Protozoa

This presentation explores the world of protozoa - single-celled eukaryotic organisms that play
significant roles in human health and disease. We'll examine their general properties, life cycles,
and the medical importance of key species.
Learning Objectives
1 Understand Protozoan 2 Identify Key Species
Characteristics
Recognize the major protozoan
Describe the general characteristics of parasites that affect human health.
medically important parasitic protozoa.

3 Comprehend Life Cycles 4 Apply Clinical Knowledge

Understand the life cycles and Identify clinical manifestations,
transmission methods of pathogenic diagnostic approaches, and treatment
protozoa. options.
Key Terminology
Infective Stage Pathogenic Stage
The form of the parasite that is capable of The stage responsible for producing organ
establishing infection in a new host. This is damage, leading to clinical manifestations.
the stage that is present in the source of
infection.

Encystation Excystation
Process by which trophozoites differentiate Process by which cysts differentiate into
into cyst forms for survival outside the host. trophozoite forms after entering a new host.
General Properties of Protozoa
Single-celled Eukaryotes Microscopic Size Reproduction Methods
Spherical to oval or elongated in Require microscopic examination Reproduce primarily via binary
shape with complex cellular for identification and diagnosis. fission (flagellates, cilia, amoeba),
structures. Classification mainly although sporozoans can divide
based on organ of locomotion. sexually and asexually.

Parasitic Lifestyle
Many species are parasitic, though some can exist in free-living states (e.g., Acanthamoeba and Naegleria)

Not all protozoa are parasitic.

Trophozoite is the motile, feeding, dividing stage of the parasite. This is the pathogenic stage.

Cyst is the dormant, non-motile form of the parasite. This is the infective stage, except for T. vaginalis where cyst
forms are not found.
Classification of Protozoa

Sarcodina Mastigophora Ciliophora

Move using pseudopods Move using flagella. Move using cilia. Example:
(false feet). Examples: Examples: Giardia, Balantidium coli.
Entamoeba, Trichomonas.
Acanthamoeba.

Sporozoa
Non-motile, reproduce through both sexual and asexual means.
Intestinal and Urogenital Protozoa
Entamoeba Giardia lamblia Trichomonas
histolytica vaginalis
Causes giardiasis, a
Causes amoebiasis, common intestinal Causes trichomoniasis, a
affecting the intestines infection worldwide. sexually transmitted
and potentially the liver. infection.

Balantidium coli
Largest protozoan parasite of humans, causing balantidiasis.
Entamoeba histolytica: Overview
Subphylum: Sarcodina

Intestinal and tissue Two-stage life cycle Colonizes the colon

ameba
Exists as cysts (infective) Can invade intestinal wall
The only known pathogenic and trophozoites and spread to other organs.
intestinal ameba in humans. (pathogenic). Trophozoite is
found in intestinal and
extra-intestinal lesions, and
diarrheal stools. Cyst in
non-diarrheal formed stool.
Entamoeba histolytica: Microscopic
Entamoeba histolytica: Microscopic
Entamoeba histolytica: Morphology
Trophozoite Cyst

Size: 8-65 μm Size: 8-22 μm

Shape: Irregular Shape: Spherical to round

Motility: Yes, with finger-like pseudopodia Motility: No

Nuclei: One with small central karyosome Nuclei: One to four with small central karyosome

Peripheral chromatin: Fine and evenly distributed Peripheral chromatin: Fine and evenly distributed

Cytoplasm: Finely granular Cytoplasm: Finely granular

Distinctive feature: Contains ingested red blood cells Distinctive feature: Chromatoid bars and glycogen
mass in young cysts
Entamoeba histolytica: Epidemiology &
Pathogenesis
Facts

E. histolytica infection is found worldwide but is mote common in tropical countries in areas with poor sanitation.

Primarily transmitted via fecal-oral route through ingestion of contaminated food and water.

Water serves as the major source of infection of the parasite.

Sexual transmission through unprotected sex with woman who has vaginal amoebiasis or through anal intercourse.

