Faculty of Life Sciences,

JSS Academy of Higher Education & Research

Mysuru

Assignment on

Trypanosoma cruzi

Submitted to

Dr Sumana K
Assistant Professor,
Department of Microbiology

Submitted by

CHETHAN M P
Reg No: MSCLS2000296
Paper : Virology
Department of Microbiology
Date of submission: 17/03/2021
 CONTENTS

 Introduction

 History

 Scientific classification

 Life cycle & Transmission

 Epidemiology

 Diagnosis

 Treatment

 Prevention

 Bibliography
 TRYPANOSOMA CRUZI

Introduction
Trypanosoma cruzi could be a protozoan parasite and therefore the agent of human
Chagas malady. Chagas malady is that the highest impact communicable disease in
geographical area and therefore the most typical explanation for infectious
myocardial inflammation within the world (Feldman and McNamara, 2000). though
human Chagas malady could be a Brobdingnagian public unhealthiness, humans
square measure really solely incidental hosts for T. cruzi. Trypanosoma cruzi is
extremely cosmopolitan in several wild and domestic mammals and so can ne'er be
eradicated. However, there's one major profit to animal disease infections like T.
cruzi: the various hosts that T. cruzi infects besides humans, together with rodents,
canines, and anthropoid primates, create outstanding models for learning the
medicine of T. cruzi infection, providing extremely reliable data relevant to the
human infections. Descriptions of the response to T. cruzi square measure
everywhere the map, from suppressed and ineffective to overexuberant and malady
promoting. However, the wealth of proof shows that immunity to T. cruzi is usually
extremely effective, leading to glorious management of parasite load and, often,
complete microorganism clearance. sadly, the consequence of the additional
common ‘control while not elimination’ outcome is that the accumulative tissue
harm and increasing probabilities of clinical malady that become additional severe
with increasing length of infection.

History
T. cruzi likely circulated in South American mammals long before the arrival of humans on
the continent. T. cruzi has been detected in ancient human remains across South America,
from a 9000-year-old Chinchorro mummy in the Atacama Desert, to remains of various ages
in Minas Gerais, to an 1100-year-old mummy as far north as the Chihuahuan Desert near
the Rio Grande. Many early written accounts describe symptoms consistent with Chagas
disease, with early descriptions of the disease sometimes attributed to Miguel Diaz
Pimenta (1707), Luís Gomes Ferreira (1735), and Theodoro J. H. Langgaard (1842).

Scientific Classification

Domain: Eukaryota
Life cycle & Transmission
Phylum: Euglenozoa

Class: Kinetoplastea

Order: Trypanosomatida

Family: Trypanosomatidae

Genus: Trypanosoma

Species: cruzi

An infected triatomine insect vector takes a provender and releases trypomastigotes in its
dejection close to the location of the bite wound. Trypomastigotes enter the host through
the wound or through intact membrane membranes, like the mucosa. Common triatomine
vector species for trypanosomiasis belong to the genera Triatoma, Rhodnius, and
Panstrongylus. within the host, the trypomastigotes invade cells close to the location of
vaccination, wherever they differentiate into animate thing amastigotes. The amastigotes
multiply by binary fission and differentiate into trypomastigotes, so area unit free into the
circulation as blood trypomastigotes. Trypomastigotes infect cells from a range of tissues
and rework into animate thing amastigotes in new infection sites. Clinical manifestations
may end up from this infective cycle. The blood trypomastigotes don't replicate (different
from the African trypanosomes). Replication resumes only the parasites enter another cell
or area unit eaten by another vector. The “kissing bug” becomes infected by feeding on
human or animal blood that contains current parasite. The eaten trypomastigotes rework
into epimastigotes within the vector’s midgut. The parasites multiply and differentiate
within the midgut and differentiate into infective metacyclic trypomastigotes within the
viscus. Trypanosoma cruzi may be transmitted through blood transfusions, organ
transplantation, transplacentally (from mother to unborn baby), and in laboratory accidents.

Vector-borne transmission
The vector-borne transmission route, occurring exclusively in the Americas, is still the
predominant mechanism for new human infections. The feces of infected bugs contain
metacyclic trypomastigotes that can enter the human body through the bite wound or
through intact conjunctiva or other mucous membranes.

