INFECTIOUS PROTOZOAL DISEASE
Amebiasis Babesiosis
• caused by facultative
parasitic ameba that can
infect human and other
animals including dogs.
• It is characterized by
persistent profuse watery
or bloody diarrhea.
Entamoeba histolytica
– a unicellular eukaryotic
parasite
– resides in the lumen of the
large intestine and cecum.
Amebiasis refers specifically
to E. histolytica infection.
Acanthamoeba castellani,
A. culbertsoni
Etiology – free living specie
– found in fresh water, soil
and sewage.
E. histolytica
The pathogenic trophozoites
inhabit the colonic wall
damaging the intestinal
epithelial cells by secreting
enzymes that
leads in lysis of cells and
disruption of intercellular
connection.
Pathophysiology
Acanthamoeba spp
Upon penetration,
hematogenous spread or
directly through nasal cavity
to the central nervous
system can occur resulting in
amebic
meningoencephalitis.
Replication
Balantidiasis
• A tick-borne protozoal
disease invading the dog’s
red blood cells.
• The severity of the disease
depend on the rate of
anemia that result from
immune-mediated
hemolysis due to damage
caused by piroplasm
(merozoites).
Babesia canis
• B. canis vogeli
– US, Africa, Asia, Australia
• B. canis rossi
– Africa
• B. canis canis
– Europe, Asia
Babesia gibsoni
– worldwide distribution
Theileria annae
– Spain and Europe
The multiplication causes the
rupture and destruction of
rbc (intravascular hemolysis)
leading to anemia,
hemoglobinuria, and
jaundice.
Destruction of the rbc
releases the parasite antigen
triggering immune response
that result to inflammation
and damage to various
organs like liver, spleen,
and lymph nodes.
the babesia parasite invade
the red blood cells by
attaching on the surfaces
where they reproduce
asexually.
Coccidiosis
• is a disease primarily
affecting pigs but can also
affect other animals
including dogs and
humans.
Balantidium coli
– large ciliated protozoa
infecting mainly pigs
The trophozoites
inhabit the colon, producing
cyst that are passed in the
feces. Invasion of layer
between the mucosa and
submucosa result in
ulceration with
hemorrhagic diarrhea.
Cryptosporidiosis
• An enteric protozoal
disease of dogs
primarily affecting
puppies.
• Many species
(Hammondia, Isospora,
and Sarcocystis) infect
the intestinal tract of dog
and appear to be host-
specific.
• The most common
coccidia affecting dogs
is Isospora
Isospora burrowsi
Isospora canis
Isospora neorivolta
Isospora ohioensis
PP: 3 weeks
Paratenic Host: rats, mice
Sporulation: 6 hours in warm,
moist, and oxygenated
conditions but usually takes
7–10 days.
often associated with
concurrent infection and
immunosuppression.
Heavy infections leading to
intestinal damage can
produce decreased nutrient
absorption, loss of fluid
and electrolytes, and,
hemorrhage.
Giardiasis
• A highly prevalent
protozoal disease affecting
a wide range of animals
including dogs and human
with worldwide distribution.
Cryptosporidium parvum
– main specie infecting dogs,
also a zoonotic protozoal
parasite
Large number are excreted
during the patent
period resulting in heavy
environmental contamination.
Infection occurs when
sporulated oocyst are ingested
and sporozoites are released
affecting the epithelial cells
where they multiply asexually.
Infection persist until the host’s
immune response eliminates
the parasite.
Concurrent infection with other
enteric pathogen can lead to
severe diarrhea.
Neosporosis
• An intestinal infection
in dogs caused by
protozoan flagellate
Giardia spp.
• The disease has
worldwide distribution
affecting domestic
animals, and wildlife.
• It is also a common
human infection
Giardia duodenalis
– ( also known as G. lamblia
and G. intestinalis)
– comprised eight
assemblages (A to H) with
some having wide host
range
o assemblage A and B
infects humans and range
of animals),
o C and D infect dogs:
o while other assemblage
have host specificity
Because of the wide host
range of some assemblage
and genotype of G.
duodenalis, between-specie
transmission and zoonotic
transmission from dogs to
their owners is possible.