"Flask-shaped" ulcer associated with the local necrosis brought about by the enzyme secreted by E. histolytica
trophozite.
Entamoeba histolytica: Life Cycle
Amoebiasis: Clinical Manifestations
Asymptomatic Carrier State Acute Intestinal Amoebiasis Extraintestinal Amoebiasis

Occurs under the following Bloody, mucus-containing diarrhea Occurs when parasite enters the
conditions: a) low-virulence strain, (dysentery) with abdominal circulatory system. Amoebic liver
b) low parasite load, or c) intact discomfort, flatulence (release of abscess is the most common
immune system. Patient has no gas) and tenesmus (feeling of extraintestinal form of amoebiasis.
symptom but parasite is passed incomplete defecation). In some Abscess found on the right lobe of
out in feces. patients, a lesion called amoeboma the liver may penetrate diaphragm
may form in cecum or ad cause lung disease (amoebic
rectosigmoid area of colon which pneumonitis). Other organs that
may be mistaken for a tumor. may be infected include
pericardium, spleen, skin, and brain
(meningoencephalitis).
Amoebiasis: Diagnosis and Treatment
Diagnosis Treatment

• Finding trophozoites in diarrheic stools • Metronidazole is the DOC for symptomatic

• Finding cysts in formed stools intestinal amoebiasis or hepatic abscess

• Identifying ingested red blood cells in • Tinidazole for both intestinal and
trophozoites extraintestinal infection

• Examining specimens within one hour of • Diloxanide furoate, metronidazole, or

collection paromomycin for asymptomatic carriers

• Serologic testing for invasive amoebiasis • Possible surgical drainage for amoebic liver
abscess
Amoebiasis: Prevention and Control
Personal Hygiene Water Safety Food Safety
Proper hand washing, Proper waste disposal to Avoid using human feces
especially for food avoid fecal contamination as fertilizer; wash and
handlers. of water sources. cook vegetables
thoroughly.

Health Education
Educate communities about transmission and prevention methods.
Giardia lamblia: Overview
Subphylum: Mastigophora

Intestinal Flagellate Two-Stage Life Cycle

Also known as Giardia intestinalis or Exists as trophozoites (pathogenic) and
Giardia duodenale or previously known as cysts (infective).
Cercomonas intestinalis.
Giardia lamblia: Morphology
Trophozoite Cyst

Pear-shaped or teardrop-shaped Oval and thick-walled

Four pairs of flagella Contains four nuclei

Distinctive "falling leaf" motility Fully mature cyst has four nuclei with four
median bodies
Resembling an old man with whiskers ("old man
facies") Each cyst gives rise to two trophozoites during
excystation
Possesses a suction disk for attachment

Two nuclei giving "face-like" appearance

Giardia lamblia: Microscopic
Giardia lamblia: Microscopic
Giardia lamblia: Life Cycle

The cyst enters the stomach and is stimulated by gastric

acid to undergo excystation in the duodenum. The
trophozoites then attach themselves to duodenal
mucosa through sucking discs. Damage to the intestines
is not due to invasion of the parasite but because of
inflammation of the duodenal mucosa, leading to
diarrhea with malabsorption of fat and proteins.
Giardia lamblia: Epidemiology &
Pathogenesis
G. lamblia has worldwide distribution through contaminated water sources.

About 50% or half of infected individuals show no symptoms but can spread the parasite.

Infection is common among individuals engaging in oral-anal contact.

High incidence in daycare centers and patients in mental facilities.

Primarily transmitted through fecal-oral route from contaminated food and water.
Giardiasis: Clinical Manifestations
Asymptomatic Carrier State Giardiasis (Traveler's Diarrhea)
No symptoms, but infected individuals pass Non-bloody, foul-smelling diarrhea with
parasites in feces, contaminating water nausea, loss of appetite, flatulence, and
sources. abdominal cramps. May lead to presence
of fat in stool (steatorrhea). May also have
malabsorption of fat-soluble vitamins, folic
acid, and proteins.
Giardiasis: Diagnosis and Treatment

Diagnosis Treatment

• Demonstration of cysts or trophozoites in • Metronidazole, tinidazole, and nitazoxanide

stool samples are the primary choice of treatment per
• String test (Entero-Test) for duodenal CDC recommendation
sampling may be done if microscopic stool
exam is negative
Giardiasis: Prevention and Control
Water Treatment Personal Hygiene Waste Management
Boil, filter, or use iodine to Proper hand washing Proper disposal of human
treat drinking water, before eating and after waste to prevent
especially in endemic using the toilet. contamination of water
areas. supplies.

