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APICOMPLEXA

VIENNA MARIE B. ECHALAR, RMT


MLS221 CLINICAL PARASITOLOGY LECTURE
L E A R N I N G O B J E C T I V E S

01 Classify the individual apicomplexa specie as intestinal or extraintestinal.

02 Identify the apicomplexa specie by scientific name, common name, and morphologic form.

03 Identify and state the purpose of the designated characteristic structure(s).

04 Construct, describe, and compare and contrast the life cycles of eachapicomplexa specie.

05 Determine specimen(s) of choice, alternative specimen type(s) when appropriate, collection


protocol(s), and laboratory diagnostic technique(s) required for the recovery of each of the
apicomplexa specie.
APICOMPLEXA

Has an apical complex at the anterior end These organisms have been reported
which consists of polar rings, subpellicular practically from all organ systems of both
tubules, conoid processes, rhoptries, and humans and animals, specifically in the
micronemes. gastrointestinal tract, genitourinary tract,
central nervous system, respiratory tract,
These structures are involved in the reticuloendothelial system, blood and blood
penetration and invasion of target cells. cells, eyes, skin, and even the oral cavity
CLASSIFICATION OF SPOROZOA

Intestinal Species Tissue Species Blood Species

Isospora belli Toxoplasma gondii Plasmodium spp.


Sarcocystis species Babesia spp.
Cryptosporidium parvum
INTESTINAL SPECIES
01 Cystoisospora belli

Common associated disease and condition names: Isosporiasis

Previously known as Isospora belli

Causes isosporiasis, which is characterized by mild diarrhea to

severe dysentery

Transmission is by ingestion of the infective oocyst in

contaminated food and water.

Humans are the definitive host; there are no intermediate hosts


Oocyst
The oval oocyst ranges in size from 25 to 40 um in
length.
The young oocyst divides into two sporoblasts.
Each sporoblast continues to mature and
eventually becomes a sporocyst, which consists of
a mature roundish sac containing four sausage-
shaped sporozoites
The cytoplasm is granular and contains two
sporocyst that contain four sporozoites each.
LIFE CYCLE
Transmission is by ingestion of the infective oocyst in
contaminated food and water.
The sporozoites excyst in the small intestine releasing
sporozoites, which penetrate the epithelial cells, thus
starting the asexual stage or the schizogonic phase of the
life cycle.
The sporozoites excyst in the small intestine releasing
sporozoites, which penetrate the epithelial cells, thus
starting the asexual stage or the schizogonic phase of the
life cycle.
Some of the merozoites undergo gametogony to produce
macrogametes and microgametes, which fuse to form a
zygote that eventually matures to form an unsporulated
oocyst.
Sporulation usually occurs within 48 hours after passage
with the stool.
PATHOGENESIS AND
CLINICAL MANIFESTATION

Isosporiasis
Patients produce foul-smelling stools that are pale
yellow and of a loose consistency.
Fecal fat levels is increased.
Infected patients may shed oocysts in their stools
for as long as 120 days.
Death may result from such severe infections.
DIAGNOSIS
The oocysts of C. belli may be detected in the feces by direct
microscopy or formalinether/ethyl acetate concentration.
Permanent staining (Ziehl-Neelsen method, Phenol-auramine,
Kinyoun’s stain)
String capsule (Enterotest®

TREATMENT
The treatment of choice for asymptomatic or mild infections
consists of consuming a bland diet and obtaining plenty of rest.
Patients suffer ing from more severe infections respond best to
chemotherapy, consisting of a combination of trimethoprim and
sulfamethoxazole or pyrimeth amine and sulfadiazine.

PREVENTION AND CONTROL


Proper personal hygiene
Adequate sanitation practices
Avoidance of unprotected sex, particularly among homosexual
men.
02 Sarcocystis species

Common associated disease and condition names: Sarcosporidiosis or


sarcocystosis.

There are about 130 recognized species under Sarcocystis including S.


hominis and S. suihominis.
Sarcocystis hominis is found in cattles
Sarcocystis suihominis is found in pigs
Humans serve as definitive hosts for the two species, but occasionally,
humans can act as intermediate hosts.
Zoite

The simplest form.


A bananashaped cell, with a pointed anterior
end, also known as the apical complex.
Possesses micronemes, micropores, and
rhoptries, and believed to be associated with
host cell penetration and creation of an
intracellular environment suitable for parasite
growth and development.
Oocyst

Oval shaped, transparent.


