PARASITOLOGY

NAEGLERIA FOWLERI
⮚ The “brain-eating amoeba”

⮚ Free-living with 2 forms: ameba (trophozoite form) & flagellate (swimming form)

⮚ Dormant cyst forms when conditions not favorable

⮚ 2 forms of trophozoites: ameboid (form found in humans) & ameboflagellate

⮚ Thermophilic

⮚ Only Naegleria fowleri is pathogenic to humans

⮚ 3 stages: cyst, trophozoite, flagellated form

▪ Cyst
o 7-10 micrometers long
o Smooth double cyst wall
o Resting domant form
o Resists drying & chlorination
▪ Trophozoite – amoeboid form
o 10-20 micrometers long
o Rounded pseudopodia (lobopodia)
o Spherical nucleus & pulsating vacuoles
o Feeding, growing & replicating form
o INFECTIVE STAGE
o Thrives in vegetation, mud & water
▪ Trophozoite – flagellate form
o Transient
o Pear-shaped
o Has 2 flagella
 ⮚ Life cycle
o Infective form: amoeboid trophozoite
o Human infection via swimming or diving in water containing amoeboid forms
o Incubation period: 1-7 days

Naegleria fowleri has three stages in its life cycle: cysts (1), trophozoites (2), and flagellated
forms (3). The trophozoites replicate by promitosis (nuclear membrane remains intact) (4).
Naegleria fowleri is found in fresh water, soil, thermal discharges of power plants, geothermal
wells, and poorly chlorinated recreational and tap water. Trophozoites can turn into temporary
non-feeding flagellated forms which usually revert back to the trophozoite stage. Trophozoites
infect humans or animals by penetrating the nasal mucosa, usually during swimming or sinus
irrigation (5), and migrating to the brain (6) via the olfactory nerves causing PAM. Naegleria
fowleri trophozoites are found in cerebrospinal fluid (CSF) and tissue, while flagellated forms
are occasionally found in CSF. Cysts are not seen in brain tissue.

⮚ Causes PRIMARY AMOEBIC MENINGO-ENCEPHALITIS (PAM)

o Pathogenesis: water carries N. fowleri into nasal cavity 🡪 N. fowleri attaches itself
to olfactory nerves & “eats” its way up to the brain through the cribriform
plate 🡪 the amoeba attacks the olfactory bulb, leading to inflammation &
infection of the brain
⮚ Clinical Manifestations
o severe frontal headache, fever, nausea, vomiting
o stiff neck, seizures, altered mental status, hallucinations, coma

⮚ Lab diagnosis of PAM

o CSF exam
▪ cloudy to purulent

▪ increased neutrophil count

▪ elevated proteins

▪ low glucose levels

▪ no bacteria found
o wet film – presence of trophozoites
o autopsy – trophozoites in brain tissue
o Wright or Giemsa stain – (+) trophozoites
o Fluorescent Ab staining – (+) amoeba
⮚ Treatment
o Amphotericin B = 1 mg/kg/day for several days
o Ketoconazole 800 mg daily (oral) for 1 month
o New drug: Miltefosine
o Therapeutic hypothermia
BALANTIDIUM COLI

⮚ A parasitic species of ciliate protozoan responsible for the disease Balantidiasis

