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PROTOZOOLOGY -definite hosts include domestic cat,

jaguarundi, ocelot, mountain lion, leopard cat,

Eimeria tenella Developmental cycle

-most pathogenic of avian coccidian Two cycles of development:
-developmental stages occurs in cecum 1. enteroepithelial
-sporulation is stimulated by the presence of 2. extraintestinal
carbon dioxide and trypsin and bile in the SI
-affects frequently birds aged 4 weeks
-infection is noticeable at about 72 hours
after infection Enteroepithelial cycle:
-chicken droops,cease feeding huddle to keep Occurs in cat and is similar to that of other
warm coccidia consisting of enteroepithelial
-at 96 hours blood appears in droppings multiplicative stages and gamonts resulting in
oocyst production with sporogony.
Eimeria necatrix It is induced by feeding cyst containing
-asexual development in SI,gametogony cycle bradyzoites( slowly multiplying stages) derived
in cecum from the brain of mice. Prepatent period is 3-5
-lesions are found in the middle third of SI days and peak oocyst production occurs from 5-
-wall of SI is markedly swollen, hemorrhagic, 8 days.
and the contents filled with unclotted blood
Multiplicative stages of Enteroepithelial
Eimeria acervulina cycle:
-responsible for subacute or chronic intestinal 1. Type A- appears 12-18 hours after
coccidiosis of older birds and chickens at the infection, it is the smallest of the
point of lay multiplicative types and is evident as
-developmental stages occur in the anterior collection of two to three organism in
part of SI the jejunum. Division is by internal
-clinical signs include weight loss and watery budding
whitish diarrhea 2. Type B- occurs 12- 54 hours after
infection. It has a centrally located
Eimeria maxima nucleus, a prominent nucleolus and
-developmental stages in SI divides by internal budding
-SI has marked production of mucus, the 3. Type C- occurs 24-54 hours after
mucosa is thickened, there is loss of tone and infection and divides by schizogony.
intestine becomes flaccid and dilated They are elongated and have a
subterminal nucleus.
Eimeria mivati 4. Type D- occur from 32 hours to 15 days
-developmental stages in SI but may extend after infection and accounts for all 90 %
from duodenum to rectum ofToxoplasma in the SI.Divide by
internal budding , schizogony and by
Eimeria mitis separation of single merozoites from the
-developmental stages occur in the anterior SI nuclear mass
occasionally in post SI 5. Type E- resembles Type D and occurs 3-
15 days after infection
Eimeria brunetti
-developmental stages in SI, cecum, and Gamoonts stage: Occurs throughout the SI
cloaca and aqre common in the ileum 3-15 days after
-cause severe disease in chicken between 4th infection
and 9th weeks of age
-lesions are confined to the posterior intestine Oocyst stage: Oocyst formation occurs in
bet the yolk sac and ceca the epithelial cells of SI. Oocysts are discharged
-causes “rectal coccidiosis” from the epithelial cells and shed in to feces.

Genus Toxoplasma Extraintestinal cycle:

