In the ppt. Babesia is explained along-with its species, its life cycle, treatment and prevention. It explains Babesia and answers questions like, What is Babesiosis? What are the species of Babesia? What is the host of Babesia? How they are spread across the globe? What are their mode of reproduction? What is their life cycle? What is the historical background of Babesiosis? How scientist named the disease? What is the morphology of Babesia? What are the stages of Life cycle of Babesia? How Babesiosis is treated? How can we prevent Babesiosis?

1. Family Babesiidae
By: Hooria Parvez

2. Morphological
Charateristics:
• Babesiids are usually described from their stages in the red
blood cells of vertebrates. They are pyriform, round, or oval
parasites of erythrocytes, lymphocytes, histiocytes,
erythroblasts, or other blood cells of mammals and of various
tissues of ticks.
• Their apical complex is reduced to a polar ring, rhop
microtubules.tries, micronemes, and subpellicular
microtubules.
• A cytostome is present in at least some species. Schizogony
occurs in ticks.
• By far the most important species in America is Babesia
bigemina, the causative agent of babesiosis, or Texas red-
water fever, in cattle.

3. Babesia
bigemina:
History of Disease:
By 1890 the entire southeastern United States was plagued by a disease of cattle, variously
called Texas cattle fever, redwater fever, or hemoglobinuria. Infected cattle usually had red-
colored urine resulting from massive destruction of erythrocytes, and they often died within
a week after symptoms first appeared.
The death rate was much lower in cattle that had been reared in an enzootic area than in
northern animals that were brought south. Also, it was noticed that, when southern herds
were driven or shipped north and penned with northern animals, the latter rapidly
succumbed to the disease.
The cause of red-water fever and its mode of dissemination were a mystery when Theobald
Smith and Frank Kilbourne began their investigations in the early 1880s. In a series of
intelligent, painstaking experiments, they showed that the tick Boophilus annulatus ( Fig.
9.14 ) was the vector and alternate host of a tiny protozoan parasite that inhabited red
blood cells of cattle and killed these relatively immense animals. Their investigations not
only pointed the way to an effective means of control, but were also the first
demonstrations that a protozoan parasite could develop in and be transmitted by an
arthropod

4. Babesia
bigemina: Hosts: Babesia bigemina infects a wide variety of
ruminants, such as deer, water buffalo, and zebu, in
addition to cattle.
Physical Form of parasite: When in an erythrocyte of a
vertebrate host, the parasite is pear shaped, round, or,
occasionally, irregularly shaped, and it is 4.0 μm long by
1.5 μm wide.
Nomenclature: Organisms of this species usually are seen
in pairs within an erythrocyte (hence the name bigemina
for “the twins”) and are often united at their pointed tips.
Reproduction: At the light microscope level, they appear
to be undergoing binary fission, but electron microscopy
has revealed that the process is a kind of binary
schizogony, a budding analogous to that occurring in
Haemosporida, with redifferentiation of the apical
complex and merozoite formation.

5. Babesia bigemina: (The Life Cycle)
The infective stage of Babesia in ticks is a sporozoite.
 It is about 2 μm long and is pyriform, spherical, or ovoid.
 After completing development, sporozoites in tick salivary glands are injected with its
bite.
There is no exoerythrocytic schizogony in the vertebrate. Parasites immediately enter
erythrocytes, where they become trophozoites and escape from the parasitophorous
vacuole.
They undergo binary fission and ultimately kill their host cell.
 Merozoites attack other red blood cells, building up an immense population in a short
time.
This asexual cycle continues indefinitely or until the host succumbs.
 Erythrocytic phases are reduced or apparently absent in resistant hosts.
 Some of the intraerythrocytic parasites do not develop further and are destined to
become gametocytes, called ray bodies, when ingested by a tick.

6. Life Cycle

7. Life Cycle Cont…
• Ticks of genus Boophilus transmit Babesia bigemina ; thus,
distribution of the tick limits distribution of babesiosis. Boophilus
annulatus is the vector in the Americas. It is a one-host tick, feeding,
maturing, and mating on a single host.
• After engorging and mating, a female tick drops to the ground, lays
her eggs, and dies. The larval, six legged ticks that hatch from eggs
climb onto vegetation and attach to animals that brush by the plants.

8. Life Cycle Cont…
• TRANSOVARIAL TRANSMISSION: One would think that a one-host
tick would be a poor vector—if they do not feed on successive hosts,
how can they transmit pathogens from one animal to another? This
question was answered when it was discovered that the protozoan
infects the developing eggs in the ovary of the tick, a phenomenon
called transovarial transmission.
• After ingestion by a feeding tick, the parasites are freed by digestion
from their dead host cells, and they develop into ray bodies. These
are bizarrely shaped stages that have a thornlike process and several
stiff, flagella-like protrusions.