⮚ The largest protozoan and the only ciliate known to parasitize humans

⮚ Found worldwide esp. in Bolivia, Papua New Guinea, Philippines

⮚ Principal host: humans. Also reported to be found in dogs, pigs and monkeys

⮚ Site of infection in humans: large intestine, caecum

⮚ Morphology: trophozoite & cyst

⮚ Cyst
o Spherical
o 40-60 um across
o Covered with thick hard cyst wall with cilia
o Infective stage
o Non-reproductive
o Has macronuclei
⮚ Trophozoite
o Oval shape, pointed at anterior end
o 50-130 um long
o Covered in cilia
o Non-infective stage
o Reproduces by binary fission & conjugation
o Has micronuclei & macronuclei
⮚ Life cycle of B. coli
o Completed in single host
o Pigs are accidental hosts
o Reproduction: asexual (binary fission) & sexual (conjugation)
o Infective stage = cyst
o Once the cyst is ingested via contaminated food or water, it passes through the
human digestive system 🡪 excystation occurs in small intestine 🡪 trophozoites
are released & travel to large intestine 🡪 the motile trophozoites reside in the
lumen of the colon & undergo reproduction
o Some trophozoites may become invasive & penetrate the wall of the colon
o Trophozoites encyst in the colon 🡪 mature cysts are released with the feces
Cysts are the stage responsible for transmission of balantidiasis . The host most often
acquires the cyst through ingestion of contaminated food or water . Following ingestion,
excystation occurs in the small intestine, and the trophozoites colonize the large intestine .
The trophozoites reside in the lumen of the large intestine and appendix of humans and
animals, where they replicate by binary fission, during which conjugation may occur .
Trophozoites undergo encystation to produce infective cysts . Some trophozoites invade
the wall of the colon and multiply, causing ulcerative pathology in the colon wall. Some return
to the lumen and disintegrate. Mature cysts are passed with feces.
⮚ Signs & symptoms of balantidiasis
o Most cases are asymptomatic
o May have diarrhea, dysentery, colitis, abdominal pain
⮚ Diagnosis
o Detection of trophozoites in stool exam or tissue collected during sigmoidoscopy
o Cysts are less encountered
o Once outside the colon, B. coli is rapidly destroyed 🡪 may need to repeat stool
exams frequently
⮚ Treatment
o Tetracycline 500 mg 4 x day for 10 days
o Metronidazole 750 mg 3 x day for 5 days
o Iodoquinol 640 mg 3 x day for 20 days
⮚ Control & prevention
o Avoid ingestion of material contaminated with animal feces
o Sanitary disposal of human & pig feces
o Prevent fecal contamination of food & water
o Cysts may be resistant to environmental conditions and may survive for long
periods of time, they are easily inactivated by heat and by 1% sodium
hypochlorite
o Ordinary chlorination of water is not effective against B. coli cysts.
FLAGELLATES
⮚ Two groups:
o Lumen-dwelling flagellates: intestinal/oral/genital tract parasite

o Hemoflagellate: blood & tissue parasite

▪ Leishmania sp. in reticulo-endothelial cells
o Trypanosoma brucei in connective tissue & blood
o Trypanosome cruzi in RE cells & blood

⮚ Lumen-dwelling flagellates
Genus Parasite Habitat
Giardia G. lamblia Duodenum
Chilomastix C. mesnilli Caecum
Enteromonas E. hominis Colon
Retromonas R. intestinalis Colon
Pentatrichomonas P. hominis Ileocecal region
Trichomonas T. vaginalis Vagina & urethra
T. tenax Teeth & gums
Dientamoeba D. fragilis Colonic mucosal crypts
GIARDIA LAMBLIA

⮚ Most common protozoan pathogen with worldwide distribution

⮚ Epidemiology
o Seen in areas with poor sanitation, especially in tropics & subtropics
o Common in younger age groups
o May cause Traveller’s diarrhea in tourists who drink contaminated water
⮚ Habitat
o Duodenum & upper part of jejunum
o The only protozoan parasite that is found in the lumen of the small intestine
⮚ Morphology – exists in cyst & trophozoite forms
o Trophozoite
▪ Teardrop-shaped, has pair of ovoid nuclei (one on each side of midline)

▪ Bilaterally symmetrical with distinct medial line called an AXOSTYLE

▪ Propelled by 4 pairs of flagella

▪ Divide via longitudinal binary fission

▪ Found in diarrheic stool 🡪 trophozoites do not survive in environment

o Cyst
o Ovoid
o Young cysts have 2 nuclei; mature cysts have 4 nuclei
o Have flagella retracted into axonemes
o Has median bodies & a tough hyaline cyst wall
o Infective & diagnostic stages: mature cysts
⮚ Mode of transmission
o Cysts from animals or human feces are transferred to the mouth via
contaminated hands, food or water
o Cysts excyst in the duodenum 30 minutes after ingestion 🡪 develop into
trophozoites
o Trophozoites attach to intestinal villi & cause damage 🡪 trophozoites may be
found in jejunum
 o The parasite encysts once it is in the colon
o Mature cysts are passed out in the feces 🡪 infectious