Congenital transmission
Between 1 and 10% of infants of T. cruzi-infected mothers are born with congenital Chagas'
disease. Congenital transmission can occur from women themselves infected congenitally,
perpetuating the disease in the absence of the vector. Factors reported to increase risk
include higher maternal parasitemia level, less robust anti-T. cruzi immune responses,
younger maternal age, HIV and, in an animal model, parasite strain.

Blood-borne transmission
Transfusional T. cruzi transmission was postulated in 1936 and first documented in 1952.
The risk of T. cruzi transmission per infected unit transfused is estimated to be 10 to 25%;
platelet transfusions are thought to pose a higher risk than other components such as
packed red cells. In 1991, the prevalence of T. cruzi infection in donated blood units ranged
from 1 to 60% in Latin American cities. Since then, blood donation screening has become
accepted as an important pillar of the Chagas disease control initiatives. Serological
screening of blood components for T. cruzi is now compulsory in all but one of the countries
in Latin America where the disease is endemic, and the prevalence of infection in screened
donors has decreased substantially. Nevertheless, Chagas' disease screening coverage by
country was estimated to vary from 25% to 100% in 2002, and the risk of transmission,
though much decreased, has not been eliminated. The residual risk in Latin America where
screening has been implemented is estimated to be 1:200,000 units.
Organ-derived transmission
Uninfected recipients who receive an organ from a T. cruzi-infected donor may develop
acute T. cruzi infection. However, transmission is not universal; in a series of 16 uninfected
recipients of kidneys from infected donors, only 3 (19%) acquired T. cruzi infection.
Nineteen instances of transmission by organ transplantation have been documented in the
literature (13 kidney, 1 kidney and pancreas, 3 liver, and 2 heart transplants). The risk from
heart transplantation is thought to be higher than that from kidney or liver transplantation.
One case of transmission through unrelated cord blood transplantation has been reported.

Oral transmission
Recently, increasing attention has focused on the oral route of T. cruzi transmission; several
outbreaks attributed to contaminated fruit or sugar cane juice have been reported from
Brazil and Venezuela. Most outbreaks are small, often affecting family groups in the Amazon
region, where the palm fruit açaí is a dietary staple that appears to be particularly
vulnerable to contamination, perhaps from infected vectors living in the trees themselves.
The largest reported outbreak to date led to more than 100 infections among students and
staff at a school in Caracas; locally prepared guava juice was implicated.

Epidemiology
Chagas unwellness, or yank trypanosomiasis, is caused by the parasite Trypanosoma cruzi.
Infection is most ordinarily unfolded through contact with the poop of Associate in Nursing
infected triatomine bug, a blood-sucking insect that feeds on humans and animals.
Infection may occur from:

 Mother-to-baby (congenital),
 Contaminated blood product (transfusions),
 An organ transplanted from Associate in Nursing infected donor,
 Laboratory accident (rare),
 Contaminated food or drink (rare).
Chagas unwellness is common in components of United Mexican States, Central America,
Associate in Nursing South America wherever a calculable eight million individuals square
measure infected. The triatomine bug thrives in poor housing conditions (for example, mud
walls, thatched roofs), and in countries wherever the bug is gift, individuals living in rural
square measures are at greatest risk for obtaining infected. Efforts by the general public
health community to stop transmission of T. cruzi have resulted in a very decrease within
the variety of recent T. cruzi infections and, in some areas, have fully stopped transmission
of the parasite by triatomine bugs. several countries wherever Chagas unwellness is
common have conjointly started screening given blood for this unwellness. However, new
cases of Chagas unwellness transmitted through infected organs, or by mother-to-child
(congenital) transmission will still occur.
Diagnosis
During the acute phase of infection, parasites may be seen circulating in the blood. The
diagnosis of Chagas disease can be made by observation of the parasite in a blood smear by
microscopic examination. A thick and thin blood smear are made and stained for
visualization of parasites. Diagnosis of chronic Chagas disease is made after consideration of
the patient’s clinical findings, as well as by the likelihood of being infected, such as having
lived in a country where Chagas disease is common. Diagnosis is generally made by testing
for parasite specific antibodies.

