1. No category

Keskes and Muhie, African Journal of Applied
Microbiology Research, 3(1): 1-11, May 2014
Available online at http://scienceparkjournals.com/ajamr
(ISSN 2315-5396) 2014 Science Park Journals
Full Length Research Paper
TOXOPLASMOSIS: EMERGING AND RE-EMERGING ZOONOSIS
Yibeltal Muhie1, 2 and Simenew Keskes 1, 3*
1
College of Veterinary Medicine and Agriculture, Addis Ababa University, Debre Zeit, Ethiopia
2
College of Veterinary medicine, Jigjiga University, Jigjiga, Ethiopia
3
College of Agriculture and Natural Resources, Dilla University, Dilla, Ethiopia
Accepted 18 April 2014
Abstract: Comprehended review was done to discuss about toxoplasmosis in animals and human.
Toxoplasmosis is a zoonotic disease with potential transmission to people from livestock and vic-versa.
Consumption of undercooked meat is one of the principal risk factors for Toxoplasma infection.
Encephalitis is the most important manifestation of toxoplasmosis in immunosuppressed patients as it
causes the most severe damage to the patients. The socio-economic impact of toxoplasmosis in humans
suffering and the cost care of sick children, especially those with mental retardation and blindness are
enormous. The clinical disease usually occurs sporadically and has low levels of incidence. However,
occasionally there are small epidemics attributed to the consumption of infected meat or contaminated
water. Collaborative and focused control strategies should be implemented for this serious disease.
Key Words: Toxoplasmosis, Veterinary and public health, immune compromised individuals,
production and productivity
INTRODUCTION
Worldwide infectious and parasitic diseases still cause untold suffering and enormous physical, economic
and social toll on human existence, causing 33% of deaths worldwide, with more than half of the victims
under the age 5 years. But the figure is much higher in developing countries. For example, in Africa it is
estimated that 68% of all deaths are as the result of infectious diseases (Zowghi, 2008). In 1992, "new,
reemerging or drug-resistant infections whose incidence has been increased within the past two decades
or whose incidence threatens to increase in the near future" were defined as "Emerging Infections".
Previously, zoonoses were defined as "diseases and infections which are naturally transmitted between
________________________________________________________________
*Correspondence: Email: drsimenew@yahoo.com, simenew.keskes@aau.edu.et
2
Afr. J. App. Microbiol. Res.
vertebrate animals and man". Thereafter, WHO noted zoonotic diseases caused either by totally new or
partially new agents, or by microorganismsm previously known (Zowghi, 2008). The majority of infectious
diseases that affect humans are zoonoses and they constitute as much as 70 % of the emerging
diseases (Jones et al., 2008). Environments where wild animals, domestic animals and humans live in
close proximity with no or small boundaries in the ecological system favor the emergence of new or
already known diseases, as it also favors the transmission of diseases between animals and humans
(Elwing, 2013). The above described situation is more common in low income countries where humans
and animals live in high density and zoonoses are generally more common. These diseases do not only
constitute a threat to human and animal health, but also reduce the production capacity of livestock and
contribute further to sustained poverty (Magnusson, 2009).
The zoonotic diseases also constitute a possible global health problem due to their pandemic potential to
spread over the world. Regarding pandemic and emerging zoonotic diseases, there is a strong
consensus that these are most efficiently fought at the origin of the epidemic, i.e. mostly in low income
countries (Jones et al., 2008). Zoonotic diseases make up 26 % of the infectious disease burden in low
income countries in terms of lost disability adjusted life years (DALYs) (Grace et al., 2012). DALY is the
present value of future years lost due to premature death or being alive with poor health. Among high
income countries, zoonoses are responsible for just 0.7 % of the infectious disease burden (Elwing,
2013).
