OTHER MEDICALLY

IMPORTANT PROTOZOANS
INTESTINAL COCCIDIANS
• Apicomplexans found in the small intestine
• intracellular
• Final host commonly man
• Reservoir hosts: animals
• Partially acid fast: possess mycolic acid
▪ Use modified acid-fast technique (change in the staining procedure)
• Infective stage: sporulated oocyst (contains sporozoites inside)
• Mode of transmission: ingestion of sporulated oocyst (contaminated food
and water)
• Diseases primarily diarrhea or gastroenteritis
CRYPTOSPORIDIUM
• Asexual and Sexual Life Cycle
• Sexual and asexual cycle happens only in one host (no
intermediate hosts)
CRYPTOSPORIDIUM
 CRYPTOSPORIDIUM
Sporozoites become trophozoites then trophozoites become meronts
• Type 1 Meront
o Asexual reproduction (merogony)
o Contains merozoites o Meront ruptures to release the merozoites
o Merozoites infect other intestinal cells
o After many cycles, some merozoites become Type 2 meront
• Type 2 Meront
o Sexual reproduction (sporogony/gametogony)
o Release merozoites
o Merozoites become gamonts (sexual cells)
▪ Macrogamont
▪ Macrogamont
o Microgametes and macrogametes released
▪ Fuse to form zygote
o Zygote eventually becomes an oocyst (already sporulated, already has 4 sporozoites
inside)
 CRYPTOSPORIDIUM
Sporozoites become trophozoites then trophozoites become meronts
• Two types of oocyst
o Thin-walled oocyst
▪ Remains in small intestine
▪ Associated with autoinfection (deadly among immunocompromised)
▪ Eventually ruptures and releases sporozoites inside the small intestine
o Thick-walled oocyst
▪ This type is the one seen in the stool
 Cryptosporidium spp.
• Cryptosporidium hominis
• Most common species infecting man
• Formerly known as Cryptosporidium parvum antroponotic genotype
(but they found out this does not usually infect humans, usually
infects animals)
• Infective stage: ingestion of sporulated oocyst
• Habitat: small intestine (jejunum)
• Target cells: enterocytes (intestinal cells, columnar cells with microvilli,
brush border)
• Low infective dose (important cause of outbreak of diarrhea, ingest
around 10 cysts only)
• Large multiplication capability: because of the autoinfection caused
by the two types of cysts
 Cryptosporidium spp.
Mode of Transmission
• Ingestion of sporulated oocyst
• Drink contaminated water
• Swim in recreational pools that are fecally contaminated (accidentally
drink the water)
Disease Manifestation
Healthy Immunocompetent Patients
• Watery diarrhea (5-10 frothy bowel movements)
• Usually self-limiting (disappears in 2-3 weeks)
• Important cause of outbreaks of diarrhea (can be considered as a bioterror agent)
Immunocompromised patients (AIDS patients)
• Chronic diarrhea
• Extraintestinal infections
• Severe and life threatening
• Immune system is weak, so they cannot control the parasites
• Severe dehydration, electrolyte loss, excessive fluid loss
• Chronic respiratory infections may also occur (pneumonia, dyspnea, bronchiolitis, chronic cough)
• Cholecystitis: affecting bile ducts of the gall bladder
 Cryptosporidium spp.
Pathology
• Changes in the morphology of the villi
o Becomes blunted and infiltrated by inflammatory cells
o Important for absorption of nutrients
o Atrophy of villi (becomes smaller)
Diagnosis
• Preferred sample: stool
o More watery: better (high detection rate)
• Concentration techniques
o Sheather’s Sugar Floatation
▪ Same principle as brine floatation
▪ But you use sucrose solution
▪ Better than FECT because Cryptosporidium is small (FECT involves
sedimentation)
o FECT
• Fecal smear using Modified Kinyoun Method (fastest and cheapest)
o Because the organism is partially acid fast o Modify a step in the staining
procedure: the decolorizer (use 1% H2SO4 instead of 2-3% HCl and 95%
alcohol found in acid alcohol)
 Cryptosporidium spp.
