PROTOZOOLOGY

Protozoa are unicellular animals or organisms in which are performed all functions/activities of life – digestion, nutrition,
respiration, reproduction, excretion, secretion, locomotion. They belong to the animal kingdom. (The other animals which are
multicellular are metazoa). The comparable form of protozoa in the plant kingdom is the prophyta.

Some organisms have characteristics of both plants and animals (kingdom protista). Living things are divided into five kingdoms,
namely:
1. Animalia 3. Monera (algae, bacteria) 5. Protista
2. Plantae 4. Fungi

Differences between prophyta and protozoa

a. Morphology – prophyta have rigid and thick cell wall of
cellulose and nuclear material dispersed in cell (prokaryotic).
Protozoa have non-rigid and twin cell wall allowing marked
variation in size and shape and well defined nucleus
(eukaryotic) enclosed in a membrane.
b. Method of nutrition – protophyta is basically holophytic.
CHO’s are synthesized in the chlorophyll containing
chromotophores (photosynthesis). Protozoa are basically
holozoic. Utilizing preformed food materials derived from
living plants or animals.
c. Method of reproduction – prophyta divide by binary
fission along transverse axis except in ciliates.

STRUCTURE OF PROTOZOA

The two main components of a protozoan cell are the nucleus and cytoplasm.

1. Nucleus – usually single but some with two similar or
dissimilar nuclei.
Roles of the nucleus
1. Controls the life and activities of the cell
2. Stores DNA and RNA
Types of Nuclei
a. Vesicular – with a central body (endosome or karyosome
or nucleolus). It consists of nuclear membrane which
bound the nucleoplasm in which the central body
(endosome (karyosome) or nucleolus) lie. Nucleolus is a
ribosome factory. Nucleolus contains deoxyribonucleic
acid – composed of chromosomes, responsible in the
transmission of hereditary characteristics.
b. Compact or homogenous – little nucleoplasm and
large amount of chromatin distributed throughout the
nucleus. Found in ciliates.
Two kinds Nuclei
a. Micronucleus – controls reproductive function of the
cell/organism.
b. Macronucleus – controls vegetative function of the
organism
2. Cytoplasm – two portions: the outer ectoplasm and the
inner endoplasm.
a. Ectoplasm – is a homogenous and hyaline in
appearance.
b. Endoplasm – contains granules, vacuoles,
pigments, fluids, and organelles.

Cytoplasm is surrounded by the periplast (pellicle in ciliates). Organelles found in the cytoplasm are mitochondria
(powerhouses of the cell that contain enzymes, final stage of respiration takes in). Ribosomes are site of protein synthesis, Golgi
bodies (collected dehydrated proteins). Lysosomes (enzymes for digestion) while Contractile vacuole (responsible for
eliminating of waste materials) and food vacuoles (digestion).

Micron – is the unit for measurement

1 micron = 0.001mm
1000 microns = 1mm locomotion

Protozoa may move by means of Pseudopodia, Flagella, Cilia or by Gliding

1. Pseudopodia (false feet) – these are temporary extrusion of 3. Cilia – fine, short flagella-like structures with axoneme,
cytoplasm, formed and retracted as needed. cytoplasmic sheath and basal granule. May also function as
2. Flagellum/flagella – filamentous structures consisting of a tactile organs and aids in the ingestion of food.
central axial filament (axoneme) and surrounded by a. Ex. Balantidium coli
cytoplasmic sheath. Axoneme arises from the basal body or 4. Gliding – body glides smoothly without locomotory
blepharoplast. In some species the flagellum passes along the organelles
undulating membrane. a. Ex. Toxoplasma, Sarcocystis, Coccidia sporozoites
a. Ex. Trypanosoma sp., Trichomonas sp. and merozoites
 PHYSIOLOGY OF PROTOZOA

Nutrition of parasitic Protozoa

1. Holozoic protozoa utilize preformed food derived from
living animals or plants. Food is ingested by pseudopodia or
ingested either through permanent opening a cytosome or
temporary opening in the body wall. Pinocytosis – ingestion
of nutrient materials through temporary opening in the body
wall. Food vacuole for digestion (ciliates). Some ingest host
tissue cells (amoeba). Some have micropore (micropyle) for
ingestion of fluids or solids.
2. Sporozoic protozoa – absorbs nutrients through the body
wall by diffusing and utilizing directly by the organism.
3. Some are holophytic - Carbohydrates are synthesized on
leaves of chlorophyll carried in chromotophores
4. Autotrophic nutrition – live on organic compounds
Phytoflagellates – proteins, carbohydrates, lipids are
synthesized from organic compounds

EXCRETION OF PROTOZOA

Either thru the body wall (by diffusion) or via the contractile vacuole or water vacuole more important as osmoregulatory organelle:
1. Regulate osmotic pressure within the cell in relation to fluid balance
2. Removal of excess water

Indigestible materials are extruded out by temporary opening or permanent – cytpyge.

Respiration: most protozoa utilize free molecular oxygen for respiration but many derived oxygen by splitting complex oxygen
containing substances in tissue of host.
Reproduction: may be asexual or sexual

A. Asexual ( without male and female involvement)

1. Binary fission – most common method. Each 3. External budding – a small daughter individual is
individual divides into two daughter cells thru the long separated off from the side of the “parent cell” and
axis except ciliates (transverse) grows full size
Ex. Trypanosomes – nucleus divides first followed Ex. Babesia sp.
by cytoplasm Ectopolygent – more than two daughter cells
2. Multiple fission (schizogony) – nucleus divides several are formed by external budding.
times before cytoplasm does. Dividing cells are called 4. Internal budding or endocyogeny
schizonts, daughter cells – merozoites (schizozoites) in Two daughter cells are formed within the mother cell
Coccidia, Plasmodia, etc. and then breaks off destroying it
 Ex. Toxoplasma sp. and Sarcocystis sp.

B. Sexual (involvement of male and female individuals)

1. Conjugation – two individuals come together Ex. Balantidium coli
temporarily and fuse along one of their sides as in 2. Syngamy – two gametes of different sexes fuse to form
ciliates. Their macronuclei degenerate, micronuclei a zygote which then divides by multiple fission to form
divide and one of the resultant haploid pronuclei passes sporozoites
from each conjugant (wandering) into the other a. Isogamy – gametes are similar in appearance
conjugant (stationary) forming a synkarion, then Ex. Babesia sp. In ticks
separate and nuclear reorganization takes place. b. Anisogamy – gametes are dissimilar
Synkarion nucleus divides, macronucleus is formed, Ex. Plasmodium sp. In mosquito
and finally two new individuals are produced from each
cell.

Gametes are produced by special cells known as gamonts or gametocytes. The process is known as gametogony. The process of
forming sporozoites is known as sporogony.
Example: Coccidia
Gametogony Syngamy Sporogony
In plasmodia In the ground
In mosquito

Effects of Protozoan Infection in general

1. Absorb nutrients - Trypanosomes – glucose 4. Destroy tissues - Coccidia – haemorrhage
2. Interfere with normal metabolism – Giardia – absorption of food 5. Destroy blood cells – haemopoetic organs
3. Production of toxin – Sarcocystis – sarcocystin 6. Premunity

CLASSIFICATION OF SUB KINGDOM: PROTOZOA

Protozoa are classified into five phyla according to organ of locomotion

I. Phylum Sarcomastigopora III. Phylum Microspora – produce spores with polar

a. Subphylum Sarcodina – with pseudopodia filament
b. Subphylum Mastigophora – with one or more flagella IV. Phylum Myxozoa – with amoeboid germinal elements
II. Phylum Apicomplexia – produces spores, no organ of in multicellular spores, Trypozoites are multicellular
locomotion V. Phylum Ciliophora – with cilia

Subphylum Sarcodina

Characteristics:
1. Move by means of pseudopodia 3. Reproduction usually by binary fission (any plane)
2. Cytoplasm distinctly differentiated into ectoplasm and 4. Nutrition is holozoic being predatory on bacteria, protozoa
endoplasm and some metazoa

Families:
Family Amoedidae: free living amoeba. Occur in stagnant water/pools, soil, canal, etc. some may become pathogenic
1. Naegleria fowleri – causes “amoebic meningoencephalitis” in man.
Route of infection – intranasally
2. Acanthamoeba culbertsoni – produce meningoencephalitis in mice and monkey if introduce intranasally.
Family Endamoebidae
1. Contains parasitic amoeba which occur in the digestive tract of vertebrates and invertebrates.
2. Multiply by binary fission and form cysts

Genus Endamoeba:
1. Nucleus with well define small endosome (nucleolus)
2. Occurs in vertebrate animals
3. Cysts contain 1-8 nuclei
4. Entamoeba species may be divided into 4 groups according to morphology of mature cyst.
 a. Cysts with 8 nuclei. ex. Entamoeba coli
b. Cysts with 4 nuclei ex. Entamoeba histolytica
c. Cysts with 1 nucleus ex. Entamoeba bovis
d. Cysts with unknown number of nuclei ex. Entamoeba gingivalis

Entamoeba histolytica
This is the only species of importance as a pathogen causing “amoebic dysentery” in man and monkeys. Occurs sometimes in
dogs, rarely in cats, pigs and cattle.

Morphology
1. The active trophozoite stage ranges from 10-60 microns in diameter. Produces long finger-like pseudopodia.
2. Endoplasm contains food vacuoles with RBC, WBC, tissue cells, etc. cysts are spherical ranging from 5-20 microns in
diameter. Cysts are initially uninucleate but finally become tetranucleate with chromatoid bodies and glycogen vacuoles.

Life cycle and Development:

The trophozoite (active stage) multiplies by binary fission in the intestinal tract and liver of the host. Later, they become
sluggish, ceased to feed and start to encyst. Cystic forms are passed out with the feces of the host. The stages are precystic,
uninucleate cyst, binucleate cyst and tetranucleate cyst. The latter represents the mature and only infective form.
Upon ingestion, the tetranucleate cyst encysts in the small or large intestine the newly released metacystic form undergoes
division resulting in the formation of 8 young uninucleate amoebae. In the large intestine, they grow and invade the tissues. Two forms
are recognized – the small and large forms.

Pathogenesis and Clinical signs

1. Only the large form of Entamoeba histolytica is pathogenic.
Small forms are non-pathogenic. Tissue penetration is
brought about by lysis of intestinal epithelium by proteolytic
enzymes, trypsin and pepsin.
2. Following tissue invasion. The amoeba multiply, forming
colonies, penetrate deeper to reach the submucosa and
finally producing ulcer usually in the cecum and colon.
There is usually enteritis with persistent dysentery
(diarrhea), an excess of mucus and blood appearing in the
feces. Frequent attempt to defecate with straining.
3. Amoeba may enter the lymphatic vessels and mesenteric
venules and invade other tissues of the body particularly the
liver, lungs, brain and skin producing amoebic abscesses.