Toxoplasmosis is a cosmopolitan zoonotic disease caused by the coccidian protozoan Toxoplasma
gondii, an obligatory intracellular parasite capable of infecting all warm-blooded animals including
mammals, birds and humans. The parasite has a worldwide distribution and it is mainly transmitted by
food contaminated with oocysts dispersed by cats and other felines, definitive hosts, undercooked meat
containing tachyzoites stages, and transplacentally (Clementino et al., 2007). All forms of toxoplasmosis
that occur in normal individuals may also occur in immunocompromised patients. People who have
previously acquired toxoplasmosis, with or without manifestation of the disease may suffer a devastating
relapse if their immune defenses, particularly cell-mediated immunity are impaired as in the case of
Acquired Immuno Deficiency Syndrome (AIDS) (Negash et al., 2008). Toxoplasmosis is a major public
health problem, with a high socioeconomic impact in terms of human suffering including the cost of caring
sick, mentally retarded and blind children. The parasite is an extremely successful pathogen, responsive
for significant morbidity and mortality, especially in congenitally infected and immuno-compromised
individuals, although some subjects experience infection without overt disease or with mild symptoms
(Molawi et al., 2008).
In animals, the infection not only results in significant reproductive and economic losses, but also has
implications for public health, since consumption of infected meat or milk can facilitate zoonotic
transmission (Clementino et al., 2007). Toxoplasma gondii-specific IgM plus detection of Toxoplasma
gondii DNA by PCR in CSF or aqueous humor correlates well with clinical disease (Lappin, 2000).
Considering its public health and veterinary importance, the objective of this paper is therefore to make
an insight review on toxoplasmosis by consulting relevant sources around the world.
Etiology
The organisms were first isolated in 1908 by Nicole and Manceaux from desert rodents which were
maintained in the Pasteur institute. The rodents are called Gondi. Hence the name of organisms is
Toxopalsma gondii (Mandal, 2006). The causative agent Toxoplasma gondii is a protozoan and a
member of the sub order Eimeria. It is specific parasite of the definitive host members of the Felidae
family, but has a wide range of intermediate hosts (Blood and Radostits, 1989).
Keskes and Muhie
3
Life Cycle
Toxoplasma gondii can complete its evolutionary cycle in the intestine of the cat and other felines, which
are the definitive hosts. In addition it can, and usually does, take advantage of an intermediate host,
which may be any of some 200 species of vertebrates. The fact that man is an intermediate host makes it
medically important (Acha and Szyfres, 2003). When the parasites are ingested by a cat, they invade the
feline intestinal cells and multiply asexually by merogony for several generations. They can multiply
sexually by gametogony and produce immature oocysts that cause the host cells to rupture, after which
they are eventually evacuated in the feces. Outside the host the oocysts mature 1-5 days, depending on
the temperature and humidity of the environment, at which point they form sporulated oocysts (Acha and
Szyfres, 2003).
Extra intestinal cycles occurs in the intermediate host only but in this regard there is also variation. This
cycle may occur in the definitive host simultaneously. In the extra intestinal cycles two types of
multiplicative stages are formed (Mandal, 2006). Bradyzoites (resting stage) are slowly multiplying
organisms contained in tissue cysts usually localized to muscle and brain. They live in the host cells for
months to years. Once ingested, gastric enzymes degrade the cyst wall liberating viable bradyzoites
takes place. Tachyzoites (tachy mean fast) are rapidly dividing organisms found in tissues during the
acute phase of infection. The tachyzoites are the forms responsible for tissue destruction. Multiplication
continues until either cyst formation or host cell destruction occurs. After cell death, the free tachyzoites
invade other cells and resume rapid multiplication (Hakeen, 2010).
EPIDEMIOLOGY
Distribution
Occurrence in Animals
Epidemiological investigation in the US and elsewhere indicates that 60% cats are serologically positive
to Toxoplasma antigen, the majority acquiring infection by predation (Urquhart et al., 2001). In Europe,
parasitism rates in excess of 50% have been found in the meat of sheep and swine slaughtered in
abattoirs. In Canada, the infection was found in 3.5% to 13.2% of pigs that underwent federal inspection,
while in Japan, the rates are much lower. Cattle, on other hand, are more resistant to the infection; they
have low, brief serological titers, and parasites are isolated from them only rarely (Acha and Szyfres,
2003).
