Trypanosoma cruzi (Chagas disease)

Definitions & Key takeaways

Trypanosoma cruzi is a parasitic protozoan that causes Chagas disease, a serious illness common in Central and South America. The disease is transmitted to humans through the feces of infected triatomine bugs, commonly known as "kissing bugs," which are found in the walls and roofs of poorly constructed houses in rural and suburban areas.

Symptoms of Chagas disease may include fever, fatigue, body aches, and swelling at the site of infection, followed by more serious complications such as heart disease, digestive problems, and neurological damage as the infection progresses. The disease can be life-threatening if left untreated.

Treatment of Chagas disease typically involves antiparasitic medications, such as benznidazole or nifurtimox, which are most effective in the early stages of the disease. However, these medications may not be effective in treating the chronic form of the disease or in advanced cases.

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Chagas Disease, also called American trypanosomiasis, is a parasitic disease common in Central and South America, caused by a protozoan called Trypanosoma cruzi or T.
cruzi for short. T.
cruzi is transmitted through the feces of the insect triatominae. Triatominae is a type of reduviid bug also called the kissing bug because it typically bites people on the face as they sleep at night - one heck of a good night kiss, huh?
The disease gets its name from Carlos Chagas, the physician who first described it. The life cycle of T.
cruzi starts with the epimastigote T. cruzi which sits in the lumen of the Reduviid bug’s midgut.
–Mastigote refers to the whip-like structure called a flagellum which protrudes from the center of the T. cruzi and helps it move around.
While in the midgut, the epimastigote multiplies through binary fission. Over time, the epimastigote transforms into a trypomastigote and at that point it loses its ability to divide, but the trade-off is that it gains the ability to invade human cells.
In fact “trypo” means to bore or punch into. Reduviid bugs feed off the blood of humans, and they prefer biting a person’s face, which is why they’re also called kissing bugs.
But unlike a normal kiss, the reduviid bug then defecates at the bite site, and if the reduviid bug is infected with T. cruzi, the feces can contain trypomastigotes.
These trypomastigotes can then infect human skin cells at the bite location; or at mucous membranes, particularly the conjunctiva of the eyes.
That can happen if a person unknowingly transfers the trypomastigotes by rubbing the bite site on their face and then touching their eyes.
Once the trypomastigote invades a human cell, it transforms into an amastigote meaning that it loses its flagellum. The amastigotes multiply intracellularly, again through binary fission, and then transform into blood trypomastigotes which can move through the blood and lymph to other tissues.
The blood trypomastigotes then invade more cells, and then again turn into amastigotes to multiply intracellularly again - and that’s how the cycle goes.
Now, a person infected by a T. cruzi infected reduviid bug, can then get bitten by a brand new reduviid bug.
In that case, that reduviid bug might get infected by the trypomastigotes, and those trypomastigotes would make their way into the reduviid bug’s midgut and then differentiate into epimastigotes - completing the life cycle.
Transmission from the reduviid bug to a person can also happen through infected organ and blood donations, which is why blood screening is super important, and it can also spread from mother to child during a pregnancy.
Now when a person is infected with Chagas disease, there’s initially an incubation period of up to two weeks. During that incubation period, T.
cruzi trypomastigotes invade host cells, amastigotes multiply, and blood trypomastigote levels begin to increase in the blood.
Usually there’s local inflammation as immune cells move towards the area of tissue damage. When this happens at the bite site it’s called a chagoma, and if it happens around the eye, it can cause eyelid swelling which is called a Romaña's sign.
Further inflammation can also lead to meningoencephalitis, which is inflammation of the membranes covering the brain and brain tissue, and hepatosplenomegaly, which is when the liver and spleen become enlarged.
Trypomastigotes have a tendency to target certain tissues and cells - like smooth muscle, cardiac muscle, and skeletal muscle, as well as neurons.
When those cells are damaged it can lead to problems like a pericardial effusion where fluid collects around the heart which disrupts its function, or issues with the electrical signals in the heart leading to heart block.
Generalized tissue damage can also lead to symptoms like fevers and fatigue. The acute phase resolves when T.
cruzi trypomastigotes are cleared from the blood, and over time, antibodies against T. cruzi gradually decrease, indicating that the infection has been cleared.
However, in some individuals, that doesn’t happen, and they go on to the chronic phase of the infection. In the chronic phase amastigotes linger in infected cells, and there are elevated levels of T.
cruzi antibodies even though trypomastigotes aren’t usually in the blood. The chronic phase can be asymptomatic, but some individuals develop progressive symptoms from nerve and muscle damage.
The most notable symptom is cardiomyopathy, where the heart gets really large, which in turn can cause arrhythmias like ventricular fibrillation and heart failure.
There can also be nerve damage; and gastrointestinal tract symptoms, like enlargement of the esophagus and colon - called megaesophagus and megacolon.
The most definitive diagnosis for the acute phase is made by microscopic detection of blood trypomastigotes in a blood smear or buffy coat preparation.
Polymerase chain reaction to detect T. cruzi DNA is also possible for certain sub-species, even at very low levels in the blood.
But there’s no “gold-standard” for diagnosing the chronic phase of the infection. Some helpful tools are serology which identifies antibodies or molecular tests that look for the presence of T.
cruzi antibodies or antigens. There’s also xenodiagnosis which is when a reduviid bug’s midgut is tested for T.
cruzi. Finally, imaging like a chest X-ray to look at the size of the heart or a barium swallow study to look for swelling of the colon can be helpful.
Finally, in the advanced stages, an electrocardiogram can be done to identify arrhythmias. Treatment depends on the phase of the diseases.
The most effective way to resolve the acute phase beginning anti-parasitic medication, like benznidazole or nifurtimox, early after infection and continuing for 2 to 4 months.
The chronic phase is mostly about managing the symptoms of cardiomyopathy, like with pacemakers or anticoagulation medications, and treated cases of reactivation with anti-parasitic medication.
A heart transplant may become necessary in advanced stages. Alright, as a quick recap: Chagas disease is caused by an infectious parasite, Trypanosoma cruzi that is most commonly transmitted through the feces of a reduviid bug after a bite.
In the acute phase, symptoms include inflammation and fever; and in the chronic phase there’s gastrointestinal disease and cardiomyopathy.