Epidemiology
1. E. histolytica is primarily a parasite of man. Infection is by ingestion of mature tetranucleate cysts.
2. Trophozoites may survive in water at room temperature for 5 weeks. Cysts are transmitted through contaminated food, or
water, raw vegetables by flies.
Diagnosis
1. Finding cysts and trophozoites in the feces, stains with 2. Clinical signs – persistent diarrhea/dysentery with or
hematoxylin without mucus or blood in the feces
Flotation technique – using zinc sulfate solution 3. Fluorescent antibody technique

Treatment (based on human therapy)

1. Etotamide 4. Diloxamide furoate (furamide) 6. Furazolidone
Nimorazole (naxogin) 5. Metronidazole – drug of choice 7. Tetracyclines (chlortetracyclines
2. Fumagillin flagentyl (secnidazole) (flagyl: metroxyn) 2x daily for 5- & oxytetracyclines)
3. Tinidazole (fasigyn) 10 days or more

Control
1. Good sanitation 3. Personal hygiene
2. Proper sewage disposal 4. Avoid fecal contamination of food and water

Other species are usually non-pathogenic: more of a commensal

Entamoeba coli – colon and cecum of man, monkey, dog, pigs Entamoeba gingivalis – mouth of man and dog
Entamoeba canibucalis – mouth of dog Entamoeba equi – horse cecum and colon
Entamoeba suis – digestive tract of pig Entamoeba muris – rat
Entamoeba bovis – digestive tract of cattle Entamoeba caviae – Guinea pig
Entamoeba bubalis (dilimanni) – digestive tract of carabao Entamoeba cuniculi – rabbit
Entamoeba ovis – digestive tract of sheep

SUBPHYLUM MASTIGOPHORA

Order Protomonadina
Characteristics
1. With 1 or more flagella. A few have pseudopodia as well. 3. Reproduction by longitudinal binary fission
Some have undulating membrane. 4. Many are free living and a few parasitic form cysts
2. Nucleus vesicular

Family Trypanosomatidae
1. Many are parasites of insects but others are heteroxenous
(spending part of life-cycle in vertebrate and partly in
invertebrate host)
2. Haemoflagellates are parasitic in the blood, lymphs and/or
tissues of mammals and birds
3. Leaf-like or rounded body with one nucleus and one
flagellum. Undulating membrane present in some genera
4. At least two development stages are undergone during the
life cycle except in a few mammalian forms

Morphology
Developmental stage of Haemoflagellates
1. Trypanosome (trypomastigote) stage – leaf like kinetoplast
post to the nucleus near the posterior end. Undulating
membrane present. Occurs in the vertebrate host but also in
arthropods as infective stage (metacyclic trypanosome) for
vertebrate host.
2. Critidial (epimastigote) stage – leaf-like; kinetoplast anterior
and near the nucleus. Short undulating membrane. Occurs in
arthropods and vertebrate host.
3. Leptomonad (promastogote) stage – leaf-like; kinetoplast
near the anterior end. No undulating membrane. Occur in
arthropods and plants.
4. Leishmania (amastigote) stage – rounded/ovoid kinetoplast
present but without free flafellum. Occurs in the vertebrate
and arthropods. All stages may occur in the culture medium

Only two genera under family Trypanosomatidae are parasitic to domestic animals and man
1. Leishmania
2. Trypanosoma

Genus Leishmania

Characteristics
1. Heteroxenous 4. Leishmania form are found in macrophages, monocytes,
2. Parasite primarily of man, dogs, and rodents polymorhonuclear leucocytes and endothelial cells of
3. Vector and transmitters are sandflies – Phlebotomus sp.
 mammalian host, leptomonads occur in the intestine of sand 6. Round or oval, 2.0-5 x 1.5-2 microns
flies 7. Only the nucleus and kinetoplast are ordinarily visible in
5. All species are morphologically similar. They are stained preparations
differentiated only according to pathogenecity and
geographical distribution.

Life cycle in general

1. Phlebotomus or sand fly ingest infected WBC (leucocytes)
2. Leishmania are liberated in the midgut ----- transform into
leptomonad (promastigote) and multiply repeatedly by
binary fission.
3. Finally leptomonads migrate to the esophagus and pharynx
where they multiply further to the extent that they block the
food canal.
4. When they fly feeds again, it dislodges the plug of
organisms into the vertebrate host.
5. Leptomonads invade macrophages and endothelial cells and
finally transformed into Leishmania which also multiply by
binary fission

Species of Leishmania
1. Leishmania donovani
1. Causes of “kala-azar”, visceral Leishmaniasis or “dumdum
fever” in India, Africa, China, South America.
2. Man and dogs are principal hosts
3. Occurs in the macrophages and endothelial cells of blood
and lymph vessels of spleen, liver, bone marrow, kidneys,
lungs and skin.

Pathogenesis and clinical signs

1. Highly fatal in man 4. Ascites in advance cases
2. The parasite multiply and destroy macrophages and 5. In dogs cutaneous lesions – ulcer and eczema
endothelial cells of visceral organs 6. Mortality rate 75-95% if not treated; death occurring in few
3. In chronic cases marked emaciation and anemia; distended weeks to several years after infection.
abdomen due to hepatomegaly and splenomegaly

2. Leishmania tropica
1. Causes “cutaneous leishmaniasis” or “oriental sore” 3. Cutaneous ulcers may be “dry, moist or wet”
2. Occurs in monocytes, polymorphonuclear, endothelial cells 4. Ulcers usually heal within a year living depressed pigment
of skin of man, dogs and rodents in Africa, Egypt, India, scar
Pakistan

3. Leishmania braziliense
1. Causes “American mucocutaneous leishmaniansis” or 3. Occurs in the macrophages and endothelial cells of skin and
“espundia” in south America, “uta” in the mountains of peru mucous membranes of the nose, lips and pharynx.
2. Host – man, dog, cat, mouse, rats Granulomatous lesions and deformed earlobes
4. Ulcers usually heal in 7-8 months but may last for 20 years 5. In extreme cases, nose, lips, soft palate and surrounding
tissues completely destroyed.

Diagnosis
1. Demonstrations of organisms from biopsy samples of 3. Culture of biopsy specimens on NNN medium (blood agar
spleen, bone marrow, lymph nodes, liver. medium with locke’s solution)
2. Stained scrapings from periphery of skin ulcers and 4. Formol-gel test
eczematous areas. 5. Urea stilbamide test

Treatment
1. Antimony compounds 3. Nostibosan, solustibosan 10-12 4. Stilbamide
2. Tartar emetic I.V. for 25-30 days days

Prevention
1. Control sandflies D.O.T., gammexane 2. Treatment of infected dogs, human cases 4. Control rodents
3. Destroy stray dogs

Genus Trypanosoma
1. Heteroxenous 4. Transmission
2. May undergo four stages of development: trypanosome a. Cyclical by arthropods
stage occurs usually in vertebrate host b. Mechanical by arthropods
3. Some are monomorphic, others polymorphic c. Both cyclical and mechanical

Trypanosoma species

The genus is divided into 2 sections on the basis of morphology and life-cycle
Section 1: salivaria (anterior station group). Transmission is thru insect bite
Section 2: stercoraria (posterior station group). Transmission is thru insect fecal contamination of wound/mucous membrane

Section 1: Salivaria group

Morphology
1. Kinetoplast small, terminal or subterminal in position 4. Undulating membrane varies in development
2. Blunt posterior end
3. Free flagellum may be absent

Biology
1. Trypanosome stage continue to multiply by binary or
multiple fission in the vertebrate host
2. “Metacyclic trypanosomes” occur in the “anterior station”
of the arthropod intermediate host (Glossina sp.) and 3.
transmission is by inoculation or insect bite. Metacyclic
trypanosome are the infective stage (smaller than those
found in the vertebrate host).
Often highly pathogenic
4. Some species under this section are transmitted Example: T. evansi and T. equinum spp., T.
mechanically only (non-cyclically) equiperdum by coitus

Section 2: Stercoraria (posterior station group)

Morphology (general)
1. Kinetoplast large and not terminal in position 3. Free flagellum present
2. Posterior end tapering 4. Undulating membrane not well developed

Biology
1. Multiplication in the vertebrate host may occur in 2. Posterior station development in the arthropods and
trypanosome, critidial or leishmanial forms (T. cruzi). transmission is by contamination with feces containing
Reproduction is usually with the criditial and leishmanial “metacyclic trypanosome” or trypomastigotes.
forms. 3. Often non-pathogenic

Pathogenecity of trypanosomes in general

1. Pathogenecity of trypanosomes varies with the species, strain and type of final host.
Ex. In South Africa trypanosomes are generally not pathogenic to wild game animals which serve as reservoir hosts.
In asia, T. evansi is not pathogenic to cattle and water buffaloes but highly pathogenic to horses.

Clinical manifestations
1. Trypanosomiasis is usually a chronic disease characterized
by intense anemia and emaciation. The usual clinical signs
are interminent fever associated with accumulation of
parasites in the blood (paroxysym of parasitemia). As the
disease progresses, the number decreases and the clinical
signs disappear except progressive loss of weight in spite of
good posture and fairly good appetite. Edema of the
subcutaneous tissue may be marked.
2. Tissue invasion - Some trypanosomes may be markedly
invasive, it injures the wall of the blood capillaries, invades
the bone marrow causing anemia. Heart muscles may be
attached causing cardiac disturbances. It may also cause
nerve lesions and capillary embolism.
3. Blood changes - The most noticeable pathological change is
progressive anemia which is due to failure in production
rather than destruction of the RBC. As the disease
progresses, there is hypoglycaemia due to exhaustion of
glucose glycogen reserves.
4. Cause of death - One theory is that in severe infection, there
is decrease in blood sugar accompanied by increased lactic
acid concentration in the blood. The increase lactic acids
causes asphyxia by interfering with the absorption of
oxygen by the haemoglobin. Another theory is that
destruction of the glucose throws a stain on the liver which
results in liver disfunction and a resulting toxaemia.

Transmission
1. Sucking flies: 2. Coitus – Trypanosoma equiperdum
a. Mechanical – tabanids – Trypanosoma evansi 3. Intrauterine
b. Cyclic – tsetse flies – Trypanosoma brucei 4. Milk/colostrums
5. Ingestion of infected blood organ
− feed contamination – Trypanosoma
6. Needly passage: blood transfusion
theileri

Section Salivaria (anterior station forms)

a. cyclically transmitted forms
b. mechanically transmited forms

A. cyclically transmitted forms

1. Trypanosoma vivax 2. Trypanosoma uniforme 3. Trypanosoma. congolense

Hosts:
Principally ruminants (cattle, buffaloes, sheep, goats) but all other animals are affected, wild game animals act as reservoir.
Distribution – Africa, Central and South America
Transmitters – tsetse flies (Glossina morsitans, G. palpalis, G. tachinoides)
Pathogenecity – mild diseases in cattle, sheep, goats
In horses – chronic course; low/depress spirit (nagana), anemia, weakness, Emaciation, edema of subcutaneous tissues
and swollen lymph nodes

Diagnosis – 1. lymph nodes smear 2. blood smear

4. Trypanosoma simiae – polymorphic
5. Trypanosoma suis – monomorphic
Host: pigs, warthogs, camel
Distribution: Africa
Transmitter – tsetse flies (Glossina sp.)
6. Trypanosoma brucei

Morphology - Polymorphic (slender, stumpy and intermediate forms)

Undulating membrane – conspicuous
Distribution: Africa
Host – horses, mules, donkeys, camel, dogs, sheep and goats are very susceptible
Causes fatal disease known as “nagana”
Cattle and pigs are resistant
Transmitter – cyclically by tsetse flies (Glossina palpalis and G. moritans) also mechanically by biting flies (Tabanus and Stamoxys)

Pathogenecity:
1. Causes severe disease in equine, may cause death in 4-8 2. Important signs – anemia, lethargy, dullness, prostration:
days after infection, but usually 2 weeks to few months (nagana) loss of condition, muscular stiffness, unsteady gait,
corneal opacity and edema of the legs and abdomen.
Diagnosis:
1. Blood smear: thick smear in chronic form a. Causes Rhodesian or African sleeping
2. Lymph node smear sickness in man
3. Mouse inoculation – may be patent in 3-4 days b. Human trypanosomiasis
7. Trypanosoma gambiense c. Affects wild and domestic animals
Causes “Gambian sleeping sickness” in man or (zoonotic)
human “trypanosomiasis” d. Transmitted by tsetse flies
Morphology: similar to T. brucei e. Morphology similar to T. brucei
Transmitted by tsetse flies f. All the species transmitted by tsetse flies.
Host – man in Africa Development occurs in the midgut and
8. Trypanosoma rhodesiense proboscis

B. Non-cyclically or mechanically transmitted forms

A. Trypanosoma evansi
Morphology: a. monomorphic
b. kinetoplast – subterminal
c. undulating membrane – well developed
d. free flagellum well developed

Hosts: horse, dogs, camel, carabao, cattle, pig, cat, other mammals
Distribution – widely distributed in the far east, near east, Philippine, central and south America, Indian subcontinent.

