Babesiosis Lecture MVSC

Piroplasms: Babesia & Theileria
MP Gupta
Piroplasms
Piroplasms or Piroplasmida are an
order of the Phylum Apicomplexa
They are very small parasites of
mammals and ticks
There are two genera which cause
import disease in livestock (and
occasionally in humans): Babesia &
Theileria
mohangupta63@gmail.com
Babesiosis
(Piroplasmosis,Tick fever, Texas
cattle fever,Red fever (Cf. Red
water is Theleriosis), Spleenic
fever,Biliary fever in horse)
Classification of Babesia
Phylum:
Class:
0rder:
Family:
Genus:
-Apicomplexa
-Piroplasma
-Piroplasmida
-Babesiidae
-Babesia
It is a tick transmitted
haemoprotozoan infection of cattle,
buffaloes, horse, pig, dog, sheep, goat,
wild animals and man characterized by
fever, anaemia, haemoglobinaemia,
haemoglobunaria and death.
Epidemiology
Babesia has a wide geographical distribution
particularly in tropics and subtropics.
Mostly animals of more than 2.5 yrs age are
affected.
More marked in exotic breeds than
indigenous.
Extreme climate may favor the disease.
Stress due to vaccination or pregnancy may
also affect the susceptibility.
Epidemiology
Mostly ticks are responsible for
transmission. Trans-ovarian
transmission is also common.
Contaminated needles and surgical
instruments can also transmit infection
physically.
Babesia has seasonal occurrence.
Greatest incidence soon after peak of
tick population in summer and autumn.
Morbidity and mortality: 90%
Etiology
Animal
Species involved
Cattle, Buffaloes
Babesia bigemina, B. bovis,

B. divergens, B. major
Horse
Babesia equi(now called Theleria

equi); Babesia caballi
Sheep
Babesia ovis; B. motasi
Pig
Babesia trautmanni
Dog
Babesia canis; Babesia gibsoni
Cat
Babesia felis
Man
Babesia microti
B.bovis and B. bigemina
10
B.microti
B.canis
11
Devastating outbreaks follow the big cattle

drives
In the 1860s and 1870s Texas longhorns
were driven in huge numbers to the
railheads in Kansas (from there they
went by train to the slaughterhouses of
Chicago and other big nothern cities)
Farmers in Kansas and Missouri were
plagued by outbreaks of Texas fever in
their herds which they linked to the
cattle drives
Several standoffs ensued as local
farmers tried to block drives
Theobald Smith and Frederick

Kilbourne show (1889-1893) that
the disease is caused by a
protozoan parasite transmitted by
ticks (first disease shown to be
transmitted by an arthropode).This
findings led others to work out life cycles of
malaria , kala-azar ,sleeping sickness 12
etc.to
consider arthropods as vectors.
Babesia bigemina causes

Texas cattle fever
B. bigemina
Mortality in acute untreated cattle

50-90%
Rapid rise in temperature (105-108
F)
Fever persists for a week or more
Loss of appetite, dull, listless
Severe anemia due to rapid loss of
red blood cells
Hemoglobinuria (red colored urine)
due to massive RBC lysis
Infected RBCs adhere to vasculature
of organs (likely similar in
mechanisms to Plasmodium)
Evidence for comparable clonal
antigenic variation
Cattle may die within 3-8 days 13
Babesia bigemina causes

Texas cattle fever
Older cattle is much more likely
to develop severe disease than
calves
In endemic areas calves get
infected and mortality is low
In the case of epidemics adults
without previous exposure get
infected resulting in massive loss
This explains the massive loss of
cattle in Kansas despite the fact
that the longhorns coming from
Texas (where the disease was
endemic) seemed perfectly
healthy
What makes the difference
between Texas & Kansas?
14
Distribution of Tick fever

caused by B. bigemina
Babesiosis coincides with the distribution of the main

vector ticks Boophilus annulatus & microplus (Winter
temperatures limit distribution)
15
Mode of Transmission
Parasites undergo developmental
stages within the body of ticks before
they are conveyed in the saliva in an
infective form.
16
Mode of Transmission
Bovine babesiosis (India)-Boophilus microplus
and B. annulatus.
Horse- Dermacentor,
Hyalomma,Rhipicephalus
Pig- R. sanguineus
Dog- Dermacentor,
Haemaphysalis,Hyalomma,Rhipicephalus
Man- Ixodes sp.
17
18
19
Life cycle
Babesia spp. do not parasitize any vertebrate host
cell other than erythrocytes.
Each sporozoite (merozoite) penetrates the cell
membrane of an erythrocyte with the aid of a
specialized apical complex.
Once inside, it transforms into a trophozoite
from which two merozoites develop by a process
of merogony (binary fission).
20
In the passage of host blood to the midgut of the tick