Epidemiology
• Found worldwide
• Zoonotic infection
• Implicated in outbreaks (children at risk)
• Infective upon release
• Highly resistant to disinfectants
o not killed by chlorination Treatment
• no standardized treatment (because if you’re healthy, it will go away after 2 weeks)
• can give Nitazoxanide
• immunocompromised patients: improvement of immune status
 CYCLOSPORA CAYETANENSIS
• Species name refers to Cayetano Heredia University in Lima, Peru (where epidemiological
and taxonomic work was done)
• Formerly classified as CLB (cyanobacterium like body)
• Appearance almost the same as Cryptosporidium
o Bigger size: 8-10 um
• Life cycle almost the same as Cryptosporidium o Infective stage: sporulated oocyst
o Slight change in morphology of sporulated oocyst (presence of sporocyst)
o Sporocyst: contains 2 sporozoites inside
o 4 sporozoites in 1 oocyst
o Oocyst released is unsporulated (not infective)
o Morula formation: undeveloped/undifferentiated structures inside the
unsporulated oocyst
o Sporulation happens in the environment (5-10 days)
 CYCLOSPORA CAYETANENSIS
Mode of transmission
• Ingestion of sporulated oocyst
• Drinking/eating contaminated food and water
• Associated with eating salads, strawberries, raspberries, basils, vegetables, fruits
(raw and not thoroughly washed)
Disease manifestation
• Intermittent watery diarrhea
• Development of d-xylose malabsorption
• Usually self-limiting
• Some cases: can become a chronic type of diarrhea
o Now being considered as an emerging cause of diarrhea
• Only infects humans (no animal reservoirs, more easily controlled)
 CYCLOSPORA CAYETANENSIS
Diagnosis
• Same with Cryptosporidium (Also stain using modified kinyoun method)
o 8-10 um size (larger)
• Fluorescence microscopy
o Capable of autofluorescence (blue or green, depends on wavelength used)
• Safranin staining
• Microwave heating (preparation of the smears)
Epidemiology
• Oocysts not infective once released (unsporulated)
• Implicated in outbreaks of diarrhea (ingestion of fecally contaminated raspberries,
basil leaves, and other leafy vegetables)
Treatment
• Self-limiting (no need for treatment)
• Co-trimoxazole (sulfamethoxazole-trimethoprim)
 CYSTOISOSPORA BELLI
• Formerly known as Isospora belli
• Least common infecting man
• Largest oocyst
• Infective stage: sporulated oocysts
o Oval-shaped, 2 sporocysts with 4 sporozoites each (total of 8 sporozoites per
sporulated oocyst)
• Life cycle almost the same with Cryptosporidium
o Release unsporulated oocyst
o Sporoblasts: undifferentiated structures inside
o 48 hours for sporulation to take place in the environment

Mode of transmission
• Oral-fecal
 CYSTOISOSPORA BELLI
Disease Manifestation and Pathogenesis
• Intermittent diarrhea
• Infects intestinal cells of humans (duodenum)
• Usually asymptomatic
• Diarrhea with fever, malaise, anorexia, abdominal pain, and flatulence
• Seen in immunocompromised patients
Diagnosis
• Similar to cryptosporidium
• Entero-test
• Duodenal aspirates
Epidemiology
• More common among children, AIDS patients, MSMs
Treatment
Trimethoprim-Sulfamethoxazole
 OTHER MEDICALLY
IMPORTANT PROTOZOANS
TISSUE COCCIDIANS
 TOXOPLASMA GONDII
Life Cycle in Cats
Cats eat intermediate hosts (rats, small animals with tissue cysts)
• Tissue cysts contain bradyzoites
• Sexual and asexual cycle in the small intestine
Oocyst from zygote
• Oocyst: shed in feces (Unsporulated)
Sporulation in environment
• 3-5 days
• Sporulated oocyst: 2 sporocysts with 4 sporozoites each (total of 8 per
oocyst)
Life Cycle in Humans and other animals
Accidentally ingest sporulated oocyst
• Oocyst will become tissue cysts
• Life cycle will not completely happen in humans
• Oocysts never found in humans
 TOXOPLASMA GONDII
• Parasite of cats
• Complete life cycle happens in cats
• Humans: intermediate host only (accidental)
o We can also be dead-end host (life cycle stops once in our bodies)
