MEDICAL

BIOLOGY
Lesson 1
Medical parasitology studies animal
parasites in men and develops
treatments for parasitic diseases

Parasite is an organism, which uses another

living organism as food source and
environment and entrust the host organism
regulate their common relationships with
eternal environment.

Valentin Dogel, Russian zoologist and

parasitologist
Key points of medical parasitology
Parasite name (Latin and common) --- disease, symptoms
geographical distribution
intermediate and definite hosts
habitats in nature and location (also called habitat) in the
host body
transmission vectors
route of infection, infective stage
life cycle
symptoms
diagnostic methods, diagnostic stage, diagnostic samples
 feral-herd or feral-nidal infection is a
natural focal disease which affects people
Zoonosis is an infective diseases transmitted
naturally from animals to people

Anthroponisis is an infective diseases transmitted

from people to people

disease vector is any agent (animal, or

microorganism) that carries and transmits an
infectious pathogen into another living organism.

disease agent is a biological pathogen that

causes a disease, such as a virus, parasite, fungus,
or bacterium
There is a
great variety
of Protista in
nature; in our
course, we
discuss only
human
parasites.
 EUGLENOZOA
BLOOD AND TISSUE FLAGELLATES
Trypanosoma brucei Sleeping sickness (African
gambiense trypanosomiasis) chronicle form
Trypanosoma brucei Sleeping sickness, (African
rhodesiense trypanosomiasis acute form)
Trypanosoma cruzi Chagas disease or American
trypanosomiasis
at least 20 Leishmania species affect humans
Leishmania major Cutaneous leishmaniasis
zoonotic type
Leishmania tropica Cutaneous leishmaniasis
anthroponotic type
Leishmania donovani Visceral leishmaniasis (kala-azar,
black fever, Dum-dum fever)
Leishmania brazilensis Mucocutaneous leishmaniasis
 Trypanosoma brucei
Two subpecies T. brucei rhodesiense and T. brucei gambiense

GEOGRAPHICAL DISTRIBUTION: T.b.

rhodesiense - East Equatorial Africa, T.b.
gambiense- West and Central Equatorial
Africa
DISEASE: trypanosomiasis, sleeping sickness
HABITAT: in fly - midgut, saliva glands, in man –
various body fluids, e.g. blood, limph, and
spinal fluid
RESERVOIR HOST: wild or domestic animals
TRANSMISSION VECTOR tsetse fly Glossina
spp.
INFECTVE FORM: metacyclic trypomastigotes
DIAGNOSTIC FORM: trypomastigotes
MODE OF INFECTION: specific inoculation
SPECIMEN SOURCE: wild animals or domestic
animals and people
Trypanosomatids morphological
stages and structure

a– amastigote; b – promastigote;
c - epimastigote; d – trypomastigote.
 Blood smear from a patient with T.
b. rhodesiense. 41-year-old man
◄
who had returned from a trip to
Tanzania.

Blood smear from a patient (a U.S. traveler) Typical trypomastigote stage with a
with T. b. rhodesiense. A dividing parasite is posterior kinetoplast, a centrally
seen at the right. Dividing forms are seen in located nucleus, an undulating
African trypanosomiasis, but not in American membrane, and an anterior
trypanosomiasis (Chagas disease). flagellum.
Trypamosomiasis vector
Glossina brevipalpis (tsetse fly)

Tsetse’s proboscis
Glossina sp. dorsal view
Trypanosoma brucei
At Risk 60 million - sub-
Saharan Africa
Humans Infected 300-500
thousand

Disease Outcome Uniformly

fatal within two years

Vaccine Prospects Poor due to

antigenic variation

Available Drugs Toxic, difficult

to deliver

Drug Resistance Documented

West Africa – T.b. gabiense

East Africa – T.b. rodesiense
 African Sleeping Sickness presentation

Chancre

utter
exhaustion
Trypanosomiasis, Human African (HAT, African Sleeping Sickness)

•Infectious Agent
•Two subspecies of the protozoan parasite Trypanosoma brucei (T. b.
rhodesiense and T. b. gambiense) cause infection.

•Mode of Transmission
Infection occurs through vector-borne transmission by the bite of an infected
tsetse fly (Glossina spp.). Transmission via bloodborne or congenital routes
can occur but is rarely reported.

