CLINICAL PARASITOLOGY LECTURE

WEEK 4: The Flagellates and Hemoflagellates

 Found in the stool
What’s Ahead  Trophozoites in outside environment – depends
I. Key definitions on the specific flagellate
II. Morphology and Life Cycle Notes  Cysts in outside environment – survive
III. Laboratory Diagnosis o They continue to develop in “outside
IV. Pathogenesis and Clinical Symptoms world” for subsequent entry into
V. Classification of the Flagellates unsuspecting human – new cycle begins.
VI. Intestinal Species
a. Giardia intestinalis LABORATORY DIAGNOSIS
b. Chilomastix mesnili  Specimen of choice for recovering most
c. Dientamoeba fragilis intestinal flagellates
d. Trichomonas hominis o Stool
e. Enteromonas hominis  Specimen of choice for recovering
f. Retortamonas intestinalis extraintestinal flagellates varies by species but
VII. Extraintestinal Species includes:
a. Trichomonas tenax o Mouth scrapings
b. Trichomonas vaginalis o Centrifuged urine
VIII. Looking Back o Vaginal/urethral discharge
o Prostatic secretions
THE FLAGELLATES
KEY DEFINITIONS PATHOGENESIS AND CLINICAL SYMPTOMS
Flagellate  Most intestinal flagellate infections are
o Single-celled parasite that moves by means asymptomatic.
of taillike structure known as a flagellum (pl. o Diagnosis of nonpathogenic flagellates –
flagella) important finding suggests ingestion of
Axostyle contaminated food or drink may have
o Rod-like support structure in select occurred.
flagellates  Only intestinal flagellate considered pathogenic
Axoneme with characteristic symptoms – Giardia
o Intracellular portion of a flagellum intestinalis
Cytostome
o Rudimentary mouth present in some CLASSIFICATION OF THE FLAGELLATES
flagellates
Median bodies
o Comma shaped structures inside Giardia
intestinalis
o Structure associated with energy,
metabolism, or support
Undulating membrane
o Fin like structure
Costa
o Rod like structure located at the base of the
undulating membrane INTESTINAL SPECIES