• Infective stage: sporulated oocyst or tissue cysts

Mode of transmission
• Ingestion of sporulated oocyst or tissue cysts
o Oocyst: ingestion of cat feces
o Tissue cysts: ingestion of contaminated meat (can be rat meat,
undercooked, raw meat), organ transplants
• Eating contaminated food/drink with feces of cat
• Vertical transmission (especially if mom is infected during pregnancy
• Eating cats (possible)
 TOXOPLASMA GONDII
Diagnostic stage
Tissue cysts
• Bradyzoites
o Multiply slowly
o Develop mostly in neural and muscular tissues
o May also develop in visceral organs
o Late stages of infection
o Enclosed in a tissue cyst
• Tachyzoites
o Rapidly multiply
o Infect cells of the intermediate hosts and non-intestinal epithelial
cells of cats
o Found in early stages of infection
o Crescent-shaped
 TOXOPLASMA GONDII
Disease manifestation and Pathogenesis
• Infections are usually asymptomatic (in immunocompetent individuals)
o May exhibit flu-like symptoms
o People: almost all of us are actually exposed or positive for the parasite
▪ Most people would have antibodies against Toxoplasma
• Immunocompromised patients (AIDS patients)
o Lead to encephalitis
o Formation of multifocal brain lesions
o May lead to blindness (can affect the eyes)
o Retinochoroiditis
o Lymphadenopathy
o Splenomegaly
• Ocular infections (chorioretinitis)
• Transplant patients: multiorgan failure
TOXOPLASMA GONDII
• Congenital infections
o Stillbirth, abortion
o Triad of toxoplasmosis (if baby lives)
▪ Hydrocephalus
▪ Chorioretinitis
▪ Intracranial calcification (calcium deposits on brain)
o Microcephaly may also occur
o TORCH Test (screening during pregnancy)
▪ Toxoplasmosis
▪ Other infections (coxsackievirus, chickenpox, chlamydia, HIV, human
Tlymphotropic virus, syphilis)
▪ Rubella
▪ Cytomegalovirus
▪ Herpes simplex
 TOXOPLASMA GONDII
Pathogenesis
• Obligate intracellular parasites (invade nucleated cells including macrophages)
• infected cells rupture leading to dissemination
• mostly asymptomatic among healthy people (because of humoral and cell
mediated immunity)
Diagnosis
• usually biopsy - examine tissues and look for bradyzoites and tachyzoites
• preferred method: Serology
o detect antibodies
o Sabin-Feldman Test (uses methylene blue, most important, classic method)
▪ Sensitive and specific
▪ Specimen: serum sample
▪ Reagent: Live Toxoplasma
▪ Positive result: non-uptake of the dye (colorless)
▪ Negative result: blue color
▪ Titer: highest solution of antibody
• High titer: >1024 indicates acute infection
 TOXOPLASMA GONDII
Epidemiology
• Worldwide distribution (majority are seropositive)
• People at risk of severe toxoplasmosis
o Infants born to exposed mothers (during pregnancy)
o Immunocompromised
Treatment
Pyrimethamine and Sulfadiazine
Prevention
• Thoroughly cook meat
• Proper hygiene
• Disinfect and clean daily cat litter pans
• Pregnant women: avoid cats
• Avoid cats
 SARCOCYSTIS SPP.
Sexual Cycle
In final host, sarcocyst releases zoites
• Zoites infect and produce gametes (microgametes and macrogametes)
• Zygote formed
• Zygote forms oocyst (sporulated in human host)
• Sporulated oocyst: contains 2 sporocysts, each with 4 sporozoites (total of 8)
Sporulated oocyst released in feces
• Ingested by intermediate host
Asexual Cycle
Sporozoites form merozoites
• Merozoites form 2nd and 3rd generation meronts
• Meronts form sarcocyst
 SARCOCYSTIS SPP.
• Infects a wide variety of animals and sometimes humans
• S. hominis: involves cattle
• S. suihominis: involves pigs (-suis: related to pigs)
• Final host: humans
• Intermediate hosts: pigs and cattle
• Infective stage to final host: sarcocyst (tissue cysts found in muscle and tissues of pigs and
cattle)
o Sarcocysts contain zoites
• Man can sometimes be an intermediate host (accidentally ingest sporulated oocyst)
o Dead-end host

Mode of transmission
• Ingestion of infected meat
 SARCOCYSTIS SPP.
