Cardiac Involvement with Parasitic Infections

Block CVS-206
Coordinators: Prof. Ahmad Kamal Diab Prof. Hanan EM Eldeek
Lecture 17 - 2nd Week - (2022-2023)
Prepared by: Prof. Hanan EM Eldeek
Professor of Parasitology- Faculty of Medicine- Assiut University

Learning objectives (2nd week/Lecture 17)

After the lecture, students should be able to:
A17.1. List parasites causing myocarditis and pericarditis.
A17.2. Recall the infective and diagnostic stages of each parasite.
B17.1. Demonstrate the pathological lesions in the heart caused by each parasite.
B17.2. Explain host-parasite relationships (pathogenesis and main clinical presentations )
B17.3. Describe laboratory diagnosis, imaging and pathological studies of the disease
related to each parasite and recall treatment and prevention of them.

A) Parasites that directly affect the heart including:

 Parasites causing carditis (myocarditis/ Pancarditis):
1. Trypanosoma cruzi (Chaga’s disease).
2. Trypanosoma brucei rhodesiense and Trypanosoma brucei gambiense (African
trypanosomiasis).
3. Toxoplasma gondii (toxoplasmosis)
4. Taenia solium (Cysticercosis).
5. Trichinella spiralis (Trichinosis)
6. Severe cases of visceral larval migrans (eosinophilic myocarditis)
 Parasites causing pericarditis:
1. Entamoeba histolytica (amoebic pericarditis).
2. Echinococcus granulosus (hydatidosis)
B) Parasites that have indirect effects on the heart:
 Infection with Plasmodium falciparum may cause pulmonary edema and a shock-
like syndrome, thus indirectly affecting the heart.
Lecture (17) Parasitology: By Prof. Hanan EM Eldeek

 Infections with Schistosoma spp. may cause pulmonary hypertension and cor
pulmonale without directly infecting the myocardium.
 The anemia that accompanies severe hookworm infections and visceral
leishmaniasis may cause heart failure.

1. Trypanosoma cruzi “Chaga’s disease”

Disease: American trypanosomiasis “Chaga’s disease”

Geographical distribution: Central and South America.
Host: Man, especially infants and young children.
Reservoir host: The most important reservoir hosts are armadillos. The dogs, cats, rats
and possibly pigs are considered other reservoirs of infection.
Vector: Triatoma megista (Reduviid bug; called kissing or cone-nosed or winged-bug).
Habitat: Cells of the heart muscle, smooth muscles, blood, bone marrow, lung, liver,
spleen, brain and macrophage-phagocyte (reticulo-endothelial cells.)
Infective stage: metacyclic trypomastigotes
Transmission: By Triatoma megista, posterior station transmission (Contaminative).
Mode of infection:
1- Contamination of the bite site by feces of kissing bug which defecates during the
process of feeding. The insect deposits infective feces near or at the bite site and most
human infections occur when feces are rubbed into the eyes or mucous membranes
following a bite.
2- Accidental ingestion of bugs.
3- Transmission by blood transfusion.
4- Via the placenta from the mother to fetus (congenital transmission).
5- Organ transplants using organs from infected donors.
 The Morphology and Life cycle of Trypanosoma cruzi was described before at the
Infection and Immunity block; INI-205 (lectures 46-47-48)
Pathophysiology:
The clinical manifestations of Chagas disease are due to cell death in the target tissues that
occurs during the infective cycle. In the acute phase of the disease, signs and symptoms

