Jameieka Price

Trypanosoma Cruzi DNA in Cardiac Lesions of Argentinean Patients with End-Stage

Chronic Chagas Heart Disease.
Schijman, G,A.et al (2003).
Introduction
Changas is an illness spread by insects and is common in South and Central America.
Trypanosoma Cruzi (T. cruzi) is a protozoa that feeds on blood and is known as Chagas
disease1. The parasite is found circulating the blood and is spread by the bite of reduvid
bugs and is starting to become a huge health concern in South America4. Chagas is
problematic because it has an acute and chronic phrase, after an infection the disease is
inevitable and typically last a few weeks or months. Chronic Chagas Heart Disease
(cChHD) is the main cause of chronic myocarditis that is shown 130 years after initial
infection. The main concerns about acquiring Chagas are complication of heart rhythm
abnormalities that can lead to death. A dilated heart, which effects the way blood is being
pumped and a host of other concerns. People are more susceptible to getting Chagas
disease if they live in a hut where the bugs live in the wall, live in poverty, received a
blood transfusion from a person who carries the parasite, but does not have active Chagas
disease. This disease affects 20 million people and 50 thousand people die each year from
it and this is primarily a disease that happens in South America (Schijman et al 2003).
Researchers wanted to determine if the increase rate of fibrosis, heart inflammation, and
chronic Chagas heart disease is caused by the parasite5. The researchers used the
polymerase chain reaction (PCR) method to analyze the proportion of DNA of the
parasite found in different parts of the heart from dead patients that were at different
stages of heart disease. This was done to show a significant association between the
detection of parasite DNA with inflammation, fibrosis, and clinical progression of
cChHD. PCR is an autoimmune process. Furthermore, it was also to prove that people
with cChHD would be at a higher stage of myocarditis than people who had non chagasic
cardiomyopathy with heart failure when they died using PCR, which was used as control
group.
Materials and Methods
Three different heart patient necropsy study groups were used.
Group A was hearts from six cChHD patients without symptoms of heart failure the mean
age for this group is 54. Group B was hearts from ten patients with severe cChHD who
had died or were treated with heart transplants 50 years old is the mean age. Group C
hearts were from six patients with non-chagasic cardiomyopathy with heart failure the
mean age for this group is 47. In order to diagnosis Chagas disease there had to be
positive results in at least two of three conventional serologic assays, which are
complement fixation, indirect hemagglutination, and indirect immunofluorescence 3. The
serological assays are laboratory tests that uses blood samples to detect abnormities and
all three tests detects antibodies. Patients that undergone transplants gave informed
consent to have their explanted hearts analyzed. The other hearts were obtained from
necropsy specimens. Patients were classified into four groups based on their progression
of the cardiomyopathy. Zero being the least affected and three being the most affected.

Two sections from different parts of each heart were cut and collected as samples and
were looked at under twenty high power fields at 400X magnification. The two sections
included one that had the lowest degree of inflammation and the other was the highest
degree5. This was after analyzing a host of different parts of the heart; it was determine
that two sections would suffice. The parasites DNA was extracted for the heart and PCR
administered. Different statistical analysis was used to determine the number of
inflammatory cells and fibrosis. Mycarditis was detected by using the Dallas Criteria. The
Dallas criteria provides a histopathological categorization to identify the different stages
of myocarditis (low inflammation 10 mononuclear cells, moderate inflammation 10-19
MNC, and high inflammation at least 20 MNC 2. Fibrosis was detected by using the
Kunkel grading system. IF there was less than 10% of fibrosis the patient had Mild
fibrosis, between 10%-20% moderate fibrosis, and more than 20% severe fibrosis.
Results
The results for Group A showed no evidence of heart failure at the time of death and the
follow-up was 864 days. Group B showed evidence of heart failure, which caused their
death and 925 days for follow-up the clinical symptoms for heart failure, was 17 months.
Group C with heart failure at the time of death the follow up was 426 days duration of the
clinical symptom of heart failure 25 months. In 3 of the 16 hearts borderline myocarditis
was detected and active myocarditis in 12 of the 16 hearts from cChHD patients. 2 of the
6 DCM hearts had borderline myocarditis and none had active myocarditis. There was a
positive correlation between the inflammation and fibrosis measured of patients who had
Chagas disease. None of the 12 heart specimens from hearts of Dilated Cardiomyopathy
(DCM) patients were positive for T. Cruzi. Group A had moderate inflammation at 11
MNC, Group B had high inflammation at 31 MNC and Group C had low inflammation at
7 MNC. Group A had mild fibrosis at 15.5% Group B had severe fibrosis at 20.5%,
Group C had mild fibrosis at 10.5%. Group B had higher counts of MNC and percentages
of fibrosis compared to Group A and C.
Discussion
People who had cChHD are at a higher stage for myocarditis and fibrosis vs. DCM
patients. It was proven that using PCR it determined that inflammation and fibrosis was a
result of T.cruzi. It was determined that parasites reach the heart from the coronary
vessels based on the inflammation of hearts. This was not the case for DCM patients,
where the different locations of fibrosis were in the myocardial of cChHD with heart
failure followed the pattern of inflammation. The PCR shows different sequencing of
parasites in biopsy specimens from the hearts of patients with chronic Chagas disease
from South America. The data showed a strong correlation between the histologic
evidence of heart tissue damage and T.cruzi. The parasite invades the myocardium and it
gets destroyed at a quicker pace. The progression of the disease indicates that there needs
to be an anti-parasitic drug created, that has good efficacy5.

Reference
1. American Trypanosomiasis. www.cdc.gov. 19 July 2013. Web. 01 Mar. 2015
2.Baughman, K.L. Diagnosis of myocarditis: death of Dallas criteria. Circulation. 113
2006:593-595
3.Britannica encyclopedia. www.britannica.com. 2015. Web 15 Mar.2015
4. Chagas Disease. www.nlm.nih.gov. Medline Plus, Web. 01 Mar. 2015
5. Schijman, A. et al. Trypanosoma Cruzi DNA in Cardiac Lesions of of Argentinean
Patients with End-Stage Chronic Chagas Heart Disease. www.ajtmh.org. Web. 28 Feb.
2015