Isospora belli

Isospora belli
Also known as Cystoisospora belli

a spore-forming coccidian protozoan

Disease: Isosporiasis/ Cystoisosporiasis
Morphology
The Isospora belli parasite is 30 micrometers long by 12
micrometers wide.
Immature oocysts are ellipsoid or spindle shaped with
tapered ends.
An undivided mass of protoplasm exists inside the
immature oocysts. This protoplasm divides to form two
sporoblasts. The oocyst forms heavy cyst walls and the
sporoblasts are now called sporocysts. These are 11 by
9 micrometers and within each sporocyst develop four
curved, sausage shaped sporozoites. Throughout the
oocysts development, the sporoblast and sporocysts are
surrounded by a two-layered, colorless, smooth cell wall.

Life Cycle
Immature, unsporulated oocyst
is excreted through feces.
Sporoblast divides into two
Each sporoblast develops into a
sporocyst with 4 sporozoites,
resulting in mature oocysts. The
time spent in stages 1 through 3
is 2-3 days.
Mature oocyst is ingested.
Oocyst bursts. Sporozoites are
released and lodge into the
intestinal lining. Sporozoites
undergo asexual reproduction to
form merozoites. The merozoites
mature into gametes which
undergo fertilization to produce a
new oocyst.
Epidemiology
Humans are the only known host for I. belli.

The

frequency of asymptomatic infection with this
parasite is unknown.

Infection is more common in tropical and
subtropical climates

and in areas of poor
sanitary conditions.

The mode of transmission of isosporiasis is fecal-
oral, ie, through food or water contaminated with
human feces.

Isospora belli has been reported as a cause

of
travelers diarrhea in visitors to endemic areas
and

of institutional outbreaks.

Protracted, foul-smelling, watery

diarrhea is
the most common symptom.

Severity

of infection ranges from self-limiting in
immunocompetent hosts

to life threatening in
immunocompromised patients,
particularly

people with human immunodeficiency
virus (HIV) infection.


Oocysts are passed unsporulated

and require
exposure to oxygen and temperatures lower
than 37C

(98F) before becoming infectious.

Oocysts are resistant

to most disinfectants and
may remain viable for months in a

cool, moist
environment.

The incubation period is thought to be 8 to 10
days.

Symptoms of isosporiasis
watery diarrhea
abdominal pain
anorexia
and low-grade fever.
Treatment
Initial management of patients with intestinal
cystoisosporiasis requires adequate rehydration and
replacement of any deficient electrolytes. A 10-day
course of trimethoprim-sulfamethoxazole is
recommended as the initial antimicrobial treatment of
choice. The alternative regimens of pyrimethamine
(Daraprim) or ciprofloxacin (Cipro) are reserved for
those unable to take trimethoprim-sulfamethoxazole
Control and Prevention
The most effective means of prevention is
improved sanitation standards and practices.
Increased awareness and attention should be given
in areas of higher Isosporiasis occurence and
with immunocompromised patients.

Isosporiasis. Oocysts of Isospora belli also can be stained with acid-fast
stain and visualized by epifluorescence on wet mounts, as illustrated.
Dirofilaria immitis
Heartworm
Taxonomy
Taxonomy
CLASS: SECERNENTEA
SUBCLASS: SPIRURIA
ORDER: SPIRURIDA
SUPERFAMILY: FILARIOIDEA
FAMILY: ONCHOCERCIDAE
Scientific name - Dirofilaria
immitis
Common name - Heartworm

Dirofilaria immitis
Commonly called as
heartworm
a parasitic roundworm that is
spread from host to host
through the bites
of mosquitoes

Primary Definitive Host:
dogs Intermediate Hosts:
may belong to several
species of mosquitos such as
the Aedes, Anopholes, and
Culex.
Morphology
Adults are long, white, thread-
like worms
Females 25 to 30cm long
Males 12 to 16 cm long with
spirally coiled tail
give live birth and the baby
worms are called
Microfilariae
Microfilariae
Sheathless
218 to 329m long
have a long pointed tail

Life Cycle
Geographic Distribution
Worldwide
More commonly
found in tropical,
subtropical and
temperate regions,
particularly humid
areas and river
valleys where
environmental
conditions harbor
the breeding of
mosquito vectors.
Pathogenesis of the Heart
Heavy infections(over 25
worms for a 40 lb dog)
worms begin to back up into
the right ventricle
less blood pumped.
Over 50 worms, the
ventricle is full and the
atrium begins to contain
worms.
Over 100 worms, the entire
right side of the heart is
filled
phenomenon is called
"Caval Syndrome" and
most dogs do not survive it.

Clinical Signs
Affected dogs most often show coughing, and
dyspnea/tachypnea, exercise intolerance, loss of
condition and syncope may also be seen. In
severe cases the pulmonary vessels may rupture,
leading to hemoptysis or epistaxis. There is a
tendency for signs to only manifest during
exercise, and so patients with a sedentary
lifestyle may never show overt disease. Right-
sided congestive heart failure may ensue when
worm burden is high, and signs can include
jugular distension, ascites, marked exercise
intolerance and hepatomegaly. A systolic murmur
is sometimes audible on cardiac auscultation.
Treatment
Adulticide
Melarsomine dihydrochloride (Immiticide

)
Intramuscular injection into lumbar muscles
Complications include thrombosis (clogging) of pulmonary
arteries due to dead worms

Microfilaricide
macrocyclic lactone (ML) anthelminthics, i.e.,milbemycin oxime,
selamectin, moxidectin and ivermectin
Commonly used in heartworm preventative

Entamoeba Hartmanni
E. hartmanni is a
nonpathogen, and
causes no disease.
This small amoeba
is commensal in man,
colonizing the colon. It
is morphologically
identical
to Entamoeba histolytic
a, for which it is often
mistaken. Size and
appearance after
staining are factors in a
correct diagnosis.

Morphology
Both the trophozoite (usual size, 4-12 m) and
cyst forms (usual size, 5-10 m) can be found in
clinical specimens.
Trophozoite
Cyst
Life Cycle
Both cysts and trophozoites of these species are
passed in stool and considered diagnostic (1).
Cysts are typically found in formed stool, whereas
trophozoites (the active stage) are typically found in
diarrheal stool. Colonization of the nonpathogenic
amebae occurs after ingestion of mature cysts in
fecally-contaminated food, water, or fomites (i.e.,
inanimate objects or substances capable of
transferring pathogens) (2).
Excystation (release of the trophozoite from the
cyst) occurs in the small intestine (3)
and the trophozoites migrate to the large intestine.
The trophozoites multiply by binary fission and both
trophozites and cysts are passed in the feces
Life
cycle
Because of the protection conferred by their cell
walls, the cysts can survive days to weeks in the
external environment and are responsible for
transmission. Trophozoites passed in the stool
are rapidly destroyed once outside the body and
if ingested would not survive the gastric
environment.
Mode of Transmission:
Fecal-oral transmission via cyst form; contaminated
food and water

Geographical Distribution:
Worldwide
primarily human-to-human transmission

Treatment:
None

Control:
Improved hygiene, adequate disposal of fecal
waste, adequate washing of contaminated fruits and
vegetables