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 TOXOPLASMA GONDI AND
BABESIA
TOXOPLASMA GONDI : is a single-celled, obligate
intracellular protozoan parasite belonging to the phylum
Apicomplexa. It is one of the most common parasites infecting
humans and warm-blooded animals worldwide. It is commonly
found in cat faeces and can be transmitted through ingestion of
contaminated food or water.also it is transmitted through
food chains, mainly through carnivores and scavengers .

 Features of T.gondi
 Worldwide distribution
 Zoonotic parasite; Toxoplasma is an opportunistic
pathogen.
 Infects animals, cattle, birds, rodents, pigs, sheep,
and humans.
 Causes the disease Toxoplasmosis.
 Intracellular parasite.
 Final host (Felidae family, cat)
 Intermediate host (mammals )

Epidemiology of toxoplasmosis
Toxoplasmosis infection was reported in warm-blooded animals and
humans, and the distribution was reported throughout the world. It
affected almost all species, from mammals to various bird species .
In the case of humans, toxoplasmosis was reported in nearly all parts
of the world, and about one-third of human populations were
vulnerable to latent infection. The incidence of toxoplasmosis in
developing and underdeveloped nations is reported to be very high;
however, it is noted that the infections were low in developed
countries. High prevalence of toxoplasmosis was reported in Africa,
parts of south-east Asia, Middle East, parts of Central/Eastern
Europe, and Latin America. . Food preparing habits such as
thoroughly cooked foods (meat) or half-cooked were the critical
factors influencing transmission ). Eating raw mussels, clams, and

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oysters have been predicted as a significant risk factor of
toxoplasmosis in various countries, including the USA ). It was
estimated that about 25–30% of human populations infected with T.
gondii . Many climatic factors that influence the survival rate of
oocysts and ruminants play a significant role in transmitting disease.
Also, seroprevalence was observed to be higher with aged people ;
however, the infection rate was largely associated with older age
adults and varied based on individuals' socio-economic conditions.
Water carries oocysts, and the consumption of unfiltered water or
water in recreation facilities contributed to disease transmission. The
socio-economic level has been an influencing factor on
toxoplasmosis infection.

Distribution of toxoplasmosis in Ethiopia In

Ethiopia the risk factor
associated with seropositivity to toxoplasma infection were
consumption of raw or undercooked meat and presence of cat in
the households . There are no reports of clinical toxoplasmosis
in animals. Serological surveys indicate a high prevalence of T.
gondii antibodies in sheep and goats. Recently reported 52.8% in
Small Ruminants from Yabello, Borana Zone and reported 74.
9% from central and southern regions of Ethiopia.

The studies have found a seroprevalence of 85.4% of feral cats

sampled in Ethiopia . The overall prevalence recorded in sheep
in Ethiopia and other African countries is 54.7% [56-60].
Ethiopia reported prevalence of toxoplasmosis in the general
population ranging from 20.2% to 97.7%.

Cats are the definitive host and are the only species know
complete the sexual phase of T. gondii culminating in the

passage of oocysts in feces.invertebrates can serve as transport

hosts by mechanical carriage of T. gondii oocysts.

Toxoplasmosis is is an infection with a parasite

called Toxoplasma gondii.
1. All parasite stages are infectious.
2. Risking group: Pregnant women, meat handlers (food
preparation) or anyone who eats the raw meat

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3.Immune sup present people like HIV AIDS people
Toxoplasma gondii exists in three forms
.. All parasite stages are infectious
1. Tachyzoites
2. Tissue cysts (bradyzoit)
3. Oocysts
Tachyzoite stage

 Rapidly growing stage observed in the early stage of

infection. (Acute phase) habits in the body fluid.
 Crescent-shaped. One end is more pointed than the other
subterminal placed nucleus.
 Asexual form.
 Multiplies by endodyogeny.
 It can infect phagocytic and non-phagocytic, cells.

Bradyzoites stage

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 Are slow-growing stage inside the tissue cysts.
 Bradyzoites mark the chronic phase of infection.
 Bradyzoites are resistant to low pH and digestive
enzymes during stomach passage.
 Protective cyst wall is finally dissolved and
bradyzoites infect tissue and transform into
tachyzoites.
 Bradyzoites are released in the intestine and are
highly infective if ingested.

Oocyst stage

 The oocyst is noninfectious before sporulation.

