Protozoa 4b): Chagas Disease Flashcards
Which organism causes chagas disease and how is it different to T brucei gambiense/rhodensiens?
Chagas Disease is mainly in Latin America but has migrated to other continents.
- It is a vector-borne parasitic disease.
- The parasite responsible for the disease is Trypanosoma cruzi.
Which bug spreads Chagas and why is it such a challenging disease?
Mammals are the main reservoir for infection: dogs, rodents and marsupials.
- The main route of infection is via the Triatomine bug. The bug takes a blood meal and defecates next to the bite. The faeces contain the trypomastigotes that enter via the bite or via the mucous membranes. (The bug often bites near the mouth where the trypomastigotes gain entry – hence the name “kissing bug”). Often exhibits marked oedema at the site of the insect bite
- Congenital infection will occur in 5-10% of seropositive women.
- Infection can occur via infected donor blood transfusion or organ transplant
- Infection can also occur via food/drink contaminated with Triatomine faeces.
- Once inside humans, trypomastigotes infect various cells and transform into intracellular amastigotes that multiply. This results in the clinical features.
It is asymptomatic in most cases
All stages can transmit the disease but only adults can fly. A female usually lays 2–3 eggs per day. These develop fairly slowly through 5 nymphal instars. Each nymphal instar stage requires a blood feed to develop into the next stage. Young nymphs can ingest ten times their own weight and may be so bloated with blood that other nymphs and adults actually feed on them!
A blood feed takes 10–30 minutes and bugs usually defaecate at the start of or during the feed. This is significant regarding the transmission of Chagas’ disease.
Triatomines normally deliver a painless bite. They are night-biters and seldom wake their victims. Human blood loss from bites can be as much as 2 ml per night. Hence anaemia is very common in endemic areas
How many people are affected by Chagas?
What is the life cycle of T. cruzi?
An infected triatomine insect vector (or “kissing” bug) takes a blood meal and releases trypomastigotes in its feces near the site of the bite wound. Trypomastigotes enter the host through the bite wound or intact mucosal membranes, such as the conjunctiva . Inside the host, the trypomastigotes invade cells near the site of inoculation, where they differentiate into intracellular amastigotes . The amastigotes multiply by binary fission and differentiate into trypomastigotes, and then are released into the circulation as bloodstream trypomastigotes . Trypomastigotes infect cells from a variety of tissues and transform into intracellular amastigotes in new infection sites. Clinical manifestations can result from this infective cycle. The bloodstream trypomastigotes do not replicate (different from the African trypanosomes). Replication resumes only when the parasites enter another cell or are ingested by another vector. The “kissing” bug becomes infected by feeding on human or animal blood that contains circulating parasites . The ingested trypomastigotes transform into epimastigotes in the vector’s midgut . The parasites multiply and differentiate in the midgut and differentiate into infective metacyclic trypomastigotes in the hindgut . Other less common routes of transmission include blood transfusions, organ transplantation, transplacental transmission, and foodborne transmission (via food/drink contaminated with the vector and/or its feces).
What is the pathophysiology of the disease?
What are the symptoms of Chagas disease?
The indeterminate phase in most people will last up to 30 – 40 years.
40% of those who enter the chronic phase will suffer from cardiomyopathy (-> sudden cardiac death
Some will develop megaoesophagus or megacolon
- Achalasia with mega-oesophagus is typical. Symptoms may resemble a pyloric stenosis with both aspiration pneumonia and loss of weight as common accompaniments. Destruction of Auerbach’s intramural plexus also causes megacolon so that some cases present with constipation and abdominal distension. Cardiac arrhythmias, including heart block, may also occur due to intracardiac neuronal destruction.
Can lead to apical aneurysms of the heart
How do we diagnose Chagas disease?
- In the acute stage: thick and thin blood films for trypomastigote visualisation
- In chronic stage: Serology antigen-antibody tests
- In acute and congenital infection: Molecular PCR DNA tests on blood/tissue/CSF
- Xenodiagnosis: allow “clean bugs” to feed off pt and then dissect bug after 4/52
- Investigations may show end-organ damage e.g. ECHO/ECG – cardiomyopathy
- An Electrocardiogram (ECG) is part of the initial investigations for Chagas disease. If it is abnormal, then a full cardiological assessment is necessary
How do we treat Chagas?
How do we control outbreaks of Chagas disease? SAQ: A region in Bolivia has been identified as having a high prevalence of American Trypanosomiasis. You are sent with a team to one of the villages in this area with the aim of (i) treating cases and (ii) reducing the incidence of infection. What measures would you take?
• Vector control has been key to bringing incidence down:
o Indoor residual spraying (pyrethroid)
o Home improvements to reduce bug-friendly habitats: plaster walls, etc.
- T. cruzi (adults and nymphs) live in the plaster cracks and crevices of many adobe homes in Central and South America. Nymphs and adults of both sexes come out to feed at night. Huge numbers of infective bugs have been found in single dwellings. Proper housing would go a long way to eliminating the disease. However ancillary methods such as using insecticides on walls, eliminating animal reservoirs such as rodents and marsupials and screening of blood for antibodies all help.
o ITNs
o Bug collection initiatives
• Vertical transmission
o PCR screening of women prior to pregnancy
o PCR screening of infants and children if mother tested positive
- Covering food/drink to prevent contamination, also in commercial food
- Donation transmission: Testing of all blood and organ donation for T. cruzi
- Public Health Education
- There is no vaccine; wild animal reservoir control is not used.
MCQ top tips 1
Difference T cruzi and T brucei
- T. cruzi has a large kinetoplast (mass of circular DNA inside a mitochondrion) whereas T. brucei has a relatively small one. In addition T. cruzi trypomastigotes usually have an easily distinguished ‘C’ shape
MCQ top tips 2
Histology specimens of T cruzi amastigotes are common in the exam (typically in heart muscle). Amastigotes of T cruzi are morphologically indistinguishable from Leishmania parasites (another common histology slide for the exam) but the latter are always in macrophages.
Further microscopy image