-oocyst with two sporocyst each with four These stages are the only forms in the life
sporozoites cycle which occurs in the non-felids. It may also
-definite hosts are felids occurs in felid and may start simultaneously
with the enteroepithelial cycle of development -clinical signs includes intermittent pyrexia,
in that animal. reduced milk yield, loss of condition, and
difficulty in breathing.
Tachyzoites formation ( rapidly multiplyinf 2. Sarcocystis bovifelis- definitive hosts are cat
stages): and feral cat.
Seen especially in the visceral 3. Sarcocystis homonis- definitive hosts are
infections.Occurs in the lamina propria, man, rhesus monkey baboon, and not
mesenteric lymph nodes and distant organs. In pathogenic in cattle
other animals it begins by ingestion of
sporulated oocyst. Organism multiply in the by Sarcocystis in Sheep:
endodyogeny and eventually 8-16 more 1. Sarcocystis ovicanis- highly pathogenic for
organisms accumulate in a host cell which then lambs which become anorectic weak and
disintegrates and new cells are infected may die. At necropsy the heart is the
severely affected organ, schizonts being
Bradyzoites formation: ( slowly multiplying found in the epithelial cells.
stage) 2. Sarcocystis tenella- non- pathogenic
Contained in cyst are characteristics of
chronic infection and occur mainly in the brain, Sarcocystis of man:
heart and skeletal muscles. Multiply slowly 1. Sarcocystis hominis
mainly by internal budding. The cyst containing 2. Sarcocystis porcihominis
thousands of these forms may persist for * S. hominis and S.porcihominis infection in
months or years after infection. Bradyzoites man is associated with anorexia, nausea and
resist peptic and typtic digestion diarrhea
3. Sarcocystis lindemanni- intermediate host is
TOXOPLASMOSIS IN MAN man and final host is unknown
Can be :
1. Congenital-occurs when a woman has Genus Plasmodium:
primary infection during pregnancy. The Contains malarial organisms of man and other
outcome varies according to fetal mammals and vertebrates. Schizogony occurs in
damage which in turn depends on the the red blood cells and also in the endothelium
virulence of the strain of organism. In of inner organs while the sexual phase occurs in
severe infection abortion is common blood sucking insects. For mammalian forms
sequel. these are anopheline mosquitoes and for avian
2. Acquired- suspected when there is forms culiciline mosquitoes.
lymphadenopathy, fever, lymphocytosis,
meningoencephalitis, eye lesions of Avian malaria
doubtful origins or myocarditis. Species with round or irregular gamonts which
displace the nucleus of the host cell
Genus Sarcocystis: 1. Plasmodium cathemerium- transmitted by
several soecies of Culex and Aedes; there
Life cycle: Infective sporocysts, derived from is marked enlargement of liver and spleen
the feces of final hosts are ingested. Sporozoites with anemia and subcutaneous
are released in the intestine and they invade hemorrhages
many tissues. Schizogony occurs in the 2. P. gallinaceum- exoerythrocytic stage
endothelial cells of blood vessels in most organs occurs in the endothelial cells; chicken is
preceding the development of typical cyst in the particularly susceptible. Birds become
striated muscles. Two recognizable regions are progressively emaciated as the disease
recognizable within the cyst. The peripheral progresses
region contains globular forms called the 3. P. juxtanucleare- highly pathogenic
metrocytes which by internal budding produce especially the Brazilian strain. Chicken
two daughter cells and these after several becomes listless, weak with anemia and