Transmission:
Mechanically by Tabanus sp. (Stomoxys, Haemotobia, Lyperosia spp) because of their interrupted feeding habits. Dogs may be
infected by ingestion of infected blood or organs.

Pathogenecity and Clinical Manifestations:

1. The most severe disease occurs in horses, camel and dogs.
This is the most pathogenic protozoan parasite of horses in
the Philippines. The disease in horses is called “surra” a
hindu word meaning “rotten”. It is always fatal if not
treated. The most common signs are anemia, emaciation in
spite of fairly good apetite, edema of the legs and lower
parts of the body (breast and abdomen). Intermittent fever,
weakness of the hind quarters, dullness, prostration,
droopiness and sometimes stiffness of one or both legs.
Urticarial plagues may appear in the neck and flanks which
may necrose in the center.
2. In cattle and carabaos, occasional outbreaks may occur. In
acute cases animals may die suddenly following stress even
in apparently healthy animals with blood teeming with
trypanosomes. In the bull, there may be edema of the
scrotum and loss of condition even if kept in good pasture.
In general, cattle and carabaos carry the organisms without
showing any clinical signs hence they serve as reservoir
host. During summer when pasture is dry, cattle may
succumb to infection.
3. On post-morthem, the important gross lesions are enlarged
spleen and lymph nodes, anemia, emaciation, congested
liver, kidneys, etc. in pig – chronic form. In dogs – T. evansi
is highly fatal causing emaciation, weakness, and edema but
may run a chronic course, 6 months or more. In camel, it is
a chronic course which may last for 3 years or more
characterized by emaciation. In Sudan they call it “gufar”.
4. In elephant “surra” is a chronic type characterized by
emaciation and weakness. In Panama it is called “murina” in
 horses, and in Venezuela, “derrengadera” in horses;
Philippines – “Bayawak” in horses.

Diagnosis
1. Clinical signs
2. Blood smear examination in acute form – direct smear;
stained smear
3. Biotest or laboratory animal inoculation in chronic type – 2-
5cc of blood to rats I.P. 0.5-1ml in mice I.P. guinea pig,
rabbits more blood IP to cat and dog
4. Serologic tests
a. mercuric chloride test – consist of adding one drop
of suspected serum to 1ml of a 1:30,000 solution of
mercuric chloride in distilled water. A white
opalescence indicates infections of one or more
month standing

B. Trypanosoma equinum
Monomorphic
Similar to T. evansi except the axoneme arises from the small blepharoplast.
Distribution – central and south America
Hosts – chiefly equines, being most seriously affected causing “mal de caderas” (bad hind quarters)
Transmission - Mechanical by Tabanus, Stomoxys and Lyperosia spp

Pathogenecity
1. Causes emaciation, marked weakness of the hind quarters “ 2. In post-morthem, the spleen and lymph nodes are enlarged
mal de caderas” resulting in staggering gait. Finally animals and cadaver is extremely anemic.
become recumbent and die in few weeks; 2-6 months in
chronic form. Causes high mortality in equines.

Diagnosis
1. Blood smear emacination – direct, stained 2. Lab animal inoculation – dogs, cats, rabbits, mouse, rats

C. Trypanosoma equiperdum
Causes a veneral disease called “dourine” (Arabic term for “unclean”) or “mal de coit”
Morphologically identical to T. evansi
Distribution – Asia, north and South America, south eastern Europe
Hosts – horse and ass

Transmission
1. Usually through coitus 3. Contamination of mucous membrane
2. Rarely by biting flies

Clinical signs: the Disease progresses thru 3 distinct phases following incubation period of 2-12 weeks or several months
I. Stage of edema May persist for few hours or 3-4days, then disappear but may
Mucoid vaginal or urethal discharges, or a degree of reappear again. Plaques are almost pathognomonic of
nymphomania, mild fever, with edema of genitalia, chest and “dourline” or “mall de coit”
belly. III. Paralysis
II. Urticarial phase Muscle of the face and nostrils are usually affected followed
Appearance of edematous “plaques” under the skin. Plaques with complete paralysis and recumbency then death. Mortality
are circumscribed, 1-4 inches in diameter (“dollar spots”) is 50-70% if not treated.
since they appear as if a silver dollar is inserted under the skin.

Diagnosis
1. Clinical signs 4. Laboratory animal inoculation
2. Parasite not readily detected in the blood 5. C.F test
3. Examination of vaginal and preputial discharges or fluids
of urticarial plaques

Section stercoraria (posterior station forms)

Transmitted by contamination with feces. Not very pathogenic. Does not multiply fast.

A. Trypanosoma theileri may interfere with surra diagnosis. It is bigger than T.

Hosts – antelopes, cattle, carabaos, buffaloes
Distribution – in the Philippines
Transmitted – clinically by Tabanus sp., Haematopota sp.
Has been associated by “turning sickness” in
Uganda, associated with abortion, and decrease milk yield
evansi. 65% prevalence in cattle and carabaos on culture.
Negative on mouse test.
Blood concentration technique – microhematocrit
 Transmitted cyclically by rat flea – Ceratophilus fasciatus
B. Trypanosoma melophagium – sheep common in P.I.
- cyclically transmited by Melophagus ovinus or
sheep ked D. Trypanosoma canorini – monkeys, rats, common in P,I
- Intermediate hosts – Triatoma or kissing bugs
C. Trypanosoma lewisi – rats

E. Trypanosoma cruzi
Causes “chagas disease” in man
Distribution – south America
Morphology: cresent-shaped
Kinetoplast usually large

SUBTERMINAL
Host: Man
Reservoir: dog, cat, pig, foxes, monkeys, opossums, armadillo
Transmitter: Cyclically by Triatoma sp.
Infection is thru contamination of wounds, m.m., nearly the eyes or lips
where they usually feed.

Clinical signs:
1. Edema at the site of bites 4. Affection of the heart result in degeneration of cardiac
2. Death may occur in 2-4 weeks in acute form in children muscle, central nervous involvement in others
3. Chronic form in adult is characterized by debility, anemia
and splenomegaly

Diagnosis:
1. blood smear in acute form 3. “Xenodiagnosis”: Feeding Triatoma on the suspect or
2. chronic form- sub-inoclutation to guinea pigs allowing bugs to feed on patient blood. Laboratory-
reared Trypanosoma cruzi- free bugs are used. Then
 examinations of the bug 7-10 days post-feeding 4. Complement Fixation Test (C.F.T.)
metacyclic trypanosomes are present in feces or in 5. Culture media
digestive tract.

Avian Trypanosomes
1. Trypanosoma avium- birds 2. Trypanosoma gallinarum- chickens 3. rypanosoma. calmetti- ducklings
Other species reported in Philippines
1. Trypanosoma chattoni- frogs 2. Trypanosoma miyagii- frogs 3. Trypanosoma palawanense- rat
Treatment of Trypanosomeiasis

Trypanosomicidal drugs may be curative or prophylactic in 3. Antrycide

nature. a. antrycide methyl sulfate
1. Tartar emetic (old treatment)- 1 gram in 20-35 ml saline 3 mg/kg in 10% solution, sub-cutaneous
solution given I.V. 6-8 times at weekly intervals. b. antrycide chloride (prosalt)
Necrosis may occur if the drug leaks from the vein 12 mg/kg protection – 70 days
2. Suramin (Naganol)- 7-10 mgs/kg in 10% solution. I.V. 4. Ganaseg- 2-4 mg/kg, body weight of a 5% solution,
Single dose or in divided doses for 3 weeks. To T. intra-muscular berenil
evansi, 1-2 grams/100 kgms B.W. 5. Trypamidium (Isometamedium)- 0.5-1 mg/kg, body
weight, intra-muscular/ intravenous

In the control of Trypanosomes, the following factors should be considered:

1. Drug resistant strains- recurrence after treatment 4. Mechanical transmitter- Tabanus, Lyperosia and Stomoxys
2. Reservoir hosts- wild game animals, domestic animal in the 5. Feeding of infected raw blood/organs, most probable cause
case of some Trypanosomes of infection in dogs with T. evansi
3. Interior host- Tsetse flies (Glossina morsitans, G. palpalis, 6. Mass vaccination- use of different needles
G. tachinoides), kissing bugs, Triatoma sp.; shepherd (M. 7. Blood transfusion
ovinus), etc.

Order Polymastigida
Characteristics:
1. 3-8 flagella 3. One or two axostyles present 5. Cysts are produced in some forms
2. One or more nuclei 4. Multiply by binary fission

Family Trichomonadidae
Morphology:
1. Pyriform in shape 3. One posterior flagellum 5. Cysts are not formed
2. 3-5 anterior flagella 4. Undulating membrane 6. One nucleus, one axostyle

Genera: Tritrichomonas- 3 anterior flagella

Trichomonas- 4 anterior flagella
Pentatrichomonas- 5 anterior flagella

Genus Tritrichomonas

Tritrichomonas foetus- occurs in the genital tract of cows and in the preputial cavity of bulls. It causes a venereal disease known
as bovine trichomoniasis which is characterized by infertility, pyometra and abortion.

Morphology:
1. 15-25 μm in size 2. 3 anterior flagella, one posterior 3. undulating membrane runs the whole length of
flagellum the body

Clinical Signs:
1. Early signs are vaginitis and periodic mucopurulent vaginal
discharge. Purulent endometritis, there may be prolonged
anestrus with pyometra due to early death of the fetus. Fetus
may not be expelled but macerated.
2. Placentitis frequently develops resulting in the detachment
of the placental membranes and death of the fetus. This
leads to abortion which is typically early (not later than the
16th week after service). If abortion occurs too early (1-2
 weeks after service) fetus and membranes may be expelled mount the female. As the condition becomes chronic, pain
unnoticed. and swelling disappear.
3. In the bull, the signs are slight swelling of the prepuce, pain
during micturition or service and the bull may refuse to

Transmission:
1. Coitus 3. Instruments, hands, gloves during veterinary examination
2. Artificial insemination

Epidemiology:
Once the bull is infected, it should be regarded as permanent source of infection (carrier). In the cows, however, the disease is
self-limiting or self-cure (parasite may disappear completely and may conceive without fear of abortion later).

Diagnosis:
1. Herd history. Trichomoniasis should be suspected when: Close orifice, massage, collect, centrifuge
a. Cow requires several services and examine sediment.
b. Failure to conceive Organisms present intermittently- repeat
c. Early abortion examination as necessary. 3 negative
d. pyometra result.
2. demonstration of organisms from the following: 3. Serological test
a. stomach of aborted fetus a. Blood agglutination test- blood mixed with antigen
b. amniotic fluid (T. foetus culture)
c. discharges following abortion b. Mucus agglutination test- mucus from vagina is
d. washings from vagina mixed with glucose saline – diluted- mixed with
e. mucus from anterior end of vagina (most abundant suspension of T. foetus ---- + agglutination
14-18 days after service/infection) 4. Culture in diamonds media or beef extract glucose- peptone
f. preputial washings serum (BGPS)
Introduce 100 cc of saline solution or 5
dextrose in saline into the preputial cavity.

Treatment:
1. Washing with either 4-5% sodium perborate or 1-3% lugols 4. Sodium Iodide- given at the rate of 5 grams/100 lbs body
or chlorine solution weight. Intra-venous; 5 consecutive doses at 48 hours
2. Application of 1% acriflavine solution or ointment to the intervals (given concurrently with local treatment)
penis of preputial sheath injected into the urethra 5. Dimentridazole P.O./I.V. or injected into the urethra in bull
3. Ganaseg 1% SOLUTION. Introduce 100-150 ml to the
preputial cavity. Let it stand for 15 minutes. Massage
thoroughly

Prevention:
1. slaughter of infected bulls and cows (carriers) 3. use of clean bulls for A.I.. T. foetus may survive in frozen
2. avoid practice of communal bull semen.