Occurrence in Humans
Toxoplasma gondii has a worldwide distribution in human population infecting up to one third of the global
population and wide range of other mammalian and avian species. The prevalence rate is usually higher
at lower elevations and in older persons. In most animals and people, primary infection results in
detectable antibody titer for the life of the host, therefore, sero-prevalence increases with age (Acha and
Szyfres, 2003). Serologic prevalence data indicate that toxoplasmosis is one of the most common of
human infections throughout the world. High prevalence of infection in France has been related to a
preference for eating raw or under cooked meat, while prevalence in Central America has been related to
the frequency of stray cat in a climate favoring survival of oocyst and soil exposure. The overall
seroprevalence in the US among adolescents and adults, as determined with specimens collected by the
NHANES III between 1988 and 1994, was found to be 22.5%, with the Seroprevalence woman of child
bearing age (15-44 years) of 15% (Jenkins, 2009). A study in Malaysia shown that, the Seroprevalence of
4
Afr. J. App. Microbiol. Res.
toxoplasmosis in HIV/AIDS patients and HBD were 21% (21/100) and 28.1% (57/203) respectively as
indicated in Table 1. Studies have shown that between 16% and 40% of the population in the US and
Great Britain and from 50% to 80% of people in continental Europe and Latin America have antibodies to
the parasite, indicating that they have been infected at some time. Bossi et al., (1998) found that 399
(24.5%) of 1,628 AIDS patients had encephalitis caused by Toxoplasma, which is rare in
immunocompitent persons; 97% of patients had antibodies to the parasite, 30% had relapses, and 84%
died during the course of study. A study in Thailand revealed an infection rate of 30.1% in pregnant
woman who were HIV negative and 21.1% in woman who were HIV positive (Acha and Szyfres, 2003).
Sources of Infection and Methods of Transmission
It appears that cats are significant factor in the contamination of parasites, because single infected cat
produces millions of oocysts, which survive in the ground for almost a year as long as they are protected
from the sun and from drying out (Acha and Szyfres, 2003). Contamination of water sources and soil with
the feces of wild or domestic cats is more difficult to control and can lead to infection following ingestion of
oocysts on unwashed, uncooked vegetables or in contaminated water. Cockroaches and coprophagic
flies may also serve as mechanical vectors of Toxoplasma, resulting in infectious oocysts with
contamination of food, water and utensils. Contact with contaminated soil or sand, such as in a garden or
sand box, may also be associated with toxoplasma infection (Weese, 2008). Most cats become by
ingesting Toxoplasma infected animals, usually rodents, whose tissues contain tachyzoites or
bradyzoites, although direct transmission of oocysts between the cats also occur. The ingestion of mature
bradyzoites is the most routes and results in the shedding of higher numbers of oocysts than when
infection is acquired from other stages (Urquhart et al., 2001).
Evidence has recently been presented indicating that fecal transmission of Toxoplasma gondii is possible
with Toxocara cati as the vector and Tsunoda in Japan has observed transmission Toxoplasma from
swine to swine via lung worms (Schwarble, 1969). The common of spread in ruminants is the ingestion of
feed contaminated by cat feces which contain infective oocysts. This is well established as the means of
transmission in sheep. In sheep, a high rate of infection has been shown to be related to a high rainfall
which allows longer survival of oocysts on pasture. There is the interesting observation that sheep raised
in cat free populations have almost no toxoplasmosis whereas sheep raised in similar environments with
cats have an infection rate as high as 32% (Blood and Radostits, 1989). The major modes of
transmission in intermediate hosts include consumption of undercooked meat containing toxoplasma
cysts, fecal-oral transfer of Toxoplasma oocysts from cat feces (either directly or in contaminated food,
water or soil), and vertical transmission from mother to fetus if primary infection occurs during pregnancy
(Weese, 2008).
Congenital transmission is infrequent in all animals except sheep and goats. It occurs in lambs only when
the ewe is infected during pregnancy. When the fetus is infected between days 45 and 55 of gestation, it
usually does; if infection is acquired in the third month of pregnancy, the lambs are born but they are sick;
if it occurs after four months, the lambs may be born with the infection but they are asymptomatic.
Congenitally infected lambs lack muscular coordination, they are physically weak, and they are unable to
feed themselves. Some authors have defended the use of sheep rather than mice as animal models for
the human infection, because the clinical characteristics of ovine congenital toxoplasmosis are similar to
those seen in man as indicate in figure 1 below (Acha and Szyfres, 2003).