 Unsporulated oocysts are subspherical to spherical.
 Sporulated oocysts are subspherical to ellipsoidal.
 Each oocyst has two ellipsoidal sporocysts.
 Each Sporocyst contains four sporozoites .
 Shedding occurs 3-5 days after ingestion of tissue cysts
 Sporulated oocyst remain infective for month.

Oocysts in the feces of cat

 Cat ingests tissue cysts containing bradyzoites.
 Gametocytes develop in the small intestine.
 Sexual cycle produces the oocyst which is excreted in
the feces.
 Oocysts appear in the cat’s feces 3-5 days after
infection by cysts.
 Oocysts require oxygen and they sporulate in 1- 5
days.

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 The life cycle of Toxoplasma

Life cycle of toxoplasma can be divided into two stages;

I, The asexual cycle :with little host specificity i.e., the stage
that occurs in sheep, humans, rodents and birds.
II, The sexual stage of the life cycle, confined to the intestinal
epithelial cells of cats,which results in the production of oocysts.
The lifecycle of T. gondii is unique among the parasite and
includes asexual as well as sexual reproduction . Further, three
different infective stages representing invasive tachyzoite
(rapidly dividing), bradyzoite in tissue cysts (slowly dividing),
and the sporozoite (environmental stage) are common.
Sporozoite form of life is protected inside the oocysts and is an
environmental stage. T. gondii at various stages are
approximately 2 m wide and 5 m long, crescent-shaped cells, a
rounded posterior end, and a pointed apical end. The motility
and structural integrity of the cells are governed by the
cytoskeleton. They contain apicoplast, a multiple-membrane-
bound plastid-like organelle, endoplasmic reticulum, ribosomes,
Golgi complex, and a mitochondrion. This parasite is also
associated with endosymbiosis of various algae . The parasite's
cytoskeletal structure helps to invade the cells and various
secretary organelles such as micronemes, dense granules, and
rhoptries .

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 Cats and some felines are the definitive hosts of T. gondii . It
can develop its life cycle in the intestinal epithelium of these
animal . Once infected cats excrete their wastes (oocysts) to
the environment, it may infect any vertebrate animal that
consumes the oocysts, including humans . Ingestion and
manipulation of raw or undercooked meat, unwashed vegetables
and fruits, the consumption of the unboiled water and contact
with cats are risk factors that increase the likelihood of ingesting
oocysts and consequently the development of Toxoplasmosis. In
humans, if the infection happens during the stage of pregnancy,
the Toxoplasma gondii can be transmitted vertically to
the fetus through the tachyzoites , invade the cells and infect all
the organs of the fetus , primarily retina, brain, muscle and
heart.
Toxoplasmosis is an infection caused by the protozoan parasite
Toxoplasma gondii. It is one of the most common parasitic
infections in humans, with an estimated one-third of the world's
population infected.
Toxoplasmosis is primarily transmitted through contact with cat
feces or by ingesting raw or undercooked meat from infected
animals (e.g., pork, lamb, venison). Cats become infected by
eating rodents or other small animals that carry the parasite.
toxoplasmosis often causes no symptoms or only mild, flu-like
symptoms that may go unnoticed. However, it can be more
severe in certain populations, including:
• Pregnant women: Infection during pregnancy can lead to
congenital toxoplasmosis in the fetus, which can cause serious
birth defects or miscarriage.
• Immunocompromised individuals: People with weakened
immune systems are at risk of developing severe toxoplasmosis,
which can affect the brain, eyes, or other organs.
Ocular toxoplasmosis is a common manifestation of
toxoplasmosis, characterized by inflammation and scarring of
the eye's retina. It can lead to vision impairment or even
blindness.