Public Education
Educate communities about transmission and prevention methods.
Trichomonas vaginalis: Overview
Subphylum: Mastogophora

Urogenital Flagellate Single Life Stage Sexual Transmission

Only exists as trophozoites
Pear-shaped organism (infective and Primarily transmitted
with four anterior flagella pathogenic); no cyst stage through sexual
and an undulating has been identified. intercourse.
membrane.
Trichomonas vaginalis: Epidemiology

Not an intestinal pathogen.

Infection is highest among sexually-active women in their 30s and lowest in post-menopausal
women. Infants may be infected through infected birth canal during delivery.
Trichomonas vaginalis: Microscopic
Trichomonas vaginalis: Life Cycle
Trichomoniasis: Clinical Manifestations
Infection in Men Infection in Women Infection in Infants
Usually asymptomatic. Men Ranges from asymptomatic May occur during vaginal
serve as reservoir for to severe vaginitis with foul- delivery, potentially causing
infection in women. When smelling, greenish-yellow conjunctivitis or respiratory
symptomatic, may present discharge, itching (pruritus), infection.
with urethritis, prostatitis, and burning sensation in the
and urinary discomfort. vagina. The cervix appears
Persistent or recurring very red, with small
urethritis is the most punctuate hemorrhages,
common symptomatic form giving rise to a strawberry
of infection. cervix.
Trichomoniasis: Diagnosis and
Treatment
Diagnosis Treatment

• Wet mount microscopy of vaginal or • Metronidazole is the DOC.

prostatic secretions • Treatment of all sexual partners
• Identification of characteristic trophozoite simultaneously to prevent "ping-pong
motility infections".
Trichomoniasis: Prevention and Control

Safe Sex Practices Health Education Partner Treatment

Consistent and correct use of Educate about sexually Simultaneous treatment of
condoms can limit transmitted infections and all sexual partners to prevent
transmission. prevention methods. "ping-pong" infections.

Vaginal Health
Maintenance of normal vaginal pH may help prevent infection.
Balantidium coli: Overview
Phylum: Ciliophora

Largest Protozoan Complex Morphology Two-Stage Life Cycle

Parasite
The only ciliated Has a cytostome Exists as trophozoites
protozoan known to infect (primitive mouth), a (pathogenic) and cysts
humans. nucleus, food vacuoles, (infective).
and a pair of contractile
vacuoles.
Balantidium coli: Morphology
Trophozoite Cyst

Large size (40-70+ μm) Spherical shape

Covered with cilia for rotary motility Thick-walled

Contains two nuclei: Contains two nuclei (micronucleus may not be

visible)
• Large kidney bean-shaped macronucleus
• Small dot-like micronucleus Infective stage of the parasite

Has a cytostome (cell mouth)

Balantidium coli: Microscopic
Balantidiasis: Clinical Manifestations
Asymptomatic Acute Infection Chronic Infection
Infection
Dysenteric diarrhea with Tender colon, anemia,
Most infected individuals blood, pus, and mucus. weight loss, and alternating
show no symptoms. diarrhea and constipation.

Extraintestinal Infection
Rare involvement of liver, lungs, or urogenital tract.
Balantidiasis: Clinical Manifestations

Asymptomatic Acute Infection Chronic Infection

Infection
Dysenteric diarrhea with Tender colon, anemia,
Most infected individuals blood, pus, and mucus. wasting, and alternating
show no symptoms. diarrhea and constipation.