Disease
Sarcosporidiosis or Sarcocystosis
• Invasive form (rare)
o Accidentally ingest sporulated oocyst
o Vasculitis o Myositis: inflammation of heart muscle
o If we become intermediate host
• Intestinal form (more common)
o Human: final host
o Nausea, abdominal pain, and diarrhea
o Usually mild, less severe (for 48 hours lang)
o Self-limiting
• Other manifestations
o Acute fever, myalgia, bronchospasm, elevated ESR, elevated Creatine
Kinase enzyme (elevated in muscle pain), symptoms may last
up to 5 years
 SARCOCYSTIS SPP.
Diagnosis
• muscle biopsy (definitive diagnosis)
o sarcocysts: microscopic in cattle (S. hominis)
o sarcocysts: macroscopic in pigs (S. suihominis) ▪ stain: H&E; PAS
(confirmatory)
• stool exam: detection of sporocyst
o concentration methods: floatation
• PCR
Treatment
• Rarely required (because asymptomatic)
• May use albendazole, metronidazole, co-trimoxazole
Prevention
• rare in humans
• thorough cooking of meat
• freezing of meat (low temp kills sarcocysts)
 OTHER MEDICALLY
IMPORTANT PROTOZOANS
HEMOFLAGELLATES (BLOOD AND
TISSUE FLAGELLATES)
• Flagellates found in blood, tissues, and CSF
• Medically important genera: Trypanosoma and Leishmania (only these two infect humans)

FOUR MORPHOLOGICAL FORMS

1. Amastigote
• Also called Donovan Leishman Body
• Oval-shaped
• Has the following structures:
o Nucleus
o Kinetoplast (anterior to nucleus)
o axoneme
o Basal body
o Has no flagella
• Intracellular stage (inside the host cell)
2. Promastigote
• Also called Leptomonas
• More elongated and longer
• Has the following structures:
o Kinetoplast (still located anterior to nucleus)
o Basal body
o Axoneme
o 1 anterior flagella
3. Epimastigote
• Also called Crithidia
• Elongated, wider than promastigote
• Structures:
o Nucleus
o Kinetoplast (still located anterior to nucleus)
o 1 anterior flagellum
o Undulating membrane (1/2 body length)
4. Trypomastigote
• Also called Trypanosome
• Elongated, but with different forms
o C-shape and U-shape
• Structures
o Nucleus
o Flagellum
o Undulating membrane (full body length)
o Kinetoplast (located posterior to nucleus)
o Presence of metachromatic granules (Volutin granules)
 TRYPANOSOMA CRUZI
Human Stages
Triatomine bug takes a blood meal
• Triatomine bug
o Female
o Also known as Assassin bug
o Bites during the night
o Also known as kissing bug because they prefer to bite in mucosal
areas or in the lips
Triatomine bug defecates on the wound
• Infective stage to humans: feces of the bug
o Metacyclic trypomastigote
o Feces enters bite wound (it is not injected)
Metacyclic trypomastigote penetrates different kinds of cells
• Metacyclic trypomastigote becomes an amastigote inside host cells
• Amastigotes reproduce asexually (binary fission)
 TRYPANOSOMA CRUZI
Human Stages
Host cells release amastigotes
• Amastigotes transform into trypomastigotes (diagnostic stage)
• Enter the bloodstream
• Trypomastigotes infect other host cells
• Become amastigotes again inside the host cells
• Clinical manifestations can arise from this cycle
 TRYPANOSOMA CRUZI
Triatomine Bug Stages
Triatomine bug bites human
• Acquires trypomastigote (infective stage to the bug)
In midgut of triatomine bug
• Trypomastigotes become epimastigotes (via longitudinal fission)
• Multiply
In hindgut of triatomine bug
• Epimastigotes become metacyclic trypomastigotes
• Fast transformation
o That’s why promastigote sometimes not presented (but the stages
happen in the insect)
• Triatomine bug bites human, transfers metacyclic trypomastigotes via feces
• Amastigote in tissue specimens: intracellular
• Trypomastigote in blood: extracellular
 TRYPANOSOMA CRUZI
• All four morphological forms are found
• Belongs to Trypanosome Group Stercoraria
• Primarily infects: myocytes, heart cells, and RESs (reticuloendothelial system: monocytes,
macrophages, skin, gonads, intestinal mucosa, placenta etc., so it is intracellular)
• Causes Chagas’ Disease (Dr. Chagas first to study the disease) or American Trypanosomiasis
(because of high prevalence in America)
• Found in the PH (but no cases)
o Found in squalid areas or dirty areas, mud walls
• Infective stage to humans: metacyclic trypomastigote
• Multiply within the mammalian host in a discontinuous manner
• Zoonotic mammalian reservoir hosts: domestic animals, armadillos, raccoons, rodents,
marsupials, and some primates
 TRYPANOSOMA CRUZI
Mode of transmission
• Feces of vector entering bite wound
• Blood transfusion
• Transplacental (vertical, can cross placenta during pregnancy)