further replications, give rise to banana shaped CNS involvement may be seen
bradyzoites. Infection of the final host is by
ingestion of muscle cysts containing
4. P. relictum- highly pathogenic for pigeons,
bradyzoites. Schizonts and metrocytes are not 5. P. griffithsi-
infective for the definitive host.
Species with elongate gamonts which do not
Sarcocystis in Cattle: usually displace the host cell nucleus
1. Sarcocystis cruzi- most pathogenic species 1. Plasmodium circumflexum
DH- dog, wolves,cayotes,raccoons,hyenas 2. P. durae
3. P. elongatum
4. P. fallax 2. Babesia bovis- small piroplasm larger than
5. P. hexamerium B. divergens. There is no usually divergent
6. P. lophurae forms lying superficially in the red blood
7. P. polare cell and vacuolated signet ring forms are
8. P. rouxi particularly common.
9. P. vaughani Ticks involved: Ixodes ricinus, I.
persulcatus, Boophilus calcaratus, B.
Malarial parasites of man microplus and R. bursa
Endogenous developmental cycle 3. Babesia divergens- smaller than B. bovis
-following the bite of infected mosquito, the and appears as paired, divergent forms
sporozoites remain in the blood for a short time lying superficially on the red blood cell.
but after an hour the blood is no longer infective 4. Babesia major- resembles B. bigemina
for another host. Sporozoites enter the except that it is smaller and lies in the
parenchyma cells of the liver and here develop center of the erythrocytes.
into preerythrocytic schizont (cryptozoites). The
exoerythrocytic forms are confined to the liver Genus Theleria
in mammalian malaria. The hepatic form grows -organisms multiply schizogony in
to become a large schizont, the time for this and lymphocytes and finally invade erythrocytes.
the size of the mature form depending on the
species of parasite. Following exoerythrocytic Thelaria species of cattle:
development merozoites invade the 1. Thelaria parva- causes East Cost Fever or
erythrocytes. bovine theleriasis. Zebu cattle has high
natural resistance to it.
Species of the Plasmodia of man 2. Thelaria lawrenci
1. Plasmodium falcifarum- the cause of 3. Thelaria annulata
malignant tertian malaria, falciparum 4. Thelaria mutans
malaria or subtertian malaria. There is
tendency for the infected rbc to clump. The Thelaria species of sheep:
gamonts are sausage-or cresent shaped 1. Thelaria hirci- highly pathogenic to sheep
and appear in the peripheral blood. and goats
2. P. malariae- the cause of quartan malaria. 2. Thelaria ovis
The schizont appear in the circulating blood
and frequently assume a band across the
3. P. ovale-the cause of mild tertian malaria. A Organism of this class possess cilia for
distinctive feature of parasitized rbc is the locomotion. They are highly organized form
appearance of Schuffer’s dots, and the cell possessing two nuclei, a macronucleus which is
is fimbriated. This species is present in the large and massive and responsible for the
Philippines. cytoplasmic activities of the organism and a
micronucleus concerned with reproductive
4. P. vivax- the cause of benign tertian or
process. Reproduction is asexual by transverse
vivax malaria which is the most common in
binary fission or in sexual phase by conjugation
the world
Genus Balantidium:
Genus Babesia
-oval to ellipsoidal in shape in outline, there is
Organism multiply in the erythrocytes by
distinct macronucleus and small micronucleus.
asexual division, producing two, four, or more
non-pigmented amoeboid parasites. When
Balantidium coli
stained with Romanowsky stain, they show a