Extraintestinal Infection
Rare involvement of liver, lungs, mesenteric nodes, or urogenital tract.
Balantidiasis: Diagnosis and
Treatment
Diagnosis Treatment

• Finding trophozoites or cysts in stool • Oxytetracycline and iodoquinol are the

specimens current recommended treatment for
• Easily detected due to large size balantidiasis
• Metronidazole - may be used as an
alternative
Balantidiasis: Prevention and Control
Water Safety Animal Management Personal Hygiene
Proper treatment of Proper disposal of pig feces Proper hand washing,
drinking water and and separation of pig especially after contact with
protection of water sources rearing from human animals or before handling
from contamination. dwellings. food.

Sanitation
Improved sanitation facilities and waste management in communities.
Blood and Tissue Protozoa
Acanthamoeba (Free-living
Amoebae): Overview
Subphylum: Sarcodina

Environmental Opportunistic Two-Stage Life Cycle

Organism Pathogen
Found in soil, freshwater Usually causes infection in Exists as trophozoites
lakes, and other water immunocompromised (pathogenic) and cysts
environments. It is able to individuals. (infective).
survive in cold water.
Acanthamoeba: Epidemiology and Pathogenesis

Exposure Entry Dissemination

Contact with contaminated water Through respiratory tract, corneal Migration through bloodstream to
or inhalation of cysts from dust. abrasions, or skin ulcers. target organs.

Has been recovered from contact

lenses, lens cases, and contact lens
solutions.

Invasion
Penetration of central nervous system or corneal tissue.
Acanthamoeba: The Free-
Living Threat
Keratitis Granulomatous
Infection of the cornea
Encephalitis
causing severe eye pain and Rare but serious brain
vision problems. May lead to infection, often fatal even
corneal perforation. with treatment.

Diagnosis
Finding trophozoites and cysts in cerebrospinal fluid, brain tissue,
or corneal scrapings. Calcofluor white, a stain usually used to
demonstrate fungi, may be used to demonstrate the parasite in
corneal scrapings.
Acanthamoeba Treatment Options
Systemic Medications For eye and skin Prevention
involvement:
• Boil water adequately
• Pentamidine • Miconazole • Disinfect contact lenses
• Ketoconazole • Chlorhexidine
• Flucytosine • Itraconazole • Avoid homemade saline
• Ketoconazole solutions

• Rifampicin
• Propamidine
Acanthamoeba: Prevention and Control
Contact Lens Hygiene Water Precautions Eye Care
Proper cleaning and storage Avoid swimming with contact Prompt treatment of eye
of contact lenses using lenses or in potentially injuries and regular eye
commercial solutions. contaminated water. examinations.

Water Treatment
Proper filtration and disinfection of water supplies.
Naegleria: Overview
Subphylum: Sarcodina

Habitat Morphology Transmission

Found worldwide in soil The known pathogen Acquired through
and contaminated water, worldwide is Naegleria swimming in
including thermal springs fowleri which is the only contaminated water or
(unlike Acanthamoeba). amoeba with three inhaling dust containing
identified morphologic the parasite.
Just like Acanthamoeba,
forms: trophozoite,
Naegleria is also a free-
flagellate, and cyst.
living organism.
Naegleria fowleri: Epidemiology &
Pathogenesis
Transmission Infection
Usually acquired transnasally when Unlike Acanthamoeba, infection is
swimming in contaminated water produced in otherwise healthy individuals,
usually children.
Naegleria fowleri: Morphology
Trophozoite Flagellate Cyst
Exhibits the typical Pear-shaped and Non-motile form
amoeboid motility equipped with two flagella
described as "slug-like". responsible for the
parasite's jerky or
The amoeboid trophozoite
spinning movement
form is the only form
known to exist in humans.
Naegleria fowleri: Life Cycle
Naegleria Disease Manifestations
Primary Amoebic Asymptomatic Colonization
Meningoencephalitis (PAM) Most common presentation in patients with
Rapidly fatal brain infection colonization of nasal passages

Usually complains of sore throat, nausea,

vomiting, fever, headache, meningeal irritation
(e.g., Kernig's sign) as well as alteration to
senses of smell and taste.

Primary amoebic meningoencephalitis (PAM) results from brain colonization by amoeboid trophozoites,
causing rapid tissue destruction. Without treatment, death typically occurs within one week after
symptoms begin.
Naegleria Diagnosis and Treatment
Diagnosis Treatment

Based on finding amoeboid trophozoites in cerebrospinal fluid. Often ineffective due to rapid disease progression. Early
detection is crucial.

