Coccidia

6 Genera of Coccidia Infecting Humans

Toxoplasma
Isospora
Cryptoporidium
Cyclospora
Sarcocystis
Plasmodium
ISOSOPORA BELLI

Intestinal parasite
No reservoir host
Direct infection (feco-oral route); ingestion of food
and drink contaminated with feces containing ripe
oocysts
Infects human and animals
Diagnostic stage: oocyst in stool (immature)
Life cycle: direct with no intermediate host
Mucosal epithelium of small intestine
Diarrhea for few days (self limiting) or chronic
infection persist for months
In immunocompetent host chronic
Number of oocyst passed the stool had to be few
and are lysed
Treatment: Trimethoprim Sulfamethoxazole (TMPSMX)
o
Alternate
drug:
Nitrofurantoin/Primaquine
SO4,
Chloroquine SO4
CYCLOSPORA

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.

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 22C to 32C, resulting in
division of the sporont into two sporocysts,
each containing two elongate sporozoites.
Fresh produce and water can serve as vehicles for
transmission and

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Coccidia
the sporulated oocysts are ingested (in contaminated
food or water) .
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 and
sexual development to mature into oocysts, which will be
shed in stools.
The potential mechanisms of contamination of food and
water are still under investigation.

Infective stage: sporozoite inside the oocyst (round)

Diagnostic stage: unsporulated oocyst
Ingestion of mature oocyst small intestine
asexual sexualproduct: immature cyst

CRYPTOSPORIDIUM

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.
Following ingestion (and possibly inhalation) by a
suitable host,
excystation occurs.
,
The sporozoites are released and parasitize
epithelial cells of the gastrointestinal tract or other tissues
such as the respiratory tract.
,
,
In these cells, the parasites undergo asexual
multiplication (schizogony or merogony)
and then sexual multiplication (gametogony) producing
microgamonts (male)
and macrogamonts (female).
, oocysts produced by fertilization of the macrogamonts
by the microgametes develop that sporulate in the infected
host.
,
Two different types of oocysts are produced, the
thick-walled, which is commonly excreted from the
host
, and the thin-walled oocyst
, which is primarily
involved in autoinfection.
Oocysts are infective upon excretion, thus permitting
direct and immediate fecal-oral transmission.

Sporulated oocysts, containing 4 sporozoites, are

excreted by the infected host through feces and possibly
other routes such as respiratory secretions.

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

Diagnostic stage: thick walled oocyst (immature)

Feco-oral route
Contaminated water reservoirs
C. parvum
o
Infect human
C. felis
o
Immunocompromised and children
o
cryptosporidiosis
C. melgridis
o
Immunocompromised only
Infects epithelial cell lining the GI and respiratory
tract
Immunocompetent persons severe, self-limiting
diarrhea
Immunocompromised (patients with HIV)
generally younger, children increased infection
rate
No treatment self limited
TOXOPLASMA GONDII

Included in TORCH
Reservoir: cats

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Coccidia

Cats are the only definitive host

Reservoir: Man
Tissue cysts or oocyst ingested by cat tachyzoite
released and invade epithelial cells
Human ingest undercooked infected meat;
ingestion of oocyst from fecally contaminated food
Cats shed oocyst for only 1 to 2 weeks resistant to
disinfectants, freezing and drying
Usually asymptomatic
Flu-like illness with cervical LADP
Benign and self-limited
Symptoms resolve within a few months to a year
In
AIDS
patient

TOXOPLASMIC
ENCEPHALOPATHY most common cause of
intracerebral mass
Toxoplasmosis (congenital)
o
Acute primary infection acquired by
mother during pregnancy
Toxoplasmosis of mother
o
Decreased incidence and decreased
sequelae in infant
Prompt and accurate diagnosis is important
Most infants with subclinical infection at birth will
subsequently develop signs and symptoms of
congenital toxoplasmosis
Diagnosis:
o
observation of parasite in bronchoalveolar
lavage
o
isolation of parasites from blood
o
serology
Treatment:
o
Pyrimethamine + Sulfadiazine
o
Spiramycin + Sulfadiazine
o
Spiramycin +Pyrimethamine