Keskes and Muhie
5
PUBLIC HEALTH SIGNIFICANCE
Modes of Transmission
Transmission of Toxoplasma gondii to humans occurs through accidental ingestion of sporulated oocysts
or the consumption of raw or undercooked meat. Among meat producing animals pigs, sheep and goats
relatively often harbor Toxoplasma gondii cysts in edible tissue and therefore raw or undercooked meat
from this animal constitutes major risk to humans. In area where goat milk is utilized, unpasteurized milk
from acutely diseased goats is also an important source of infection to children, Toxoplasma gondii can
also be transplacentally transmitted from the mother to offspring if the infection is contracted during
pregnancy (Negash et al., 2008).
Recent studies have suggested that coprophilic flies and cockroaches may act as transport host carry
cat’s fecal oocysts to human feed, which would account infection in vegetarians. Contamination of the soil
with oocyst from wild feline would account for infections contracted by indigenous people living alone the
bank of Xingu River in Brazil, who do not keep domestic cat and who do not eat raw meat (Acha and
Szyfres, 2003). Consumption of undercooked meat is one the principal risk factor for Toxoplasma
infection and people who handle raw meat, such as abattoir workers may also be commonly exposed to
parasite. The importance of this varies factors likely varies, considerably between ethnic groups due to
differences in cultural habits regarding exposure to undercooked meat, soil and cats (Weese, 2008).
Infection Risk for Humans
Most infections in humans are asymptomatic, but at times the parasite can produce devastating disease.
Infection may be congenitally or postnatal acquired. Congenital infection occurs only when a woman
st
becomes infected during pregnancy. Congenital infections acquired during the 1 trimester are severe
nd
rd
than those acquired in the 2 or 3 trimester while the mother rarely has symptoms of infection, she does
have a temporary parasitemia. Focal lesions develop in the placenta and the fetus may become infected.
st
At the 1 trimester there is generalized infection in the fetus. Later, infection is cleared from the visceral
tissues and may localize in the central nervous system. The socioeconomic impact of Toxoplasmosis in
humans suffering and the cost of care of sick children, especially those with mental retardation and
blindness are enormous (Lawley et al., 2006). Under normal circumstances, a female that has been
exposed to Toxoplasma 4-6 months prior to pregnancy will develop sufficient immunity to protect herself
and the fetus for the rest of her life. However, if the immune response is suppressed by drug therapy or
disease such as HIV/ AIDS in the humans, both the mother and fetus may become susceptible to
infection again (Weese, 2008).
In toxoplasmosis both humeral and cell-mediated components appear to be involved in the immune
response. However, the relative importance of their roles remains to be ascertained, although it is
generally believed that antibody formation by the host leads to a cessation in the production of
tachyzoites and to the development of the latent bradyzoite cyst. It is believed that recrudescence of
tachyzoites activity may occur if the host becomes immunosuppressed as a consequence of therapy or
some other disease (Schwarble, 1969). Postnatal acquired infection may be localized or generalized.
Oocyst-transmitted infections may be more severe than tissue induced infections. Enlarged lymph nodes
are the most frequently observed clinical form of toxoplasmosis in humans. Lymphadenopathy may be
associated with fever, fatigue, muscle pain, sore throat, and headache. Toxoplasmosis ranks high on the
list of diseases which lead to death of patient with AIDS. Although in AIDS patients any organ may be
6
Afr. J. App. Microbiol. Res.
involved, including the testis, dermis, and the spinal cord, infection of the brain is most frequently reported
(Lawley et al., 2006).
Clinical Manifestations
The symptoms of congenital toxoplasmosis are highly varied. Early infection can cause pre-natal or postnatal death or severe damage to the fetus. Later infection can cause generalized disease in utero,
subsequent infection of the nervous system, and the birth of children with sequel such as hydrocephaly,
chorioretinitis, or cerebral calcification. When the infection occurs shortly before the delivery, the child
may be born with an in apparent infection; or with fever, eruptions, hepatomegally, spleenomegally, or
pneumonia; or with generalized infection that compromises the hematopoietic, reticuloendothelial, or
pulmonary systems. Ocular toxoplasmosis deserves special mention. The most common manifestations
are retinochoroiditis, but there can be other lesions, and alterations, such as strabismus, nystagmus, and
microphtalmia. Ocular lesions are common in new born infants is with toxoplasmosis, and they are almost
bilateral. Later manifestations of the lesions tend to be unilateral (Acha and Szyfres, 2003). Encephalitis
is the most important manifestation of toxoplasmosis in immunosuppresed patients as it causes the most
severe damage to the patients. Infection may occur in any organ and patients may have headache,
disorientation, drowsiness, hemi paresis, reflex changes and convulsions, and may become comatose.
