidazole 5 -7 mg/kg/day (30 -120
days)
4. Allopurinol

Prevention
Vaccine with Trypanosoma rangeli
produced positive results in Animal models
DNA vaccine for immunotherapy of acute
and chronic Chagas disease is being
tested
0.5g/L of gentian violet kills T. cruzi
Antifungal agent amphotericin B has been
proposed as a second line treatment but
high cost and relatively high toxicity of the
drug have limited its use

Management of Clinical
Manifestations
Pacemakers

and medications for

irregular heartbeats
Direct stem cell therapy of heart
muscle using the bone marrow cell
transplantation has shown to
decrease heart failure
Surgery for mega intestine
New drug targets may be revealed
following the sequencing of

Trypanosoma cruzi

Control/Prevention

Housing improvement lower bug colonization

Residual spraying with insecticides:
Fumigation canisters releasing pyrethroid
insecticide fumes when lit reduce bug
population in households & disease
prevalence
Insecticide paints used by spry teams:
Reduce prevalence of disease
Reduce house infestation by vectors
Gentian violet or amphotericin B is used to
kill T. cruzi in blood before blood transfusion
Health Education

References

Gordon C. Cook and Alimuddin I. Zumla.

Mansons Tropical Diseases, 22nd Edition
Saunders Elsevier 2009