Parasites affecting the CVS
Parasitic infections produce a wide spectrum of cardiac manifestations. They
may involve various anatomic structures of the heart and are manifested
clinically as myocarditis, pericarditis, pulmonary hypertension and hear
failure.
1.
Trypanosoma cruzi (Protozoa).
2.
Trichinosis (Nematode).
3.
Visceral larva migrans (Nematode).
4.
Hydatid disease (Cestode).
5.
Cysticercosis (Cestode).
6.
Sparganosis (Cestode).
41
Protozoal infections
Hemosomatic flagellates
(Hemoflagellates)
Genera: Two medically important genera-Trypanosoma and Leishmania.
Overview:
-Important pathogens of humans and livestock.
-All species are transmitted by insects.
-All have more or less complex cycles alternating from one morphologic form
to another.
-Distinguishing structural characteristics-flagellum, kinetoplast.
-Basic morphologic stages:
1. Promastigote
2. Epimastigotes.
3. Trypomastigote
4. Amastigote
42
Differences between forms of blood flagellate
Differences
Promastigote
Epimastigote
Trypomastigote
Amastigote
Body
Elongated
Elongated
Elongated
rounded
Kinetoplast
Anteriorly
In front of the
nucleus.
posteriorly
Beside the
nucleus
Undulating
membrane
Absent
short
Long
Absent
Free
flagellum
Present
Present
Present
Absent
Habitat
Leishmania
assume this form
in culture and
inside insect
vector.
Trypanosome
Present in the blood
assume this form and lymph.
inside the body
and inside insect
vector. vector
43
InR.E.S,some
trypanosomes
assume this
form in tissues
American Trypanosomiasis
(T.Cruzi)
Distribution:
South and Central America.
Morphology:
The parasite takes two forms:
1. Trypomastigote form in the blood, it is commonly C or U shaped with a
central nucleus and a large kinetoplast, the posterior end is sharp. It does not
multiply in the blood.
2.Amastigote form in the cardiac muscles and reticulo-endothelial cells,
(bone marrow, lungs ,spleen and liver), it divides by binary fission.
44
Transmission:
1
Vector: Winged bug-kissing bugs [Triatoma infestans].
2
Reservoirs: armadillo, dogs and rodents.
-The main method is through bugs’ bite, the infective stages are in the
feces.
-Blood transfusion.
-Organ transplantation
Life cycle:
1. The winged bug transmits T.cruzi, metacyclic trypanosomes in the
feces of the bug contaminating skin abrasion will be engulfed by the
skin macrophages (local histiocytes) and transform inside into
amastigote forms which multiply by binary fission forming pseudocyst.
2. This produces a swelling in the skin called chagoma, after a period, the
amastigote forms passing through a transitory epimastigote stage get
metamorphosed into trypomastigote forms which reach the blood
stream.
3. The cardiac muscle, R.E.S and the thyroid gland are
invaded by the trypanosomes that cause damage to the affected organ.
45
Chagas disease
The disease is characterized by:
1.
Chagoma in the skin (bite reaction-non pustular, itchy painful
swelling).
2.
Acute stage , malaise, restlessness, lymphadenitis, hepatomegaly,
splenomegaly, acute myocarditis with generalized edema.
3.
Contamination of the eye could occur. The trypanosomes proliferate
locally and produce unilateral orbital edema with enlargement of the of the
ipsilateral lymph nodes. This is called Romana’s sign.
4.
Acute stage when affecting the children could end with CNS
invasion.
5.
Thyroid insufficiency.
6.
Cardiac affection with arrhythmia, in chronic phase, cardiomegally
46
and heart failure may develop.
7.
Megaoesophagus and megacolon occur in chronic phase due to
destruction of the parasympathetic nerve ganglia that leads to organ dilatation.
Diagnosis:
A) Direct methods:
1. Blood film examined as fresh smear or giemsa stained smear for detection
of trypomastigotes.
2. Culture on N.N.N medium.
B) Indirect methods:
1.
Sero-diagnosis:
IHA -ELISA for detection of antibodies against T. cruzi antigens.
2.
PCR:
for
3. Intradermal test:
detection
Cruzin test
trypanosomes have been tried.