•Occurrence
HAT is transmitted only in rural sub-Saharan Africa. The two human-infective
subspecies of T. brucei do not overlap in geographic distribution.
T. b. rhodesiense is found in eastern and southeastern Africa. Over 95% of the
cases of T. b. rhodesiense infection occur in Tanzania, Uganda, Malawi, and
Zambia.
T. b. gambiense is found predominately in Central Africa and in limited areas of
West Africa. Over 95% of the cases of T. b. gambiense infection are reported
from the Democratic Republic of Congo, Angola, Sudan, Central African
Republic, Republic of Congo, Chad, and northern Uganda.
Clinical Presentation Stage I
• Haemolymphatic
CLINICAL SYNDROMES stage
Depend on whether parasite is well • Fever, myalgia,
adapted to humans (slow/chronic illness) headache
or primarily a zoonosis (rapid/ acute • Itching,
illness)
lymphadenopathy
• Symptoms and signs of T. b. rhodesiense infection
generally appear within 1–3 weeks of the infective bite.
These may include high fever, a chancre at the site of
the infective bite, skin rash, headache, myalgia, Stage II
thrombocytopenia, and less commonly, splenomegaly, • Meningoencephalitis
renal failure, or cardiac disfunction. Central nervous
system involvement can occur within the first month of • Reversal of sleep–
infection. wake cycle (hence
‘sleeping sickness’)
• Symptoms of T. b. gambiense infection are nonspecific.
Symptoms and signs may include fever, headache, • Confusion/behaviour
malaise, myalgia, facial edema, pruritus, change
lymphadenopathy, and weight loss. Central nervous • Weakness and wasting
system involvement occurs after months of infection
and is characterized by somnolence, severe headache, • Convulsions
and a wide range of neurologic manifestations, (uncommon)
including mood disorders, behaviour change, focal
deficits, and endocrine disorders. Tremor, ataxia, coma

• Untreated HAT infection is eventually fatal.

Philippa C. Matthews 2012. TROPICAL MEDICINE NOTEBOOK

HAT caused devastating epidemics during the 20th century.
Thanks to sustained and coordinated efforts during the past 15 years
the number of reported cases has fallen to a historic low. The number of
new human African trypanosomiasis cases reported between 2000
and 2012 dropped by 73%. Fewer than 3,000 cases were reported in
2015, and the disease is targeted for elimination by the World Health
Organization (Büscher Philippe et al. WHO).

https://infograph.venngage.com/p/98426/african-sleeping-disease-health-campaign-infographic

the WHO
neglected
tropical
diseases
roadmap
targeted its
elimination as
a public
health
problem by
2020.
Trypanosoma cruzi
DISEASE: Chagas disease or American
Trypanosomiasis.
GEOGRAPHICAL DISTRIBUTION Mexico,
Central and South America
TRANSMISSION VECTOR: Reduviid bug;
Triatoma and Panstrongylus species
RESERVOIR HOST: Various mammals.
INFECTIVE FORM: Metacyclic
trypomastigotes.
DIAGNOSTIC FPORM trypomastigotes
PATHOGENESIS: frequently fatal; localized
severe inflammation, organomegaly
cardiomyopathy; HABITAT: Circulatory,
central nervous, and reticuloendothelial
systems; heart muscle.
bone marrow. intestine
MODE OF INFECTION: Fecal contamination
after the bite (specific contamination)
SPECIMEN SOURCE: Blood of infected
animals and people
In 1908 Cruz became Head of the Institute for Tropical Diseases at Rio,
and remained its Director until his death. One of his pupils was Carlos
Chagas, who discovered the causative agent of South American
trypanosomiasis and named the organism Trypanosoma cruzi in honour of
Cruz.
Oswaldo Cruz (1872–1917),
Carlos Chagas (1879–1934), discoverer of the
causative agent of South American who performed public health
trypanosomiasis researches in southern America

From Cook G.C. 2007. TROPICAL

MEDICINE: AN ILLUSTRATED
HISTORY OF THE PIONEERS
 During the day, triatomines hide in
crevices in the walls and roofes
The bugs emerge at night, when
the inhabitants are sleeping.
Because they tend to feed on
people's faces, triatomine bugs are
also known as "kissing bugs".

Triatoma rubida

Triatoma dimidiata
Trypanosoma cruzi life cycle
 Summary of the life cycle
of Trypanosoma cruzi, in the vector (1–
4) and mammalian host (5–7).