vector, the development of two populations of ray bodies
from the gamonts (gametocytes) occurs.
The ray bodies undergo further multiplication within the
erythrocytes (?) which continues after they have
emerged.
Large aggregations of multinucleated ray bodies form, but
once division is complete, single- nucleated ray bodies
that are now haploid and assumed to be gametes
emerge from the aggregates and then fuse together in pairs
(syngamy) to form a spherical cell (zygote) .
21
The zygote selectively infects the digestive cell of the tick

gut where they multiply and then the basophilic cells where
further multiplication occurs with development to kinetes
that escape into the tick hemolymph.
In the gut cells, schizogony occurs with the formation of
polyploid kinetes (large merozoites) .
These motile club-shaped kinetes then escape .into the
hemolymph and infect a variety of cell types and tissues,
including the oocytes where successive cycles of
secondary schizogony occurs.
22
Thus, trans ovarial transmission occurs with

further development occurring in the larval
stage.
Kinetes enter the salivary glands and are
transformed into multinucleated stages
(sporogony) and these then break up to
form sporozoites.
23
24
Babesia
Merozoites (piroplasms) multiply
in RBCs of the mamalian host
Tick takes up sexual stages with
blood meal, gamete formation,
fertilization
Kinetes infect various organs of
the tick including ovary
(transovarial infection of next
generation of ticks)
In the larvae the kinetes invade
salivary gland cells, massive
replication results in the
production of ten thousands of
sporozoites which are injected
upon feeding
25
Transmission
26
Life Cycle of Babesia bigemina

1. An infected tick bites cattle releasing
__________________________ into the
cow bloodstream.
2. Sporozoite penetrates a rbc and

becomes a _______________________.
3. Trophozoite undergoes binary fission
- 2 trophozoites often appear attached
anteriorly (diagnostic!).
4. Rbc is destroyed and trophozoites
reinvade new rbc's
this asexual cycle continues
indefinitely until the host dies.
27
5. Feeding tick picks up rbc's with

trophozoites.
6. Trophozoites penetrate cells of many
organs and undergo schizogony to
release __________________________.
7. Some merozoites enter the tick's
ovaries and eggs & are transmitted to the
next generation of ticks by
________________________________.
8. Merozoites undergo schizogony in
tick offspring and infective stage
_____________________________
are produced
sporozoites migrate to the tick
salivary glands
transmitted to cattle with next tick
bite.
28
Boophilus is a single host tick

In the U.S. & Mexico Babesia
bigemina is transmitted by
Boophilus annulatus
Boophilus are one host ticks:
larvae hatch from the eggs on
the ground and attach to a
host
Ticks stay on host and feed
and molt several times until
they are adults
Engorged and fertilized female
drops of to lay eggs and dies
Transovarial infection is very
important for effective
transmission in one host ticks
29
Pathogenesis
Pathogenic effect is intra-vascular hemolysis.
The vasodilatation accompanied by

increased vascular permeability leading to
circulatory stasis and shock.
Proteolytic enzymes liberated from infected

RBCs, interact with blood componenets and
produces erythrocytic fragility, hypotensive
shock and intra-vascular coagulation.
30
When a few RBCs are destroyed, free Hb is transferred

into bile pigments in liver and excreted in the bile but
when destruction is heavy; excess Hb is excreted in
urine (Hburea) and icterus is manifested.
In severe cases anemia and nutritional disturbances

lead to fetal termination.
Death occurs due to anemic anoxia.
When a cow become affected during pregnancy