Tritrichomonas suis- gastro-intestinal tract and nasal passages of pigs

Tritrichomonas equi- cecum, colon of equine

GENUS Trichomonas

Trichomonas gallinae
Causes “avian trichomoniasis” of upper intestine of pigeon in particular. Chickens, turkeys and other birds may be affected. It
causes a serious disease of pigeons.

Morphology:
1. pyriform 3. with 4 anterior flagella 4. V.M. ends at about 2/3 of the
2. 5-10μ in size body

Symptoms:
1. great majority of pigeons (80-90%) 3. acute outbreaks may occur in squabs characterized by
2. may carry T. gallinae without showing signs weakness and death
Pathogenesis:
The earliest visible lesions are yellowish nodules which increases in size until the mouth, eosophagus and trachea are blocked.
Nodules are also found in the crop and proventriculus. Nodules contain caseous materials “yellow buttons” filled with T. gallinae.
Pigeons become emaciated due to failure to ingest feed.
a. “pigeon’s milk” b. Contaminated drinking water c. Contaminated feed

Diagnosis:
a. Occurrence of characteristic nodules in the mouth cavity, b. Demonstration of organisms from mouth and crop
esophagus and crop contents or caseous materials

Treatment:
1. Enheptin- 30mg/kg daily for 7-14 days 3. Furazolidone- 25-30 mg/day for 7 days. Carrier adults
2. Dimetridazole should be treated

Trichomonas gallinarum- occurs in lower intestine and liver of chickens in particular. May occur in other birds.

Morphology:
1. pear shaped 3. 4 anterior flagella
2. 6-8 μx 9 x 12μ 4. posterior flagellum ends at about the same point as the tip
of the axostyle

Symptoms:
As a rule, it is not very pathogenic
Liquid pale yellow diarrhea
Nuffled feathers, loss of weight, loss of appetite

Pathology: Trichomonas gallinarum produces circular necrotic lesions of the liver similar to histomoniasis. Lesions have irregular
outline and raised surfaces.

Transmission: Ingestion of contaminated feed and water

Treatment:
1. Enheptin (2-amino-5-nitrothiazole) 2. Furazolidone- 25-30 mg/kg with the feed
0.1% of the feed

Other species:
Trichomonas anseri- ceca of geese Trichomonas tenax- mouth of man, monkeys (between gum and
Trichomonas anatis- ceca of duck teeth). Most commonly associated with dental disorders and
Trichomonas ovis- cecum of sheep pyorrhea
Trichomonas felistomae- mouth of cat Pentatrichomonas hominis -5 anterior flagella. Intestine of man,
Trichomonas canis- intestine of dog monkeys, gibbon and other animals
Trichomonas vaginalis- vagina, prostate and urethra of man.
Laboratory animals causes vaginitis
FAMILY HEXAMITIDAE
General Characteristics:
1. binucleated without undulating membrane 4. reproduce by binary fission
2. 8 flagella produce cysts
3. 2 needle-like axostyles

Genus Hexamita
Hexamita meleagridis- small intestine of turkeys, causing a condition known as Hexamitiasis or Catarrhal enteritis

Morphology:
1. pyriform 4. 6 anterior flagella 7. multiply by binary fission
2. bilaterally symmetrical 5. 2 posterior flagella 8. moves very rapidly
3. 2 nuclei 6. 2 axostyles 9. cyst is formed with fibrils

Symptoms:
1. a disease particularly of young turkeys 3. affected birds appear nervous, depressed, ruffled feathers with foamy,
2. mortality may reach 80% watery diarrhea
4. loss of condition, dehydration and death

Pathology: Catarrhal
• inflammation of the intestine
• intestinal contents are thin, watery and foamy

Diagnosis:
1. demonstration of organisms in freshly killed birds 2. organisms are difficult to demonstrate in birds 1-2 hours after death

Treatment:
1. Furazolidone- 50 mg/lb of feed 4. Nithiazide- 0.02% of drinking water
2. Oxytetracycline- 25 mg/lb feed 5. Enheptin- 30 mg/kg body weight for 7 days
3. Chlortetracycline- 200 mg/lb feed

Prevention:
1. raise young poults away from adults 3. treatment of carrier adults
2. general cleanliness

Hexamita columbae - pigeon

Genus Giardia

Giardia lamblia (intestinalis)- occurs in the small intestine of pig, monkey and man causing a condition known as “giardiosis”.
Common in Philippine Island.

Morphology:
1. bilaterally symmetrical
2. pyriform
3. with 2 nuclei
4. 2 axostyles
 5. two well developed sucking disk
6. 8 flagella
7. convex dorsally and concave or flattened ventrally

Symptoms:
1. most cases are asymptomatic
2. chronic diarrhea
3. there may be large amount of mucus in the feces but no blood

Pathogenesis: Diarrhea and dysentery

Diagnosis:
1. demonstration of trophozoites and cysts in the feces

Treatment:
1. Atabrin, quinacrine 2. Chloroquin 3. Camoquin 4. Metromidazole

Giardia canis- dogs, Philippine Island

G. cati- cats
G. bovis- cattle
G. caprae- goats

ORDER RHIZOMASTIGIDA

General Characteristics:
1-4 flagella with pseudopodia

FAMILY MASTIGAMOEBIDAE
Genus Histomonas
Histomonas meleagridis
• Occurs in the liver and ceca of turkeys, chickens, quail, pheasant peafowl, partridge
• A serious disease of turkeys causing a disease known as “histomoniasis”, enterohepatitis or “black head”

Morphology:
1. pleomorhic 7. cysts are not formed
2. 8-15μin diameter 8. reproduce by binary fission
3. one nucleus 9. in the lumen of the ceca, it has 1-4 flagella
4. large endosome 10. in the liver and cecal tissue, they are actively amoeboid with blunt rounded
5. no axostyle pseudopods (no flagella)
6. no undulating membrane 11. may occur singly or in cluster

Transmission:
• Infection is either direct by ingestion of infected feces or indirectly through ingestion of infected Heterakis eggs or infected
earthworms. (Heterakis are cecal worms, Histomonas are attracted by the developing heterakis ova, becomes enclosed by the egg
shell. Earthworms can transmit Heterakis eggs with Histomonas)

Epidemiology:
• Chickens are important reservoirs • Earthworms may harbor Heterakis eggs with Histomonas
• May carry the organisms without showing signs for long period
• Infected Heterakis eggs may survive in soil for 1-2 years

Symptoms:
1. combs and wattles may become cyanotic (black head) 3. vent smeared with sulfur yellow feces
2. sulfur-yellow droppings 4. droopiness, ruffled feathers, loss of appetite

Pathogenesis:
• In the liver, characteristics are circular, depressed, yellowish • It is more of a disease of young turkeys 3 to 12 weeks of age
areas of necrosis (the various sizes of a 50 centavo coin) one • Chickens are resistant
to three cm. occur • Losses 50-100%
• These are the pathognomonic lesions: the ceca ulceration
and neorosis of the cecal wall which become thickened,
containing yellowish caseous exudate.

Diagnosis:
1. Clinical signs, sulfur-yellow droppings is very suggestive 3. Histologic examination of liver and cecal section and
2. Pathological lesions, necrotic lesions of the liver and finding organisms
cecum

Treatment:
1. furazoline 3. carbasone 5. dimetridazole, ronidazole
2. enheptin 4. nithiazide

Prevention:
1. do not raise turkeys with the 3. pasture rotation at regular 6. raise turkeys on wire floorings
chickens intervals 7. continuous medication with the
2. remove droppings regularly 4. elevated waterers and feeders feed with the above therapeutic
5. phenothiazine with the feed agents

Phylum Apicomplexia
Class: Sporozoa
• no organ of locomotion except in the gamete stage a. asexually by binary fission or multiple fission
• produces oocysts, spores and sporozoites (Schizogony)
• reproduced: b. sexually by gametogony/syngamy and
sporogony

Subclass: Coccidia
• parasites of the epithelium of the digestive tract and related organs chiefly of vertebrates

Two important families:

1. Family Eimeriidae
2. Family Sarcocystidae

FAMILY EIMERIIDAE

Schizogonic, gametogonic and syngamy take place in one and the same host. Sporogony occurs outside the host. No intermediate host.

A macro and microgametocyte develop independently. One macrogametocyte develops into one macrogamete while one
microgametocyte develops into several microgametes.
A zygote is formed by the union of one macrogamete and one microgamete. The zygote secretes membrane (cyst wall) around itself
and becomes an oocyst. By a process known as sporogony, a variable number of spores or sporocysts are formed. Sporozoites are
produced in each spore/sporocyst. The different gene5ra of the Family Eimeriidae are differentiated by the number of spores or
sporocysts and sporozoites in each sporulated oocysts.

Six genera of veterinary importance are the following:

1. Cryptosporidium 4. Eimeria
 No sporocyst or spore  4 sporocysts
 4 sporozoites  2 sporozoites in each sporocyst
2. Tyzzeria 5. Wenyonella
 No sporocyst or spore  4 sporocysts
 8 sporozoites  4 sporozoites in each sporocyst
3. Isospora 6. Klossiella
 2 sporocysts or spores  No spore
 4 sporozoites in each sporocyst  Produce sporoblast/sporozoites
Life cycle of Coccidia in general:
The asexual phase (Schizogony) starts with the trophozoite, a round or oval body inside a tissue cell. The trophozoite
enlarges, nucleus divides into several nuclei which leads into the formation of a schizont. Each nucleus acquires a small portion of the
cytoplasm resulting in the formation of spindle-shaped and motile merozoites. Affected host tissue cell ruptures releasing the first
generation merozoites.

Some merozoites invade other tissue cells and repeat the process of schizogony producing second generation schizonts. This
process may be repeated several times.
As a possible response to developing immunological reaction, some merozoites become differentiated into male and female
forms and the sexual phase of the life-cycle is initiated. The sexual forms are known as gamonts or gametocytes. The male form
(microgametocyte), divides into several motile microgametes while the female form (macrogametocyte) develops into a single
macrogamete. One microgamete fertilizes a macrogamete to form a zygote. The latter secretes a cyst wall and becomes oocyst. The
oocyst is extruded from the host tissue and pass to the outside with the feces. This is the resistant stage in the life cycle.

In the ground, the oocyst sporulates (sporogy) to form sporoblast which latter develops into sporocyst or spore. Sporozoites
are formed inside each sporocyst. In Eimeria, 4 sporocysts or spore develop, each with 2 sporozoites. In Isospora, 2 sporocysts each
with 4 sporozoites are formed.
Sporulated oocysts are infective. Infection is through the ingestion of sporulated oocyst with contaminated feed and water or
feces. In the intestinal tract, the oocyst exists and the sporozoites are released. Sporozoites enter epithelial cells (host cell) and the
schizogonic process is repeated.
Pathogenesis:
Depends on:
• number of Schizogonic generations • number of merozoites • type of host cell affected
• size of infective dose • host resistance

Destruction of the host cells leads to:

1. Diarrheal enteritis with or without 2. Discharge of large amount of 4. Poor feed conversion
bloody droppings mucus 5. Weakness, emaciation, anemia
3. Poor weight gain, stuntedness 6. death

Immunity:
Specific resitance to reinfection is characteristic of Coccidiosis. In chickens, resistance to further infection begins to develop sometime
after exposure. In layers, mild gradual exposure to Coccidia is necessary to produce immunity.

Epidemiology:
In general, adults are resitant to Coccidiosis, young stock are highly susceptible. Infective (sporulated) oocysts are resistant and can
survive long period of time. Transmission is thru water and feed contamination. Mechanical vectors are flies, beetles, rodents, man and
animals.