Miles M. 2008 Ch.76 from Cook_Zumla (eds.)

2008 Manson's Tropical Diseases 22nd
Edition5

Philippa C. Matthews 2012. TROPICAL MEDICINE NOTEBOOK

 Trypanosoma cruzi native geografical
distribution

7–8 million people are infected

worldwide
Transmission cycles of Trypanosoma cruzi. (A) An example of separate silvatic and
domestic transmission cycles, in Bahia
State, Brazil:
T. cruzi I in the silvatic cycle (principal
silvatic host the opossum, Didelphis
albiventris, vector Triatoma
tibiamaculata, and T. cruzi II in the
domestic transmission cycle (vector
Panstrongylus megistus).

(B) An example of overlapping silvatic

and domestic transmission cycles, in
parts of
Venezuela: T. cruzi I in both the
domestic and silvatic transmission
cycles (vector Rhodnius prolixus in
houses and in palm trees).

(C) Enzootic
transmission in the Amazon basin:
sporadic cases of Chagas’ disease
occur due to adult bugs flying to palm
presses (orally transmitted outbreaks)
or houses but not forming domestic
colonies; also forest workers harvesting
the piassaba palm may be attacked by
Rhodnius brethesi. (Courtesy of
J. S. Patterson.)
Miles M. 2008 Ch.76 from Cook_Zumla (eds.) 2008 Manson's Tropical Diseases 22nd Edition
 Chagas disease presentation

chagoma, ‘Romaña’sign’

‘Chagas heart’
Megacolon
Trypanosomiasis, American (Chagas Disease)

Infectious Agent
American Trypanosomiasis is caused by the protozoan parasite, Trypanosoma
cruzi.

Mode of Transmission
Infection occurs through vector-borne transmission in endemic counties via the
feces of the triatomine insect (reduviid bug), which may be inadvertently inoculated
into the skin, the mucosa of eye, nose, or mouth when the insect’s bite is scratched
and rubbed
Through transfusion or organ transplantation
From mother to infant (transplacentally)
Through occupational exposure in research workers

Occurrence
Approximately 7.6 million people are infected with Chagas disease, according to the
most recent estimates. The disease is endemic in Mexico, Central and South
America. Rare cases of Chagas disease attributed to local vector-borne
transmission have been reported in the United States.
 Clinical Presentation
• The acute phase of Chagas disease lasts up to 90 days, followed by
asymptomatic chronic infection, usually undetectable by
parasitologic methods. Most infected individuals never develop
symptoms but remain infected throughout their lives. Those who
develop acute illness will do so at least one week following
exposure. A chagoma may develop, which is an area of edema and
erythema at the site of infection; the classic picture is Romaña’s
sign, which presents as edema of the lid and ocular tissues when
the entry site was the conjunctiva. Approximately 20%–30% of
infected patients will develop manifestations of chronic Chagas
disease, usually involving the heart. Clinical signs include
conduction system abnormalities, ventricular arrhythmias, and in a
late stage disease, congestive cardiomyopathy. Chronic
gastrointestinal problems may ensue when Chagas causes
megaesophagus or megacolon. Reactivation of the disease may
occur in immunocompromised patients.
 (Miles M. 2008 Ch.76 from Cook_Zumla (eds.) Manson's Tropical Diseases 22nd Edition)

Thanks to Chagas’ disease control the incidence

of new infections by T. cruzi in the whole
continent has decreased by 70%.
Patrícia da Silva LOPES et al., 2015.
Revalence of chagas disease among
blood donor candidates in Brazil

Cases of Chagas disease recorded in

Hemominas, in Ituiutaba town, Minas
Gerais State, Brazil.
“An estimated 8 million people are infected worldwide, mostly in Latin America.”
“It is estimated that over 10 000 people die every year from clinical
manifestations of Chagas disease, and more than 25 million people risk
acquiring the disease.”
 Genus Leishmania
GEOGRAPHICAL DISTRIBUTION:
prevalent in the tropics and subtropics.
DISEAS cutaneous, muco-cutaneous, visceral,
viscerotropic leishmaniasis depending on the
species
HABITAT: vector (sand fly) alimentary canal
in man - skin and nearly all internal organs,
particularly liver and spleen
RESERVOIR HOST: rodents, canids, some other
mammals
TRANSMISSION VECTOR sand flies of genera
Phlebatomus and Lutzomyia
INFECTIVE FORM: promastigote
DIAGNOSTIC FORM both amastigote and
promastigote
MODE OF INFECTION: specific inoculation
SPECIMEN SOURCE: wild animals, infected
people or both
Lieutenant-General Sir William Boog Leishman (1865–1926)