Treatment:
-Primaquine
-Nifurtimox (Lampit).
-Beznidazole (Radanil).
Prevention and control:
-Control of winged bugs.
-Treatment of cases.
-Destruction of the reservoir hosts.
47
of
parasite
DNA.
using an antigen prepared from cultured
Helminthic infections
Trichinellosis
(Intestinal and tissue nematodes)
Infection with Trichinella spiralis is common in countries where pork is eaten
raw or insufficiently cooked.
Life cycle:
Habitat: Small intestine embedded by its anterior part in the mucosa.
Definitive host: Man.
Intermediate host: Pigs.
Reservoir host: Rats.
Infective stage: The trichina capsule.
Stages in the life cycle: Larva-trichina capsule adult.
48
Trichina Capsule:
-It is the larval stage of Trichinella spiralis.
-It is common in the striated active muscles as diaphragm,
intercostal, deltoid, laryngeal and extra-ocular muscles.
-It is ellipsoidal in shape.
-Its size is about 0.5 X 0.2 mm.
-It contains a larva coiled upon itself.
-It becomes infective after 15 days from reaching the muscles.
-Trichina capsule becomes calcified within 18 months but the larva inside
remains viable for years.
49
Method of infection:
Trichina capsule is the infective stage.Eating insufficiently cooked infected
pig’s meat (pork) infects man.
Life cycle:
1.
The adults live in the small intestine of man and animals specially pigs
and rats.
2.
After fertilization males die and expelled. Females penetrate deeply in
the mucosa and lay larva. Each female lays about 1500 larvae in its life span
(about 2 months).
3.
Larvae find their way to the circulation and passing through the
pulmonary filter, they are distributed all over the body. They are found mainly
in the skeletal muscles where they are encysted.
4.
Larvae coil and encyst, they grow to reach a size of 1 mm taking about
two weeks to become infective.
5.
Man gets the infection through ingestion of raw or undercooked pork
containing the trichina capsule.
6.
Ingested larvae are liberated from the cyst in the small intestine where
50
they mature to adults. (Within 5 days after matting the female burrows deep in
the mucosa and give birth to larvae.
Pathology:
1.
Stage of intestinal invasion by adult worms.
2.
Stage of migration of the new born larvae: (7-21 days): Damage of the
blood vessels occurs resulting in localized edema specially in the face and
hands. Headache, fever, skin rash and edema of both eye lids with chemosis of
the conjunctiva .
3.
Stage of muscular penetration and encystment (after the third week):-
The presence of trichina capsule in the muscles causes myositis with muscle
tenderness and spasms In heavily infected cases , there is intense muscular
pain, difficulty in breathing or swallowing with weakness of pulse The
muscular invasion is followed by fibrosis and calcifications, that lead to
muscle atrophy and weakness.
4. In heavy infection: myocardial involvement is common and it is considered
as an important cause of death in fatal cases. The larvae that disseminate to the
myocardium set up multifocal interstitial inflammatory lesions& no true cysts
are formed in the cardiac muscle causing myocarditis. Electrocardiographic
changes involve sinus tachycardia, prolongation of the P-R interval, primary
T-wave changes and low QRS voltage. Various nervous disorders including
hallucinations can occur.
Diagnosis:
1. Clinical diagnosis:
a) Larvae in blood stream (periorbital edema).
b) Larvae in blood and the start of muscles' invasion (conjunctivitis-fever and
chills-muscle pain-headache-eosinophilia-skin rashes-painful breathing).
51
c) Larvae in myocardium (tachycardia-edema of legs-hypotension-ECG
changes and elevated cardiac enzymes.
d) Larvae in brain meninges (headache -delirium-apathy or altered
consciousness-stiff neck).
2. Laboratory Diagnosis:
A) Blood examination: during the second week blood is examined for
migrating larva.
B) Muscle biopsy: Biopsy is taken from superficial muscle as the deltoid or
intercostal. The excised muscle is examined either by:
i)
Compression: between 2 slides and examined for trichina capsule.
ii) Sectioning and examined for trichina capsule.
iii) Digestion in artificial gastric juice and the mixture is examined for
the free larvae.