Consists of two mature sporocysts that each
average from 10 to 18 µm in length.
Each sporocyst is equipped with four sausag
shaped sporozoites.
A double-layered clear and colorless cell wall
surrounds the sporocysts.
PATHOGENESIS AND
CLINICAL MANIFESTATION

Sarcocystis
Patients present fever, severe diarrhea, weight
loss, and abdominal pain.
Muscle tenderness and other local symptoms are
exhibiting symptoms caused by Sarcocystis
invasion of the striated muscle.
LIFE CYCLE
Humans are infected by consumption of uncooked or undercooked meat of
intermediate host that contains sarcocysts.
The parasite undergoes sexual reproduction within the intestines.
After sarcocysts are ingested and the wall is digested, bradyzoites become
motile. Active bradyzoites enter intestinal cells and change into the male
and female forms, microgamonts and macrogamonts, respectively.
Fusion of a macrogamont and a microgamont creates a fertilized cell called
a zygote, which develops into an oocyst.
The oocyst is passed through the feces.
After oocysts are ingested by a susceptible intermediate host the
sporocysts pass to the small intestine.
The plates forming the sporocyst wall separate, releasing the four
sporozoites into the intermediate host’s body.
The sporozoites migrate through the gut epithelium and eventually enter
the endothelial cells in small arteries where they undergo the first two
generations of asexual reproduction .
Merozoites emerge from the second generation meronts and enter the
mononucleate cells where they develop to become metrocytes and encyst
in the muscles, initiating sarcocyst formation.
DIAGNOSIS
Specific diagnosis is done through stool examination.However,
in many cases, the oocysts have already ruptured and only the
sporocysts are visible on examination of the stool specimen.
Flotation methods based on high-density solutions incorporating
sodium chloride, cesium chloride, zinc sulfate, sucrose, Percoll,
Ficoll-Hypaque, and other density gradient media are preferred
over formalinether/ethyl acetate and other sedimentation
methods.

TREATMENT
The treatment protocol for infections with Sarcocystis spp. when
humans are the definitive host is similar to that for Isospora belli.

PREVENTION AND CONTROL


Adequate cooking of beef and pork.
Proper sanitation and personal hygiene practices.
Proper disposal of human waste and animal stool.
03 Cryptosporidium

Common associated disease and condition names:


Cryptosporidosis

Cryptosporidium hominis found mainly in humans.


Cryptosporidium parvum is the only species that infect
mammals
In patients with acquired immunodeficiency syndrome
(AIDS), Cryptosporidium infections are an important cause
of death due to dehydration.
In the immunosuppressed patient, the parasite causes a
wide range of debilitating problems, including malabsoiption
and stomach, liver, and respiratory disorders.
Oocyst

The oval oocyst ranges in size from 4 to 6 jam.


Oocysts contain four sporozoites enclosed
within a thick cell wall.
The cytoplasm may contain several dark
granules.

Schizonts and Gametocytes

Schizonts contains four to eight merozoites,


microgametocytes, and macrogametocytes.
The average size of these forms is a mere 2 to
4 µm.
LIFE CYCLE
All stages of development are completed in the gastrointestinal tract of
the host.
Infection starts with the ingestion of oocyst.
The oocyst develops to become sporozoites which attaches to the
surface of epithelial cells of the gastrointestinal tract.
The sporozoites develop into small trophozoites and become
intracellular but extracytoplasmic, and attach to the brush borders.
The trophozoites divide by schizogony producing merozoites that infect
other cells.
Macro- and microgametocytes are eventually produced, and the
macrogamete is fertilized by the microgamete to produce a zygote.
There are two types of oocysts resulting from the zygote: the thin-
walled and the thick-walled oocysts.
The thin-walled oocysts infect other enterocytes thus resulting in
autoinfection, which is possibly responsible for the chronicity of the
infection among the immunocompromised.
On the other hand, the thick-walled oocysts are passed out with the
feces that may contaminate food and water, which are ingested by the
same or another host.
PATHOGENESIS AND
CLINICAL MANIFESTATION

Cryptosporidiosis
Patients present with self limiting diarrhea.
Infected immunocompromised individuals,
particularly AIDS patients, usually suffer from severe
diarrhea. Malabsorption may also accompany
infection in these patients. In addition, infection may
migrate to other body areas, such as the stomach
and respiratory tract. A debilitating condition that
leads to death may result in these patients.
DIAGNOSIS
Microscopic detection of acid-fast oocysts in stool or small bowel mucosal
epithelial cells
Sheather sugar flotation
Enterotest, enzyme-linked immunosorbent assay (ELISA), and indirect
immunofluorescence

TREATMENT
No treatment has been proven to be effective. However, the use of spiramycin,
even though still in the experimental stage, has preliminarily proven helpful in
ridding the host of Cryptosporidium.