 Development of clinical toxoplasmosis is dependent on both

host and parasite. Some strains of T. gondii may be more

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 pathogenic than others, and some strains may have specific
tissue affinities, such as a tendency to cause ocular disease in
cats. If a poor immune response is mounted after primary
infection, overwhelming tachyzoite replication that results in
tissue necrosis is the major cause of disease. Eosinophilic
fibrosing gastritis was recently described in a T. gondii–
infected cat.
Fatal extra intestinal toxoplasmosis in cats can develop from
overwhelming intracellular replication of tachyzoites following
primary infection; hepatic, pulmonary, CNS, and pancreatic
tissues are commonly involved.Kittens infected by the
transplacental or transmammary routes develop the most
severe signs of extra intestinal toxoplasmosis and generally
die of pulmonary or hepatic disease. Common clinical signs
in cats with disseminated toxoplasmosis include lethargy,
anorexia, and respiratory distress.
Transmission of Toxoplasmosis
Transmission of the disease reported to occur mainly through
water, from contaminated food, ingestion of the tissue cysts,
congenital transmission, or ingestion of oocyts. However, this
disease's transmission varied widely among populations, mainly
based on food habits and culture. The infection can get through
unpasteurized milk and contamination of blood products by
tachyzoite. Tissue cysts are located in the brain and muscle of
most of the intermediate hosts. Cats reported to acquire
toxoplasmosis through contaminated prey such as birds or
rodents and act as hosts to continue sexual reproduction,
enteroepithelial cycle, and oocyst production . Carnivorous
animals from wild habitats such as skunks, raccoon, fox, bears
also acquire toxoplasmosis through the ingestion of cysts from
tissues.
 Human beings acquire toxoplasmosis by consuming half-
cooked contaminated meat, such as lamb or pork . The
ingested tissue cyst is digested by the action of various
proteolytic enzyme activities in the stomach of the host
organism and release the parasite in the form of bradyzoites.
The parasite is observed to be highly resistant to protease
and survive in the host organism's small intestine. A report

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 estimated more than 10 million cyst removal through fecal
materials in cats within two weeks of ingestion. The released
oocyst sporulates within five days of release in the
environment. In the soil sample, the sporulated organism
remains alive for about one year .

 Generally, eating contaminated vegetables, fruits, or

contaminated food with oocysts were the major risk factors
of disease transmission. These risk factors and modes of
actions were assessed previously by and . In human beings,
oocyst induced infections are highly complex and more
severe than cyst acquired infections . Among cats, oocyst
shedding happens for a short duration, and the fastidious
nature of cats, the passing of non-infective oocysts, direct
contact with cats is no risk to any kind of infection from cats .
In seawater, oocysts are stable for six months, and this
revealed that the coastal environment is an essential source
of infection. Also, the oocysts transfer from one host to
another . Oocysts could tolerate a wide environment and
survive in fishes such as sardines and anchovies (filter
feeders), and it remained in the alimentary canal of the
organism and be viable The congenital transmission is also
reported, and this stage of transmission happens when the
time of toxoplasmosis is at the acute phase. Tachyzoites form
of parasite from the mother crosses the placenta and causes
infection in the fetus. The effect of maternal toxoplasmosis is
based on the stage of pregnancy. During the earlier stages of
pregnancy (first trimester), maternal toxoplasmosis is very
low; however, at the later stages of pregnancy, the
transmission rate increased by about 80% Maternal
toxoplasmosis in earlier stages caused various problems,
including mental retardation, hydrocephaly, and spontaneous
abortion. However, during the final trimester transmission
rate was very high, and various subclinical interventions such
as recurrent chorioretinitis, subclinical interventions
potentially blindness or vision problems reported in children.

In general toxoplasmosis transmitted by

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Contaminated water or food by oocysts
Ingestion of tachyzoites and bradyzoites
(cysts) in flesh of infected host.
Undercooked meat.
Mother to fetus.
 Organ transplant (rare).
Blood transfusion (rare)
Pathogenesis of toxoplasmosis
The virulence factors of the parasite and immune defenses of the
host might drive the species-dependent susceptibility to
toxoplasmosis Obviously, the immune status of the host also
influences the development of the disease. It considered the most
frequent opportunistic pathogen in AIDS patients and there are
numerous reports of infections after immunosuppressive.
Toxoplasma infection, with the infection usually being in
apparent or producing only transient mild symptoms during the
acute phase, although the host remains chronically infected for
its lifetime .

Toxoplasma gondii infection outcome varies depending on the

genetic background and immune status of the host, as well as on
the parasite genotype. The resistance or susceptibility to
infection seems to differ depending on the host species and even
the subspecies, as has been demonstrated in the case of rodents.
T. gondii infection influencing a range of human behaviors and
personality disorders were evaluated psychiatric patients the
primary diagnoses like alzheimer's, schizophrenia, major
depression, schizoaffective, or bipolar .

DIAGNOSIS OF TOXOPLASMOSIS

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The diagnosis of T. gondii infection is crucial for the
surveillance, prevention and control of toxoplasmosis .