PP: 3-10 days
No intracellular stages
trophozoites usually live in
the proximal portion of the
small intestine and migrate
down the intestine during the
course of infection,
encysting in the small or
large intestine.
The cysts are passed in the
feces and are immediately
infectious.
trophozoites inhabits the
lumen of the small
intestine and attach to the
brush border of epithelial
cell, causing
malabsorption of sugar,
vitamin B12, folate and
triglycerides
They multiply in the
epithelial cells by binary
fission
Toxoplasmosis
• a disease characterized by
necrosis of nerve tissue
and muscle from cyst
rupture and tachyzoite
invasion in dogs.
Neospora caninum
– a coccidian parasite with
tachyzoite and cyst that
resemble T. gondii under light
microscope
Dogs – act as a definitive
host where sexual cycle
occurs; excrete oocyst in
feces; oocyst sporulate and
is infective after 24h; infective
to dogs and IH
Cattle, horse, sheep, goat
and other wild animals – act
as intermediate host; can
cause bovine abortion and
stillbirth
• It is a multisystemic
disease affecting dogs
and other animal with
cats being the definitive
host.
• Severity of the disease
depend on the organ
affected and of the
injury caused by cyst.
• It has worldwide
distribution.
Toxoplasman gondii
– an obligate intracellular
coccidian protozoa
Immunosuppression or
concomitant illness allows
proliferation of the T.
gondii causing acute
inflammatory response.
In some instances
however, chronically
infected tissue cyst form
to produce low-grade
disease that is not
clinically apparent.
Clinical disease in dogs
with toxoplasmosis are
asymptomatic. Serious
infection occurs
mostly in cats.
the organism spread to
the extraintestinal organs
via blood or lymphatics
lodging to different
organs in the body like the
heart, eye, and central
nervous system causing
focal necrosis of the
affected tissue.
 E. histolytica
– ingestion of cyst through
human feces
– Encystment of trophozoites
seldom occurs in dogs so
transmission from pets
to human rarely occurs.
Transmission
Acanthamoeba spp
– infection through inhalation
of organism from
contaminated water
or colonization of skin or
cornea.
– Fulminating dysentery in
acute case which may be
fatal can progress to
chronicity or resolve
spontaneously.
– Chronic cases – weight
loss, anorexia, tenesmus,
and chronic diarrhea or
dysentery, which may be
continual or intermittent.
– Colitis and severe
dysentery can result in
dehydration and
Clinical Features electrolyte imbalance.
– Disseminated infections –
amebic abscesses,
resulting in more
generalized signs,
including fever, signs of
generalized abdominal
pain, and hepatomegaly.
– May invade perianal skin,
genitalia, liver, brain,
lungs, kidneys, and other
organs.
• Microscopic examination –
colonic biopsies is the
most reliable method.
• Trophozoite in feces –
demonstration using
methylene blue stain
• Elevated WBC, protein,
xanthochromia in CSF –
granulomatous amebic
meningoencephalitis
Diagnosis
– Bite from infected tick from
genus Rhihicephalus and
Dermacentor
– Blood transfusion
– Transplacental
– Acute babesiosis generally
runs a course of ~1 week
or less
– Lethargy
– Anorexia
– Weight loss
– Pale mucous membrane
– Fever
– Splenomegaly
– Lymphadenopathy
– Hemoglobinemia
– Icterus
– GIT signs including
vomiting, diarrhea, dark
feces
– o Renal urologic disease
resulting in renal failure
• CBC – mild to severe
regenerative anemia,
moderate to severe
thrombocytopenia can also
occur without anemia,
variable leukocytosis or
leukopenia.
• Biochemical profile and
urinalysis – mildly elevated
liver enzyme, renal failure
and metabolic acidosis,
bilirubenemia and
hemoglobinuria.