9. Life Cycle Cont…
• Fusion of two ray bodies forms a zygote, which becomes a primary kinete.
• The primary kinetes leave the intestine and penetrate various cells, such as
hemocytes, muscles, Malpighian tubule cells, and ovarian cells including
oocytes.
• They enlarge and become polymorphic, dividing by multiple fission into a
number of cytomeres, which differentiate into new kinetes.
• Some secondary kinetes migrate to the salivary glands, penetrate gland
cells, and become polymorphic.
• They stimulate host cells and nuclei to hypertrophy. When a host begins to
feed, parasites rapidly undergo multiple fission to produce enormous
numbers of sporozoites about 2 μm to 3 μm long by 1 μm to 2 μm wide.
• These sporozoites enter the channels of the salivary glands and are
injected into the vertebrate host by the feeding tick.

10. Life Cycle Cont…
Although this is the life cycle as it occurs in a one-host tick, two- and
three-host ticks serve as hosts and vectors of B. bigemina in other parts
of the world. With these ticks transovarial transmission is not required
and may not occur. All instars of such ticks can transmit the disease.

12. Life Cycle of Babesia
cannis

14. Life Cycle of Babesia cannis:
• ( 1 ) Sporozoite injected with saliva of feeding tick.
• ( 2, 3 ) Asexual reproduction in red blood cells of vertebrate host by
binary fission, yielding merozoites.
• ( 4 ) Merozoites in erythrocytes are ingested by tick.
• ( 5, 6 ) Gametocytes form protrusions after ingestion by tick and
become ray bodies.
• ( 7–9 ) Two ray bodies fuse to form zygote.
• ( 10 ) Zygote becomes motile kinete.
• ( 11 ) Kinetes leave intestine, enter other cells, and form new
kinetes.
• ( 12 ) Kinetes that enter cells of salivary gland give rise to thousands
of small sporozoites.

15. Pathogenesis:
Babesia bigemina is unusual in that the disease it causes is more severe in adult
cattle than in calves.
 Calves less than a year old are seldom seriously affected, but the mortality rate
in acute cases in untreated adult cattle is as high as 50% to 90%.
 The incubation period is 8 to 15 days, but an acutely ill animal may die only four
to eight days after infection.
 The first symptom is a sudden rise in temperature to 106°F to 108°F; this may
persist for a week or more.
 Infected animals rapidly become dull and listless and lose their appetite.
Up to 75% of erythrocytes may be destroyed in fatal cases, but even in milder
infections so many erythrocytes are destroyed that a severe anemia results.
Mechanisms for clearance of hemoglobin and its breakdown products are
overloaded, producing jaundice, and much excess hemoglobin is excreted by the
kidneys, giving the urine the red color mentioned earlier.
Chronically infected animals remain thin, weak, and out of condition for several
weeks before recovering. Levine described damage to internal organs.

16. Cattle that recover are usually immune for life with a sterile immunity or, more commonly,
premunition.
There are strain differences in the degree of immunity obtained; furthermore, little cross-
reaction occurs between B. bigemina and other species of Babesia.
TREATMENT:
For unknown reasons drugs that are
effective against trypanosomes are
also effective against Babesia spp. A
number of chemotherapeutic agents
are available, some allowing
recovery but leaving latent infection,
others effecting a complete cure. It
should be remembered that
elimination of all parasites also
eliminates premonition.

17. Prevention:
Infection can be prevented by tick control, the means by which
red-water fever was eliminated from the United States.
 Regular dipping of cattle in a tickicide effectively eliminates
vectors, especially if it is a one-host species.
 Another method that has been used is artificial premunizing of
young animals with a mild strain before shipping them to
enzootic areas.

18. Babesia microti: Historical background:
 Prior to 1969 Babesia infections in humans were rare.
 There have been a few reports of infections caused by species normally
parasitic in other animals.
 In several cases, three of which were fatal, patients had been
splenectomized some time before infection, and it was believed that the
disabling of the immune system by splenectomy rendered the humans
susceptible.
 However, human infection with Babesia in a nonsplenectomized patient
was reported from Nantucket Island off the coast of Massachusetts in
1969.
 Since then, hundreds of cases have been recorded, most in the northeast
United States but some in Wisconsin, Washington, and California.
 These have all been infections with B. microti, a parasite of meadow voles
and other rodents that can also infect pets.
 The vector is Ixodes scapularis, whose adults feed on deer. Deer are
refractory to infection with B. microti, and the infection is transmitted
among rodents and to humans by nymphs of I. scapularis and among
rodents by I. muris, which does not feed on humans.
 It is unclear why this formerly rare infection has now become almost
common. However, as with Lyme disease ,the explanation probably lies in
the increased contact of humans with ticks and the reservoir hosts.

19. Other Species of Babesiidae:
• Cattle seem particularly suitable as hosts to piroplasms.
• Other species of Babesia in cattle are B. bovis in Europe, Russia, and
Africa; B. berbera in Russia, North Africa, and the Middle East; B.
divergens in western and central Europe; B. argentina in South America,
Central America, and Australia; and B. major in North Africa, Europe, and
Russia.
• Several other species are known from deer, sheep, goats, dogs, cats, and
other mammals as well as birds. Their biology, pathogenesis, and control
are generally the same as for B. bigemina.
• Babesia divergens occasionally occurs in splenectomized humans in
Europe, and two such cases have been reported in the United States.
• Another Babesia sp. occurs in rabbits ( Syvilagus floridanus ) in the United
States. It is morphologically and genetically similar to B. microti and B.
divergens but will not grow in bovine erythrocytes in vitro.