• Amphotericin B in combination with Miconazole and

Rifampicin
Preventing Naegleria Infections

Chlorinate swimming pools Disinfect hot tubs

Maintain proper disinfection levels Regular cleaning and maintenance

There is no guaranteed method to prevent Naegleria infection, but reducing exposure to

contaminated water sources is the best approach. Adequate chlorination of swimming facilities is
essential.
Leishmania: Overview
Subphylum: Mastigophora // Hemoflagellate parasite

Vector Transmission Intracellular Parasitism Reservoir Hosts

Female sandflies of Phlebotomus and Obligate intracellular parasites that Rodents, anteaters, dogs, and cats
Lutzomyia genera transmit the invade macrophages serve as natural reservoirs
parasite

Morphological Forms
Has 3 morphologic forms: promastigote (infective; may be seen only if blood is collected and examined immediately after
transmission), amastigote (diagnostic; found in tissue and muscles, and CNS), and epimastigote (found primarily in the
vector) stages.

Typical amastigote is round to oval in shape and has a nucleus, a basal structure called blepharoblast, and a small parabasal
body located adjacent to it. Both blepharoblast and parabasal body are collectively known as kinetoplast.
Leishmania: Epidemiology &
Pathogenesis
Three major strains:

Leishmania Leishmania tropica Leishmania

donovani braziliensis
Causes cutaneous
Causes visceral leishmaniasis, affecting Causes mucocutaneous
leishmaniasis (kala-azar), the skin leishmaniasis, affecting
affecting internal organs skin, cartilage, and
mucous membranes
Leishmania: Life Cycle
Leishmania donovani complex
Causative agent of visceral leishmaniasis (also known as kala-azar or dumdum fever)

The complex consists of 1) L. donovani chagasi mainly seen in Central America (Mexico, West Indies, South America) and
transmitted by Lutzomyia sandly; 2) L. donovani donovani mainly seen in Africa and Asia (Thailand, India, China, Burma, East
Pakistan) and transmitted by Phlebotomus sandfly; and 3) L. donovani infantum also trasnmitted by Phlebotomus sandly and seen
in Europe, Africa.

Transmission Transformation Organ Invasion

Promastigotes injected through Parasites lose flagella, are engulfed Reticuloendothelial system (liver,
sandfly bite by macrophages, become spleen, bone marrow) becomes
amastigotes infected

Disease Progression
Fever, weakness, weight loss, and massive splenomegaly develop
Visceral Leishmaniasis: Clinical
Features
Incubation Period
2 weeks to 18 months before symptoms appear

Initial Symptoms
Intermittent fever, weakness, and progressive weight loss

Characteristic Signs
Massive splenomegaly, hepatomegaly, and hyperpigmentation in light-
skinned patients (kala-azar means "black sickness" or "black fever")

Hematological Effects
Anemia, thrombocytopenia, and leukopenia due to bone marrow
involvement
Diagnosing Visceral Leishmaniasis
Screening Test
Montenegro skin test (similar to tuberculin skin test) for population screening

Definitive Diagnosis
Demonstration of amastigotes in Giemsa-stained specimens from blood, bone marrow,
lymph nodes, or biopsies

Additional Methods
Culture to show promastigote forms and serologic tests (IFA, ELISA, DAT)
Treating Visceral Leishmaniasis
First-Line Alternative Option Combination Therapy
Treatment
Sodium stibogluconate,
Liposomal amphotericin B though resistance may Gamma interferon with
(Ambisome) is the current develop pentavalent antimony
drug of choice shows favorable
responses in some
patients
Preventing Leishmaniasis
Vector Control Personal Protection Environmental
Measures
Controlling sandfly
populations is crucial for Using insect repellents and Installing screens on
prevention wearing protective windows and doors
clothing

Treatment
Prompt treatment of infected individuals helps prevent disease spread
Leishmania braziliensis complex
Causative agent of mucocutaneous leishmaniasis (also called espundia)