Diagnosis:
1. Clinical manifestations 2. finding large number of oocysts in the feces 3. pathognomonic lesions on autopsy

Treatment:
I. SULFONAMIDE PREPARATIONS II. COMMERCIAL SULFA PREPARATIONS
SULFAMERAZINE BELMET SULQUIN
SULFAQUINIDINE TRIOS ESB POWDER
SULFAQUINOXALINE ABIZET RE-O-SAL
SULFAMONOMETHXINE SULMET
SULFAMETHAZINE

Prevention:
1. coccidiostats with feed/water amprol pul; clopidol, 3. regular removal of droppings (daily/twice a week)
robenicdine 4. maintain cleanliness
2. avoid overcrowding 5. mild exposure to produce immunity

Difference between Coccidiosis and Coccidiasis:

coccidiosis – a clinical disease condition cause by coccidian (eimeria, isospura, etc.) and treatment is needed
coccidiasis – the presence of oocyst in the intestinal tract without producing clinical manifestation (subclinical infection). Treatment is
not necessary

Coccidia of mammals
In general, coccidial infection in mammals is not a problem. It usually occurs as mild infection. Many animals harbor oocysts
without showing clinical signs (coccidiasis).

Coccidia of Cattle, Carabaos, Buffaloes.

1. Eimeria zuernii – most pathogenic. Small and large 3. Eimeria auburnensis – cause mild coccidiosis
intestines 4. Eimeria ellipsoidalis
2. Eimeria bovis – next to E. zuernii in pathogenicity 5. Eimeria bukidnonensis

Clinical signs
1. Calves below one year – usually infected 2. Watery diarrhea with mucus and blood
3. Tail and hind quarters soiled with feces 5. Loss of appetite, dehydration, loss of weight, death
4. Abdominal pain and straining during defecation

Diagnosis
1. finding oocysts in the feces 3. smears from the mucosal scarpings on
2. clinical signs ost mortem

Treatment
1. Sulfonamides 2. Amprolium

Coccidia of sheep and goat

• Eimeria ahsata – most pathogenic • Eimeria arloingi – most • Eimeria crandallis

• Eimeria faurei – mildly pathogenic common • Eimeria granulosa

Clinical Signs
Clinical coccidiosis is confined only to young animals (Kids and lambs). Significant sign is diarrhea. Mortality rate with E. arloingi.
May reach 10%.
Coccidia of swine
Usually occur in low grade infection (Coccidiasis). Generally not pathogenic
1. Eimeria debliecki – most common 3. Eimeria scabra
2. Eimeria spinosa 4. Isospora suis

Clinical Signs
Profuse Diarrhea, may occur concurrently with colibacillosis/scouring in piglets

Coccidia of Horses
Occurs in low grade infection
1. Eimeria leuckarti 3. Eimeria uniungulati
2. Eimeria solipedum 4. Klossiella equi

Coccidia of Dogs and Cats

Eimeria canis Isospora canis
Eimeria felina Isospora bigemina (now Sarcocystis bigemina)
Eimeria cati Isospora rivolta
Isospora felis
Normally, the oocysts are unsporulated when voided with the feces.

In Isospora felis and Isospora rivolta extra-intestinal tissue forms (zoites) are seen in the liver, brain, spleen, lymph nodes of
cats, puppies and even in rats and mice. This peculiarity is also exhibited by Toxoplasma normally and therefore interfere with correct
diagnosis.

Clinical signs
1. bloody diarrhea 2. weakness 3. anorexia 4. emaciation and death

Coccidia of rabbits
Pathogenic species
1. Eimeria perforans 4. Eimeria intestinalis
2. Eimeria media – G.I. tract causing diarrhea 5. E. stiedai – liver (bile ducts)
3. Eimeria magna, Irresidua C.S.I
Rats
1. Eimeria separata, E. nieschultzi

Mouse
1. Eimeria falciformis
2. Cryptosporidium muris, C. parvum

G. Pig
1. E. cavial colon
2. Cryptosporidium wrairi
 Klossiella kobayae – kidney

Fish
1. Eimeria aurata – gold fish 2. E. carpelli – carp 3. E. cyprinid – carp 4. E. truttae –
salmon

Diagnosis, Treatment and Preventation – the same as that of cattle

COCCIDIA OF POULTRY

Coccidia of Chickens
Coccidiosis of chickens is of great economic importance. Heavy mortality occurs in severe infection.

Subclinical infection – common, no mortality but causes poor feed conversion, poor weight gain and low egg production. More or
less organ specific
1. Eimeria tenella – most common and most pathogenic species causing “cecal” coccidiosis. Usually affects chicken 3-5 weeks
of age. Mortality may range from 80-90% in severe untreated cases

Clinical signs:
• Bloody droppings • Anemia • Dehydration
(most significant sign • Weakness • Death

Pathology
1. Hemorrhagic ceca – the most significant lesion. Severe
hemorrhages occur 5-6 days post-infection. If the bird
survives 48 hours following hemorrhage, “cheesy necrotic
core” (accumulation of clotted blood, tissue debris and
oocysts in the ceca persist. Occysts are produced and seen
more abundantly on feca. Examination 9-11 days after
infection. Mortality is highest between the 4th and 6th day
post infection. Continues mild exposure induce strong
immunity.
2. Eimeria necatrix – next to tenella in pathogenicity.
Causes distention of the middle intestine (ballooning). 2-3
times the normal diameter. Filled with unclotted blood.
Affects even older birds/layers may die of severe
infection. 8-12 weeks or older, induce poor immune
response.

Other species:
• Eimeria acervulina – duodenum, characterize by • Eimeria mivati – duodenum; middle intestine
numerous gray or whitish transverse pathes. • Eimeria maxima – S.I. qualification necrosis/ sloughing
• Eimeria praecox – duodenum of the mucosa
• Eimeria hagani – duodenum; less pathogenic • Eimeria mitis – S.I., cecum less pathogenic

Diagnosis:
1. finding large number of oocysts b. Distended or ballooned middle intestine – E.
2. clinical manifestations necatrix
3. post-mortem exam of some birds: c. Hemorrhagic duodenum – E. acervulina
a. Hemorrhagic ceca – E. tenella d. Sloughing of mucosa – E. brunette
Treatment
• Sulfonamides e. Sulfanonomethoxine
a. Sufamonomethozine (Daimeton soda) f. Belmet – sulfanerazine, sulfadiazine,
b. Sufamethazine sulfamethazine
c. Sulfaquinoxaline g. ESB power (sulfachloropyrazine)
d. Sulmet – sodium sulfamethylpyrimedine h. Sulquin 6-50 solution
i. Abizet

Medication – 3-2-3 program (3 day treatment 2 days non-medication and 3 days medication)

Prevention:
1. continuous medication with the feed using coccidiostats 2. all-in, all-out system of management – through cleaning
(inhibitory) coccidiocidal (kills) and disinfection in between batches (at least 2 weeks
a. coopidol vacant)
b. cycostat 3. elevated waterers, raise birds on-slated floor/wire
c. monensin 4. in cases where drug resistance occur change coccidiostats.
d. salinomycin Regular switching of coccidiostats
e. amprolium 5. frequent removal of litter if possible

Coccidia of Turkeys
• Eimeria adenoides – lower SI and LI most pathognenic
bloody droppings and mortality of up to 100%
• E. gallopavovis – lower SI, ceca, rectum
• E. meleagritis – 1-90% mortality; bloody diarrhea;
necrotic entritis
Pigeon
• Eimeria columbae – SI non-pathogenic
• E. lasseana – SI pathogenic to squabs
o Blood tinged diarrhead
• E. tropicalis – pathogenic to squabs

Geese and ducks Coccidia of ducks

• Eimeria truncata – kidney, very pathogenic to gooseling; 1. Eimeria anatis
may cause 100% mortality 2. E. bocchadis – kidney
• E. anseris – SI moderately pathogenic 3. E. matthae - ballooning of SI; hemorrhagic enteritis of 2-3
week old ducklings
4. E. saitame

Causes of ballooning of Small Intestine – hemorrhagic enteritis of ducklings 2-3 weeks of age

Cyptosporidium sp. – oocysts produced on mucosa or surface epithelium of digestive and respiratory tracts causing respiratory
symptom emerging disease of and high mortality can be mistaken for chronic respiratory disease (CRD), coryza, etc.
Cryptosporidium tyzzeri – chicken cecum (extracellularly or the microvilli)
Cryptosporidium melagridis – turkey, diarrhea and some mortality
Wenyonella anatis – ducks
Wenyonella philiplevinei – ducks
Wenyonella gallinae – chickens
Tyzzeria perniciosa – ducks S.I.
Tyzzeria anseris – Geese S.I.
 FAMILY SARCOCYSTIDAE

Reproduction occurs in two hosts. Part of the subclass coccidian intermediate and final hosts are vertebrae
• Intermediate Host – asexual reproduction takes place
• Final Host – sexual reproduction takes place
• Oocysts are reduced

A. Asexual reproduction occurs in a variety of vertebrate I.H multiply by

a. Binary fission
b. Endocyogeny
c. Endoplygeny
d. Pseudocysts/cyst formation
B. Sexual reproduction occurs in another vertebrate host which is the primary or final host
• Schizogony and gametogony – syngamy --- oocysts formation occur in the intestinal tract usually of carnivores (Dogs,
cats, etc.)
• Genera
a. Toxoplasma
b. Sarcocystis
c. Besnoitia
d. Hammondia
e. Frenkelia

GENUS Toxoplasma

• Cyst not septate/lobulated

• Toxoplasma gondii – intracellular parasite of many types of tissue cells = endothelial, parenchymal, epithelial, muscular, blood
and other cells of almost all animals including man (zoonotic).

Morphology:
Occurs in 3 forms:
1. Trophozoite – banana shaped, reproduced by binary
fission, endodyogeny and endopolygeny in tissue cells of
various vertebrate IH. These are also known as
tachyzoites, the rapidly multiplying forms
2. Pseudocysts or cyst – contains many zoites or bradyzoites
(slow multiplying form) – found in the brain, lungs, liver
and other organs of vertebrae I.H.
3. Oocysts – produced after schizogony, gametogony and
syngamy in the intestinal epithelium of cats and other
animals of the feline family only (which are the F.H.)
sporulation takes place in the ground. Sporulated oocyst
has two sporocysts, each with 4 sporozoites (similar to
Isospora)

Life cycle:

When other trophozoites (tachyzoites) pseudocysts (bradyzoites) or sporulated oocyts (sporozoites) are ingested by cats (F.H.).
the zoites invade the epithelial cells of the small intestine and undergo schizogony and gametogony oocysts is voided out with the
feces and sporogony occurs in the ground in 3-4 days. The cycle is repeated when the sporulated oocysts are again ingested by cats.

If animals other than the cat family like cattle, goat, pig, dog, man, etc. which serve as initial hosts ingest the zoites
(spurozoited, tachyzoites and bradyzoites) the organisms invade tissue cells of various organs brain, spinal cord, liver, lungs, spleen,
lymph node etc. where they multiply asexually by binary fission, endodyogeny or endopolygeny or form pseudocyst where they
produce various clinical signs.

Prepatent period
1. 3-5 days if tachyzoites an bradyzoites are ingested 2. 20-25 days if sporozoites are ingested

Transmission and Mode of Infection

1. congenital – transplacental a. infected meat, organ or whole animal
2. ingestion of infective materials (Trophozoites, (rodents/birds)
Bradyzoites, Sporozoites) b. cat feces with sporulated oocysts
 c. venereal – coitus g. handling hand, gloves on vet exam
d. lactation – milk h. secretions and excretions – nasal discharges,
e. blood transfusion saliva
f. organ transplant

Pathogenesis
1. Asymptomatic in most cases 2. organisms invade fetus causing abortion and stillbirth

Clinical Manifestation: depends on organs affected, infection may be direct or indirect

Life Cycle of Toxoplasma gondii

1. Attacks the central nervous system causing encephalitis,
incoordination, paralysis, blindness and concunctivitis
2. lymphadenitis
3. fetal abnormalities – hydrocephalus and ascites,
undeveloped eyes incomplete lens etc.
4. pneumonitis due to destruction of lung tissues
5. acute form – fever, anorexia, jaundice, tremor in pigs,
asymptomatic form in 20% (serologically).