MORPHOLOGY AND LIFE CYCLE NOTES Giardia intestinalis

Two possible flagellate morphologic forms:  Laboratory diagnosis
1. Trophozoites o Stool, small intestine biopsies: Standard
2. Cysts methods
 Ingestion of infected cysts when present – o Duodenal contents obtained by aspiration
initiation of human intestinal infection or Enterotest (string test)
 Trophozoites emerge in intestine o Fecal antigen detection using enzyme
 Trophozoites in intestinal tract immunoassays (EIA) and enzyme linked
o Actively multiply by asexual binary fission immunosorbent assays (ELISA)
 Changes in intestinal environment – excystation, o Direct fluorescence
when cysts are present o Western immunoblotting (blot) has shown
 Results in diagnostic stages of: promising results
o Cysts and/or o Real time polymerase chain reaction (RT
o Trophozoites that do not/cannot make the PCR)
conversion in time
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 Life cycle notes  Also known as traveler’s diarrhea
o After human ingestion  Diarrhea, abdominal pain and
 Gastric acid in stomach stimulates cramping, weight loss, anorexia,
cysts to transform (excyst) into chronic fatigue, flatulence
 Established trophozoites multiply  Severe cases may result in:
every 8 hours by longitudinal binary  Fat soluble vitamin deficiencies
fission.  Folic acid deficiencies
 Trophozoites use sucking discs to  Hypoproteinemia with hypogamma
attach to duodenum mucosa. globulinemia
 Trophozoites may also invade:  Intestinal villi structural changes
 Bile duct  Typical course of infection
 Gallbladder o Incubation period of 10 26 days
 Changes in the trophozoites o Self limiting condition – typically over in 10-
environment result in: 41 days
 Unacceptable conditions for the  Chronic infection
trophozoites o Multiple relapses may occur.
 Trophozoites respond by o Individuals with an IgG deficiency seem to
converting to cysts be susceptible to recurring infections.
(encystation) as they migrate to  Treatment
the large bowel o Metronidazole (Flagyl)
 Resulting cysts exit the human host o Tinidazole (Tindamax)
through the feces. o Nitazoxanide (Alinia)
 Cysts may remain viable for as long  Prevention and control
as 3 months in water. o Proper water treatment
 Any trophozoites that exit the human o Proper food handling/ preparation
host disintegrate due to their fragile o Adhering to protected sex
composition. o Protect food from insects
 Epidemiology
o Avoid using human stool as fertilizer
o Worldwide in multiple water sources
 Parasite name note
o Transmitted via:
o G. intestinalis has had two previous names,
 Contaminated food/water
most recently G. lamblia
 Hand to mouth o The name G. intestinalis is gaining
 Unprotected sex popularity.
 Circulating flies and cockroaches o Some consider G. duodenale as a
o Considered one of the most common synonym.
intestinal parasites, especially among o The nomenclature of this parasite is
children currently under review.
o Cysts resistant to routine water chlorination Trophozoite
 Chemical and filtration processes
required
o Contamination of food possible after
exposure to infected water
o Populations at risk:
 Children in day care centers
 Individuals in areas of poor sanitation
 Travelers to and who drink
contaminated water in known
endemic areas
 Individuals who practice unprotected
sex: Homosexual males
o Several known animal reservoir hosts:
 Beavers, muskrats, water voles
 Domestic animals (e.g., sheep, dogs,
cattle), which can directly transmit the
parasite to humans
 Clinical symptoms
o Asymptomatic (carrier)
o Symptomatic intestinal amebiasis
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Cyst

Chilomastix mesnili
 Laboratory diagnosis
o Stool – standard methods
 Epidemiology
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o Cosmopolitan – prefers warm climates
o Mode of transmission:
 Consumption of contaminated food and
water
 Hand to mouth contamination
 Clinical symptoms
o Usually, asymptomatic
 Treatment
o Treatment usually not indicated
 Prevention and control
o Good sanitation and personal hygiene
practices
o Protection of food from insects
Trophozoite

Cyst

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WEEK 4: The Flagellates and Hemoflagellates
 Diarrhea and abdominal pain
– Diarrhea alternating with
constipation
 Bloody or mucoid stools
 Flatulence
 Nausea or vomiting
 Weight loss
 Fatigue or weakness
 Low grade eosinophilia
 Pruritis
 Treatment
o Although there is some uncertainty about its
pathogenicity, treatment may be indicated
in symptomatic cases.
 Iodoquinol, tetracycline, paromomycin
(Humatin)
Dientamoeba fragilis  Prevention and control
 Laboratory diagnosis o Exact measures unclear due to unknown
o Stool – standard methods life cycle
o Multiple samples necessary to rule out its o Measures believed to minimize spread:
presence  Good sanitation and personal hygiene
o Conventional and real time (RT) PCR practices
methods used (RT PCR most sensitive)  Adhering to protected sex
 Life cycle notes
o Life cycle poorly understood
o Only known morphologic form –
trophozoites
o Location after human ingestion:
 Mucosal crypts of large intestine
 No evidence of surrounding tissue
invasion
o Known to rarely ingest RBCs
 Epidemiology
o Exact mode of transmission – unknown
o Possible theory: D. fragilis may be
transmitted via select helminth eggs
(Chapter 8):
 Enterobius vermicularis (pinworm)
 Ascaris lumbricoides (large intestinal
roundworm)
o Evidence suggests:
 Most likely distributed in metropolitan
areas; geographic distribution unknown
 At risk populations: children,
homosexual men, individuals in
semicommunal or institutional
environments
 Possible transmission routes: person to
person, oral anal
o The difficulty in correctly identifying D.
fragilis likely inhibits epidemiologic
information.
 Parasite tends to blend in with Trichomonas hominis
background material.  Laboratory diagnosis
 Clinical symptoms o Stool – standard methods
o Asymptomatic  Life cycle notes
o Symptomatic – D. fragilis infection o Only known morphologic form: trophozoites
 Symptoms vary and include:  Epidemiology
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CLINICAL PARASITOLOGY LECTURE
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o Found worldwide particularly in
metropolitan areas of warm and temperate
climates
o Most likely mode of transmission –
ingestion of trophozoites possibly in
contaminated milk
 Clinical symptoms
o Usually asymptomatic
 Treatment
o Usually not indicated
 Prevention and control
o Good sanitation and personal hygiene
practices
Trophozoite