Microscopic diagnosis
These techniques imply the detection of the parasite based on
light microscopy. Despite having been traditionally used, they
have a low sensitivity and require skilled personnel to obtain
reliable detection results . Oocysts could be identified on faecal
(felids), water, soil, or food (i.e., susceptible to T. gondii
presence like vegetables or fruit) samples, and even in aerosols,
after filtration and centrifugation processes .

Bioassay: Cats are the most sensitive bioassay model for the
detection of T. gondii in meat because an animal can be fed with
much larger volumes of tissues (500 g or more) and can excrete
millions of oocysts after ingesting only one bradyzoite .

Molecular methods -DNA detection

PCR-based diagnosis methods cover the inherent limitations of
traditional diagnostic methods, being much more sensitive and
specific. Nested-PCR targeting multicopy genes, usually used
for the detection of T. gondii in biological samples, where in
some cases the parasite burden is extremely low (e.g., blood
samples) . PCR amplification is very important for detection of
T. gondii DNA in body fluids and tissues and enables an [88]
early detection of T. gondii DNA in brain tissue, cerebrospinal
fluid (CSF), Vitreous and aqueous fluids, bronchoalveolar
lavage (BAL) fluid and blood .

Serological assays
The serologic tests for demonstration of specific antibody to T.
gondii are the initial and primary method of diagnosis. Based on
specific antibodies detection (indirect diagnosis) to determine
the time point of infection (recent/chronic), a valuable
alternative is the detection of circulating antigens in serum

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(direct diagnosis) in ELISA has been designed .A combination
of serologic tests is required to measure different antibodies that
possess unique patterns of rise and fall with time after infection .
Toxoplasma l Profile (TSP), ELISA and AC/HS tests are used to
determine infection acquired in the recent or more distant past .

Treatment of toxoplasmosis
Intensive supportive treatment may be necessary in animals
with disseminated disease. Clinical cases are treated with
antibiotics. Only certain drugs, such as clindamycin and
azithromycin used alone or in various combinations, are
effective. The most effective treatment of toxoplasmosis is a
combination of the oral antibiotic drugs pyrimethamine and
sulfadiazine plus the B vitamin folinic acid. Corticosteroids may
be administered concurrently in ocular disease to reduce
inflammation. While antibiotics can suppress actively dividing
parasites, they cannot destroy tissue cysts and are unlikely to
completely eliminate T. gondii from the body .

Prevention and control

To prevent food-borne horizontal transmission of T. gondii,
meat and other edible parts of animals should not be consumed
raw or undercooked, i.e. they should be cooked thoroughly
(67°C) before consumption. Deep-freezing meat (−12°C or
lower) before cooking can reduce the risk of infection. In
addition, meat should not be tasted during seasoning or cooking
The main strategies for controlling of toxoplasmosis involve
transmission control, it depends on the host species on which we
were focused but they are always based on reducing the
exposure to T. gondii oocysts in the environment and avoid the
ingestion of meat potentially contaminated with tissue cysts .

The implementation of farm biosecurity protocols, hygienic

measures and management practices should be adopted in all
farms, mainly for reducing the level of environmental
contamination with T. gondii oocysts via cat faeces or limiting

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the access of felids to abortion-derived tissues. Basic
measurements are: avoiding cat access to farm areas, especially
to those housing pregnant ruminants, troughs food warehouses
and water supplies; promptly removing any abortion-derived
tissue as well as appropriately disposing of animal carcasses
[109] and establishing rodent control. In humans, consumption
habits, preventing to eat raw or undercooked meat in which
possible tissue cysts remain viable or washing vegetables and
fruit before consumption, as well as to the way we handle
domestic c

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 BABESIA
Babesia :also called Nuttallia and
an apicomplexan parasite that infects red blood cells and
is transmitted by ticks. Originally discovered by the
Romanian bacteriologist Victor Babeș in 1888, over 100
species of Babesia have since been identified.
Babesia comprises more than 100 species of tick-borne
parasites that infect erythrocytes (red blood cells) in many
vertebrate hosts.
Babesia species infect livestock worldwide, wild and
domestic vertebrate animals, and occasionally humans,
where they cause the disease babesiosis.
B. microti is the most common strain of the few which
have been documented to cause disease in humans and
a
 Phylum: Apicomplexa
 Class: Sporozoa
 Order: Piroplasmida
 Family: babesidae
 Genus : Babesia
Classification
Babesia species are classified into four major clades
based on their genetic characteristics:
Clade I:
• Babesia divergens
• Babesia odocoilei
• Babesia venatorum
Clade II:
• Babesia bovis
• Babesia bigemina
• Babesia caballi
Clade III:

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 • Babesia duncani
• Babesia gibsoni
• Babesia microti
Clade IV:
• Babesia canis
• Babesia felis
• Babesia vogeli
Additional species:
• Babesia lengau
• Babesia ovata
• Babesia starlingi

Clade I: Babesia species are primarily found in North

America and Europe and infect a wide range of
mammals, including humans. Babesia divergens is the
most common Babesia species that infects humans in
North America and Europe.

Clade II: Babesia species are primarily found in

tropical and subtropical regions and infect cattle and
other large mammals. Babesia bovis and Babesia
bigemina are the most common Babesia species that
infect cattle and cause significant economic losses in the
livestock industry.

Clade III: Babesia species are primarily found in Asia

and Africa and infect a wide range of mammals,
including humans. Babesia gibsoni is the most common
Babesia species that infects humans in Asia and can
cause severe and even fatal infections.

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 Clade IV: Babesia species are primarily found in
Africa and infect dogs and cats. Babesia canis is the most
common Babesia species that infects dogs and can cause
severe and even fatal infections.

Babesia spp Animals Principal Tick vectors

affected Geographical
distribution
Babesia bovis Cattle, deer, America, Ixodes ricinus, I.
Water buffalo, Europe, persulcatus, B. calcaratus,
Wild ruminants Australia, Rh. Bursa
Middle East,
Africa
Babesia bigemina Cattle Zebu, America, Boophilus annulatus, B.
Water buffalo, Europe, microplus, B. australis B.
Deer, Wild Australia, calcaratus, B. decoloratus,
ruminants Russia Rhipicephalus everts Rh.
bursa, Rh. appendiculatus
Haemaphysalis punctate
Babesia divergens Cattle Europe I. ricinus

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Distribution in Ethiopia
Ethiopia has the largest livestock population in
Africa
The presence of diseases caused by haemoparasites
is broadly related to the presence and distribution
of their vectors.Arthropod transmitted
haemoparasitic disease of cattle is caused by the
trypanosome,babesia,theileria and anaplasma species
In Ethiopia, now days no adequate emphasis has been
given to livestock disease, particularly, to Bovine
Babesiosis, despite of its devastating effect on
cattle and other livestocks.Bovine Babesiosis is one
of the most important diseases in the country
because it occurs sometimes in acute forms with
serious recognized clinical manifestations yet
lowering the productive performance of the affected
animals.Generally bovine babesiosis is one of the
most important diseases that seriously hinder cattle
production in Ethiopia and other part of the world.
Transmission and life cycle
Babesia species are transmitted to humans and other
animals through the bite of an infected tick. Ticks become
infected with Babesia parasites when they feed on an
infected animal. The parasites then multiply in the tick's
gut and salivary glands. When the tick bites a new host,
the parasites are transmitted through the tick's saliva.

Babesia species can also be transmitted through blood

transfusions or organ transplants from an infected donor.
Transmission of Babesia species:
• Babesia divergens and Babesia odocoilei are transmitted
by the blacklegged tick (Ixodes scapularis) in North
America.
• Babesia microti is transmitted by the deer tick (Ixodes
dammini) in North America.
• Babesia bovis and Babesia bigemina are transmitted by the
cattle tick (Rhipicephalus microplus) in tropical and
subtropical regions.

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• Babesia gibsoni is transmitted by the dog tick
(Rhipicephalus sanguineus) in Asia and Africa.
• Babesia canis is transmitted by the brown dog tick
(Rhipicephalus sanguineus) in Africa.

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Life Cycle

The Babesia life cycle involves two hosts, which includes a rodent,
primarily the white-footed mouse, Peromyscus leucopus, and a tick in the
genus, Ixodes. During a blood meal, a Babesia-infected tick introduces
sporozoites into the mouse host . Sporozoites enter erythrocytes and
undergo asexual reproduction (budding) . In the blood, some parasites
differentiate into male and female gametes although these cannot be
distinguished at the light microscope level . The definitive host is the tick.
Once ingested by an appropriate tick , gametes unite and undergo a
sporogonic cycle resulting in sporozoites .