⮚ Life cycle of Giardia lamblia

⮚ Cysts are resistant forms and are responsible for transmission of giardiasis. Both cysts
and trophozoites can be found in the feces (diagnostic stages) (1). The cysts are hardy
and can survive several months in cold water. Infection occurs by the ingestion of cysts
in contaminated water, food, or by the fecal-oral route (hands or fomites) (2). In the
small intestine, excystation releases trophozoites (each cyst produces two trophozoites)
(3). Trophozoites multiply by longitudinal binary fission, remaining in the lumen of the
proximal small bowel where they can be free or attached to the mucosa by a ventral
sucking disk (4). Encystation occurs as the parasites transit toward the colon. The cyst is
the stage found most commonly in nondiarrheal feces (5). Because the cysts are
infectious when passed in the stool or shortly afterward, person-to-person transmission
is possible. While animals are infected with Giardia, their importance as a reservoir is
unclear
⮚ Pathogenesis
o With the help of a sucking disc, they adhere to the convex surface of epithelial
cells & crypts of the intestinal mucosa
o It does not invade the tissues.
o May cause abnormalities of villous architecture by apoptosis
o Capable of producing harm via toxic effect (produces variant specific surface
proteins), irritative effect, or spoliative action (diverts nutriments)
o To avoid the high acidity of the proximal duodenum, Giardia often localizes in
the biliary tract (gall bladder)
⮚ Clinical features
o Incubation period: about 2 weeks
o Silent cases (asymptomatic)
o Diarrhea is the most common symptom, occurring in 89% of cases. It is followed
by malaise and flatulence.
o Spontaneous recovery occurs within 6 weeks in mild to moderate cases
o Acute cases:
▪ abdominal pain, described as cramping, associated with diarrhea

▪ excessive flatus with an odor of “rotten eggs” due to hydrogen sulfide.

▪ abdominal bloating, nausea, and anorexia

o Chronic infection:
▪ steatorrhea, or the passage of greasy, frothy stools

▪ Periods of diarrhea alternate with normal or even constipated bowel

periods
▪ weight loss, profound malaise, and low-grade fever. In developing
countries

⮚ Lab diagnosis
o Stool exam
▪ Identification of cysts in formed stool, or trophozoites & cysts in diarrheic
stool or after a purgative
▪ In asymptomatic carriers, only cysts are seen

▪ Macroscopy: offensive odor, pale-colored, fatty stool

▪ Microscopy: use saline & iodine wet preparations

 ▪ Trophozoites in direct fecal smears may be characterized as having a
floating leaf-like motility

o Enterotest (string test)

o Method for obtaining duodenal specimen
o Performed when the physician suspects a parasitic infection in a patient
with a negative stool sample
o Sensitivity of test is similar to duodenal aspirate 🡪 no need for duodenal
intubation
o Procedure:
▪ A coiled string with a small weighted gelatin capsule is swallowed
by the patient & the free end of the string is attached to the side
of the patient’s face
▪ The capsule dissolves in the stomach and the string (weighted at
the distal end) passes into the duodenum
▪ After 2-4 hours, the string is withdrawn and placed in a saline
solution 🡪 shake solution
▪ The centrifuged deposit of saline is observed by wet mount
technique to detect the motility or presence of Giardia
trophozoites. May also be used to detect larvae of Strongyloides
stercoralis.

o Serodiagnosis – antigen detection in feces (if antigen present, there is active

infection)
o ELISA
▪ Giardia-specific Ag 65 (GSA 65) can be detected
o IIF (indirect immunofluorescent tests)
o Immune-chromatographic strip test
o Sensitivity = 95%, specificity = 100%
o Not for routine use 🡪 for epidemiological & control purposes
o Note: ELISA and IIF can also be used for antibody detection
▪ Cannot differentiate between recent & past infection