C) Intra-dermal test (Bachman’s test): The antigen used is a purified
extract of larvae collected by digestion of the infected pig’s meat .Intra-dermal
injection of 0.1 ml of the antigen is followed by an immediate reaction in the
forearm, a wheel surrounded by erythema appearing within 10-20 minutes.
D) Serological tests: As the Bentonite flocculation test, ELISA, IFA and
countercurrent electrophoresis.
Treatment:
1
2
3
Corticosteroids.
Fluids and electrolyte balance.
Mebendazole.
52
Prevention and control: Trichinosis is common in countries consuming
raw or insufficiently cooked pork. Rats are considered the reservoir hosts
while pigs are the only source of infection to man.
Visceral arva migrans
(Tissue nematodes)
It is the invasion of humans' viscera by the larvae of:
1.
Dog Ascarides (Toxacara canis).
2.
Cat Ascarides (Toxacara cati).
Also human Ancylostoma, Ascaris and Strongyloides sterocaralis larvae.
Pathology and clinical picture:
Visceral larva migrans affects mostly children, probably because they
are more likely to come in contact with dogs and cats ascarid eggs.
Hypereosinophilia is very common, hepatomegally may be seen. In some
cases pulmonary infiltration is seen with cough and fever (loeffler’s
syndrome). Ocular larva migrans (granulomatous ophthalmitis) is rare, but its
consequences may be severe. Toxocaral granuloma may be misdiagnosed as
retinoblastoma. Cardiac involvement could occur with acute myocarditis in
early phase and heat failure in chronic latent phase.
Diagnosis:
1.
Persistent eosinophilia, hepatomegally, loss of weight, joint pain is
suspicious.
2.
Biopsy from different organs may reveal the granuloma containing the
larvae which are the only confirmatory method.
3.
Cardiac manifestations and ECG changes.
53
4.
Serologic and intradermal tests.
Treatment:
1.
Diethylcarbamazine (Hetrazan).
2.
Thiabendazole (Mintezol).
3.
Steroids.
54
Hydatid disease
(Hydatidosis-Hydatid cyst)
(Tissue Cestode)
It is the presence of hydatid cyst (Larval stage of E.granulosus) in the human
tissues.
Methods of infection:
Man is infected with hydatid cyst by swallowing the eggs of
Echinococcus granulosus that are voided in the feces of dogs and wolves.
Sites of hydatid cyst:
Hydatid cysts may be found in any organ. The distribution as 58% in the
liver, 27% in lungs and 15% in other organs including the heart.
Pathology and clinical manifestations:
It depends on its site.
1. Cardiac hydatid cyst: Cardiac hydatid cyst causes myocarditis in
early phase, pericarditis with pleural effusion manifested by exertional
dyspnea accompanied by a dry cough. Symptoms related to heart
failure may develop in latent phase.
2. Hepatic hydatid cyst: discomfort in the right hypochondrium,
hepatomegally , indigestion and jaundice.
3. Pulmonary hydatid cys: causes cough, chest pain and hemoptysis.
4. Cerebral hydatid cyst: symptoms of increased intra-cranial tension
and epilepsy.
55
5. Osseous hydatid cysts: spontaneous fractures.
6. General: When hydatid cyst ruptures , escape of the fluid leads to
allergic manifestations that vary from moderate as urticarial rash to
severe anaphylactic shock.
Diagnsosis:
1. Clinically by eliciting hydatid thrill and signs and symptoms according
to the location.
2. ECG changes in cardiac involvement.
3. Ultrasonography and CT scan.
4. Laboratory techniques
Indirect Techniques:
A)
Intradermal test (Casoni test): The antigen used is prepared from
hydatid cysts of sheep. This is performed by intradermal injection of 0.25 ml
of the antigen in one arm, in the other arm a control test is done. -The positive
reaction is indicated by a wheel surrounded by erythema reaching its
maximum width within 10-20 minutes.
B)
Serological tests as ELISA, complement fixation test andslide
flocculation test.
Direct Techniques:
Biopsy is not preferable due to the fear of rupture of the cyst and the
resultant complications'. Left thoracotomy and pericardiotomy are
performed through to drain of hydatid fluid in case of pericardial
effusion.
Treatment:
1.
Surgical removal.
2.
Medical treatment: Mebendazole or Albendazole.
56