-widespread in swine and appears as the
blue cytoplasm and a red chromatin mass
primary host. Generally it is a commensal of the
usually at one pole.
large intestine
Babesia of Cattle:
Genus Ichthyophthirius
1. Babesia bigemina- cause of cattle tick
-found mainly as parasites of fish in thew gills
fever, red water fever, piroplasmosis. A
and skin
large piroplasm and characteristically pear
shaped and lie in pairs forming an acute
Ichthyophthirius multifilis- the cause of “ich” or
angle in the red blood corpuscle.
white spot disease and occur in all fresh water
Ticks involved: Boophilus annulatus, B.
fishes. Penetration of the tomite causes severe
decoloratus, B. microplus, Rhipicephalus
irritation accompanied by mucous secretion and
evertsi, R. bursa, R. appendiculatus,
hyperplasia of the epithelium
Haemaphysalis punctata,
ORDER RICKETSIALLES Anaplasmosis is not contagious. Numerous
species of tick vectors ( Boophilus ,
Genus Anaplasma
-appear As small, spherical bodies, red to dark Dermacentor , Rhipicephalus , Ixodes ,
red in color inside the rbc of cattle, deer, sheep Hyalomma , and Ornithodoros ) can transmit
and goats.
1. Anaplasma marginale- located at the margin Anaplasma spp . Not all of these are likely
of infected cells significant vectors in the field, and it has been
2. Anaplasma centrale- centrally placed in the
erythrocyte shown that strains of A marginale also co-evolve
3. Anaplasma ovis with particular tick strains. Boophilus spp are
major vectors in Australia and Africa, and
Anaplasmosis, formerly known as gall sickness,
Dermacentor spp have been incriminated as the
traditionally refers to a disease of ruminants
main vectors in the USA. After feeding on an
caused by obligate intraerythrocytic bacteria of
infected animal, intrastadial or trans-stadial
the order Rickettsiales, family Anaplasmataceae,
transmission may occur. Transovarial
genus Anaplasma . Cattle, sheep, goats, buffalo,
transmission may also occur, although this is
and some wild ruminants can be infected with
rare, even in the single-host Boophilus spp . A
the erythrocytic Anaplasma . Anaplasmosis
replicative cycle occurs in the infected tick.
occurs in tropical and subtropical regions
Mechanical transmission via biting dipterans
worldwide (~40° N to 32° S), including South
occurs in some regions. Transplacental
and Central America, the USA, southern Europe,
transmission has been reported and is usually
Africa, Asia, and Australia.
associated with acute infection of the dam in
The Anaplasma genus has recently been
the second or third trimester of gestation.
expanded to include species transferred from
Anaplasmosis may also be spread through the
the genus Ehrlichia , now named Anaplasma
use of contaminated needles or dehorning or
phagocytophilum (compiled from species
other surgical instruments.
previously known as Ehrlichia phagocytophila , E
There is a strong correlation between age of
equi , and human granulocytic ehrlichiosis
cattle and severity of disease. Calves are much
agent), A bovis (previously E bovis ), and A
more resistant to disease (although not
platys (previously E platys ), all of which invade
infection) than older cattle. This resistance is
blood cells other than erythrocytes of their
not due to colostral antibody from immune
respective mammalian hosts. Bovine
dams. In endemic areas where cattle first
anaplasmosis is of economic significance in the
become infected with A marginale early in life,
cattle industry.
losses due to anaplasmosis are minimal. After
Etiology: recovery from the acute phase of infection,