• Microscopic examination –
can be used as a definitive
diagnosis, use modified
Wright’s stain.
• Serological examination –
Immunofluorescent
antibody
• PCR – to test the presence
of Babesia DNA in
biologica sample.
– ingestion of water or feeds – ingestion of oocysts in the – through accidental ingestion – Fecal-oral route – Transplacental – hence – through ingestion of cyst
contaminated with pig’s feces once infective. from contaminated water, – direct contact with infected congenital infection occurs or oocyst.
feces. food and direct contact from animal or cyst – Ingestion of sporulated cyst
infected feces. contaminated environment from dog’s feces or from
• Giardia cyst are tissues of IH
immediately infectious after
excretion and very resistant
to environmental desiccation
that result in increase
environmental
contamination. Increase
humidity favors survival of
cyst.
Clinical signs of hemorrhagic– Diarrhea can be profuse – All clinical cases occur in – Infection may be present – Usually, subclinical infection – In young dogs,
colitis: watery, mucoid or sometimes dogs less than 6 months old without clinical signs and – In young dogs <6 months generalized infection with
– Mucoid bloody diarrhea with blood that can persist for with no breed and sex diagnosed only during o ascending paralysis with o fever
– Chronic weight loss weeks predilection routine fecal checks. gradual muscle atrophy. o weight loss
– Anorexia and dehydration – Both I. canis and I. ohioensis – Can be asymptomatic with – Can be associated with – Litters or individual puppies o anorexia,
– Retarded growth may cause bloody diarrhea and oocyst shedding chronic diarrhea or o develop progressive o tonsillitis,
poor growth. – Small bowel diarrhea steatorrhea, which can be hindlimb paresis o dyspnea
– Isospora burrowsi may not continual or intermittent, associated with o diarrhea and
cause clinical disease. particularly in puppies. polyradiculoneuritis, o vomiting.
– Isospora neorivolta – Feces usually are soft, o myositis – In older dogs,
occasionally causes diarrhea. poorly formed, pale, o muscle atrophy. localized infection with
malodorous, contain – Adult dogs may have neurologic manifestations
mucus, and appear fatty. o encephalomyelitis, including
– Watery diarrhea is o focal cutaneous nodules o inflammation,
unusual, and blood is or ulcers, o seizures,
usually not present in o pneumonia, o tremors,
feces. o peritonitis o paresis
– Vomiting is unusual but o hepatitis, o paralysis
may occur. o myocarditis, o tetraparesis
o sometimes associated
with use of – Involvement of the
immunosuppressive muscular system is also
drugs. apparent.
– Ocular and cardiac
invlovement in dogs are
rare and not clinically
apparent, respectively.
• History of contact with pig’s • Fecal examination – to • Identify oocyst in feces – • Zinc sulfate concentration • CBC, biochemical panel – • CBC – normocytic,
feces and clinical signs demonstrate Isospora spp accomplished by using sugar technique (ZSCT ) – gold nonspecific normochromic anemia
oocyst. and zinc sulfate flotation. standard for diagnosis
• Fecal flotation technique – Stain used for smear is best • Creatinin kinase and AST – • Serum biochemical
may detect B. coli • CBC and biochemical achieved with modified acid • ELISA kits – have false remarkable when there is profile – increased in
trophozoites and cyst panel – reflect fluid and fast oocyst appear orange- negative rate of 31.6% and muscle involvement AST and ALT with
stained using methylene electrolyte loss from red. Negative staining gives high specificity of 95.7% icterus and
green (1 g methylene green diarrhea a clear view of oocyst using • Immunofluorescent hypoalbuminemia
mixed with 1 ml glacial Crystal violet. • Immunofluorescence antibody – from CSF and
acetic acid and 100 ml assay – more sensitive serum • ELISA – IgM and IgG
water) • PCR – not commonly used and specific for detecting and antigen serum
for diagnostic techniques, low cyst numbers even • ELISA – available for titers give the most
• Fresh fecal smear mixed but more sensitive than other with stored feces sample. testing cattle definitive information
with saline can also techniques. from samples. IgM is
demonstrate trophozoites • Direct fecal smear – • PCR – differentiate N. the single serologic titer
• Intestinal biopsy – identify trophozoites and caninum from T. gondii in of choice for diagnosis
demonstrate organism in cyst in feces. CSF and N. caninum from of active infection,
epithelial cells but can Hammondia cyst in feces. elevate 2 weeks
produce false positive result. postinfection. IgG rise 2
to 4 weekspostinfection.