PREVENTION AND CONTROL


Proper treatment of water supplies, handling known infected material by
using gloves and wearing a gown (when appropriate)
Proper hand washing, and properly disinfecting potentially infected
equipment with full-strength commercial bleach or 5% to 10% household
TISSUE SPECIES
01 Toxoplasma gondii

Common associated disease and condition names: Toxoplasmosis,


congenital toxoplasmosis, cerebral toxoplasmosis.

Common cause of congenital infection


Toxoplasma is an intracellular parasite, which infects different
kinds of nucleated cells including macrophages.
Oocyst in cat feces may infect man
.
Oocyst
The typical infective form of Toxoplasma gondii, the oocyst, is similar in appearance to that of Isospora belli. The most
notable difference between the two organisms is that T. gondii is smaller.
The transparent oocyst contains two sporocysts, each with four sporozoites. The organism is bordered by a clear,
colorless, two-layered cell wall.
Tachyzoite
The actively multiplying, crescent-shaped.
Each tachyzoite is equipped with a single centrally
located nucleus, surrounded by a cell membrane.
A variety of other organelles are present, including a
mitochondrion and Golgi apparatus; however, these
structures are not readily visible.

Bradyzoites
The typical bradyzoite basically has the same physical
appearance as the tachyzoite, only smaller.
Gather in clusters inside a host cell, develop a
surrounding membrane, and form a cyst in a variety of
host tissues and muscles outside the intestinal tract.
LIFE CYCLE
The infective stages include the tachyzoite, the bradyzoite, and
the oocyst. The complete life cycle occurs only in the members
of the cat family (Felidae), which serve as definitive hosts.
It follows a typical coccidian life cycle consisting of schizogony,
gametogony, and sporogony in the intestinal epithelium. The
extraintestinal stages are the asexual stages: tachyzoites and
bradyzoites.
The oocyst are passed out with the cat's feces and can be
ingested together with contaminated food or water by another
host.
When the mature oocyst reaches the intestine of the new host,
it excysts and releases four sporozoites which can penetrate
the lamina propria.
The parasites gain entry to the lymphatics then spread to the
different organs, tissues, and fluids of the body
PATHOGENESIS AND
CLINICAL MANIFESTATION

Toxoplasmosis in Immunocompromised Patients


Clinical manifestations become apparent when the
immune system is suppressed as in old age, drug-
induced immunosuppression after organ
transplantation, or in the case of AIDS.
The most common manifestation is encephalitis,
myocarditis, and focal pneumonia.
PATHOGENESIS AND
CLINICAL MANIFESTATION

Cerebral Toxoplasmosis in AIDS Patients


AIDS patients suffering from infection with T. gondii
may experience early symptoms of headache, fever,
altered mental status (including confusion), and
lethargy. Subsequent focal neurologic deficits, brain
lesions, and convulsions usually develop.
The T. gondii organisms do not spread into other
organs of the body but rather stay confined within the
CNS.
PATHOGENESIS AND
CLINICAL MANIFESTATION
Congenital toxoplasmosis
Occurs in approximately one to five of every 1000 pregnancies.
Transmission of the disease occurs when the fetus is infected
(via transplacental means) unknowingly by its asymptomatic
infected mother.
Typical symptoms in an infected child include hydrocephaly,
microcephaly, intracerebral calcification, chorioretinitis,
convulsions, and psychomotor disturbances. Most of these
infections ultimately result in mental retardation, severe visual
impairment, or blindness.
Stillbirth and abortion may result when mothers acquire the
infection during the first trimester of pregnancy.
DIAGNOSIS
The recommended test for the determination of immunoglobulin M (IgM)
antibodies present in congenital infections is the double-sandwich ELISA
method.
Sabin-Feldman dye test -Methylene blue staining of tachyzoites is inhibited
by prior addition of patient serum containing antibodies to Toxoplasma

TREATMENT
The treatment of choice for symptomatic cases of T. gondii infection consists of
a combination of trisulfapyrimidines and pyrimethamine (Daraprim).

PREVENTION AND CONTROL


Avoidance of contact with cat feces.
Avoidance of ingesting contaminated meat.
Keeping cats away from potentially infective rodents, feeding cats only dry or
cooked canned cat food, and/or not having cats at all.
END

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