Enteromonas hominis
 Laboratory diagnosis
o Stool – standard methods
o Careful screening required due to small
parasitesize
 Epidemiology
o Worldwide distribution in warm and
temperate climates
o Primary mode of transmission – ingestion of
infected cysts
 Clinical symptoms
o Usually asymptomatic
 Treatment
o Usually not indicated
 Prevention and control
o Good sanitation and personal hygiene
practices
Trophozoite

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CLINICAL PARASITOLOGY LECTURE
WEEK 4: The Flagellates and Hemoflagellates

Retortamonas intestinalis
 Laboratory diagnosis
o Stool – standard methods
o Careful screening required due to small
parasite size
 Epidemiology
o Warm and temperate climates
o Primary mode of transmission –
consumption of infected cysts
 Clinical symptoms
o Usually asymptomatic
 Treatment
o Usually not indicated
 Prevention and control
o Good sanitation and personal hygiene
practices

Cyst
Trophozoite

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CLINICAL PARASITOLOGY LECTURE
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Trichomonas tenax
 Laboratory diagnosis
o Mouth scrapings, tonsillar crypts, pyorrheal
pockets
 Standard methods
 Culture on appropriate media
 Life cycle notes
o Lives in gumline; exists as scavengers
o No known cyst stage
o Trophozoites unable to survive stomach
juices
 Epidemiology
o Healthy and unhealthy mouths in all
populations studied to date
o Exact mode of transmission: unknown
 Evidence suggests transmission may
occur via:
 Contaminated dishes/utensils
Cyst  Droplet contamination
 Clinical symptoms
o Typically asymptomatic
o Respiratory tract involvement in patients
with select pulmonary issues
 Treatment
o usually not indicated
 Prevention and control
o Practicing good personal oral hygiene

Trophozoite

EXTRAINTESTINAL SPECIES

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CLINICAL PARASITOLOGY LECTURE
WEEK 4: The Flagellates and Hemoflagellates
 Foul smelling, greenish yellow,
liquid vaginal discharge
 Burning, itching, chafing
 Infant infections
 Respiratory, conjunctivitis
 Treatment
o Metronidazole (Flagyl)
o Treatment of all sexual partners
recommended
 Prevention and control
o Adhering to protected sex
o Prompt diagnosis and treatment
o Avoidance of potentially infective towels,
sponges, underclothing
o Avoid sharing douche equipment

Trophozoite

Trichomonas vaginalis
 Laboratory diagnosis
o Standard techniques; saline wet preps often
preferred
 Spun urine
 Vaginal or urethral discharge
 Prostatic secretions
o DNA based assay has been developed
o InPouch TV culture system
 Women: vaginal swabs
 Men: urine sediment, semen sediment
 Involves incubation of up to 3 days
 Life cycle notes
o Reside on the mucosal surface of the
vagina in women
 Trophozoites replicate by longitudinal
binary fission.
 Trophozoites feed on bacteria and
leukocytes.
 Trophozoites thrive in slightly alkaline
or slightly acidic pH environment (like
that in an unhealthy vagina).
o Reside in the prostate gland region and the
epithelium of the urethra in men
 Detailed life cycle in men – unknown
 Clinical symptoms
o Asymptomatic
o Symptomatic
 Persistent urethritis
 Enlarged tender prostate
 Dysuria
 Nocturia
 Epididymitis
 Persistent vaginitis