• PCR – samples from
CSF, aqueous humor, or
infected tissue can
differentiate T. gondii
from neosporosis
infection, but not
commercially available.
 Metronidazole – 20 mg/kg, Imidocarb dipropionate –
PO, q12h for 7 days Preferred therapy, can
completely clear B. canis but
not B. gibsoni.
Diminazine aceturate –
efficacy is similar to
imidocarb dipropionate.
Metronidazole,
Clindamycin, Doxycycline–
decreases clinical signs but
Treatment do not clear the infection
Prednisone – used to treat
immune-mediated
component of anemia
Metronidazole – 15-30 Sulfadimethoxine
mg/kg PO q12h for 7 days
Trimethoprim-sulfadiazine
Tetracyclines – 22 mg/kg –TMS can produce
PO q8h for 10 days keratoconjunctivitis sicca in
dogs with reduced Schirmer
tear test.
Amproline – as feed
additive
Usually self-limiting in
immunocompetent animal
Mild diarrhea is treated on
out-patient basis
Paromomycin
- Not approved for use in small
animals.
- Stops oocyst shedding in
dogs and cats.
- Not absorbed from the from
GI tract when intact.
- young animals and animals
with hemorrhagic diarrhea
can possibly cause renal
failure and deafness.
Disinfect using 10%
formaldehyde solution and
5% ammonia to kill oocyst but
require 18 hour exposure.
Febantel-fraziquantel-
pyrantel (Drontal Plus)
–preferred treatment due to
lack of side effects
Metronidazole –efficacious
in dogs but may affect the GI
microflora affecting the
immunologic effect of cell
population in bowel.
Albendazole –at higher
doses it can be potentially
toxic causing
myelosuppression in dogs
o Increase in epithelial
permeability, increased
numbers of intraepithelial
lymphocytes, and activation
of T lymphocytes
Prognosis – poor once
muscle contracture and
ascending paralysis occurs.
Progression of clinical signs
may be arrested with
treatment.
Clindamycin
– 12.5-25 mg/kg PO, IM q12h
for 14 days until signs
plateued.
Trimethoprim-sulfadiazine
– 15-20 mg/kg PO q12h for
14 days until signs plateued.
Pyrimethamine – 1 mg/kg
PO q24h for 14 days
combined with
Trimethoprim sulfadiazine
Clindamycin – 10-20
mg/kg PO, IM q12h for at
least 2 to 4 weeks after
clinical signs are
clear.
Azithromycin
Sulfadiazine in
combination with
pyrimethamine
Trimethoprim-
sulfadiazine combine
with brewer’s
yeast or folinic acid to
correct bone marrow
suppression caused by
TMS.
Prednisolone 1%
ophthalmic drops – 2-3
drops in infected eye q8h
for 2 weeks.

o Trophozoite toxins and T-

cell activation initiate a
diffuse shortening of brush
border microvilli and
decreased activity of the
small-intestinal brush border
enzymes, decreasing the
overall absorptive area in the
small intestine and thus an
Pathogenesis impaired intake of water,
electrolytes, and nutrients.

o Proteins secreted by
trophozoites contribute to
degrading the intestinal
mucous barriers and
disrupting the intestinal
intracellular junctions.

o Reduced activity of lipase

and the increased
production of mucin by
goblet cells lead to
steatorrhea and mucous
diarrhea.