• Transmission associated with poor living conditions
Final Host – Humans
Intermediate host/Vector
Reduviid Bug/Kissing bug (Triatoma, Panstrongylus, Rhodnius)
 TRYPANOSOMA CRUZI
Disease Manifestation
Acute phase (Initial)
• Fever and lymphadenopathy (enlargement of lymph nodes near the
chagoma)
• Diffuse or focal inflammation (affecting myocardium)
• Malaise
• Nausea
• Vomiting
• Chagoma: local inflammation, reddish nodule, furuncle-like lesions
associated with central edema, regional lymphadenopathy (at site of
bite wound)
• Romaῆa’s sign: periorbital swelling (edema of eyelid and conjunctiva)
parasite penetrates the conjunctiva, unilateral swelling (only one
eyelid affected), bipalpebral edema, conjunctivitis
• after a few months, symptoms disappear (latent phase)
TRYPANOSOMA CRUZI
Chronic Phase (after 10-20 years)
• no characteristic symptoms
• during this phase, still capable of transmitting it to other people
• amastigotes still reproducing o triggers enlargement of vital organs
o fibrotic reactions that can cause injury to the myocardium, cardiac
conduction network, and enteric nervous system (decrease in
nerve ganglia, leading to megasyndromes)
o congestive heart failure
o thromboembolism
o chest pain, palpitations, dizziness, syncopal episodes, abnormal ECG findings
o mega colon (chronic constipation)
o mega cardium/cardiomegaly (can develop arrhythmias and you can die)
o mega esophagus (achalasia)
*majority of symptomatic chronic patients manifest with the
cardiac form, rest with gastrointestinal form
 TRYPANOSOMA CRUZI
Pathogenesis
• acute inflammatory reaction on bite (Chagoma)
• uses lectin like carbohydrates for binding
• target cells: cells of RES, cardiac cells, skeletal and smooth muscles, neuroglia cells
Diagnosis
• complete patient history
o determine possible exposure, risk factors, recent transfusion, contact
o primary tool
• presence of lesions (in early phases)
o aspirate, prepare a smear, stain, then view
• cardiac symptoms present, especially if living in endemic regions
• demonstration of trypanosomes in:
o blood (thick and thin smears) for sdefinitive diagnosis
o buffy coat (concentration technique: Strout Method)
o CSF
o Lymph
o Trypomastigotes only seen in first two months of acute disease
 TRYPANOSOMA CRUZI
Epidemiology
• Occurs only in the American continent
• Highest prevalence in Brazil
• More common in rural areas (because they prefer squalid conditions, mudwalls
• Chronic disease more common
• Common in unsanitary housing conditions
Treatment
Nifurtimox and Benznidazole
*symptom-specific management
Prevention
• Vector control
• Screening of blood
• Health education
 Trypanosoma rangeli
• Nonpathogenic
• Metacyclic trypomastigote is discharged via the salivary glands
o Injected
o Not in the feces

Vector
• Rhodnius
 TRYPANOSOMA BRUCEI COMPLEX
Human stages
Tsetse fly bites human
• Takes a blood meal
• Injects metacyclic trypomastigotes
Injected metacyclic trypomastigotes transform into bloodstream trypomastigotes
(diagnostic stage)
• Goes to different parts of the body (brain and other vital organs)
• Trypomastigotes multiply (binary fission) in various body fluids (blood,
lymph, spinal fluid)
Trypomastigotes found in blood
• Tsetse fly bites human, acquires the trypomastigotes
 TRYPANOSOMA BRUCEI COMPLEX
Tsetse fly stages
Tsetse fly’s midgut
• Trypomastigotes become procyclic trypomastigotes
• Procyclic trypomastigotes multiply by binary fission
Procyclic trypomastigotes leave midgut
• Transform into epimastigotes
Epimastigotes go to salivary glands
• They multiply here
• Transform into metacyclic trypomastigotes
• Tsetse fly bites human and injects the metacyclic trypomastigotes
 TRYPANOSOMA BRUCEI COMPLEX
• Complex because it is made of two subspecies
o Rhodesiense
o Gambiense
o Belong to trypanosome family Salivaria
o Morphologically the same, different in location (endemic area – area where it is
transmitted) and severity of infection
• T. brucei brucei: primarily affects wild and domestic animals
• infective stage to humans: metacyclic trypomastigote
• only epimastigote and trypomastigote are seen
o epimastigote in insect vector
o trypomastigote in human (diagnostic stage)
▪ polymorphic (slender, short, and stumpy forms)
• trypanosomes evade immune detection through antigenic variation (VSGs)
 TRYPANOSOMA BRUCEI COMPLEX
Mode of transmission
Insect bite
*can also be through mechanical methods (accidental needle pricks), other
blood-sucking insects, vertical transmission
Intermediate Host/Vector
Tsetse Fly (Glossina spp.)