Clinical bovine anaplasmosis is usually caused cattle remain chronically infected carriers but

by A marginale . Cattle are also infected with A are generally immune to further clinical disease.

centrale , which generally results in mild However, these chronically infected cattle may

disease. A ovis may cause mild to severe relapse to anaplasmosis when

disease in sheep, deer, and goats. immunosuppressed (eg, by corticosteroids),

when infected with other pathogens, or after
Transmission and Epidemiology:
splenectomy. Carriers serve as a reservoir for (41°C) occurs at about the time of peak
further transmission. Serious losses occur when rickettsemia. Mucous membranes appear pale
mature cattle with no previous exposure are and then yellow. Pregnant cows may abort.
moved into endemic areas or when under Surviving cattle convalesce over several weeks,
endemically unstable situations when during which hematologic parameters gradually
transmission rates are insufficient to ensure all return to normal.
cattle are infected before reaching the more Bos indicus breeds of cattle appear to possess a
susceptible adult age. greater resistance to A marginale infection than
B taurus breeds, but variation of resistance of
Clinical Findings:
individuals within breeds of both species occurs.
In animals <1 yr old anaplasmosis is usually
Difference in virulence between Anaplasma
subclinical, in yearlings and 2 yr olds it is
strains and the level and duration of the
moderately severe, and in older cattle it is
rickettsemia also play a role in the severity of
severe and often fatal. Anaplasmosis is
clinical manifestations.
characterized by progressive anemia due to
extravascular destruction of infected and
Lesions are typical of those occurring in animals
uninfected erythrocytes. The prepatent period
with anemia due to erythrophagocytosis. The
of A marginale is directly related to the infective
carcasses of cattle that die from anaplasmosis
dose and typically ranges from 15-36 days
are generally markedly anemic and jaundiced.
(although it may be as long as 100 days). After
Blood is thin and watery. The spleen is
the prepatent period, peracute (most severe but
characteristically enlarged and soft, with
rare), acute, or chronic anaplasmosis may
prominent follicles. The liver may be mottled
follow. Rickettsemia approximately doubles
and yellow-orange. The gallbladder is often
every 24 hr during the exponential growth
distended and contains thick brown or green
phase. Generally, 10-30% of erythrocytes are
bile. Hepatic and mediastinal lymph nodes
infected at peak rickettsemia, although this
appear brown. There are serous effusions in
figure may be as high as 65%. RBC count, PCV,
body cavities, pulmonary edema, petechial
and hemoglobin values are all severely reduced.
hemorrhages in the epi- and endocardium, and
Macrocytic anemia with circulating reticulocytes
often evidence of severe GI stasis. Widespread
may be present late in the disease.
phagocytosis of erythrocytes is evident on
Animals with peracute infections succumb
microscopic examination of the
within a few hours of the onset of clinical signs.
reticuloendothelial organs. A significant
Acutely infected animals lose condition rapidly.
proportion of erythrocytes are usually found to
Milk production falls. Inappetence, loss of
be parasitized after death due to acute
coordination, breathlessness when exerted, and
a rapid bounding pulse are usually evident in
the late stages. The urine may be brown but, in Treatment:
contrast to babesiosis, hemoglobinuria does not Tetracycline antibiotics and imidocarb are
occur. A transient febrile response, with the currently used for treatment. Cattle may be
body temperature rarely exceeding 106°F sterilized by treatment with these drugs and
midwestern, northeastern, and western coastal
remain immune to severe anaplasmosis regions of the USA and in Europe and Asia. The
subsequently for at least 8 mo. host range of infection and illness for various
strains within this genogroup also includes
Prompt administration of tetracycline drugs horses and ruminants; dogs and cats may
(tetracycline, chlortetracycline, oxytetracycline, occasionally be infected. Anaplasma (Ehrlichia)
platys is the cause of infectious cyclic
rolitetracycline, doxycycline, minocycline) in the thrombocytopenia of dogs. The following
discussion of ehrlichiosis primarily describes
early stages of acute disease (eg, PCV >15%)
infection in dogs caused by E canis .
usually ensures survival. A commonly used
treatment consists of a single IM injection of Epidemiology:
long-acting oxytetracycline at a dosage of 20 E canis and A platys are enzootic in many parts
mg/kg. Blood transfusion to partially restore the of the USA and worldwide. These agents are
PCV greatly improves the survival rate of more transmitted by the brown dog tick,
severely affected cattle. The carrier state may Rhipicephalus sanguineus . Rhipicephalus ticks
be eliminated by administration of a long-acting become infected with E canis after feeding on
oxytetracycline preparation (20 mg/kg, IM, at infected dogs, and ticks transmit infection to
least 2 injections with a 1-wk interval). other dogs during blood meals taken in
Withholding periods for tetracyclines apply in successive life stages. Blood transfusions, or
most countries. Injection into the neck muscle other means by which infected WBC can be
rather than the rump is preferred. transferred, may also transmit the pathogens.
Imidocarb is also highly efficacious against A Other Ehrlichia and Anaplasma species have
marginale as a single injection (as the sylvan cycles in the environment involving
dihydrochloride salt at 1.5 mg/kg, SC, or as various other tick species and wildlife reservoir
imidocarb dipropionate at 3.0 mg/kg). hosts. In the USA, E chaffeensis and E ewingii
Elimination of the carrier state requires the use are transmitted by Amblyomma americanum ,
of higher repeated doses of imidocarb (eg, 5 the lone star tick. Anaplasma phagocytophilum
mg/kg, IM or SC, 2 injections of the is transmitted by Ixodes species of ticks; in the
dihydrochloride salt 2 wk apart). Imidocarb is a northeastern USA, infection is transmitted by I
suspected carcinogen with long withholding scapularis , the black-legged tick, whereas
periods and is not approved for use in the USA infection in western states is primarily
or Europe. associated with I pacificus , the Western black-