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CLINICAL PARASITOLOGY LECTURE
WEEK 4: The Flagellates and Hemoflagellates
THE HEMOFLAGELLATES
KEY DEFINITIONS
Hemoflagellate:
o Single-celled parasite that moves by
means of tail-like extensions of
cytoplasm known as a flagellum (pl.
flagella) that resides in blood and tissue
Blepharoplast:
o Basal body structure located in the
cytoplasm of the hemoflagellates
Kinetoplast:
o An umbrella term that refers to the
blepharoplast and small parabasal body
located in the cytoplasm of the
hemoflagellates
Parasitemia
o Parasite infection in the blood
LOOKING BACK
 Flagellates consist of single celled parasites that
MORPHOLOGIC FORMS
move by means of flagella.
 Flagellates are differentiated from each other
AMASTIGOTE
(and identified) based:
o Size
o Shape
o Nuclear structures
o Flagellate number/arrangement
o Cytoplasmic features
o Presence/relative size of undulating
membrane when present
 Careful examination of all specimens submitted
for parasite analysis is important.
 Suspicious flagellate forms must be evaluated
closely to ensure accurate identification.

What’s Ahead
I. Key Definitions
II. Morphologic Forms
III. General Morphology and Life Cycle
Notes
IV. Laboratory Diagnosis
V. Pathogenesis and Clinical Symptoms
VI. Classification of the Hemoflagellates
VII. Blood and Tissue Species
a. Leishmania braziliensis complex
b. Leishmania donovani complex
c. Leishmania mexicana complex
d. Leishmania tropica complex
e. Trypanosoma brucei gambiense
f. Trypanosoma brucei rhodesiense
g. Trypanosoma cruzi
h. Trypanosoma rangeli
VIII. Looking Back

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CLINICAL PARASITOLOGY LECTURE
WEEK 4: The Flagellates and Hemoflagellates

PROMASTIGOTE

TRYPOMASTIGOTE

EPIMASTIGOTE

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PATHOGENESIS AND CLINICAL SYMPTOMS
 Symptoms vary and include:
o Small red papule at bite site
o Intense itching
o Secondary bacterial infections
o Fever
o Diarrhea
o Kidney involvement
o Mental retardation
o Comatose state
o Death
o Initial skin lesions:
 Spontaneously heal
 Remain dormant for months or years

CLASSIFICATION OF THE HEMOFLAGELLATES

BLOOD AND TISSUE SPECIES

LEISHMANIA SPECIES
 Historical perspective
o Depictions of Leishmania date back to 1st
century A.D. on pottery from Ecuador and
Peru.
o Leishmaniasis is a general term
describing the diseases caused by the
parasites in the genus Leishmania
o Increased travel and exposure to different
environments have resulted in parasite
GENERAL MORPHOLOGY AND LIFE CYCLE infections in the blood (parasitemias).
NOTES
 Morphologic forms routinely seen in human DISEASES AND CONDITIONS ASSOCIATED
samples: WITH LEISHMANIASIS
o Amastigotes in tissue, muscle, and CNS  Baghdad boils
o Trypomastigotes in peripheral blood o A common name for an infection with
 Life cycles vary among the hemoflagellates Leishmania tropica
and are thus covered where appropriate later o It is a cutaneous form of leishmaniasis
in this presentation. presenting with pus-containing ulcers
 Bay sore
LABORATORY DIAGNOSIS o A common name for a cutaneous form of
 Specimens of choice vary and include: infection caused by Leishmania mexicana
o Peripheral blood  Chiclero ulcer
o Lymph node and ulcer aspirations o A form of cutaneous leishmaniasis cased
o Tissue biopsies by L. mexicana
o Bone marrow o It is commonly found in Belize Guatemala,
o CSF and the Yucatan peninsula in areas where
 Traditional, serologic, and molecular methods chicle sap is harvested for making
are available. chewing gum
 Dum dum fever