In 1900 Leishman demonstrated the causative

agent of kala-azar (dumdum fever), but he did not
publish this finding until 1903. In that year (1903),
Donovan confirmed this discovery at Calcutta
(India).
Thus, one of the visceral leishmanaisis
infective agents was called in honor of both
scientists -
Lishmania donovani

From Cook G.C. 2007. TROPICAL

MEDICINE: AN ILLUSTRATED
HISTORY OF THE PIONEERS

Charles Donovan (1863–1951)

 Leishmania spp.

Promastigote form
of Leishmania.
Leishmania
changes to several
Leishmania tropica amastigotes from a differnt forms
skin touch preparation. A still intact during its life time.
macrophage is practically filled with This form is
amastigotes, several of which have infective to
clearly visible a nucleus and a humans and pets.
kinetoplast (arrows)
Old World leishmaniasis vector :
the sand fly Phlebotomus papatasi
Phlebotomus spp.
New World leishmaniasis vector :
the sand fly Lutzomyia sp.
Leishmania geographic distribution
Leishmania life cycle
Philippa C. Matthews 2012. TROPICAL MEDICINE NOTEBOOK
 Worldwide distribution of cutaneous
leishmaniasis

90% of cases occurs in Afghanistan, Brazil, Iran, Peru, Saudi Arabia and Syria.
Zoonotic cutaneous leishmaniasis
ivfectious agent – Leishmania major
An acute form of cutaneous leishmaniasis
occurring among people living in rural areas near
infected rodents and characterized by rapidly
developing skin lesions that become severely
inflamed, with moist necrotizing sores, ulsers that
often leave disfiguring scars. Often secondary Middle East, North and
bacterial infection appears. Western Africa, Asia

Incubation period 3-4 weeks,

irregular shaped ulcers are
localized on upper and lower
limbs. wound healing begins
at 2-4 months

main source- wild rodents

 Anthroponotic cutaneous leishmaniasis
Also callled chronic cutaneous leishmaniasis,
dry cutaneous leishmaniasis, urban
cutaneous leishmaniasis

infectious agent – Leishmania tropica

incubation period 2 month -2 years and more

in urban areas in West and Central

Asia. Painless, chronic, dry
ulceration that develops normally
from two to eight months after the
bite, heals about one year often living
a scar
 Zoonotic vs. anthroponotic cutaneous leishmaniasis
Zoonotic Anthroponotic
acute form chronic form

•Leishmania major •Leishmania tropica

•Short incubation period • long incubation period

•Scarring ends in five month • scarring ends in one-two years.

 Mucocutaneous leishmaniasis
New World : infectious agent
Leishmania brazilensis
South America, especially in Brazil, Paraguay,
Ecaudor, Bolivia, Peru, Colombia, Venezuela
90% of cases occurs in Bolivia, Brazil and Peru

Old World : Leishmnia aethiopica

Ethiopia, Kenya, Namibia

inital symptoms are similar to that of cutanous form

single or multpile lesions and ulcers develop at the mucosal
regions (nose, mouth, throat cavities) and in the adjacent
tissue
extensive disfiguring of the nasal septum, lips, and palate
after several weeks, the lesions tend to heal on
their own
Leishmania mexicana specyfies on the human auricle

An inflamed and ulcerated ear of L. mexicana, or chiclero ulcer, may lead to

cartilage destruction. From James WD, Berger T, Elston DMD, eds.
Andrew’s Diseases of the Skin. 11th edn. London, Saunders; 2011.
Worldwide distribution of visceral
leishmaniasis
VL in Europe, Asia and Africa
• Karimi Abdollah, Alborzi Abdolvahab, Amanati Ali. 2016.
 Visceral Leishmanianisis
Medterranean type Indian type (kala-azar)
infectious agent – L. infantum infectious agent – L. donovani

(post-kala-azar
manifestation)

anthroponosis,
source – people
zoonosis, source – canids main victims - adults
main victims – little kids