▪ Lacks sensitivity & specificity

▪ Antibody detection (anti-Giardia IgG) can be useful for

epidemiological & pathophysiological studies
 ▪ The presence of anti-Giardia secretory IgA in breastmilk protects
breast-fed infants from giardiasis.
o Molecular method
o DNA-based techniques are available now
o PCR & DNA probes can be used to determine the genome of a parasite

⮚ Treatment
o Metronidazole 250 mg 3 x day for 5 days (cure rate is about 95%)
o Tinidazole 2 gm single dose (more effective treatment)
o Furazolidone & Nitazoxamide for children (has less adverse effects)
o Parmomycin for pregnant women

⮚ Prevention and Control

o Proper disposal of waste water & fecal material
o Proper personal hygiene, ex. handwashing, proper disposal of dirty diapers
o Prevention of food & water contamination
o Boiling/filtration of drinking water
o Note: chlorination of water is not effective against cysts
TRICHOMONAS VAGINALIS

⮚ Characteristic features
o Single-celled
o Pathogenic protozoa
o They DO NOT form cysts
o Flagellated
o Most common pathogenic protozoan in industrialized countries

⮚ Morphology
o 7-20 um long & 5-15 um wide
o With short undulating membrane
o Many granules among its axostyle
o Has hydrogenosomes
o Structure:
⮚ Trichomoniasis
o Etiologic agent: Trichomonas vaginalis
o A sexually transmitted disease
o Reservoir: human genital tract, where it replicates by binary fission
▪ Male: prostate, urethra

▪ Female: lower genital tract

o T. vaginalis does not survive well in external environment
⮚ Symptoms in women
o Prominent symptom: vaginitis with purulent discharge
▪ Discharge is yellow-green, frothy, foul-smelling (fishy odor)
o Cervicitis/Vaginitis 🡪 itching in genital area
o Lower abdominal pain
o Dysuria, dyspareunia
o Symptoms usually appear within 5-28 days of exposure
o Strawberry cervix in chronic stage
⮚ Symptoms in men
o Most are asymptomatic
o May have urethritis and prostatitis
o Non-purulent discharge that has a fishy odor
o Dysuria, dyspareunia
o Signs of inflammation on external genitals
⮚ Potential complications
o In infected pregnant women 🡪 preterm delivery, low birth weight
o Predisposition to HIV infection & cervical cancer

⮚ Diagnosis
o Direct microscopy of wet mounts of genital secretions may establish the
diagnosis by detecting actively motile organisms. This is the most practical and
rapid method of diagnosis (allowing immediate treatment), but it is relatively
insensitive.
o Direct immunofluorescent antibody staining is more sensitive than wet mounts,
but technically more complex
o Culture of the parasite is the most sensitive method, but results are not available
for 3 to 7 days. In women, examination should be performed on vaginal and
urethral secretions. In men, anterior urethral or prostatic secretions should be
examined.

⮚ Treatment
o Trichomoniasis can be cured with a single dose of metronidazole (2 gm) or
tinidazole (2 gm). May also take Metronidazole 500 mg 2 x day for 7 days.
Metronidazole is safe for pregnant women.
o Avoid alcohol during treatment and for 24 hours after intake of metronidazole
(72 hours if tinidazole) 🡪 otherwise, will get disulfiram-like reaction
**disulfiram-like reaction: a process in the body that produces symptoms
similar to those that occur when alcohol is consumed after taking
disulfiram (Antabuse).
Disulfiram is an oral drug used for treating alcoholism that causes
unpleasant symptoms when alcohol is consumed. Normally, alcohol 🡪
acetaldehyde by alcohol dehydrogenase, then acetaldehyde 🡪 acetic acid
by acetaldehyde dehydrogenase. Disulfiram inhibits acetaldehyde
dehydrogenase, leading to a buildup of acetaldehyde levels in the blood.
These high levels of acetaldehyde levels cause unpleasant symptoms
after drinking alcohol such as headache, hypotension, severe flushing,
palpitations, nausea or chest pain.
 o People who have been treated for trichomoniasis can get it again. About 1 in 5
people get infected again within 3 months after treatment. To avoid getting re-
infected, make sure that all sex partners get treated too. Retesting for T.
vaginalis is advised 3 months after end of treatment. Testing for other STDs is
also advised.
o Avoid sexual intercourse during treatment, until all partners have been treated,
and until all symptoms have resolved for all parties involved.