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o A common name for the visceral  Amastigotes continue to reproduce
leishmaniasis caused by Leishmania causing tissue damage.
donovani  Promastigotes invade
 Espundia reticuloendothelial cells and transform
o Another name for an infection resulting into amastigotes.
from Leishmania braziliensis o Diagnostic stage for human
o The principle cause of mucocutaneous  Amastigotes (and on occasion,
disease in Central and South America, promastigotes)
particularly in Brazil o Infective stage for sand fly
 Forest yaws  Amastigotes – sand fly picks them up
o Another name for an infection with during blood meal.
Leishmania guyamensis o Evolution in the sand fly
o The principle cause of mucocutaneous  Amastigotes convert to promastigotes
leishmaniasis in the Guianas, parts of in sand fly midgut.
Brazil and Venezuela; also known as pian  Promastigotes multiply and migrate to
bois salivary gland for injection into next
An human during blood meal.
 Kala-azar  Epidemiology
o Another name for the most severe form of o Central and South America
visceral leishmaniasis caused by o Mode of transmission: bite of a sand fly
members of the Leishmania donovani o Numerous reservoir hosts, including:
complex  Forest rodents
 Oriental sore  Domestic dogs
o A common reference for the cutaneous L. braziliensis Geographic distribution:
leishmaniasis caused by the infecting  Mexico to Argentina
agents comprising the Leishmania tropic Vector:
complex  Lutzomyia and
 Pian bois Psychodopygus sandflies for
o Another name for infection with L. all species comprising this
guyanensis; also known as forest yaws complex
 Uta Reservoir hosts:
o A reference to mucocutaneous  Dogs and forest rodents for
leishmaniasis in the Peruvian Andes all species comprising this
complex
LEISHMANIA SPECIES L. panamensis Geographic distribution:
 Panama and Colombia
Leishmania braziliensis Complex L. peruviana Geographic distribution:
 Laboratory diagnosis  Peruvian Andes
o Specimen of choice for recovery of L. guyanensis Geographic distribution:
amastigotes – Giemsa-stained biopsy of  Guiana, Brazil, Venezuela
infected ulcer  Clinical symptoms
o Promastigotes may be seen: o Mucocutaneous leishmaniasis
 When sample is collected  Large ulcers in nasal mucosa
immediately after parasite  Cutaneous and/or mucosal lesions
introduction into patient  Lesions that may heal on their own
 Upon specimen culture  May result in permanent
o Serologic methods disfigurement of face
 Life cycle notes  May involve destruction of nasal
o Arthropod vector septum
 Sand fly species: Lutzomyia and  Other affected areas include:
Psychodopygus — Lips
o Mode of transmission — Nose
 Sand fly blood meal; injects parasite — Other soft parts
into human  Death from secondary bacterial
o Infective stage for human infection possible
 Promastigotes  Treatment
o After entry into human: o Medication group of choice
 Antimony compounds