Eastafrican type
infectious agent – L. arshibaldi

anthropo-zoonosis, source
– rodents, people
 if not treated, VL case fatal rate is 100% within 2 years

90% of reported visceral leishmanaesis cases occur in

Bangladesh, Brazil, India, Nepal and Sudan

weight loss, which may be severe

low blood counts (pancytopenia)
enlargement of liver and spleen
(organomegaly)
fever, which is usually intermittent
high levels of immune globulin in the
blood
Kidneys and bone marrow also may be
affected. The skin may turn dark, causing
VL to be called "kala-azar," which means
"black sickness”. The disease is
complicated by serious infections
 Post-kala-azar

Post-kala-azar dermal (skin) leishmaniasis

(PKDL) is a unique eruption that develops
after apparent cure of kalaazar (KA) or
visceral leishmaniasis. It is mainly prevalent
in the countries around the Indian
subcontinent including India, Pakistan,
Bangladesh and Nepal. Other places are
Iraq, China and of late a large number of
cases are being reported from African states.
People are the the sourse of infection, which
manitests itself in a new human host first as
Kala azar visceral leishmanaisis and only later it may
turn into a dermal form.
 Diagnosis

Blood test for

antibodies against the
parasite

Microscopical identification
• . Leishmania invade the cells of the reticuloendothelial system,
such as macrophages, bone marrow cells, spleen cells and the
Kupffer’s cells of the liver. Tropism of the parasites is thought to
be dependent, in part, on the optimal temperature of growth of
the amasigotes, where Leishmania parasites with a preference
for a temperature around 35° C cause cutaneous or
mucocutaneous manifestations, while parasites that grow best
at 37° C cause the visceral manifestation of the disease.
• There are some 20 different species of Leishmania, which
infect people. The disease is endemic in the tropical and
subtropical regions of 88 countries. In total 350 million people
are at risk and 12 million people are infected. In East Africa,
India, and China, the most spread is visceral leishmaniasis or
"kala azar", while in the Middle East, there is mainly cutaneous
leishmaniasis or "oriental sore". 1.5 million of new cases are
reported annually, 500.000 of which are visceral leishmaniasis.
The diseas is a subject of thorough investigation.
• Localization of cutaneous leishmaniasis
– Old World
» L donovani - China, India, Bangladesh,
Sudan
» L tropica - Middle East, China, India,
Mediterranean
» L major - Middle East, Africa, India, Asia
» L aethiopica - Ethiopia, Kenya, Namibia
» Leishmania infantum - Asia, Africa,
Europe
– New World
» Leishmania leishmania mexicana -
Central and South America, North
America
» L leishmania amazonensis - Dominican
Republic, Central America, South
America
» L leishmania venezuelensis -
Venezuela
» L viannia braziliensis - Central America,
South America
» L viannia guyanensis - Guyana, French
Guyana, Surinam, Brazil
» L viannia panamensis - Costa Rica,
Panama, Colombia, Ecuador
» L viannia peruviana - Peru, Argentina
» Leishmania donovani chagasi - Texas,
Caribbean, Central America, South
America
• Diffuse cutaneous leishmaniasis
– Old World
• L aethiopica - Ethiopia, Kenya, Namibia
– New World
• L leishmania mexicana - Central, South America, North America
• L leishmania amazonensis - Dominican Republic, Central America,
South America
• Leishmaniasis recidivans
– Old World
• L tropica - Middle East, China, India, Mediterranean
– New World
• L viannia braziliensis - Central America, South America
• Post-kala-azar leishmaniasis
– Old World
• L donovani - China, India, Bangladesh
• L infantum - Asia, Africa, Europe
– New World
• L donovani chagasi - Central America, South America
• Mucocutaneous leishmaniasis
– Old World
• L aethiopica - Ethiopia, Kenya, Namibia
– New World
• L viannia braziliensis - Central America, South America
• L viannia panamensis - Central America, South America
• L viannia guyanensis - Guyana, French Guyana, Surinam, Brazil
• Less often seen with L leishmania mexicana - Central America, South America, North
America
• Less often seen with L leishmania amazonensis - Brazil, Panama
• Visceral leishmaniasis
– Old World
• L donovani – Asia (China, India, Bangladesh), East Africa (Sudan)
• L infantum – Mediterranean region (Asia, Africa, Europe)
• L. arshibaldi – East Africa (Sudan Kenya Ethiopia Somali Chad)
– New World
• L donovani chagasi - Central America, South America
• Viscerotropic leishmaniasis