⮚ Prevention

o Monogamous sexual relations with partner

o Should notify partner if infected so they can be treated too

COCCIDIANS
Largest group of apicomplexan protozoa falling under Class Conoidasida.
Coccidia is a subclass of microscopic, spore-forming, single-celled obligate intracellular
protozoan.
The secretion allows the parasite to enter the host cell. Coccidians infect the intestinal tract of
most phyla of invertebrates and all classes of vertebrates including humans.
The disease called coccidiosis is recognized as one of the major problems in animal farming and
in zoo management.
Opportunistic in immunocompromised and immunodeficient individuals.
Life cycle: alternation of sexual and asexual multiplication
○ Sexual/Sporogony – oocysts
○ Asexual/Schizogony/Merogony – merozoites/meront
○ Gametogony – male & female gametocytes/gamont
Species with medical significance:
i. Cryptosporidium
ii. Cyclospora
iii. Cystoisospora
iv. Sarcocystis
v. Toxoplasma

CRYPTOSPORIDIUM HOMINIS
 ➢ Found in feces of animals and humans
➢ Transmission: fecal – oral route
➢ Epidemics are unusual in North America, although there was a report of an epidemic
involving over 400,000 cases in the state of Wisconsin in the United States–f
➢ Faulty water purification system– contaminated with calf feces.
➢ Life Cycle

Sporulated oocysts, containing 4 sporozoites, are excreted by the infected host through feces
and possibly other routes such as respiratory secretions (1). Transmission of Cryptosporidium
parvum and C. hominis occurs mainly through contact with contaminated water (e.g., drinking
or recreational water). Occasionally food sources, such as chicken salad, may serve as vehicles
for transmission. Many outbreaks in the United States have occurred in waterparks, community
swimming pools, and day care centers. Zoonotic and anthroponotic transmission of C. parvum
and anthroponotic transmission of C. hominis occur through exposure to infected animals or
exposure to water contaminated by feces of infected animals (2). Following ingestion (and
possibly inhalation) by a suitable host (3), excystation (a) occurs. The sporozoites are released
and parasitize epithelial cells (b, c) of the gastrointestinal tract or other tissues such as the
respiratory tract. In these cells, the parasites undergo asexual multiplication (schizogony or
merogony) (d, e, f) and then sexual multiplication (gametogony) producing microgamonts
(male) (g) and macrogamonts (female) (h). Upon fertilization of the macrogamonts by the
microgametes (i), oocysts (j, k) develop that sporulate in the infected host. Two different types
of oocysts are produced, the thick-walled, which is commonly excreted from the host (j), and
the thin-walled oocyst (k), which is primarily involved in autoinfection. Oocysts are infective
upon excretion, thus permitting direct and immediate fecal-oral transmission.

➢ Morphology:

○ Oocysts
■ when passed out are already infective.
■ round and measure 4 to 5 µm in diameter.
■ four sporozoites
■ Infective stage
■ Sporozoites are sometimes visible inside the oocysts, indicating that
sporulation has occurred.
■ Infections that are resolving can be accompanied by increasing numbers
of non-acid-fast oocysts “ghosts.”