2
Lecture (17) Parasitology: By Prof. Hanan EM Eldeek

are caused directly by the replication of T. cruzi and the immune system's response to it.
During the chronic phase, long-term organ damage develops over years due to continued
replication of the parasite and damage from the immune system.
Clinical picture:
Chagas’ disease has two forms:
I- Acute form: common in infants and young children.
1. Romana’s sign: is swelling of the patient eyelid. The swelling is due to bug feces being
accidentally rubbed into the eye, or because the bite wound was on the same side of the
patient’s face. The tear glands become inflamed and the pre-auricular lymph nodes
enlarged. “It is a marker of acute Chagas disease.”
2. When swellings appear in other parts of the body, they are known as chagoma due to
multiplication of the parasite inside macrophage cells of subcutaneous tissue.
3. Invasion of the reticulo-endothelial cells causes generalized lymphadenopathy,
splenomegaly, and hepatomegaly.
4. Presence of anemia, continuous fever, and severe headache.
5. Fatal due to acute myocarditis or acute meningoencephalitis.
II- Chronic form: in adults
1. If the patient survives the acute phase, the disease becomes chronic.
2. The parasites are in organs (heart and nervous system) but No parasites in blood.
3. Only 10-30% of patients with chronic T.cruzi infections ever develop symptomatic
chronic Chagas' disease. Myocardial dysfunction is the most frequent consequence of
chronic T.cruzi infection.
4. The heart is affected due to the persistent presence of parasites in heart muscle which
stimulates an inflammatory process leading to organ dysfunction and in many cases
death. The inflammatory process can cause a variety of disturbance in conduction;
ventricular arrhythmia (tachycardia), right bundle branch block. These abnormalities
can cause dizziness and syncope, and sudden death is common.
5. Congestive cardiomyopathy (dilated cardiomyopathy); the heart becomes stretched
and weakened and is unable to pump effectively.

3
Lecture (17) Parasitology: By Prof. Hanan EM Eldeek

6. Destruction of autonomic nerve ganglion in muscles of hollow

organs and heart resulting in mega organ disease
 Megaesophagus (dilatation of the esophagus leading to dysphagia) and chronic
achalasia.
 megacolon (dilatation of the colon leading to constipation and
patients with advanced disease can go for weeks between bowel movements)
 cardiomegaly.
7. The lymph nodes are edematous, and there is hepatosplenomegaly.
8. Nervous system: meningitis and meningo-enchephalitis.
Diagnosis:
A. Clinical diagnosis:
 History (residence or traveling to endemic areas) and clinical picture.
B. Laboratory diagnosis:
1. In acute cases, T. Cruzi (Monomorphic trypomastigotes) can be found
in thick blood smears or in aspirates from chagoma, lymph node,
bone marrow, and CSF.
2. In light infections:

 Xenodiagnosis is applied. Allow clean winged bug (bred in the laboratory and fed on
plant juices) to feed on the blood of the suspected patient. After about 7-15 days the
insect is dissected, and the rectum is examined for developmental stages as metacyclic
trypanosomes.

 Cultivation of the suspected blood on N.N.N. medium (Novy-MacNeal-Nicolle

Medium) and examined after (1-4 weeks) to show epimastigotes and trypomastigotes.

 Inoculation in laboratory animals (mice/ rats) to show monomorphic trypomastigotes.

3. Serological tests are most useful in the diagnosis of chronic disease (complement
fixation, indirect fluorescent antibody test and ELISA). High immunoglobulin in csf.
4. PCR-based methods are useful to diagnose acute and chronic Chagas’ disease as well
as to monitor therapy.

4
Lecture (17) Parasitology: By Prof. Hanan EM Eldeek

C. ECG (Electrocardiography): To diagnose cardiomyopathy and arrhythmia.

D. Imaging methods:
 Chest X ray to diagnose heart enlargement.
 Echocardiographic methods: To diagnose myocarditis and congestive heart failure.
 X ray with Barium: To diagnose mega-organs “Megaesophagus or megacolon”.
Treatment:
1. Early stage (acute stage): anti-parasitic drugs; benznidazole or nifurtimox
2. Late stage (chronic stage): Symptomatic treatment.
 For chronic heart disease, antiarrhythmics, and pacemaker implantation for heart block
are used. Cardiac transplantation is an option.
 For gastrointestinal disease, changes in diet, the use of laxatives and/or enemas,
dilation of the esophageal sphincter.
Prevention and control:
1. Treatment of infected patient 2. Destruction of reservoir hosts.
3. Eradication of vector by, dusting or spraying.
4. Screening of blood donors in endemic areas.