– Old World
• L tropica - Middle East
• Leishmaniasis, Cutaneous (CL)
• Leishmaniasis is a parasitic disease found in parts of the tropics, subtropics,
and southern Europe. Leishmaniasis has several different forms.
• Infectious Agent Obligate intracellular protozoan parasites of the genus
Leishmania; approximately 20 species cause CL.
• Mode of Transmission
• Vector-borne, through the bite of infected female Phlebotomus, Lutzomyia
sand flies. CL also can occur after accidental occupational (laboratory)
exposures to Leishmania parasites.
• Occurrence
• In the Old World CL is found in parts of the Middle East, Asia (particularly
Southwest and Central Asia), Africa (particularly the tropical region and
North Africa), and southern Europe.
• In the New World CL is found in parts of Mexico, Central America, and
South America. Occasional cases have been reported in Texas and
Oklahoma. CL is not found in Chile, Uruguay, or Canada.
• Overall, CL is found in focal areas of ~90 countries. Most (>90%) of the
world’s cases of CL occur in eight countries: Afghanistan, Algeria, Iran, Iraq,
Saudi Arabia, and Syria (in the Old World); and Brazil and Peru (in the New
World).
• Clinical Presentation
• CL is characterized by the presence of one or more skin lesions (open or
closed sores), which typically develop within several weeks or months of the
exposure. In some persons, the sores first appear months or years later, in
the context of trauma (e.g., skin wounds or surgery).
• The sores can change in size and appearance over time. They typically
progress from small papules, to nodular plaques, to open sores, with a
raised border and central crater (ulcer), which can be covered with scales or
crust. The lesions usually are painless but can be painful, particularly if
open sores become infected with bacteria.
• Satellite lesions, regional lymphadenopathy (swollen glands), and nodular
lymphangitis can be noted.
• The sores usually heal eventually, even without treatment. However, they
can last for months or years and typically result in scarring.
• Another potential concern applies to some of the Leishmania species in
South and Central America—occasionally, these parasites spread from the
skin to the mucosal surfaces of the nose or mouth and cause sores there.
This form of leishmaniasis, mucosal leishmaniasis (ML), might not be
noticed until years after the original skin sores appear to have healed.
Although ML is uncommon, it has occurred in travelers and expatriates
whose cases of CL were not treated or were inadequately treated. The initial
clinical manifestations typically involve the nose (e.g., chronic stuffiness,
bleeding, and inflamed mucosa/sores) and less often the mouth; in
advanced cases, ulcerative destruction of the nose, mouth, and pharynx
can be noted (e.g., perforation of the nasal septum).
Leishmaniasis, Visceral (VL)
• VL has several different forms and which affects some of the internal organs of the body (e.g.,
spleen, liver, bone marrow).
• Infectious Agent Mode of Transmission – such as for CL
Congenital and parenteral transmission (through blood transfusions and needle sharing) have
been reported.
• Occurrence
• VL usually is more common in rural than urban areas; but it is found in some periurban areas
(e.g., in northeastern Brazil).
• In the Old World (Eastern Hemisphere), VL is found in parts of Asia (particularly the Indian
subcontinent and Southwest/Central Asia), the Middle East, Africa (particularly East Africa), and
southern Europe.
• In the New World (Western Hemisphere), most cases occur in Brazil; some cases occur in
scattered foci elsewhere in South and Central America.
• Overall, VL is found in focal areas of approximately 65 countries. Most (>90%) of the world’s
cases of VL occur in the Indian subcontinent (India, Bangladesh, and Nepal), Sudan, and Brazil;
none of the affected areas in these five countries are common tourist destinations.
• Clinical Presentation
• Among symptomatic persons, the incubation period typically ranges from weeks to months. The
onset of illness can be abrupt or gradual.
• Stereotypical manifestations of VL include fever, weight loss, hepatosplenomegaly (especially
splenomegaly), and pancytopenia (anemia, leukopenia, and thrombocytopenia).
• If untreated, severe (advanced) cases of VL typically are fatal.
• Latent visceral infection can become clinically manifest years to decades after exposure in
persons who become immunocompromised due to other medical reasons.