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o Alternative medications:  Dogs, cats, foxes
 Liposomal amphotericin B L. donovani Geographic distribution:
(Ambisome) donovani  Parts of Africa, India,
 Oral antifungal drugs: Thailand, Peoples
 Fluconazole (Diflucan) Republic of China,
 Ketoconazole (Nizoral) Burma, East Pakistan
 Itraconazole (Sporanox) Vector:
 Prevention and control  Phlebotomus sandfly
o Public awareness and education Reservoir hosts:
 India, none; China,
programs
dogs
o Personal protection against sand fly bites
o Prompt treatment L. donovani infantum Geographic distribution:
o Eradication of infective ulcers  Mediterranean
Europe, near East
o Control of sand fly populations and
Africa; also in
reservoir hosts Hungary; Romania,
Southern region of
Leishmania donovani Complex former Soviet Union,
 Laboratory diagnosis Northern China,
o Screening test: Montenegro skin test Southern Siberia
o Giemsa-stained slides for demonstration Vector:
of diagnostic amastigotes:  Phlebotomus sandfly
 Blood Reservoir hosts:
 Lymph node aspirates  Dogs, foxes, jackals,
porcupines
 Biopsies of infected areas
o Samples that when cultured often show  Clinical symptoms
o Visceral leishmaniasis
promastigotes
 Blood  Non-descript abdominal illness
 Bone marrow  Hepatomegaly
 Other tissues  Diarrhea
o Serologic methods  Anemia
 Life cycle notes  May progress to kidney damage
o Identical to that of Leishmania braziliensis  Darkening of the skin (kala azar black
complex with 2 exceptions: fever)
1. The specific sand fly species vary with  Chronic cases – possible death in 1 2
the members of the L. donovani years
complex.  Acute disease – debilitates patient
2. Members of L. donovani complex and becomes lethal in only weeks
invade visceral tissue.  Treatment
 Epidemiology o Liposomal amphotericin B (Ambisome) –
o Depends on the subspecies but includes: medication of choice
 India o Sodium stibogluconate (Pentosam) –
 Pakistan alternative
 Parts of Africa o Patients who also have AIDS respond well
 China to allopurinol
 Mediterranean areas  Prevention and control
o Protection against sand flies
 Former Soviet Union
o Prompt treatment of human infections
 Central and South America
o Control of sand fly population
 Middle East
o Reservoir hosts vary among the o Control of reservoir hosts
subspecies.
L. donovani chagasi Geographic distribution: Leishmania mexicana Complex
 Central America,  Laboratory diagnosis
especially Mexico, o Giemsa-stained preparations
West Indies, South  Amastigotes – lesion biopsy material
America o Culture on NNN media – promastigotes
Vector: o Serologic methods
 Lutzomyia sandfly  Life cycle notes
Reservoir Hosts:
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o Identical to that of L. braziliensis species comprising this
o Primary sand fly vector species – complex
Lutzomyia Reservoir hosts:
 Rock hyrax
L. Mexicana Geographic distribution: L. major Geographic distribution:
 Belize, Guatemala,  Former Soviet Union, Iran,
Yucatan Peninsula Israel, Jordan, parts of
Vector: Africa, Syria (esp. in rural
 Lutzomyia sandfly for all areas)
species comprising this Reservoir hosts:
complex  Gerbilis, other rodents
Reservoir hosts: L. tropica Geographic distribution:
 Forest rodents for all  Mediterranean, parts of the
species comprising this former Soviet Union,
complex Afghanistan, India, Kenya,
L. pifanoi Geographic distribution: Middle East (esp. in urban
 Amazon River Basin, areas)
Brazil, Venezuela Reservoir hosts:
L. amazonensis Geographic distribution:  Possible dogs
 Amazon River Basin,  Clinical symptoms
Brazil o Old world cutaneous leishmaniasis
L. gamhami Geographic distribution:  Small red papule occurs at bite site
 Venezuelan Andes often, with intense itching.
L. Geographic distribution:  Incubation and appearance vary
venezuelensis  Venezuela with subspecies.
 Clinical symptoms  One or more pus containing ulcers
o New world cutaneous leishmaniasis that self-heal:
 Small red papule occurs at bite site  Sometimes self-healing does
often with pruritis. not occur because of the
 Incubation times vary with each  thick plaques of skin along
subspecies. with multiple lesions/nodules.
 Spontaneous healing does not occur
due to hypersensitivity immunologic
responses.
 Prevention and control
o Protection against sand flies
o Prompt treatment of human infections
o Control of sand fly and reservoir host
populations

