COCCIDIA

-Class: Sporozoa
-Intracellular parasites with no definite organelle of
locomotion (movement: body flexion, gliding or undulating of
longitudinal ridges)
LIFE CYCLE
Reproduction
Multiplication

SPOROGONY
Sexual
Union of sex cells

SCHIZOGONY
Asexual
Segmentation/
division
Merozoites
Intermediate

End Product
HOST

Sporozoites
Definitive or final

Isospora
Eimeria,
Cryptosporidium
Sarcocystis
Toxoplasma

Asexual and sexual stages,

occurs in a single host

Human Sarcocystis Infection

Sarcocystis hominis

Disease

Needs 2 host for life cycle

Trophozoite - smallest and earliest stage of

coccidian inside a tissue cell.
Young trophozoite, inside a host cell ! mature
trophozoite, undergoes schizogony ! segmenter /
schizont, grows and later causes rupture of the host cell !
releasing the merozoites, which invade other tissue cells
and become young trophozoites again.
This process is repeated until some of the mature
trophozoites differentiate into immature sex cells /
gametocyte (male-microG, female-marcroG) ! mature
sex cells / gametes, undergo union ! zygote, secretes a
cyst wall ! oocyst, which has sporoblast, secretes a cyst
wall ! sporocyst that contains sporozoites. This is
already the mature oocyst form. The sporozoites are
released when the cyst wall ruptures. The liberated
sporozoites invade other host cells and become young
trophozoites.

Isospora belli

Life Cycle
Infective Stage
Small Intestine
Epithelial Cells
Excretion

Human coccidiosis
Worldwide, but rare
Tropical > Temperate
Sexual and asexual
Man
Distal duodenum and proximal ileum

End product
Intermediate
hosts
Definitive
host

Intestinal
sarcocystis
Oocyst
Cattle and pig
Man

Sarcocystis lindemanni
Extra-intestinal sarcocystis
/ sarcosporodiosis
Sarcocyst
Man
Unknown
(possibly carnivores: dog,
cats)

Sarcocystis hominis
Morphology

Oocyst almost identical with that of I. Belli, passed

out in the feces fully developed (oocyst of I. Belli
matures after evacuation in the stool).

Sarcocyst in the skeletal muscle, containing

numerous large round cells called metrocytes or
merozoites, wall is covered with the closely set, thin
villi giving the appearance of being striated.
Life Cycle
-Infective Stage: Sarcocyst from improperly cooked beef or
pork.
-The sarcocyst ruptures in the small intestine to release the
merozoites, which invade the lamina propia of the intestinal
mucosa and initiate the production of gametes. Sporogony
occurs resulting to formation of oocyst that matures and
later evacuated in the feces. Cattle or pig ingest the mature
oocyst and schizogony takes place in the vascular
endothelial cells. Sarcocysts develop in the skeletal and/or
cardiac muscle fibers.
Pathogenesis
-The organisms, while in the sporogony cycle, destroy the
epithelial cells of the intestine.

mature oocyst in food or drinks.

Excystation
Sporozoites ! Trophozoites
Feces (Oocyst: Diagnostic Stage)

*Clinical manifestation, method of diagnosis, and treatment

are the same as in human coccidiosis.

Sarcocystis lindemanni

Pathogenesis
-Confined to the intestinal epithelial cells, the organisms
cause destruction of the surface layer. There is
malabsorption, markedly abnormal intestinal mucosa with
short villi, hypertrophied crypts, and infiltration of the lamina
propia with eosinophils, neutrophils, and round cells.
Clinical Manifestations
-asymptomatic and self-limiting.
-Some mild gastrointestinal distress to severe dysentery
producing pale yellow and foul-smelling stools that may
suggests malabsorption process.

Diagnosis
-Fecal smears: (+) Oocyst
-Concentration procedures (Zinc sulfate), increase the yield
of positive results.
Treatment
-Rest and bland diet may be sufficient for mild or
asymptomatic cases.
-Drugs: co-trimoxazole, perimethamine and sulfadiazine.