Although oocysts are usually only shed for 1-2 weeks,

large numbers may be shed. Oocysts take 1-5 days to
sporulate in the environment and become infective.
Intermediate hosts in nature (including birds and rodents)
become infected after ingesting soil, water or plant
material contaminated with oocysts .
Oocysts transform into tachyzoites shortly after
ingestion. These tachyzoites localize in neural and muscle
tissue and develop into tissue cyst bradyzoites .
Cats become infected after consuming intermediate
hosts harboring tissue cysts .
Cats may also become infected directly by ingestion of
sporulated oocysts. Animals bred for human consumption
and wild game may also become infected with tissue cysts
after ingestion of sporulated oocysts in the environment .
Humans can become infected by any of several routes:
eating undercooked meat of animals harboring tissue
cysts .
consuming food or water contaminated with cat feces or
by contaminated environmental samples (such as fecalcontaminated soil or changing the litter box of a pet cat) .
blood transfusion or organ transplantation .
transplacentally from mother to fetus .
In the human host, the parasites form tissue cysts, most
commonly in skeletal muscle, myocardium, brain, and eyes;
these cysts may remain throughout the life of the host.
Diagnosis is usually achieved by serology, although tissue
cysts may be observed in stained biopsy specimens .
Diagnosis of congenital infections can be achieved by
detecting T. gondii DNA in amniotic fluid using molecular
methods such as PCR .
SARCOCYSTIS

The only known definitive hosts for Toxoplasma

gondii are members of family Felidae (domestic cats and
their relatives). Unsporulated oocysts are shed in the cats
feces .

Carnivorous
Intermediate host = herbivores
Definitive host = parasite is not very pathogenic
Accidental host = MAN
IH brain, muscle, and kidney tissues may be
damaged
Loss of appetite, fever, weight loss, anemia, and
death in severe infection
Gait abnormalities animals move in circles
Cause abortion
Treatment in man is not required

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Coccidia
Oocysts sporulate in the intestinal epithelium and are
shed from the host in feces .
Due to the fragile nature of the oocyst wall, individual
sporocysts may also be detected in feces.

PNEUMOCYSTIS CARNII

Both sporulated oocysts (containing two sporocysts)

and individual sporocysts can be passed in stool.
Sporocysts contain four sporozoites and a refractile
residual body. Sporocysts ingested by the intermediate
host (cattle for S. hominis and pigs for S. suihominis)
rupture, releasing sporozoites.
Sporozoites enter
endothelial cells of blood vessels and undergo schizogony,
resulting in first-generation schizonts. Merozoites derived
from the first-generation invade small capillaries and blood
vessels, becoming second-generation schizonts. The
second generation merozoites invade muscle cells and
develop into sarcocysts containing bradyzoites, which are
the infective stage for the definitive host.

Pathogenesis multiplication in the LUNGS

Stimulates the exudation of serous fluid, histiocytes,
lymphocytes, and plasma cells
Death
Agammaglobulinemia
Insidious onset
Incubation period: 1-2 months
Start as non productive cough
Loss of ventilatory capacity
Temperature is normal
Signs and symptoms
o
WBC normal or slightly elevated
o
(+) Eosinophils
o
CXR symmetric cloudiness with
alternating areas of lobular collapse and
emphysema
o
Honey comb effect
2 forms
o
Trophozoite
o
Cyst
Diagnosis
o
Biopsy
o
Demonstration in tissue and materials and
lungs
o
Demo by GOMORIS methenamine Ag
stain, HE stain, for quick staining:
Toluidine blue
Treatment
o
TMP-SMZ
o
Alternative: Pentamide
Prognosis: Poor

Humans become infected when they eat undercooked

meat containing these sarcocysts.
Bradyzoites are released from ruptured cysts in the
small intestine
and invade the lamina propria of the intestinal
epithelium .
There,
they
differentiate
into
macroand
microgametocytes. Fusion of male and female gametes
results in the formation of oocysts .

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