Leishmania tropica Complex

 Laboratory diagnosis
o Giemsa-stained preparations
 Aspiration of fluid underneath ulcer
bed for amastigotes
 Ulcer tissue culture for promastigotes
o Serological tests
 Life cycle notes
o Same as that of L. braziliensis with 2
exceptions:  Treatment
1. Vector – Phlebotomus sand fly o Sodium stibogluconate (Pentostam)
2. Attacks human lymphoid tissue of skin o Steroids
L. aethiopica Geographic distribution: o Application of heat to infected lesions
 Highlands of Ethiopia, o Meglumine antimoniate (Glucantime)
Kenya, perhaps Southern o Pentamidine
Yemen
o Oral ketoconazole
Vector:
o Paromomycin ointment (to aid in healing)
 Phlebotomus sandfly for all
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CLINICAL PARASITOLOGY LECTURE
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 Prevention and control  Clinical symptoms
o Controlling sand fly and reservoir host o West African (Gambian) sleeping sickness
populations  Painful chancre surrounded by
o Use of protective equipment: white halo at bite site
 Protective clothing  Fever, malaise, headache,
 Repellents weakness, anorexia,
 Screening lymphadenopathy
o Prompt treatment and eradication of  Winterbottom’s sign (enlargement of
infected ulcers cervical lymph nodes)
o Vaccine developed and currently in  Erythematous (red) rash, pruritis,
clinical trials localized edema
 Kerandel sign (a delayed sensation
TRYPANOSOMA SPECIES to pain)
 Historical perspective  CNS involvement possible
o Ancient papyri discussed the diseases  Coma and death
associated with Trypanosoma species –  Treatment
well described throughout history. o Treatment of choice is situation
o Trypanomaniasis is the general term dependent; choices include:
describing the diseases caused by the  Melarsoprol
parasites in the genus Trypanosoma.  Suramin
 Pentamidine
Trypanosoma brucei gambiense  Eflornithine
 Laboratory diagnosis  Prevention and control
o Specimens of choice: o Destruction of tsetse fly breeding areas
o Giemsa-stained preparations – o Proper personal protective measures:
trypomastigotes  Clothing
o IgM testing on CSF or serum  Repellents
o Serologic testing  Screening
 Life cycle notes o Prompt treatment of infected persons
o Arthropod vector
 Tsetse fly: Glossina palpalis and Trypanosoma brucei rhodesiense
Glossina tachinoides  Laboratory diagnosis
o Mode of transmission o Giemsa-stained blood preparations –
 Tsetse fly blood meal trypomastigotes
o Infective stage for humans o Microscopic examination of CSF –
 Trypomastigote trypomastigotes
o After entry into human o Serologic tests
 Trypomastigotes migrate through  Life cycle notes
bloodstream, actively multiplying. o Identical to T. b. gambiense with 1
 Invasion of CNS may occur. exception:
o Diagnostic stage for humans  Tsetse fly species: Glossina
 Trypomastigotes morsitans and Glossina pallidipes
o Infective stage for tsetse fly  Epidemiology
 Trypomastigotes – tsetse fly picks o East and Central Africa
them up during blood meal. o Reservoir hosts:
o Evolution in the tsetse fly  Cattle
 Trypomastigotes convert to  Sheep
epimastigotes during migration into  Wild game animals
salivary gland.  Clinical symptoms
 Once in salivary gland, o East African (Rhodesian) sleeping
epimastigotes convert back to sickness
trypomastigotes for injection into  Short incubation period
next human during blood meal.  Acute disease:
o West and Central Africa, especially in  Fever, myalgia, rigors
shaded areas along stream banks where  Rapid weight loss common;
tsetse flies breed CNS involvement early in
o No known animal reservoir hosts disease