➢ Clinical Manifestations
○ Immunocompetent host
 ■ may be self-limiting diarrhea lasting for 2 to 3 weeks
■ less commonly, abdominal pain, anorexia, fever, nausea, and weight loss.
○ Immunocompromised persons,
■ severe diarrhea
■ bile duct and gall bladder may become heavily infected and lead to acute
and gangrenous cholecystitis.
■ respiratory infections lead to chronic coughing, dyspnea, bronchiolitis,
and pneumonia.
■ villi of the intestines become blunted and there is infiltration of
inflammatory cells into the lamina propria and elongated crypts—
malabsorption and excessive fluid loss in immunocompromised patients
■ death
➢ Diagnositics
○ Identification of C. hominis oocyst on stool examination
○ Round, 4-5 um in diameter
○ Sheather’s sugar floatation & FECT – commonly used
○ Kinyoun’s modified acid fast stain
○ Oocysts: red-pink doughnut-shaped in a blue background
○ Biopsy – various stages seen at the microvillus region of the infected
➢ Treatment
○ There is presently no acceptable treatment for cryptosporidiosis.
○ Nitazoxanide, however, has been reported effective in preliminary trials.
Bovine colostrum, paromomycin and clarithromycin have shown promise in
treating severe diarrhea.
○ Azithromycin may also be of value.
○ In addition to chemotherapy, body fluid replacement and symptomatic
treatment are recommended for both the immunocompetent and
immunosuppressed patients

➢ Prevention and Control

○ Chlorine does not kill the oocysts.
○ Avoid ingestion or handling infected water\
○ Sanitation

CYCLOSPORA CAYATENENSIS
➢ Found in contaminated fruits and vegetables
➢ No animal reservoirs found
 ➢ Cyclosporiasis has been reported in many countries, but is most common in tropical and
subtropical areas.
➢ People become infected with Cyclospora by ingesting sporulated oocysts, which are the
infective form of the parasite.
➢ Sporozoites invade the epithelial cells of the small intestines
○ Site of predilection: Jejunum
➢ Life Cycle

When freshly passed in stools, the oocyst is not infective (thus, direct fecal-oral
transmission cannot occur; this differentiates Cyclospora from another important coccidian
parasite, Cryptosporidium). In the environment , sporulation occurs after days or weeks at
temperatures between 22°C to 32°C, resulting in division of the sporont into two sporocysts,
each containing two elongate sporozoites . The sporulated oocysts can contaminate fresh
produce and water which are then ingested . The oocysts excyst in the gastrointestinal
tract, freeing the sporozoites, which invade the epithelial cells of the small intestine . Inside
the cells they undergo asexual multiplication into type I and type II meronts. Merozoites from
type I meronts likely remain in the asexual cycle, while merozoites from type II meronts
undergo sexual development into macrogametocytes and microgametocytes upon invasion of
another host cell. Fertilization occurs, and the zygote develops to an oocyst which is released
from the host cell and shed in the stool . Several aspects of intracellular replication and
development are still unknown, and the potential mechanisms of contamination of food and
water are still under investigation.
➢ Morphology
○ INFECTIVE STAGE: SPORULATED OOCYST
○ DIAGNOSTIC STAGE: UNSPORULATED OOCYST
○ Oocysts are spherical, 7.5-10 µm in diameter and unsporulated when passed in
feces.

➢ Clinical Manifestations
○ Initial symptoms include malaise and low grade fever, which may occur 12 to 24
hours after exposure.
○ Chronic and intermittent watery diarrhea occurs early in the infection and may
alternate with constipation.
■ The diarrhea may continue for 6 to 7 weeks with six or more stools per
day.
■ Other symptoms such as fatigue, anorexia, weight loss, nausea, vomiting,
abdominal pain, flatulence, bloating, and dyspnea may develop.
○ D-xylose malabsorption has been found to develop in some of the patients.
○ Infections are usually self-limiting and immunity may result with repeated
infections.
 ○ No death associated

➢ Diagnostics
○ Direct fecal smear under high power
○ Kinyoun’s stain
○ Oocysts in fluorescent microscopy–blue or green circles
○ Safranin staining and microwave heating are also helpful
○ PCR
➢ Treatment
○ Self-limiting and treatment is not necessary for mild symptoms.
○ Only effective drug is trimethoprim-sulfamethoxazole 160/800 mg twice daily for
7 days.
○ There is no alternate treatment if patients are unable to tolerate
sulfamethoxazole.
○ Oocysts disappear from the stools a few days after treatment.
○ Recurrence of symptoms was noted in about 40% of patients within 1 to 3
months post treatment.
➢ Prevention and Control
○ Good sanitary practices should be followed to prevent the infection.
○ Only water that has been subjected to adequate treatment procedures should
be consumed.
○ Boiling water seems to be the best method since chlorination is not effective.
○ Fruits and vegetables should be washed with clean water, but it would be
prudent to avoid eating fruits and vegetables that have been exposed to natural
untreated water.