• T. b. rhodesiense – G. pallidipes, G morsitans
• T. b. gambiense – G. palparis
*has animal reservoir hosts
Final Host
Human
 TRYPANOSOMA BRUCEI COMPLEX
Disease Manifestation
Trypanosoma brucei gambiense (95% of cases)
• West and Central Africa (endemic area)
• No animal reservoir hosts involved (anthroponotic, only humans, rural
population)
• low parasitemia
• Causes Gambian or West African Sleeping Sickness
o Has a slower progression (more than 9 months – year)
o Less severe type
• Earliest sign: Trypanosomal Chancre
o Painful ulceration at site of bite
o Patients still appear healthy, but trypomastigotes already seen in the
blood smear
o Parasite goes to other body parts, patient may experience fever
once the lymph nodes are affected
▪ Lymphadenopathy (affects axillary and supraclavicular lymph nodes in
both gambiense and rhodesiense)
▪ Winterbottom’s Sign (affecting the cervical lymph node, its as big as a
plum)
 TRYPANOSOMA BRUCEI COMPLEX
• Chronic disease
o CNS invasion (goes to the brain)
o Sleeping sickness stage initiated
o Prominent lympadenopathy
o Severe headache, increasing mental deterioration and apathy, meningoencephalitis

▪ Manifestation of Kerandel’s Sign (delayed sensation to pain) and Kernig’s Sign (inability to
straighten leg when hip is flexed at 90 degrees)
o Terminal phase: coma leading to death
 TRYPANOSOMA BRUCEI COMPLEX
Pathogenesis
• Generalized lymphoid hyperplasia (increase in number of cells in lymph nodes)
• Anemia (blood loss)
• Thrombocytopenia
• Hypergammaglobulinemia (increased antibody production)
• Immune evasion through VSGs
• Acute infection for Rhodesian
• Chronic infection for Gambian
Diagnosis
• Physical findings and patient history
• Demonstration of trypomastigotes in blood, CSF, lymph node aspirate
o Early stages, examine blood for trypomastigotes
o If sleeping stage has started, examine CSF
o Abnormal CSF: increase in cell count, opening pressure, protein
concentration, and IgM levels (increase in IgM levels are
pathognomonic for the meningoencephalitic stage)
 TRYPANOSOMA BRUCEI COMPLEX
Epidemiology
• Vectors inhabit areas near river banks and streams
• Congenital transmission is possible
• Low prevalence rate (<1%)
Treatment
• Better prognosis if treatment started before CNS stage
• Pentamidine and Suramin (for blood and lymphatic stage)
• Melarsoprol (Late stage)
o Can cause Jarisch-Herxheimer reaction (due to trypanosome lysis)
• Nitrofurazone used in case of Melarsoprol failure
 LEISHMANIA SPP.