Acute forms – similar to hog cholera, petechial hemorrhages on the skin, high fever, weakness of hindlegs, anorexia, conjunctivitis

Diagnosis:
1. Serological tests • CFT (Compliment Fixation Test)
• Skin test
• IFAT (Indirect Fluorescent Antibody Test)
• IHAT (Indirect Hemagglutination – Agglutination Test)
2. demonstration of organisms in tissue smears, impression, 3. mouse inoculation/passages
blood smears

Treatment:
1. Pyrimethamine 4. sulfadiazine pyrimethamine
2. Sulfamonomethoxine • reduces oocysts output
3. sulfamonomethoxine plus pyrimethamine combination 5. clindamycin (Antibiotic)

Prevention:
1. Thorough cooking of meat 2. cats should not be fed raw meat 3. strict sanitation 4. control of rodents
Note: Not all cats carry T. gondii

Genus Sarcocystis
General Characteristics
1. Zoites are elongate 5. cysts are microscopic to macroscopic in size
2. cysts are septate, filled with spores or rainey’s corpuscles 6. sporulated oocyst/sporocysts produced in the intestinal
or bradyzoites wall of vertebrate F.H. (carnivores: dogs and cats/man
3. both IH and FH are vertebrate animals voided out with the feces
4. cyst (Sarcocyst, Miescher’s tube) found in the muscle of 7. high incidence in the Philippines
vertebrate IH

Species:
• Sarcocystis fusiformis • Sarcocystis tenella • S. bertrami
F.H. – dogs and cat F.H. – cat F.H. – dog
I. H. – carabaos (cattle) F.I. – sheep, goats I.H. - equines
• Sarcocystis cruzi • Sarcocystis ovicanis • S. miescheriana
F.H. – Dogs F.H. –dog F.H. – dog
I.H. – Carabao, cattle I.H. - sheep I.H - pig
• Sarcocystis bovicanis • S. hominis or bovi hominis • Sarcocystis porcifelis
F.H. – Dog F.H. – man F.H. – cat
I.H. – cattle I.H. – cattle I.H. - pig
• Sarcocystis levinet • Sarcocystis muris
F.H. – dog F.H. – cat
I.H. – Carabao, cattle I.H. – rats

Life Cycle:

Sporulated oocysts which are voided out with the feces or F.H., contains 2 sporocyst, each with 4 sporozoites. Oocyst wall is
delicate, usually ruptures and sprorocysts are also seen in fresh feces.

If sporulated oocysts/sporocyts containing sporozoites are ingested by suitable F.H. the sporozoites are released in the small
intestine and undergo gametogony (no schizogony and syngany). Oocyts are formed and sporulate in the epithelium of the small
intestine of dog, cat, man etc. Prepatent period is 1-3 weeks.

If infective materials (Sarcocyst, sporulated oocyst) are ingested by the I-I-, the zoites invade many tissues and undergo
schizogony in endothelial cells of blood vessels in most organs. The resulting merozoites migrate to the muscles via the blood stream
where they grow and form cyst or sarcocyst. Inside the sarcocyst, the spores (Bradyzoites) reproduce by binary fission or by
endocyogeny.
Transmission or mode of infection: Ingestion of sporulated oocyst, sporocysts containing sporozoites or meat with sarcocyst
(containing spores or bradyzoites)

Symptoms:
1. Asymptomatic in most cases 3. abortion
a. In acute cases – reduced milk yield 4. anemia, diarrhea, loss of weight
2. severe infection – muscular weakness, extreme 5. death in severe infection
submuscular emaciation, submuscular edema, toxin =
sarcocystin fever

Diagnosis:
1. finding sarcocyst in the muscle tissue (macro and micro) 3. finding sporulated oocyst/sporocyst in the feces of
in carabaos may reach an inch long carnivores
2. finding trophozoites/spores in ground muscle

Treatment: None
Prevention:
Dogs and cats should not be given raw meat since they serve as F.H. and dissimilar or sporulated oocyst /sporocyst in nature

Genus Besnoitia

Forms:
1. tachyzoites in tissues of I.H. 3. Oocyst in interior tract of carnivores (F.H.)
2. oocyst in connective tissue of I.H.

Besnoitia besnoiti
F.H. – rats
I.H. – cattle

Clinical signs
• thickened and wrinkled skin • emaciation • abortion • edema, diarrhea
• hairs fall off like in mange • some mortality below • sterility in bull • enlarged lymph nodes
but without pruritus 10% • acute fever – anorexia • rapid respiration

Transmission:
1. Ingestion of trophozoites and cyst with bradyzoites from tissues
2. ingestion of sporulates oocyst from the ground

Besnoitia benetti – equine I.H.

Genus Hammondia

Hammondia hammondi
 F.H. – Cats
I.H. – rodents
• Cyst in skeletal muscles, brain
• Tachyzoites multiply in lamina propria of intestine and muscle

Genus Frenkelia
Frenkelia microti – I.H. – mice, wolves
• Cyst in brain and spinal cord

ORDER HAEMOSPORIDIA

FAMILY PLASMODIDAE
Reproduction takes place in two hosts: schizogony (asexual) and gametogony occur in vertebrate host (secondary) while
syngamy (sexual) and sporogony take place in invertebrate host (Final or Primary host)

Genera:
1. Plasmodium 2. Haemoproteus 3. Leucocytozoon

Genus Plasmodium
Schizogony occurs in the RBC and endothelial cells of solid organs (bone marrow, liver, lungs, etc. of vertebrate host syngamy
and sporogony occur in mosquito vectors pigment granules (hemozoin) present.

I. Avian Plasmodia • P. cathemerium - sparrow • P. vinckei

• Plasmodium gallinaceum – II. Human Plasmodia IV. Simian malaria
chickens • Plasmodium ovale • Plasmodium knowlesi
• P. juxtanucleare – chickens • P. palciparum • P. cynomolgi
• • P. brazilianum
• P. relictum – pigeon P. malariae
• P. vivax • P. kochi
• P. durae – turkey • P. inui
• P. lophorae – pheasant III. Rodent malaria • P. simium
• P. elongatum – sparrow, canaries • Plasmodium berghei

Mosquito Vectors (Primary/Final Host)

I. Avian forms – culicine mosquitoes II. Mammalian forms – human, simian, rodent
a. Culex spp. a. Anopheles mosquitoes – Anopheles spp.
b. Aedes spp.

Life cycle of Avian Plasmodia

Sprozoites are inoculated by culicine mosquitoes. Enters macrophages and fibroblast of the skin – from first generation pre-
erythrocytic schizont called cryptozoite. Merozoites from the latter, envades other macrophages – form the second generation
preerythrocytic schizonts – the metacryptozoites. Merozoites from metacyptozoites enter erythrocytes and other cells of the body and
form erythrocytic and exoerythrocytic schizonts respectively. Merozoites from erythrocytic schizonts invade other RBC and either
repeat schizogonic process or proceed to gametogony forming micro- and macrogametocytes. (some erthrocytic merozoites invade
endothelial cells and produce exoerythrocytic schizonts, the phanerozoites).

Merozoites from exoerythrocytic schitionts invade RBC and initiate further erythrocytic schizogony
.
Macrogametocytes and microgametocytes are ingested by culicine mosquitoes and in the gut, macrogametocyte matures into
one macrogamete while microgametocyte matures and a number of microgametes (6-8 flagella-like) are formed and extended out
from the parent cell by exflagellation process.

Once macrogamete is fertilized by a single microgamete (syngamy) forming a motile zygote, the ookinete. The ookinete
penetrates themidgut wall and lie on the other surface of the stomach, forming oocyst sporogeny then takes place forming several
sporozoites. Oocyst ruptures and sporozoites are released, migrate to the salivary gland – proboscis and finally transmitted to birds
when the mosquito bites to suck blood. Mosquitoes are infected throughout the entire life span.
P. gallinaceum – occurs in chickens endemic in India, Pakistan and other neighboring countries not a problem in the Philippines.
Vectors are Culex and Aedes mosquitoes causes a disease condition known as “Avian malaria gallinaceum”. Gametocystes are big,
round or irregular with pigment granules. Schizonts in RBC round to irregular in shape; 6-30 merozoites. Displaces host cell nucleus.
Host cell distorted

The Lifecycle of Plasmodium sp. (Malaria)

Pathogenesis and Clinical signs

Mortality up to 80% or more in endemic areas. Progressive weakness, emaciation, severe anemia, greenish diarrhea and sometimes
paralysis due to massive number of the parasite in endothelial cells of the brain

Up top 90% of the RBC may be parasitized

Pathology
• spleen and liver are enlarged • pale muscle and mucous membrane

Plasmodium juctanucleare – chickens (wild and domestic)

• prevalent in P.I. • causes “Avian malaria juxtanucleare” • vectors – Culex sp.

Gametocytes are usually elongate – pyriform, may be round; schizonts small with 3-7 merozoites, usually in contact with the are
nucleus. Host cell not distorted, nucleus not displaced. Parasitemia usually low – 3-5% or less. Rarely higher

Symptoms: Anemia and emaciation

Low Mortality

Diagnosis: Blood smear and examination and finding schizonts and gametocytes in RBC

Treatment:
• Paludrine 7.5 MG/KGM • Sulfamonomethoxine – pyrimethamine combination
• Chloroquin – 5 MG/KGM • Trimethroprim S.Q. combination
• Plasmochin – 5MG/KGM

Human malaria – characterized by paroxisimal attack – chilling, fever and sweating

Paroxysm – is due to release of toxin upon periodic rupture of mature schizonts.

Plsmodium palciparum “malignant malaria” Quotidian malaria

- most common form of human malaria widely distributed in the tropics. – schizognic cycle takes one day. Paroxism
occurs in day 2.
 Plasmodium malariae – quartan malaria
Tertian malaria - less common in tropical and subtropical
– schizogomic cycle takes two days. Paroxism occurs in day 3.
Plasmodium ovale – mild tertian malaria
Quartan malaria - Philippines, India, Africa
– schizogonic cycle takes three days. Paroxism occurs in day 4.
Plasmodium vivax – “benign tertian malaria”
- most common and widely distributed

Genus Haemoproteus

Schizogony in endothelial cells of blood vessels especially the lungs and not in RBC. (no erythrocyctic schizogony) only
gametocytes occur in RBC. Found in blood sucking insects Hippoboscid flies and Culicoides sp of some cases. Pigment granules
present in gametocytes. Host cell not usually distorted.

H. columbae in pigeons causing “pigeon malaria” prevalent in the Philippines. Also affect doves and wild birds. Only sausage
shape gametocytes are found in RBC. Pigment granules present. Most cells usually not distorted.
Vectors are pigeon louse fly – Pseudolynchia (maura) canariensis

Life cycle:
Sporozoites introduced by pigeon lousefly endothelial cells of blood vessels schizonts cytomeres merozoites
either repeat schizogony or undergo gametogony gametocytes in RBC (micro and macro) syngamy zygote
ookinete oocyst sporozoites proboscis.

Pathogenesis
Many pigeons harbor the organism without showing signs. Heavy mortality may occur among squabs. Frequent signs are
anemia and emaciation, on post-mortem, liver and spleen are enlarged.

Control
Diagnosis is by blood examination and finding of gametocytes in RBC

Treatment
no satisfactory treatment
quinacrine may affect gametocytes but not schizonts

Prevention – control of pigeon lousefly sp (Psuedolynchia maura and canariensis)

Other species:
Haemoproteus meleagridis – turkey; gametocytes – sausage shape. Vector – unknown
H. nettionis – ducks and geese; gametocytes – susage shape. Vector – Culicoides sp
H. sacharovi – pigeons and doves; gametocytes – irregular or round. Vector – Pseudolynchia sp and Culicoides sp.