2. African trypanosomiasis
Parasites& diseases:
 Trypanosoma brucei gambiense; causing chronic sleeping sickness.
 Trypanosoma brucei rhodesiense; causing acute sleeping sickness.
The reservoir host: Wildlife animals.
The vector: Various species of Glossina (Tsetse) flies (biological transmission)
Habitat: Blood, Lymph channel, CSF, brain and reticuloendothelial system.
Transmission:
1. The disease is mostly transmitted through the bite of an infected tsetse fly.
2. Mother-to-child infection: the trypanosome can cross the placenta and infect the fetus.
3. Accidental infections have occurred in laboratories due to pricks from contaminated
needle or via blood transfusion and organ transplantation.
Clinical picture and pathogenesis:

5
Lecture (17) Parasitology: By Prof. Hanan EM Eldeek

 Local lesion at site of bite (Trypanosomal chancre)

 Enlargement of the posterior cervical lymph glands, which is called
(Winterbottom’s sign) and followed by generalized lymphadenopathy.
 Recurrent or irregular fevers due to antigenic variation
 Myocarditis with disproportionate tachycardia.
 Death may result from congestive heart failure and arrhythmias, even before CNS
disease develops, in case of Trypanosoma brucei rhodesiense.
 CNS manifestations; changes of behavior, confusion, sensory disturbances and poor
coordination. Disturbance of the sleep cycle gives the disease its name.
Diagnosis:
- Trypanosomes found in blood, lymph and cerebrospinal fluid
- Serological tests (IFAT, ELISA): High immunoglobulin in CSF.
- Antigen detection
- Animal inoculation “mice or hamster” with blood, bone marrow, lymph aspirate or
spinal fluid.
Control:
A) Chemoprophylaxis. B) Eradication of Glossina and the reservoir host.
C) Mass treatment of infected patients.

3. Toxoplasma gondii "toxoplasmosis"

Toxoplasma gondii is an obligate intracellular parasite. It is the second most common

pathogen in protozoan myocarditis after Trypanosoma cruzi.
Disease: toxoplasmosis Distribution: Worldwide
The predator host is mainly the domestic cat, while man, animals (cattle, sheep, goat,
pig) and birds (chicken, pigeon) serve as prey hosts.
Transmission
1. Ingestion of sporulated oocysts in contaminated vegetables or water or during handling
of litter trays.
2. Ingestion of tachyzoites or bradyzoites in cysts in undercooked meat or during handling
infected raw meat.

6
Lecture (17) Parasitology: By Prof. Hanan EM Eldeek

3. Trans-placental occurs in pregnant women when exposed for the first time to T. gondii
infection, blood transfusion or organ transplantation.
Pathogenesis:
The organisms are disseminated by the lymphatics and blood with subsequent invasion of
various organs and tissues producing areas of necrosis in vital organs such as the
myocardium, lungs, liver and brain.
Two categories are at high risk of infection, the immunocompromised and the pregnant
women who receive their first exposure to T. gondii while pregnant; their fetuses are at
particular risk.
Disseminated toxoplasmosis: It is commonly manifested as ocular toxoplasmosis and
fatal CNS disorders as encephalitis. Cardiac involvement as myocarditis, cardiac
hypertrophy and dilatation and pericarditis is usually associated with involvement of other
organ systems.
Diagnosis:
1. Diagnosis is typically by testing blood for antibodies or by testing amniotic fluid for
the parasite's DNA.
2. Serological tests; Sabin-Feldman dye test, IFT and ELISA.
3. Biopsy and immunohistochemistry for antigen.
4. Isolation of Toxoplasma from infected or suspected tissues
and intra-peritoneal inoculation to laboratory mice.
Treatment: Combination of pyrimethamine and sulphadiazine is the drug of choice.
Control:
1- Daily cleaning of cat litter boxes and proper disposal of feces.
2- Washing of hands after handling raw meat and before eating.
3- Rodents should be controlled. Raw meat should not be fed to cats.
4. Cysticercosis

Definition: It is the invasion of human tissues by the larval stage of Taenia solium
(Cysticercus cellulosae). Man acts as a blind intermediate host.
Geographical distribution: Worldwide, especially in big raising countries.