CYSTOISOSPORA BELLI

➢ This is the causative agent of a medical condition affecting the small bowel called
cystoisosporiasis.
➢ The other known species Isospora hominis is now taxonomically grouped under the
 genus Sarcocystis.
➢ Cystoisosporiasis is most common in tropical and subtropical areas of the world.
➢ The parasite can be spread by ingesting contaminated food or water.
➢ Life Cycle

At time of excretion, the immature oocyst contains usually one sporoblast (more rarely two) .
In further maturation after excretion, the sporoblast divides in two (the oocyst now contains
two sporoblasts); the sporoblasts secrete a cyst wall, thus becoming sporocysts; and the
sporocysts divide twice to produce four sporozoites each . Infection occurs by ingestion of
sporocysts-containing oocysts: the sporocysts excyst in the small intestine and release their
sporozoites, which invade the epithelial cells and initiate schizogony . Upon rupture of the
schizonts, the merozoites are released, invade new epithelial cells, and continue the cycle of
asexual multiplication . Trophozoites develop into schizonts which contain multiple
merozoites. After a minimum of one week, the sexual stage begins with the development of
male and female gametocytes . Fertilization results in the development of oocysts that are
excreted in the stool .
➢ Morphology
○ Oocysts are large (25 to 30 µm) and have a typical ellipsoidal shape. When
excreted, they are immature and contain one sporoblast.
○ The oocyst matures after excretion: the single sporoblast divides in two
sporoblasts, which develop cyst walls, becoming sporocysts, which eventually
contain four sporozoites each.
○ Cystoisospora will autofluoresce under ultraviolet (UV) microscopy.

➢ Clinical Manifestations
○ Immunocompetent patients:
■ Generally asymptomatic or selflimiting gastroenteritis.
■ Severe infections: severe diarrhea and fat malabsorption can occur, low-
grade fever, anorexia, vomiting, general body malaise, anorexia, weight
loss, and flatulence
■ Stools usually contain undigested food, mucus, and Charcot-Leyden
crystals. I
○ Immunocompromised
■ Ranges from a self-limiting enteritis to severe diarrheal illness resembling
that of cryptosporidiosis, giardiasis or cyclosporiasis.
■ Mucosal bowel biopsy may reveal flattened mucosa and damaged villi.
 Infiltration of the lamina propria with lymphocytes, plasma cells, and
eosinophils has been reported. However, the mechanism by which the
parasite produces these lesions is still not clear.

➢ Diagnostics
○ Oocysts may be detected in the feces by direct microscopy or
formalinether/ethyl acetate concentration, also used are zinc sulfate and sugar
flotation.
○ Alternatively, oocysts can be seen in a fecal smear stained by a modified Ziehl-
Neelsen method- they stain granular red color against a green background.
○ Phenol-auramine, as well as iodine staining of the specimen can help visualize
the organism.
○ Acid-fast stain, such as Kinyoun’s stain or an auraminerhodamine stain, is also
useful.
○ A considerable amount of stool may have to be examined because oocysts in the
samples are often few in number.
○ In blood examination, peripheral eosinophilia is common.
○ String capsule (Enterotest®) and duodenal aspirate examinations may be of
value.
➢ Treatment
○ Asymptomatic infections may be managed with bed rest and a bland diet
○ Symptomatic infections, such as those occurring in AIDS patients
■ Trimethoprim-sulfamethoxazole 160/800 mg four times per day for 10
days, then two times per day for 3 weeks.
■ Combination therapy with pyrimethamine and sulfadiazine for 7 weeks
has also been used successfully.
➢ Prevention and Control
○ Good sanitary practices
○ Thorough washing and cooking food
○ Avoid contaminated water