GENUS Leucocytozoon

Schizogony in endothelial and parenchymal cells of liver, lungs, spleen, testes, ovary, intestine etc. gametocytes in
erythocytes or leukocytes. Depending on the species. Pigment granules absent. Syngamy and sporogony in blood sucking insects.

Disease condition – leucocytozoonosis

Leucocytozoon cauleeryi – the cause of chicken leucocytozoonosis
Vectors – are biting midges Culicoides sp.
Gametocytes are found in RBC which some enlarged, distorted and damaged.

Most prevalent blood parasite of chickens in the Philippines also present in many countries of the far-east Japan, Burma,
Taiwan, Malaya, Thailand etc.
Life cycle: basically the same as H. columbae except that:
1. schizogony occurs on the endothelia and parenchymal cells 3. primary host are Culicoides sp
of solid organs – liver, lungs, spleen, testes, ovary, intestine 4. secondary host are chicken
etc. 5. self limiting – after one developmental cycle, the chicken
2. gametocytes – are round and RBC are distorted and becomes free of parasite and recover.
destroyed

Leucocytozoon simondi·Fig. 1. Life cycle of Leucocytozoon simondi in

its vertebrate hosts (domestic and wild ducks and geese) and in its vector ( spp.,
black flies). 1–5 Sporozoites injected by the Simulium fly are carried by the
bloodstream to the liver, where they enter Kupffer cells and form the
multinucleate first-generation schizonts. The latter give rise to small merozoites
(5) which may reinfect other hepatic cells (2) or invade lymphoid cells (6–8) or
erythrocytes (9.1). 6–8 After invasion of lymphoid cells or macrophages 4–6 days
after infection, large schizonts (= megaloschizonts) of 60–150 μm diameter are
formed, which via cytomeres (7) produce numerous merozoites (8). 9–12 Having
entered lymphoid cells, the majority of merozoites probably develops into
gamonts (9.2), but it is thought that some may initiate further asexual
reproduction. During the formation of the finally elongate or ovoid (20 × 5 μm)
the host cells become distorted and appear elongated-spindle-shaped (10.2).
Occasionally, spherical gamonts appear (10.1) which are thought to originate from
hepatic merozoites (5) that have penetrated erythrocytes instead of lymphoid
cells. However, there is no evidence that these differ functionally from the
elongate forms. When the vector has sucked blood, the formation of (11, 12) is
initiated inside the gut, leading, after fertilization, to an extracellular 13–17 The
immobile zygote is transformed into a motile , which enters the intestinal wall
(15), migrates through the of a gut cell and begins its transformation into an
situated between basal membrane and epithelial cells of the gut (17). 18–20
Formation of multinucleate sporoblasts (18) which give rise to numerous
sporozoites (19; SP). The latter are released into the body cavity and migrate to
the salivary glands (20). These slender sporozoites are finally injected into the
next host. CY, ; DG, developing microgamete; E, erythrocyte; HC, host cell; IE,
intestinal epithelium; L, lymphoid cell/macrophage; N, nucleus; NH, nucleus of
host cell; PV, SG, SP,

Symptoms:
– anemia, hemoptysis – greenish diarrhea – morbidity 30-50%
– depressions, dullness – ruffled feathers – mortality 0-20%
– weakness – poor apetite

Pathology:
1. liver and spleen enlarged 4. blood clot maybe present in the abdominal cavity
2. gall bladder suspended with bile 5. muscle very pale
3. hemorrhagic spots (petechiae) in the combs, liver, muscles and
other organs, may be absent.

Diagnosis:
1. blood examination 2. ring forms 3. mature gametocytes 4. developing gametocytes

Treatment and Prevention

1. sulfa monomethoxine sodium feeds 20-25, treatment 1 4. halofuginone 4-5ppm
gram/litter prophylactic 1 gram/20litters continuously 5. control of Culicoides sp. – breeding places, larvicides, good
2. sulfamonomethoxine 15ppm. Pyremethanine 3ppm drainage
3. clopidol 66ppm

L. sabrazesi- chickens mature gametocytes in spindle shaped WBC.

L. simondi- ducks and geese causing “duck and geese malaria” in the U.S, Canada, Europe. Mature gametocytes in spindle-shaped
WBC. Vectors are Similium sp. Or black flies. Gametocytes persistently present in the blood circulation.
L. simondi is markedly pathogenic to young ducks and geese death. Mortality is usually 30-50% but may reach up to 100%

Diagnosis: blood smear examination and finding spindle-shaped host cell with gametocytes
Treatment: Clopidol in feeds
Prevention:
1. control of Simuliun sp.
2. raise duckling away from carrier adults.

L. smithi turkeys caused “turkey malaria” or turkey leucocytozoonosis in US gametocytes in elongated spindle shaped WBC
Vectors – Simulium spp
Pathogenesis: Strongly pathogenic to young turkeys. Mortality may reach up to 90%
Clinical signs: Anorexia, emaciation, leg weakness, incoordination
Diagnosis: blood smear examination and finding gametocytes
Treatment:
1. sulfaquinoxaline (treatment) 2. clopidol (prevention) 3. control of black flies

FAMILY BABESIIDAE

Babesia or piroplasma – piroplasmosis or babesiosis (a disease primarily of older animals) pyriform, amoeboid intracellular,
multiply in the RBC into two or more nonpigmented pearshaped organisms. Lie charactistically at an angle with narrow ends in
apposition.
Babesia are divided into two groups:
I. large forms – more than 3u
II. small forms – less than 3u

Life cycle in general:

In the vertebrate host, multiplication occurs in the erythrocytes by budding, binary fission or multiple fission forming 2, 4 or
more trophozoites. These are liberated and invade new RBC until large number are readily transmitted mechanically by blood
inoculation. Under natural condition and transmission of Babesia in ticks is either transovarian or transtadial (stage to stage)

Life cycle of Babesia spp. in the tick and

vertebrate hosts. Events in the tick begin with the
parasites still visible in consumed erythrocytes.
Some are beginning to develop Strahlenkörper
forms (A). The released gametes begin to fuse (note
that only one of the proposed mechanisms is
pictured; one gamete has a Strahlenkörper form,
whereas the other does not) (B). The formed zygote
then goes on to infect and move through other
tissues within the tick (C) to the salivary glands.
Once a parasite has infected the salivary acini, a
multinucleate but undifferentiated sporoblast is
formed (D). After the tick begins to feed, the
specialized organelles of the future sporozoites form
(E). Finally, mature sporozoites bud off of the
sporoblast (F). As the tick feeds on a vertebrate
host, these sporozoites are inoculated into the host
(G). Not shown is the preerythrocytic phase seen in
Theileria spp. and T. equi (B. equi). Sporozoites (or
merozoites) contact a host erythrocytic and begin
the process of infection by invagination (H). The
parasites become trophozoites and can divide by
binary fission within the host erythrocyte, creating
the various ring forms and crosses seen on stained
blood smears (I). Illustrations are not to scale.
Transovarian transmission – adult female ticks takes infected RBC. The parasite enters the developing tick egg and is transmitted by
larvae, nymphs and adults of the next generation. This is the mode of transmission in one host ticks.
Example: Babesia bigemina and Babesia microplus

Development does not occur unless ticks are replete with blood otherwise the organism dies or retarted. In the tick gut epithelium, the
parasites undergo multiplication process similar to schizogony producing “fission bodies” (schizonts) containing club-shaped forms
called “vermicules” similar to merozoites.

Mature fission bodies rupture and the vermicules are released into the gut lumen. Vermicules penetrate the gut wall into the
hemonymph to enter the ovary and finally the developing eggs. When the egg hatches into larvae, the organism undergoes
multiplication (schizogony) in the gut epithelium. Vermicles enter salivary gland when the larvae molts into nymph, the vermicules
invade the salivary glands where large schizonts are again formed producing infective vermicules.

Transtadial transmission or stage to stage – Babesis ingested into larval or nymphal ticks is transmitted by the succeeding stage
(nymph or adult) occurs in 2 or 5 host ticks.
Example: B. canis in R. sanguineus

Phagocytes just beneath the hypodermis in the body cavity undergoes schizogony forms containing club shaped forms (vermicules)
club shaped forms are liberated and invade the tick. Muscle cells divide into large number of small ovoid forms. When adult emerges
from the nymph and feeds the organism migrate to the salivary glands and further reproduce by repeated binary fission into large
number of small ovoid infective dorms. Schizogony occurs in the salivary glands of nymph and adults but most transmission is by
adults.

Babesia of cattle
Babasia bigemina
B. bovis – Argentina
B. divergens

B. bigemina - CATTLE
1. Worldwide in distribution in the tropics and subtropics. 5. Pyriform in pairs, round, oval, Irregular
2. Philippines 6. Vectors are principally Boophilus sp.
3. Morphology: large piroplasm (2X4-50) 7. Intra-Uterine transmission possible
4. Round forms are 2-3U in diameter
PATHOGENESIS:
Causes disease known as “Texas Fever”, Red water, Cattle tick fever, Bovine Malaria or piroplasmosis, Bovine Babesiosis.

CLINICAL SIGNS:
1. Calves below 1yr. are resistant, frequently asymptomatic.
2. Incubation period 1-2 weeks.
3. 1st. sign-high fever(106-1080F OR 41-420C) severe
anemia develops up to 75% or RBC being destroyed,
mucous membrane becomes pale , ecteric and increase in
heart and respiratory rates.
4. Hemoglobinuria-usually present (coffee-colored urine)
5. Initially- Profuse diarrhea followed by marked
constipation, anorexia, depression, weakness, cessation or
rumination and drop in milk yield.
6. Mortality- As high as 30-90% in untreated outbreaks.
Death occurring within a week onset.
7. Animals that survive acute phase go into chronic phase
for several weeks duration. Characteristics intermittent
fever(40-40.5%) emaciation, diarrhea or constipation but
usually without marked hemoglobinuria.
8. Cerebral form is characterize by sudden onset high fever,
incoordination followed by posterior paralysis or
convulsions, coma and death.

POST MORTEM: Anemia, Icterus, Subcutaneous and intramuscular edema splenomegaly (maybe 6 times the normal size),
Hepatomegaly distended gall bladder with thick dark blue bile,red urine or dark brown in color.

IMMUNOLOGY:
1. Their is inverse age resistant . Calves resistance.
Asymptomatic and have very low parasitemia. Adults
very susceptible. Clinical signs marked. 3.
2. Accquired immunity a premunition. Immunity to
reinfection is due to continuing low grade infection. Life
long immunity for B. bigemina but may be overcome by
DIAGNOSIS:
1. Clinical signs- high fever, anemia and hemoglobinuria are 3.
suggestive of babesiosis.
2. Demonstration of organism in the peripheral blood smear 4.
especially during period of high fever.
stress (parturition,starvation etc.) if the parasite disappears
the animal becomes fully susceptible again.
Spleen plays important role in maintaining immune
status. Splenectomy is often followed by severe or fatal
released in the “premunized animals. Splenectomized
animals are also more susceptible to infection and much
more seriously affected.
Animal inoculation 50-100ml of suspected blood I.V. or
SC to splenomectomized calves.
SEROLOGICAL HEMAGLUTINATION I-F-A-T

B. bovis
Argentina cattle of temperate countries present in the B. divergens-cattle of N. Europe.
Philippines (small piroplasm (2.4-1.5u) sygnet ring forms Smallest Bebasia sp. Of cattle (1.5X.40). Usually paired and
particularly common. Also pyriform or irregular. widely diverged lying superficially in RBC.
vectors: Ixodes sp. Boophilus sp.Rhicephalus spp. Disease vectors: Ixodes ricinus
similar to but more severe than B. bigemina premunition does
not last 2 years.

DIAGNOSIS: - Smears from heart, kidney, brain, and peripheral blood obtained from tail tip.