Human stages
Sandflies bite human
• Injects promastigote into the skin
Promastigotes ingested/phagocytized by macrophages in the blood
• Promastigotes become amastigotes inside the macrophage
• Amastigotes multiply inside
Macrophages burst
• Release amastigotes
• Amastigotes: infective stage to sandflies
Sandfly stages
Sandflies bite human
• Ingests macrophages infected with amastigotes
In midgut of sandfly
• Amastigotes transform into promastigotes
• Amastigotes divide in the midgut
Amastigote migrate to proboscis
• When it bites a human, it injects the promastigotes
 LEISHMANIA SPP.
• Vector borne parasitic disease
o Sandflies: Phlebotomus spp. (infects old world, Europe), Lutzomyia (infects new world, US)
• Intracellular parasites (inside host cells)
• Diploid protozoa
• Zoonotic (dogs in urban places, rodents in urban and rural places)
• Old World Leishmaniasis: L. tropica (Asia and Eastern Europe), L. aethiopica (Africa), L.major
• New World Leishmaniasis (Mexico, Central America, South America, Amazon rainforest):
L. mexicana, L. amazonensis, L. guyanensis, L. braziliensis, L. chagasi
• Leishmania tropica
• Leishmania braziliensis
• Leishmania donovani (most severe)
• Infective stage to humans: promastigotes
• Infective stage to sandflies: amastigotes
• Targets RE cells
• Viannia subgenus produces promastigotes in the hindgut, midgut, and proboscis
(Leishmania subgenera only produces promastigoes in the midgut and proboscis)
 LEISHMANIA SPP.
Mode of transmission
• Bite of vector
• Blood transfusion
• Close contact
• Contamination of bite wounds
Intermediate host/Vector - Sandflies
Final Host - Humans
Disease Manifestation: Cutaneous Leishmaniasis
• Also known as Old World Leishmaniasis, Aleppo Button, Delhi Boil, Baghdad Boil,
Jericho Boil
• Etiologic agent: Leishmania tropica (can also be caused by L. major and L. mexicana)
o Live in skin capillaries (in the endothelial cells)
o That’s why they’re seen as lesions on the skin
o L. tropica: dry or urban oriental sore
o L. major: moist or rural oriental sore
o L. mexicana: chiclero ulcer
 LEISHMANIA SPP.
• Incubation period: weeks to months
• Painless elevated skin ulcers
o Leaves an ugly scar and is highly disfiguring (erodes the skin)
o Oriental Button: erythematous papule which forms an ulcer
• Common in Middle East and some parts of Asia
Diffuse Cutaneous Leishmaniasis
• AKA Anergic or Lepromatous Leishmaniasis
• Characterized by a localized, non-ulcerating papule
• Develops diffuse satellite lesions (affects the face and extremities)
• May be initially diagnosed as lepromatous leprosy
 LEISHMANIA SPP.
Disease Manifestation: Mucocutaneous Leishmaniasis
• Also known as American, New World Leishmaniasis
• Etiologic agent: Leishmania braziliensis
• Incubation period: weeks to months
• Habitat: tissues in nose and mucous membranes
• Initial: ulcers are similar to Cutaneous Leishmaniasis
• Later stage: spreads to oronasal and pharyngeal mucosa (can lead to dysphonia,
dysphagia, and aspiration pneumonia)
o Involvement of the mucous membranes results in nasal stuffiness,
discharge, epistaxis, and destruction of the nasal septum
o Espundia: in the nose
o Tapir Nose: also affects the nose
o Chiclero Ulcer: affects ears
 LEISHMANIA SPP.
Disease Manifestation: Visceral Leishmaniasis
• Also known as Kala-azar, Dumdum Fever (this is a place), Black Fever
• Etiologic agent: Leishmania donovani (can also be caused by L. chagasi and L.
infantum)
• Incubation period: 1-3 months
• Habitat: RES
• Dromedary fever peak: fever with twice daily elevations (Double Quotidian)
• Splenomegaly
• Cachexia
• Reticuloendotheliosis
• Hepatomegaly
• Darkening of skin (forehead, temples, around the mouth)
o That’s why its called black fever
• Dermal leishmanoid lesions (rare)
o Present if treatment is incomplete
• Post-kala azar dermal leishmaniasis (PKDL): sequela
o Cutaneous eruption resulting in hypopigmented macules, malar erythema,
nodules, and ulcerations
o Manifest a few months to several years after treatment
 LEISHMANIA SPP.