Transovarial transmission (also known as vertical, or hereditary,

transmission) has been documented for “large” Babesia spp. but not for the
“small” babesiae, such as B. microti .

Humans enter the cycle when bitten by infected ticks. During a blood meal,
a Babesia-infected tick introduces sporozoites into the human host .
Sporozoites enter erythrocytes and undergo asexual replication (budding) .
Multiplication of the blood stage parasites is responsible for the clinical
manifestations of the disease. Humans are, for all practical purposes, dead-

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end hosts and there is probably little, if any, subsequent transmission that
occurs from ticks feeding on infected persons. However, human to human
transmission is well recognized to occur through blood transfusions .

Pathogenesis of Babesia
Babesia parasites invade red blood cells and
multiply within the cells. The parasites consume the
hemoglobin in the red blood cells, which can lead to
hemolytic anemia, a condition in which red blood
cells are destroyed.

Hemolytic anemia can cause a number of symptoms,

including:

• Fatigue
• Weakness
• Shortness of breath
• Pale skin
• Jaundice
• Dark urine

In severe cases, hemolytic anemia can lead to organ

damage and even death.

In addition to hemolytic anemia, Babesia parasites

can also cause other complications, such as:

• Splenomegaly: Enlargement of the spleen

• Hepatomegaly: Enlargement of the liver
• Kidney failure
• Respiratory failure
• Neurological problems

The severity of Babesia infection depends on a

number of factors, including the species of Babesia
parasite, the immune status of the host, and the
presence of any underlying medical conditions.

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In humans, the most common Babesia species that
cause infection are:

• Babesia divergens
• Babesia microti
• Babesia duncani

These species typically cause mild to moderate

symptoms. However, in some cases, these species can
cause severe and even fatal infections.

Babesia gibsoni is a Babesia species that is found

in Asia and Africa. This species can cause severe
and even fatal infections in humans.

Overall, the pathogenesis of Babesia infection is

complex and can vary depending on the species of
Babesia parasite and the immune status of the host.

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Diagnosis for Babesia Species
Babesia infection is diagnosed with a blood test
that detects the parasites or antibodies against the
parasites.
Microscopic examination of blood smears:
• Blood smears can be examined under a microscope to
look for Babesia parasites inside red blood cells.
• This method is relatively simple and inexpensive,
but it is not as sensitive as other diagnostic
tests.
PCR (polymerase chain reaction):
• PCR is a molecular diagnostic test that detects
the DNA of Babesia parasites in the blood.
• PCR is a very sensitive and specific test, but it
is more expensive than microscopic examination of
blood smears.
Serology:
• Serology tests detect antibodies against Babesia
parasites in the blood.
• Serology tests are less sensitive than PCR, but
they can be used to diagnose Babesia infection in
people who have recently been infected or who have
low levels of parasites in their blood.
Other diagnostic tests:
• Rapid diagnostic tests: Rapid diagnostic tests are
available that can detect Babesia parasites or
antibodies against the parasites in the blood.
• These tests are less sensitive than PCR, but they
are faster and less expensive.

Treatment for Babesia species

Babesia infection is treated with antibiotics. The
most common antibiotics used to treat babesiosis
are:
• Atovaquone
• Azithromycin

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These antibiotics are typically taken for 7-10 days.
In severe cases of babesiosis, blood transfusions
may be necessary to correct anemia.
Treatment for Babesia infection is usually
effective, but it is important to start treatment as
early as possible to prevent serious complications.
Prevention and control of
Babesia species
Prevention:
• Avoid areas where ticks are known to be present.
• Wear long sleeves and pants when in areas where
ticks are known to be present.
• Check for ticks after being in areas where ticks
are known to be present.
• Remove ticks promptly and properly.
Control:
• Reduce tick populations by clearing brush and
debris from around homes and yards.
• Use tick control products on pets.
• Vaccinate pets against Babesia infection.
It is important to note that there is no vaccine
to prevent babesiosis in humans. However, the
preventive measures listed above can help to reduce
the risk of infection.
If you are bitten by a tick, it is important to
remove the tick promptly and properly. To remove a
tick, grasp the tick with tweezers as close to the
skin as possible and pull it straight up. Do not
twist or crush the tick. After removing the tick,
clean the bite area with soap and water.

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