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CLINICAL PARASITOLOGY LECTURE
WEEK 4: The Flagellates and Hemoflagellates
 Mental disturbance, lethargy,  Epimastigotes multiply and migrate
anorexia to hindgut.
 Rapid, fulminating disease  Epimastigotes convert back to
results trypomastigotes for injection into
 Kidney damage and next human during blood meal.
myocarditis, which contribute to  Epidemiology
death within 9 12 months of o Central and South America
untreated patients Highest prevalence – Brazil
 Treatment o Number of known reservoir hosts
o Identical to that of T. b. gambiense o Most commonly seen in small children
 Prevention and control  Clinical symptoms
o Destruction of tsetse fly breeding areas o Chagas’ disease
o Proper personal protective measures:  Erythematous nodule (chagoma) at
 Clothing infection site (usually on the face)
 Repellents  Edema and rash around the eyes
 Screening  Conjunctivitis
o Prompt treatment of infected persons  Eyelid edema (Romaña’s sign)
Trypanosoma cruzi o Chronic Chagas’ Disease
 Laboratory diagnosis  Myocarditis
o Giemsa-stained blood preparations:  Enlargement of the colon
trypomastigotes (megacolon) or esophagus
o Giemsa-stained lymph node biopsies and (megaesophagus)
culture of blood: amastigotes  Hepatosplenomegaly
o Serologic tests  CNS involvement
o PCR/ELISA methods  Cardiomegaly
 Life cycle notes  Brain damage
o Arthropod vector  Sudden death
 Kissing (reduviid) bug o Acute Chagas’ Disease
o Mode of transmission  Fever
 Kissing bug defecates near blood  Chills
meal site.  Fatigue
 Kissing bug subsequently rubs it  Myalgia
into the skin via the scratch in  Malaise
preparation for its blood meal.  3 possible outcomes:
o Alternate modes of transmission 1. Recovery
 Blood transfusion, sexual 2. Transition to chronic stage
intercourse, transplacental disease
 Entry through mucous membranes 3. Death a few weeks after the
when kissing bug bites site near attack
areas such as eye or mouth  Treatment
o Infective stage for human o First choice: nifurtimox (Lampit)
 Trypomastigotes o Alternatives:
o After entry into human  Benzimidazole
 Trypomastigotes convert into  Allopurinol
amastigotes.  Ketoconazole
 Amastigotes multiply and destroy  Prevention and control
host cells. o Eradication of kissing bug nests
 Amastigotes convert back into o Education programs that cover:
trypomastigotes.  Disease signs and symptoms
o Diagnostic stage for human  Disease transmission
 Trypomastigotes and amastigotes  Possible reservoir hosts
o Infective stage for kissing bug
 Trypomastigotes – kissing bug picks Trypanosoma rangeli
them up during blood meal.  Laboratory diagnosis
o Evolution in the kissing bug o Giemsa-stained blood preparations:
 Trypomastigotes convert to trypomastigotes
epimastigotes in sand fly midgut. o Serologic tests
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CLINICAL PARASITOLOGY LECTURE
WEEK 4: The Flagellates and Hemoflagellates
o PCR methods
 Life cycle notes
o Same as that for Trypanosoma cruzi with
2 exceptions:
1. Species of arthropod vector (reduviid bug)
– Rhodius prolixus
2. Vector transmits parasite via its saliva
(rather than through defecation)
 Epidemiology
o Central and South America
o Number of known reservoir hosts
 Clinical symptoms
o Generally asymptomatic
o Considered a benign infection
 Treatment
o Nifurtimox (Lampit)
o Benzimidazole
 Prevention and control
o Eradication of kissing bug nests
o Education programs that cover:
 Disease signs and symptoms
 Disease transmission
 Possible reservoir hosts

LOOKING BACK
 Hemoflagellates consist of single-celled
parasites that move by means of flagella and
reside in blood and tissue.
 There are four morphologic forms of
importance:
1. Amastigotes
2. Promastigotes
3. Epimastigotes
4. Trypomastigotes
 These morphologic forms are differentiated
based on:
o Shape
o Presence/absence of a flagellum
o Presence and length of undulating
membrane
 Good microscopy and staining techniques are
of utmost importance when identifying these
parasites using traditional methods.

Song recommendation hihi ^^

https://open.spotify.com/track/249gnXrbfmV8NG6j
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