there is no apparent infection of calf in uterus, but
there is an apparent transfer of immunity via
colostrums to new born calves.
31
IP
Cattle: 2-3 weeks
Horse: 8-10 days
32
Symptoms
High fever, 106 oF; anorexia;
depression; weakness; cessations of
urination and fall in milk yield.
Respiration and heart rates are
increased.
Brick red conjunctivitis; severe
jaundice; urine- dark red to brown;
severely affected animals die after 24
hrs. Pregnant animals may abort. In
young animalsmohangupta63@gmail.com
mild fever, but Hburea 33
Symptoms
Animals affected with B. bigemina
shows cerebral babesiosis
characterized by incordination,
posterior paralysis, mania, convulsions
and coma. Infections with B.
divergens: spasms of anal sphincter
causing the passage of PIPE STEM
FECES.
34
35
36
Horse: Symptoms
Onset of immobility; reluctance to
move; some are in lateral recumbancy;
do not respond to stimuli; fever 104 oF.
Complete anorexia,
- edema of fetlock, head and ventral
abdomen.
37
Horse: Symptoms
- Feces are mucus covered and colic
occurs.
-No Hburea in horse. Mucosa- pale pink

and tinged with jaundice. Horse may
die within 24 hrs.
38
Diagnosis
1.Hematology: decreased level of Hb
by 20% (i.e., 3 gm/dL); PCV: 16%
reduction; 20% reduction in TRC;
increased leucocyte count-- marked
neutrophilia and
increased ESR.
39
Diagnosis
2.P/M Findings:
Carcass anemic; spleenomegaly (soft,
pulpy, and enlarged);
frothy exudates in trachea, bronchi
and lungs;
distension of gall bladder
. Blood tinged fluid in pericardium. S/C
tissues and muscles are pale.
40
Diagnosis
2.P/M Findings:
Hemorrhage in kidneys, liver, gall
bladder, LNs, and GI mucosa.
Embolism in brain capillaries.
Urinary bladder: reddish brown urine
(coffee colored).
41
Bovine, brain. The

cerebral cortex is
diffusely reddened
(cerebral flush).
42
Diagnosis
3.Serology:
Capillary tube AT;
Indirect HA;
Indirect FAT;
RIA;
ELISA
43
Differential Dx
1. Anaplasmosis: less acute disease;
relapses are more common; Hburea is
rare or does not occur. Calves are
resistant.
2.Eperthrozoonosis: anemic, less
severe than Babesiosis; caused by
Rickettsia eperthrozoan. Haemotrophic
Mycoplasma???
44
Differential Dx
3.Thelariosis: T. annulata, T. parva;
Piroplasms in RBCs. LNs enlarged;
massive pulmonary edema and
hyperemia.
4.Leptospirosis: leptospirurea;
abortions common; calves have high
mortality: 50%; septicemia and
toxaemia; adults have thick orange
milk.
45
Differential Dx
5.Trypanosomiasis
6. Bacillary haemaglobinuria (caused by
Clostridium hemolyticum (Cl. Novyi Type D).
Fatal disease of cattle dies within 24-36 hrs.
7. Rabies
8. Rapeseed poisoning
9. Chronic copper poisoning
10. Post Parturient hemoglobinuria: due to
P deficiency
46
Rx: Cattle
Diminazine aceturate (Berenil): 0.8-1.6
gm/100 kg. b.wt. i/m, on alternate
day or week.
Cattle: 10 mg/kg b.wt.
Horse: 3 mg/kg. b. wt.
Quinorarium derivatives: Acaprin,
Babesan, Piveran, Piroparv,
Piroplasmin etc.
47
Rx: Cattle
Acaprin(Quinirorium derivative) @ 1 ml. /50 kg.
b. wt. s/c- single dose. Reaction with
this drug: salivation, sweating,
diarrhea, panting, collapse and death.
Use adrenalin as antidote.
Imidocarb(IMIZOLE): @ 1mg/kg, b. wt
s/c- single dose.
Trypan blue 1%: 100-200 ml i.v- single
48
dose.
Rx: Horse
1.Imicarbalide isothionate
(PHENAMIDINE), Diminazine aceturate
(Berenil); Piravan, Diampran. OTC have
been used.
2.Imidocarb: most favoured drug for
horse: 4 mg/kg, b.wt i/m at 72 hrs
interval OR, 2 mg/kg b.wt. at 24 hrs.
interval. The hcl salt of imidocarb is
more acidic and causes local reaction
so that dipropionate salt is used more 49
commonly.
Rx: Sheep & Goat