Maturation Process and Stages of Development

Disease
Distribution
Infection
Reproduction
Host
Habitat

-Chromic diarrhea ! vague abdominal pain with cramps,

weight loss, weakness, malaise and anorexia. Chronic
diarrhea may be from several months to about 15 years.

-Sarcocysts are found in either skeletal or cardiac muscles,

BUT NOT BOTH.

Morphology
-Sarcocyst several millimeters in length with tapered ends,
spindle-shaped or cylindrical in skeletal muscle, contains
metrocytes that produce and maintain the cyst wall and
generate fusiform merozoites (also called bradyzoites,
cytozoites, or zoites) within the cyst.

COCCIDIA

JC DEDACE (2013 edition)

Life Cycle
-The infection is acquired through the ingestion of mature
oocyst that came from the feces of the definitive host
(presumed to be carnivores such as the dogs and cats).
Excystation occurs in the intestine releasing the sporocyst,
which excyst to release the sporozoites.
-The sporozoites find their way to the vascular endothelium
where they develop into schizonts and produce one or more
generations of merozoites (called tachyzoites). The
merozoites then invade the striated muscle cells and
produce the sarcocyst.
Pathogenesis

Destruction of vascular endothelium

Inflammation of the involved muscle

Release of sacrcocystin from the sarcocyst may result

to hyper-sensitivity reaction

Prevention
-Proper and through cooking of meat
-Environmental sanitation
-Periodic examination of cats feces
-Public education

Cryptosporidium parvum
Disease
Distribution
Infection
Host
Habitat

Clinical Manifestations
-Myositis
-Pain and tenderness of the involved muscle
-Allergic manifestations
Diagnosis
-Biopsy of the sarcocyst
-Periodic Acid Shift (PAS) staining areas of the cytoplasm
will show PAS negative reaction.
Treatment No specific treatment
Prevention of Infection
-Protect uncooked foods from contamination with feces of
flesh-eating animals.

Toxoplasma gondii
Disease
Distribution
Infection
Reproduction
Host
Habitat

Toxoplasmosis
Cosmopolitan
Quite common, the disease is rare
Endodyogeny
Domestic cats
Acute: various tissue
Chronic: CNS
-Endodyogeny ! 2 daughter trophozoites within the parent
cell.
Morphology
Trophozoite
- pyriform or crescent-shaped, one end is more round than
the other with spherical to ovoid nucleus that is usually
nearer the blunt end.
-Tachyzoites are rapidly dividing trophozoites seen during
the acute phase of the infection.
-Bradyzoites are the slow multiplying forms within the cyst.
Diagnosis
-History and physical examination
-Organisms in biopsy material of the lymph node, bone
marrow, spleen, brain and other tissues.
-Detection of the parasites DNA through Polymerase Chain
Reaction (PCR)
-Serologic tests:
"
Complement Fixation Test.
"
Double Sandwich ELISA test.
"
Indirect Immunofluorescent antibody test.
"
Indirect Hemagglutination test.
"
Sabin-Feldman dye test.
"
Frenkel skin test, which is a type of delayed
hypersensitivity reaction

Treatment
- Pyrimethamine and sulfonamides
- Spiramycin

cryptosporidiosis
worldwide
water-borne infection or zoonotic
more common among children than
adults.
Domestic animals
Brush border: stomach, intestine, gall
bladder and the pancreatic duct