Diagnosis
• Demonstration of lesions
• Montenegro Skin Test o Also called Leishmanin Skin Test
o Test to determine if you have a previous exposure to the parasite
o Person injected with a suspension of parasites (promastigote) in the
intradermal area
o Positive result: if there is enlargement
o Negative in diffuse cutaneous leishmaniasis and kala azar
• Formol Gel Test
o Useful for donovani
o To determine if there is hypergammaglobulinemia
• Serology: IFAT, ELISA, rk39 antigen dipstick test

Treatment
• Antimony compounds (sodium stibogluconate, n-methyl-glucamine antimonite or
meglumine)
 BABESIA SPP.
Erythrocytic cycle
Sporozoites infect RBCs
• start of erythrocytic schizogony
• no exo-erythrocytic cycle in Babesia spp.
• sporozoites develop into an immature trophozoite form
• trophozoites develop into merozoites
Merozoites released from RBCs
• infects other RBCs
Gametogony
• after many cycles, gametes are produced (macrogamete and microgamete)
• no schizonts and gametocytes
Transmission of gametocytes
• gamete is ingested by another tick
• gamete: infective stage to the definitive host
 BABESIA SPP.
Sporogonic cycle
Gut/GI Tract
• macrogamete and microgamete fuse to form zygote
• fertilization
Formation of ookinete
• zygote becomes elongated and motile
o forms ookinete
o subsequent development of Babesia: development of numerous
kinetes (sporokinetes)
▪ when sporokinetes are released, they continue to infect and multiply in
various organs and the ovaries, until death ensues
• ookinete enters salivary gland
• ookinete develops into an oocyst
o sac-like structures with sporozoites
Oocyst bursts
• releases sporozoites
• already in the salivary glands
 BABESIA SPP.
• Blood-borne and vector-borne
o Transmitted by ticks (genus Ixodes)
▪ Ixodidae or hard ticks
▪ Transmission via soft tick (Ornithodoros erraticus) has been reported
▪ Other vectors: Boophilus spp., Rhipicephalus spp., Hyalomma spp.,
Haemaphysalis spp., and Dermacentor spp.
• Hemosporidian parasites
• Dr. Victor Babes: first documented Babesia in cattle (1888)
• Heteroxenous parasite: infesting more than one kind of host, requiring at least two kinds of
host to complete the life cycle (mammal as primary host and ticks as intermediate
hosts or vectors)
• has a tendency to take on pleomorphic forms (ability to alter their shape or size in
response to environmental conditions) in different hosts o obscures their
identification at the species level
• transstadial: capable of stage-to-stage passage
o each of developmental stages capable of parasite transmission to mammals
 BABESIA SPP.
• smaller forms (ex: Babesia bovis and Babesia equi more pathogenic
• larger forms (ex: Babesia bigemina and Babesia caballi) less virulent
• Sometimes mistaken for Plasmodium
o Important to differentiate them
o Babesia: blood parasite that causes malaria-like infections
o Babesia does not undergo exoerythrocytic merogony (residual bodies usually not
found in infected RBCs)
• Zoonotic infection
• Causative agents: Babesia microti (found in the Northeastern US) and Babesia divergens
(found in Europe)
o Groupings obtained through phylogenetic analyses of gene sequences of SSU rDNA
(small subunit ribosomal deoxyribonucleic acid) of Babesia spp.
 BABESIA SPP.
Mode of Transmission
• Bite of an infected tick (blood meal)
• Blood transfusion
• Vertical transmission
• Organ transplant
• Transovarian transmission (for Babesia divergens)
o Ticks can pass the parasite to its progeny/offspring
o Infect ova (egg) of the ticks
o Terminates with death of the vector
Definitive Host - Tick (Ixodes)
Intermediate Host - Mammals
• White footed mouse (most important)
• livestock
• Cattle
• Humans
• Deer: primary reservoir host
Infective stage to intermediate hosts: sporozoites (called pyriform bodies)
 BABESIA SPP.
Treatment
• Combination of Clindamycin and Quinine
• Or Azithromycin and atovaquone
• For B. equi and B. caballi in vitro
o Use arteminisin, pyrimethamine, and pamaquine
Prevention
• Avoid tick bites
• Apply insect repellants
• Screen blood donors
• Remain covered with clothing
• Immediately remove any attached ticks
• Control rodent population (since they are major carriers or reservoirs)