Genus Ehrlichia: legged tick. People, dogs, cats, and other

Classical canine monocytic ehrlichiosis is caused domestic animals are incidental hosts of these
by Ehrlichia canis , which infects the
mononuclear cells of dogs; canine monocytic pathogens.
ehrlichiosis may also be caused by E
chaffeensis , the etiologic agent of human Clinical Findings:
monocytic ehrlichiosis. A monocytic ehrlichiosis In E canis infections, signs arise from the
has been identified in cats in Africa, France, and
the USA; however, the exact species has not involvement of the hemic and lymphoreticular
been determined. E ewingi is a granulocytic
systems and commonly progress from acute to
species that has been isolated from dogs and
humans in the southern, western, and chronic, depending on the strain of organism
midwestern USA. Human granulocytic
and immune status of the host. In acute cases,
ehrlichiosis, caused by Anaplasma
phagocytophilum is seen in the northern there is reticuloendothelial hyperplasia, fever,
generalized lymphadenopathy, splenomegaly, thrombocytopenia may cause epistaxis,
and thrombocytopenia. Variable signs of hematuria, melena, and petechiae and
anorexia, depression, loss of stamina, stiffness ecchymoses of the skin. Variably severe
and reluctance to walk, edema of the limbs or pancytopenia (mature leukopenia,
scrotum, and coughing or dyspnea may occur. nonregenerative anemia, thrombocytopenia, or
Most acute cases are seen in the warmer any combination thereof) may occur. Aspiration
months, coincident with the greatest activity of cytology reveals reactive lymph nodes and,
the tick vector. usually, marked plasmacytosis. Frequently,
During the acute phase of E canis infection in polyclonal, or occasionally monoclonal,
dogs, the hemogram is usually normal but may hypergammaglobulinemia occurs.
reflect a mild normocytic, normochromic Dogs infected with A platys generally show
anemia; leukopenia; or mild leukocytosis. minimal to no signs of infection despite the
Thrombocytopenia is common, but petechiae presence of the organism in platelets. The
may not be evident, and platelet decreases may primary finding is cyclic thrombocytopenia,
be mild in some animals. Vasculitis and immune- recurring at 10-day intervals. Generally, the
mediated mechanisms induce a cyclic nature diminishes, and the
thrombocytopenia and hemorrhagic tendencies. thrombocytopenia becomes mild and slowly
Lymph node aspiration reveals hyperplasia. resolves. Other ehrlichial infections not caused
Death is rare during this phase; spontaneous by E canis appear clinically similar to acute E
recovery may occur, the dog may remain canis infection, but the clinical course is usually
asymptomatic, or chronic disease may ensue. more self-limiting. Shifting leg lameness and
Chronic ehrlichiosis caused by E canis may fever of unknown origin may be present.
develop in any breed, but certain breeds, eg, Thrombocytopenia and mild leukopenia or
German Shepherds, may be predisposed. leukocytosis may occur during the acute course
Seasonality is not a specific hallmark of chronic of infection, which is clinically more discrete.
infection, as appearance of chronic signs may be Chronic disease, as seen with E canis infection,
variably delayed following acute infection. In is not typically seen in other ehrlichial infections.
chronic cases, the bone marrow becomes Lesions:
hypoplastic, and lymphocytes and plasmacytes During the acute or self-limiting phase of E canis
infiltrate various organs. Clinical findings vary infections, lesions generally are nonspecific, but
based on the predominant organs affected, and splenomegaly is common. Histologically, there is
may include marked splenomegaly, lymphoreticular hyperplasia, and lymphocytic
glomerulonephritis, renal failure, interstitial and plasmacytic perivascular cuffing. In chronic
pneumonitis, anterior uveitis, and meningitis cases, these lesions may be accompanied by
with associated cerebellar ataxia, depression, widespread hemorrhage and increased
paresis, and hyperesthesia. Severe weight loss is mononuclear cell infiltration in perivascular
a prominent finding. regions of many organs.
The hemogram is usually markedly abnormal in
chronic cases. Frequently, severe
The drug of choice for all forms of infection
caused by these organisms is doxycycline
because of its superior intracellular penetration.
The recommended dosage is 5-10 mg/kg, PO or
IV, SID for 10-21 days. Tetracycline (22 mg/kg,
PO, TID) can also be used for ≥2 wk in acute
cases and 1-2 mo in chronic cases. Two doses of
imidocarb dipropionate (5-7 mg/kg, IM), 2 wk
apart, are variably effective against both
ehrlichiosis and some strains of babesiosis. In
acute cases receiving appropriate antibiotic
therapy, body temperature is expected to
return to normal within 24-48 hr after
treatment. In chronic cases, the hematologic
abnormalities may persist for 3-6 mo, although
clinical response to treatment often occurs
much sooner. Supportive therapy may be
necessary to combat wasting and specific organ
dysfunction; platelet or whole-blood
transfusions may be required if hemorrhage is
extensive. Concurrent broad-spectrum
antibiotics may be needed if the dog has severe
leukopenia. The E canis antibody titer should be
measured again within 6 mo of illness to
confirm a low or seronegative status indicative
of successful therapy. Serum titers that persist
at lower but positive levels should be rechecked
in another 6 mo to ensure that they are not