Morphology
-Trophozoite and schizont may measure 2 5 micrometers
and are attached to the host cell membrane
-Oocyst has 4 sporozoites but with NO sporocyst.
-Schizont produces 8 falciform merozoites
Life Cycle
-Infective Stage: mature oocysts in foods / drinks.
-Excystation occurs in the upper gastrointestinal tract.
Sporozoites escape from the oocyst and invade epithelial
cells of the GIT. The organisms occupy the apex of
enterocytes within the host cell membrane but NOT within
the cell cytoplasm. Asexual multiplication (merogony)
occurs to produce merozoite, which may invade other cells.
Some of the merozoites undergo gametocytogenesis
resulting to the production of micro- and macrogametocytes,
which when fertilization of the macrogamete occurs will
result to the development of an oocyst that contains 4
sporozoites capable of initiating a new infection.
Pathogenesis Developing organisms destroy the host
cells.
Clinical Manifestations
-Self-limiting among persons with good immune functions
-Nausea and vomiting, and abdominal cramps, weight loss,
and fever among symptomatic individuals.
-Diarrhea is a common presentation especially among
children
-Severe fluid loss due to diarrhea and vomiting may lead to
fatal outcome among children
Diagnosis
-History and PE
-DFS: (+) oocyst
-Duodenal string test (Enterotest) to recover the oocyst
-Modified acid-fast stain of stool samples will show redstained oocyst. Yeast cells stain green.
-Stool samples may be concentrated to increase the yield of
positive results.
-Serologic tests ELISA and immunofluorescence
Drugs for Treatment
-Spiramycin
-Pyrimethamine and sulphadiazine
-Somatostatin

COCCIDIA

JC DEDACE (2013 edition)

Prevention
-Proper personal hygiene
-Proper disposal of human waste
-Environmental sanitation

Prevention
-Early diagnosis and prompt treatment of the patient
-Build-up the resistance of the patient
-Public Education

Pneumocystis carinii
Disease

Interstitial plasma cell pneumonia

/ pneumocytosis
Infection
Airborne infection, transplacental
Habitat
Pulmonary alveoli
*This organism does not have yet a definition classification.
The organisms are small with uncertain affinities to other
organisms but more closely related to fungi.
Morphology
Trophozoite
Cyst

Amoeboid with a single nucleus and the

cytoplasm has vacuoles, granules, and
globules.
Thick cyst wall, usually containing 8
trophozoites (referred to as intracystic
bodies / sporozoites) each with a single
nucleus.

Pathogenesis
-It is NOT an intracellular organism NOR it invades the
pulmonary epithelial cells of the interstitium. It adheres to
the alveolar epithelium by means of its cell wall.
-The presence and multiplication of the organisms in the
lungs stimulate the exudation of serous fluid, histiocytes,
lymphocytes, and plasma cells.
-Interstitial tissues are thickened and are heavily infiltrated
with mononuclear and plasma cells.
-The lungs increase its weight and volume with thickening of
the pleura with consolidation and prominence of interlobular
septa.
-There is immunosuppression or agammaglobulinemia.
-Ventilation is impaired and death occurs due to respiratory
failure.
Clinical Manifestations
-Onset is insidious and with a gradual course.
-Incubation period is about 1-2 months.
-Illness begins with non-productive cough that gradually
progresses to serious loss of ventilatory capacity,
respiratory failure, and cyanosis.
-The physical signs in the chest, moderately deranged, with
temperature that is normal or slightly elevated with normal
or slightly increase white cell count.
Diagnosis
-History and PE
-Demonstration of the organisms in sputum, naso-tracheal
washings, bronchial scrapings, biopsy, or materials
obtained through percutaneous pulmonary needle
aspiration.
-Cysts are best demonstrated by Gomoris methenamine
silver staining. Giemsa or Papanicolaus stains may also be
used.
-Chest X-ray will show symmetrical cloudiness with ground
glass appearance that spread bilaterally from the bila.
Alternating areas of lobular collapse and emphysema may
produce a honey-comb effect.
-Immunofluorescence may also be used for diagnosis
Drugs for Treatment

Trimetophrim sulfamethoxazole

Pentamidine compounds

Trimetrexate and Leucovorin

COCCIDIA

JC DEDACE (2013 edition)