Berenil is the drug of choice. @ 3.5
mg/kg b.wt. Give 2 injs, on alternate
day or alternate week. OR, 12 mg/kg.
b.wt. -single dose i/m.
50
Disease control is mostly

through vector control
Disease can be treated with drugs

A partially effective attenuated
vaccine is available
Tick control mostly through pesticide
application remains the most
important counter measure
51
Vaccination of cows with an

antigen from the tick midgut
Antigen Bm86
gut
Host
Salivary gland
normal
vaccinated
Proteins found on the

surface of the gut
epithelium of Boophilus
ticks have be
characterized and used
to make a recombinant
vaccine (against the
tick not the parasite)
Ticks fed on vaccinated
cows are exposed to
antibody/complement
mediated attack of their
epithelium
These tick grow poorly
52
and have low fecundity
Vaccination:
a.Live vaccine: resistance in calves.
b.Killed vaccine: killed adjuvant
vaccines have been successful in
cattle. Subunit vaccine derived from
monoclonal technique were proven
effective against several clinical
diseases. Mab inhibits merozoites
invasion of RBCs.
53
Irradiated vaccine:
Irradiated B.bigemina vaccine has been
used with success.
54
Two commercial vaccines

are available for
Boophilus microplus,
both based on the Bm86
antigen: TickGARD in
Australia and GAVAC in
Cuba and parts of South
America
55
Babesia microti
VECTOR - ______________________________
- larvae and nymphs feed on meadow voles to pick up infection
- they then bite humans to transmit the disease

- no transovarian transmission
(dont confuse babesiosis with Lyme disease,
a bacterial disease, also transmitted by deer ticks)
meadow vole
Human
deer tick
56
Babesia microti
This species normally occurs in
________________________________, but recent cases of it have
been reported in humans.
Causes _________________________________________reported in Massachusetts (first report in 1975), New York, Rhode

57
Island, and Wisconsin
Transmission in man
58
Infrequent human babesiosis in

the U.S. by B. microti
Some species of Babesia
(in particular B. microti)
that naturally infect small
rodents like the whitefooted mouse can also
infect humans
B. microti is transmited by
infected Ixodes ticks (dear
ticks)
Most transmission occurs
along the North-Eastern
seaboard and infection
rates can be relatively high
locally
The epidemiological risk
factors are very similar to
59
Lyme disease
Infrequent human babesiosis in

the U.S. by B. microti
Human blood film with B. microti, Giemsa stain

Vannier & Krause 2009
Many infections likely go undiagnosed,

about a third of the infections are
asymptomatic
Most infected show mild disease with
general malaise and fatigue and fever
and chills
People who are elderly or immunecompromised (including in particular
people without a spleen) are most
likely to show severe disease
Heavy RBC infection in severe cases
can lead to acute respiratory failure,
congestive heart failure and other
complications with a mortality rate of
5-10%
Babesiosis can be treated with
antibiotics that target the apicoplast
and/or the parasite mitochondrion
60

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Piroplasms: Babesia & Theileria

Morbidity and mortality: 90%

Babesia bigemina, B. bovis,

Babesia equi(now called Theleria

Babesia ovis; B. motasi

Babesia canis; Babesia gibsoni

B.bovis and B. bigemina

Devastating outbreaks follow the big cattle

Theobald Smith and Frederick

Babesia bigemina causes

Mortality in acute untreated cattle

Babesia bigemina causes

Distribution of Tick fever

Babesiosis coincides with the distribution of the main

In the passage of host blood to the midgut of the tick

The zygote selectively infects the digestive cell of the tick

Thus, trans ovarial transmission occurs with

Life Cycle of Babesia bigemina

2. Sporozoite penetrates a rbc and

5. Feeding tick picks up rbc's with

Boophilus is a single host tick

The vasodilatation accompanied by

Proteolytic enzymes liberated from infected

When a few RBCs are destroyed, free Hb is transferred

In severe cases anemia and nutritional disturbances

Death occurs due to anemic anoxia.

When a cow become affected during pregnancy

-No Hburea in horse. Mucosa- pale pink

Bovine, brain. The

Rx: Sheep & Goat

Disease control is mostly

Disease can be treated with drugs

Vaccination of cows with an

Proteins found on the

Two commercial vaccines

- they then bite humans to transmit the disease

Causes _________________________________________reported in Massachusetts (first report in 1975), New York, Rhode

Infrequent human babesiosis in

Infrequent human babesiosis in

Human blood film with B. microti, Giemsa stain

Many infections likely go undiagnosed,

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