Treatment
Antitrypanosomal Drugs
Nifurtimox and benznidazole are the only drugs with proven efficacy against Chagas'
disease. Nifurtimox, a nitrofuran, interferes with T. cruzi carbohydrate metabolism by
inhibiting pyruvic acid synthesis. Gastrointestinal side effects are common, occurring in 30
to 70% of patients. These include anorexia leading to weight loss, nausea, vomiting, and
abdominal discomfort. Neurological toxicity is also fairly common, including irritability,
insomnia, disorientation, and, less often, tremors. Rare but more serious side effects include
paraesthesia, polyneuropathy, and peripheral neuritis. The peripheral neuropathy is dose
dependent, appears late in the course of therapy, and should prompt interruption of
treatment. Higher doses are often used in infants than in older children, and tolerance is
better in children than in adults.
Benznidazole is a nitroimidazole derivative, considered more trypanocidal than nifurtimox.
Dermatological side effects are frequent, and consist of rashes due to photosensitization,
rarely progressing to exfoliative dermatitis. Severe or exfoliative dermatitis or dermatitis
associated with fever and lymphadenopathy should prompt immediate cessation of the
drug. The peripheral neuropathy is dose dependent, usually occurs late in the course of
therapy, and is an indication for immediate cessation of treatment; it is nearly always
reversible but may take months to resolve. Bone marrow suppression is rare and should
prompt immediate interruption of drug treatment. Patients should be monitored for
dermatological side effects beginning 9 to 10 days after initiation of treatment. Benznidazole
was well tolerated in two placebo-controlled trials with children (12% had a rash and <5%
had gastrointestinal symptoms in one study; <10% had moderate reversible side effects in
the other study). Side effects are more common in adults than in children.

Treatment of Acute and Congenital T. cruzi infection

In acute and early congenital Chagas' disease, both drugs reduce the severity of symptoms,
shorten the clinical course, and reduce the duration of detectable parasitemia. The earliest
trials of antitrypanosomal drugs were conducted with patients with acute Chagas' disease in
the 1960s and 1970s using nifurtimox. Serological cure was documented at the 12-month
follow-up in 81% of those treated in the acute phase.
Treatment of Chronic T. cruzi Infection
Until recently, only the acute phase, including early congenital infection, was thought to be
responsive to antiparasitic therapy. However, in the 1990s, 2 placebo-controlled trials of
benznidazole treatment in children with chronic T. cruzi infection demonstrated
approximately 60% cure as measured by conversion to negative serology 3 to 4 years after
the end of treatment. Several follow-up studies suggest that the earlier in life that children
are treated, the higher the rate of reversion to negative serology. Together with growing
clinical experience across Latin America, these studies revolutionized management of
children with Chagas' disease, making early diagnosis and antitrypanosomal drug therapy
the standard of care throughout the region.
There is currently a growing movement to offer treatment to older patients and those with
early cardiomyopathy. In Latin America, most Chagas' disease experts now believe that the
majority of patients with chronic T. cruzi infection should be offered treatment, employing
individual exclusion criteria such as an upper age limit of 50 or 55 years and the presence of
advanced irreversible cardiomyopathy. This change in standards of practice is based in part
on nonrandomized, nonblinded longitudinal studies that demonstrate decreased
progression of Chagas' cardiomyopathy and decreased mortality in adult patients treated
with benznidazole.

Prevention
 insecticide spraying of houses and surrounding areas;
 home improvements to prevent vector infestation (such as plastering walls,
and installing concrete floors and corrugated iron roofs);
 good hygiene practices in food preparation, transportation, storage and
consumption;
 personal preventive measures such as bednets;
 screening of blood donors;
 testing of organ, tissue and cell donors and receivers;
 observance of the standard safety protocols (wearing laboratory coats, gloves,
face masks, caps and glasses) for laboratory accidents prevention
 BIBLIOGRAPHY

 Chatterjee, 1986. Medical Parasitology. Tata McGraw Hill

 Karyakarte, R.P. and Damle, 2005. Medical Parasitology. 5th edition
 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3194829/
 https://en.wikipedia.org/wiki/Chagas_disease