7
Lecture (17) Parasitology: By Prof. Hanan EM Eldeek

Mode of infection:
1. Ingestion of raw vegetables or water contaminated by infected feces containing eggs of
Taenia solium. 2. Autoinfection.
Pathogenesis and signs:
1) When man is infected with cysticerci, various clinical signs may occur
depending on the location of the cysts in vital organs, muscles or subcutaneous tissue.
2) Neuro-cysticercosis: is the most serious.
3) Cysts have been observed in the heart as incidental findings at autopsy or during
cardiac surgery for unrelated causes.
Diagnosis:
1) Clinical diagnosis.
2) Direct methods: Usually post-operative microscopic examination of biopsy specimens.
3) Serological methods: (ELISA, IHT, IFT)
4) Blood picture: Show high eosinophilia in 10% of cases.
5) Imaging techniques: Echocardiography, X-ray, CAT and MRI.
Control:
1. Proper treatment of infected patients with T. solium (avoid vomiting).
2. Avoid using human manure as fertilizer.
3. Personal hygiene and periodic examination of food handlers.

5. Entamoeba histolytica "Amoebic pericarditis"

Habitat: The parasite lives in the large intestine in colonic flexures (intestinal
amoebiasis). It may reach the liver, lung and brain causing amoebic abscesses (extra
intestinal amoebiasis).
Transmission: Faeco-oral route. Persons get infected by ingestion of the
Quadrinucleated cyst contaminating, fingers, food, flies and water.
Pathogenesis: Cyst stage
Amebic pericarditis is a rare but serious complication of liver abscess when it ruptures
into the pericardium. Cardiac tamponade (compression of the heart by an accumulation

8
Lecture (17) Parasitology: By Prof. Hanan EM Eldeek

of fluid in the pericardial sac) and even perforation can occur, but typically the course is
more insidious and involves substernal chest pain as well as congestive heart failure.

6. Visceral larva migrans

 It is a condition produced by the presence of the larvae of ascarids of dogs and cats
(Toxocara canis and Toxocara cati) in the tissues of unnatural host (man).
 Most cases of visceral larva migrans occur in children.
 Mode of infection: accidental ingestion of embryonated eggs of Toxocara canis and
Toxocara cati with food and drinks or through hands contaminated with polluted soil.
 Pathogenesis: The larvae migrate through viscera (liver, lung and heart) and form
granulomatous lesions.
 Clinical picture:
• Symptoms and duration of illness depend on the site and severity of infection.
• Light infection is asymptomatic unless affecting vital organs (eye or brain).
• Myocarditis may occur.
• In heavy infection especially in children, symptoms include tender hepatomegaly, fever
and malaise, persistent eosinophilia, cough asthma and pneumonitis.
Diagnosis:
- ELISA with larval stage antigens. - High eosinophilia.
- Hyper-gammaglobulinemia with raised IgM and IgG levels.

7. Trichinella spiralis (trichinosis)

- Cardiac pathology is a direct result of migrating larvae of Trichinella spiralis and
the local inflammatory response.
- Severe morbidity and mortality usually occur secondary to pneumonitis,
encephalitis or myocarditis and congestive heart failure.

8. Hydatid disease (Hydatidosis)

- Definition of hydatidosis: It is invasion of the human tissues by the larval stage of

Echinococcus species.
- Pressure like symptoms; according to the site infected.
- Myocarditis and pericarditis may occur.

9
Lecture (17) Parasitology: By Prof. Hanan EM Eldeek

10