Pathogen Transmission

L. braziliensis complex includes L. panamensis (Panama Transmitted by Lutzomyia and Psychodopigus

and Colombia), L. peruviana (Peruvian Andes), L. sandflies through skin bites
guyanensis (The Guianas, parts of Brazil and
Promastigotes invade reticuloendothelial cells and
Venezuela)
transform into amastigotes
Primarily affects skin, cartilage, and mucous
Reproduction of amastigotes leads to tissue
membranes
destruction
Common in Brazil and Central America, especially
Amastigotes are taken up by the vector during blood
among construction and forestry workers
meal and are transformed into promastigotes
Mucocutaneous Leishmaniasis: Clinical
Features
Tissue Destruction
Initial Lesion Lesions destroy nasal cartilage but spare
Papule forms at the insect bite site adjacent bone

1 2 3 4

Metastatic Lesions Complications

Secondary lesions develop, especially at Death can occur from secondary
mucocutaneous junctions infections
Mucocutaneous Leishmaniasis: Clinical Features
Diagnosing Mucocutaneous
Leishmaniasis
Specimen Collection Microscopic Culture
Examination
Ulcer biopsy specimens are Infected material cultured
used for diagnosis Giemsa-stained specimens to show promastigotes
reveal diagnostic
amastigotes

Serologic Testing
Additional confirmation through antibody detection
Treating Mucocutaneous
Leishmaniasis
Sodium stibogluconate is most widely used drug for treatment, although resistance may
develop.

Alternatives include liposomal Amphotericin B and oral antifungals (fluconazole,

ketoconazole, itraconazole)
Preventing Leishmaniasis
Vector Control Personal Protection Environmental
Measures
Controlling sandfly
populations is crucial for Using insect repellents and Installing screens on
prevention wearing protective windows and doors
clothing

Treatment
Prompt treatment of infected individuals helps prevent disease spread
Leishmania tropica complex
Causative agent of cutaneous leishmaniasis

The L. tropica complex includes L. tropica, L. aethiopica, and L. major, causing what is referred to
as Old World cutaneous leishmaniasis. Transmitted by Phlebotomus sandflies, these parasites
primarily attack lymphoid tissue of the skin.

The disease is also known as oriental sore, and Baghdad or Delhi boil.
Cutaneous Leishmaniasis:
Clinical Features
Initial Lesion
Small, pruritic red papule develops at the bite site

Ulcer Formation
Develops into one or several pus-containing ulcers

Resolution
May heal spontaneously in immunocompetent individuals

Complications
In patients with anergy, thick skin plaques with multiple
nodules may develop
Diagnosing and Treating Cutaneous
Leishmaniasis
Diagnosis Treatment

Microscopic examination of Giemsa-stained slides Sodium stibogluconate is the drug of choice

from fluid aspirated from beneath the ulcer bed
Steroids with application of heat to infected
Culture of specimens to show promastigote forms lesions

Serologic tests for additional confirmation Alternative drugs: meglumine antimonite,

pentamidine, and oral ketoconazole

A vaccine against L. tropica is currently

undergoing clinical trials
Trypanosoma spp.: Overview
The trypanosomes are also hemoflagellates like Leishmania. The major difference between the two is
that the diagnostic stage for Leishmania is amastigote, while is it trypomastigote for Trypanosoma.

Morphology Key Species Difference from

Leishmania
Curved trypomastigotes in Trypanosoma cruzi: Causes
C, S, or U shapes American trypanosomiasis Different diagnostic stage
(Chagas disease) (trypomastigote vs.
Kinetoplast located
amastigote)
posterior to nucleus Trypanosoma brucei:
Causes African Different vector (reduviid
Visible in peripheral blood
trypanosomiasis (sleeping bug or tsetse fly vs. sandfly)
sickness)
Trypanosoma cruzi: Epidemiology

Geographic Distribution
Primarily found in South and Central America

Vector
Transmitted by reduviid or triatomid bug (kissing bug or cone-nose bug or
Triatoma)

Transmission Routes
Feces of infected bug introduced into bite site, blood transfusion, sexual
intercourse, congenital transmission, and through mucus membranes if bite is
near mouth or eye