CLINICAL SIGNS
1. Babesia of sheep and goats 2. B.motasi-in Europe, Asia and America
SIGNIFICANT SIGNS: Fever, anemia, Haemaglobinimia
Babesia of Horses, Donkeys, Mules
Babesia caballi, B. Equi

Babesia caballi
Resembles B.begemina 2.5-4u longs.
Vectors: Dermacentor spp. Rhicephalus spp. and Hyalomma spp.

Pathogenesis:
1. Anemia icterus but Hemaglobinuria is rare and not 3. Inverted age resistance. Recoverd horses are
characteristic. premune for 1 to 2 years.
2. Paralysis common.

DIAGNOSIS
Clinical signs
1. Demonstration of organisms
2. Serological test Compliment Fixation Test, Flourescent Antibody Test
B. equi
Morphology:smaller than B. caballi 2u long and characteristically divides into 4 daughter cells which frequently form a “maltese”
cross appearance.
Vectors: Dermacentor , Rhicephalus, Hyalomma spp

Pathogenesis: More pathogenic than B. caballi. Significant signs are fever anemia, icterus, Hemoglobinuria and Edema. Paralysis
(common in caballi) is not usually seen in B. equi.
Mortality: 10-50% if not treated.

BABESIA OF SWINE BABESIA OF DOGS

B. trautmanni, Europe, Africa, USSR B. canis- dogs worldwide P.I
B. peroncitoi- Sudan B.gibsoni- dogs in S. Asia
B.vogeli-dogs S. Asia Africa

Babesia canis – dogs worldwide common in the Philippines.

1. Large (4-55 Long)cytoplasm frequently vacuolated. Pleumorphic ring, ameboid, irregular forms. Multiple infection of RBC
common up to 16 organism in a single RBC.
V ectors: Rhicephalus spp. Principally
Dermacentor spp., Haemaphysalis spp
PATHOGENESIS:
1. Causes “Biliary fever” or malignant jaundice. Puppy may
show clinical disease more severe than in adults(unlike
Babesiosis in other animals).
2. disease more severe in imported dogs
3. Incubation period 10-21 days.
4. Typical signs are fever, depression, anorexia, jaundice,
hemoglobinuria (sometimes) splenomegaly. Chronic
intermittent fever anemia, weakness, emaciation.

Atypical cases
1. respiratory type – bronchitis, pneumonia. SC, edema, ascites 3. gastrointestinal type – gastritis
2. nervous type – dist, locomotion epileptiform. Fits paresis, 4. ocular type – keratitis, iritis
coma

Immunity: recovered animals are pre-immune for life

Diagnosis – demonstration of organism in capillary blood. At a time difficult to demonstrate.

Clinical signs
1. animal inoculation – 10ml of 2. B. gibsoni – produces more 3. B. vogeli similar to B. canis but
blood to splenectomized dogs chronic disease than B. canis no cross immunity

Babesia of cat
Babesia felis – small (1.5 – 2u long) round, oval forms, divides into four: organism forming “maltese cross” arrangement. Important
signs are anemia, icterus and emaciation

Diagnosis – clinical signs, blood smear exam.

Treatment of babesiosis – piroplasmosis treatment.

Cattle:
1. trypan blue – 100ml of 1-2% solution I.V 5. diampron – 10mg/kgm I.M or SC (amicarbilide) drug of
2. acriflavine – 20ml of 5% solution I.V choice for cattle
3. ganaseg – 3mg/kgm 5% I.M (berenil) 6. imizol or imidocarb – 1mg/kgm SC or IM (imidazole)
4. pirevan – 1ml of 5%/50kgm SC (babesam/acaprin) 7. diampron – 5-10mg/kgm IM orSC
8. dogs – ganaseg 3-10mg/kgm IM
Supportive treatment
1. blood transfusions
2. hemtinics

Zoonotic Babesia
Babesia bovis Babesia microti B. divergens

Prevention and control of babesiosis

1. tick control – regular dipping of cattle
2. prophylacyic medication
a. imidocarb – 2mg/kgm SC protects cattle for 3 months
3. preimmuniztion
a. inoculation of young calve below 6 months with mild strain of B. bigemina or B. argentina with 5ml blood from carrier
cattle if clinical disease occur as a result of inoculation, treat with imidocard, ganaseg etc.

Family Theileriidae

Organism are round, ovoid, comma shaped, rod like ring or irregular form found in erythrocytes and lymphocytes of cattle,
buffaloes, sheep and goats. Produce macro schizonts (agamont) and micro-schizonts (gamonts). Pigment granules absent. Transmitted
by ticks, disease condition produced is called “theileriasis”. Not reported in Philippine Islands

Species affecting cattle and buffaloes

Theileria parva- east coast fever T.lawrenci
T. annuluta- tropical theileriosis Theileria parva - causes east coast fever or bovine theileriasis in Africa, High
T. mutans mortality among susceptible imported stock. Primary host- ticks

Life cycle
1. Sporozoites are inoculated by ticks in vertebrate host.
2. Schizonts are formed in the lymphocytes and endothelial cells.

Two forms of schizonts:

1. Macro-schizonts or agamont with large chromatin granule 2. Micro schizonts or gamonts with smaller chromatin
and form macromerozoites. Repeat the cycle until the majority granules and product micromerozoites.
of the lymphoid cells are paralyzed.

Micromerozoites attack RBC. (Mostly rod shaped). Infected RBC are ingested by ticks (especially R. appendiculatus) in the tick –
ookinete—sporozoites are produced which are infective.

Symptoms: higher fever. Up to 90% of RBC may be parasitized at the height of the fever. Dry hemorrhagic feces. Marked emotion,
weakness. Enlarged superficial lymph nodes.
Mortality up to 100%

Post mortem: Enlarge spleen and liver. Petechial hemorrhages on serous membranes. Swollen lymph nodes.

Transmission:
Normally by ticks. Inoculation of emulsified spleen and lymph nodes (T.parva, is not transmissible by blood transfusion/inoculation.

Diagnosis:
1. Clinical signs - Absence of anemia 2. Demonstration of schizonts from 3. Demonstration of forms in RBC
and icterus aid in differentiating “east the lymph nodes and spleen puncture (sometimes difficult)
coast fever” from piroplasmosis. (biopsy).

Treatment: chlortetracycline, Oxytetracycline, Halofuginone

Prevention: control of ticks

Recovered animals are immune to reinfection

T. anulata- cattle and buffaloes T. ovis-sheep and goat-benign theilerriosis

T. mutans- cattle of Africa, Asia, Australia and Soviet Union causes Haematonexus veliferus- cattle
“benign bovine Theleriasis” which is almost non-fatal. Transmitted Haematoxenus separatus-sheep
by Rhipicephalus, Haemaphysalis and Boophilus spp. Similar to theileria but RBC forms have rectangular veil
T. hirci-sheep and goat- 50-100% mortality extending from their sides.

Family Haemogregarinidae

Genus Hepatozoon
Schizogony in the endothelial cells of the liver. Gametocytes in the leucocytes and erythrocytes depending on the species.
Hepatozoon canis- dog, cat (Present in the Philippines)

Schizonts in the endothelial cells of the spleen, bone marrow and liver. Gamonts/gametocytes occurring in leucocytes forming
rectangular bodies measuring 3x12 microns by 3-6 microns surrounded by delicate capsule, stain pale blue with reddish purple
nucleus.

Developmental cycle
The dog is infected through ingestion of infected tick (R. sanguineus) which contains sporozoites in the body cavity.
Sporozoites penetrate intestinal walls of dog. Spleen Liver bone marrow and become schizonts merozoites invade leucocytes
become gametocytes/gamonts. Upon ingestion gametocytes leaves leucocytes in the alimentary canal of tick gamete male and
female gametes unite (fertilization) zygote ookinete penetrate intestinal wall of tick haemocoele sporoblast sporocyst
with sporozoites. On the ingestion of ticks oocyst and sporocyst are ruptured to release the sporozoites.

Pathogenesis and clinical signs. May be asymptomatic

Clinical signs- irregular fever, anemia, progressive emaciation with the enlargement of spleen, Lumbar paralysis may occur.
Diagnosis: demonstration of gametocyte in stained blood smear or schizonts in spleen and bone marrow.
Treatment: no known effective treatment but tetracycline and imidocarbs give best results.
Hepatozoon muris - Brown rats (Rattus norvegicus)
Hepatozoon musculi - mouse
Hepatozoon cuniculi - rabbit

Genus Anaplasma, Eperythozoon, Haemabartonella, Aegyptianella, Grakamella, Ehrlichia

1. Anaplasma marginale et centrale
Host- cattle
Disease- anaplasmosis or gallstickness

Morphology: small spherical bodies, red to dark red in the color found in the RBC.

Transmission- mechanical tick, Tabanids, Stableflies, mosquitoes, dehorning, mass vaccination or castration.

Symptoms: fever, anorexia, weakness recumbency, dehydration. Loss of weight, pale mucous membrane (anemia). Marked icterus.
Slow labored breathing, constipation. Parasitemia 30-50%. Mortality usually 10% but may reach as high as 80%.

Post mortem: watery blood, distended gall bladder, enlarged liver.

Diagnosis: anaplasmosis should be suspected when there is:

1. Icterus and anemia without Hemoglobinuria 4. Distended gal bladder and enlarged liver and spleen on post
2. Demonstration of organism in the RBC. mortem.
3. Thin and watery blood.

Treatment:
1. Tetracyclines injection
2. Imodocarb injections with supportive treatment either- blood transfusion, dextrose administration, I.V large amount of water
through s. tube mild laxative. Avoid rough handling.

Prevention:
1. Control of ticks and blood sucking flies 4. preimunization- 5ml. of blood from cattle. Eperythrozoon
2. Proper precaution in surgical operations Minute ring or coccoid shaped granular bodies in the RBC.
3. Antibiotic administration with the feed at 2-3 weeks interval
in the enzootic areas.

Eperythrozoon suis- pig E. wenyoni-cattle

E. parvum-pig E. ovis- sheep

May produce anemia and jaundice “icteroanemia” or “yellow belly” in pigs- Eperythrozoon suis is not pathogenic. May cause high
morbidity in suckling pigs.
Treatment: tetracyclines injections

Haemobartonella - round, oval bodies of the RBC ,or coccoid forms in chain

Haemobartonella felis- cats-“feline infectious anemia”

H. canis- dogs
− causes haemobartonellosis
− Causes progressive anemia and emaciation, jaundice
Diagnosis: identification of organism in the RBC.

Treatment:
1. blood transfusion 2. Tetracycline 3. Chloramphenicol 4. Thiacetarsamide
(caparsolate)

Ehrlichia- cause of Ehrlichiosis

Coccoid, introcytoplasmic forms in the WBC. Transmitted by ticks
Ehrlichia bovis E. ovina E. canis E. equi

E. canis- causes “tropical canine pancytopenia” or thrombocytopenia

Class Ciliata- the ciliates

Cilia for locomotion. Has 2 nucleus –macronucleus
-micronucleus
Reproduction- transverse binary fission (asexual) and conjugation (sexual)

Genus Balantidium
Balantidium coli- causes “balantidial dysentery”. In pigs and man. Most prevalent protozoon parasite in swine macronucleus is bean-
shaped. Micronucleus lies in a notch of macronucleus body covered with cilia. Cyst are ovoid or spherical.

Transmission: ingestion of cyst

Pathogenesis: causes mild to severe enteritis resulting to watery diarrhea and dehydration and dehydration particularly among the
weanling pigs. May cause superficial or deep ulceration of the intestines.

Diagnosis: fecal examination and finding of vegetative motile Trophozoites and cysts.

Treatment: not easy to treat. Tetracycline per os.

Tetracycline plus carbasone per os, sulfonamides.
Prevention: good management and sanitation, thorough disinfection of pig pens with boiling water or 10% formalin.

Species of uncertain classification

Pneumocystis carinii - causes interstitial pneumonia in man and animals in very young and old especially with debiletative factors
such as AIDS. Association of protozoa and fungi commonly seen in animals infected with immunosuppressive drugs.