Reservoirs
Humans, domestic cats and dogs, wild animals (armadillo, raccoon, rat)
Trypanosoma cruzi: Life Cycle
Chagas Disease: Clinical Phases
Acute Phase Systemic Symptoms Chronic Phase
Nodule (chagoma) at bite Hepatosplenomegaly,
site, unilateral eyelid Fever, chills, malaise, lymphadenopathy,
swelling (Romaña's sign) myalgia, fatigue myocarditis with cardiac
arrhythmia

Complications
Megacolon, megaesophagus, meningoencephalitis, cardiac failure
Chagas Disease: Clinical Phases
Diagnosing Chagas Disease

Blood Examination Tissue Sampling Xenodiagnosis

Finding trypomastigotes in Bone marrow aspiration, Allowing uninfected
thick or thin films of muscle biopsy, and culture laboratory-raised reduviid
patient's blood during on special media bugs to feed on patient,
acute phase then examining bug
intestinal contents
Treating and Preventing Chagas Disease

Treatment Options Prevention Strategies

Drugs of choice are benznidazole and nifurtimox Protection from reduviid bug bites
but are less effective in chronic disease
Improvement of housing conditions

Insecticide use
Alternative agents include allopurinol and
ketoconazole Education about disease transmission

Prompt treatment of infected individuals

Trypanosoma brucei: African Sleeping
Sickness
Two subspecies cause human disease: T. brucei gambiense and T. brucei rhodesiense. Both share
similar morphology and life cycles involving the tsetse fly (Glossina) as vector. The disease is
endemic in sub-Saharan Africa, the natural habitat of the tsetse fly.
Trypanosoma brucei: Epidemiology & Pathogenesis
T. brucei gambiense T. brucei rhodesiense Vector
Humans are the primary reservoir Domestic and wild animals are Tsetse fly (Glossina)
reservoirs
Causes West African or Gambian Transmits infective trypomastigotes
Sleeping Sickness Causes East African or Rhodesian
Sleeping Sickness
Found along water courses in West
Africa Found in arid regions of East Africa

Chronic disease progression More rapidly fatal infection

Pathogenesis
Spreads from skin to blood to lymph nodes and brain

Causes demyelinating encephalitis

African Sleeping Sickness: Clinical Features
Initial Lesion Early Systemic Phase Additional Symptoms
Indurated ulcer (chancre) at the Intermittent weekly fever and Red rash with pruritus, localized
site of insect bite lymphadenopathy develop edema, delayed pain sensation
(Kerandel's sign)
Winterbottom's sign: enlarged
posterior cervical lymph nodes

Neurological Phase
Headache, insomnia, mood changes, muscle tremors, slurred speech, apathy

Progresses to somnolence (sleeping sickness) and coma

T. brucei rhodesiense vs. T. brucei
gambiense
T. brucei rhodesiense T. brucei gambiense

• More virulent infection • Less virulent infection

• Shorter incubation period • Longer incubation period
• No Winterbottom's sign • Winterbottom's sign present
• No lymphadenopathy • Lymphadenopathy common
• Early CNS involvement • Late CNS involvement
• Rapid disease progression • Chronic disease progression
• Death within 9-12 months if untreated • Slower progression to death if untreated
Diagnosing African Sleeping Sickness
Blood Examination Tissue Sampling
Microscopic examination of Giemsa-stained Aspiration of chancre or enlarged lymph
slides of blood to detect trypomastigotes nodes to isolate parasites

CSF Analysis Serologic Testing

Examination of cerebrospinal fluid in patients Additional confirmation through antibody
with CNS involvement detection

Presence of IgM in CSF is considered

diagnostic
Trypanosoma brucei
Trypanosoma brucei Life Cycle
Treatment of African Sleeping
Sickness

Melarsoprol, pentamidine, and eflornithine. The choice of drug will depend on whether the
patient is pregnant or not, their age, and stage of the disease.
Prevention and Control
Prevention against bite of the fly.

Use of netting and protective clothing.

Use of fly traps and insecticides.

Clearing the forest around villages.