Most AIDS patients suffering from toxoplasmosis have bilateral, severe and persistent headache which
responds poorly to analgesics. As the disease progresses, the headache may give way to a condition
characterized by confusion, lethargy, ataxia, and coma (Lawley et al., 2006).
TOXOPLASMOSIS IN ETHIOPIA
In human a study conducted to assess the seroprevalence of Toxoplasma gondii and associated risk
factors among pregnant women in Jimma town, Southwestern Ethiopia showed that 83.6% (Zemene et
al., 2012). The study revealed that anti- T. gondii IgG antibodies were detected in 81.4% of the samples
of which 78.4% were positive for only IgG and 3.06% positive for both IgG and IgM antibodies
(Gebremedhin et al., 2013). There is also a report on isolation of viable Toxoplasma gondii from tissues
and feces of cats from addis ababa, ethiopia. In total, viable T. gondii was isolated from 27 of the 36 cats,
and these isolates were designated TgCatEt1 to TgCatEt27 and this is the first report of isolation of viable
T. gondii from any host in Ethiopia (Dubey et al., 2013a).
In addition to this there is Four genotypes were recognized, including ToxoDB #1 (Type II clonal, nine
isolates), ToxoDB #2 (Type III, five isolates), Toxo DB #3 (Type II variant, ten isolates), and ToxoDB #20
(nine isolates) study conducted from tissues and feces of 27 cats from Ethiopia (Dubey, 2013b). There
are some studies on the prevalence of toxoplasmosis in animals and human in different parts of the
country as indicated in the above table (Table 1).
ECONOMIC SIGNIFICANCE OF TOXOPLASMOSIS
Its effects are particularly important in sheep and goats because it causes abortions and disease in
newborns, resulting in serious economic losses, especially in Australia, Great Britain, and Newzealand. In
Tasmania, Australia, T.gondii was believed to have been the etiology in 46% of the outbreaks of abortion
and neonatal mortality in sheep between 1962 and 1968. Congenitally infected lambs lack muscular
coordination, they are physically weak, and they are unable to feed themselves (Acha and Szyfres, 2003).
In most countries, toxoplasmosis comes as the second in prevalence after chlamydial abortion. Prenatal
mortality rates (including ovine abortion and neonatal mortality due to T. gondii) in affected flocks can be
Keskes and Muhie
7
as high as 50% and in non-clinical cases may result in low losses. Therefore, the infection has an
economic and clinical significance in many sheep and goat producing countries (Radostits et al., 1994).
DIAGNOSIS OF TOXOPLASMOSIS
General
Examination of the fecal sample for detection of the oocysts of T.gondii is done. The oocysts are very
typical having two sporocysts. Each sporocyst has four sporozoites. The organisms are also isolated from
the infected animal, and then the organisms are inoculated in the mice. The organisms are detected in
the infected mice after considerable period. Furthermore, the cysts remain packed up with bradyzoites
and these cysts are clearly visible under the dissecting or stereoscopic microscope or emulsifying the
muscle in saline (Mandal, 2006).
Serological Tests
Immunologic testing via IFA and ELISA for IgM and IgG antibodies can be performed on serum, CSF, or
aqueous humor. Serum antibodies document exposure to T.gondii but do not diagnose disease caused
by T. gondii because clinically normal animals may have positive Ab titers. IgM Abs correlate best with
clinical disease, but failure to detect IgM Abs does not exclude toxoplasmosis as cause of disease. IgG
Abs persist for years because the host rarely clears infections completely (Morgan et al., 2003). A fourfold
rise in titers suggests recent infection. T. gondii-specific IgM plus detection of T.gondii DNA by PCR in
CSF or aqueous humor correlates well with clinical disease (Lappin, 2000).
IFA and ELISA are particularly appropriate for this purpose because they make it possible to determine
the presence of IgM antibodies, which appear and disappear before the IgG Abs. Because IgM does not
cross the placenta, the presence this Abs in the serum of newborns is reliable evidence that the fetus
developed them inutero and that the infant was born with the infection. Another procedure used for
determining the presence of acute infection is the evolution of IgG Abs titers and if the titers increase after
more than three dilutions, it may be speculated that the patient’s immune system is responding actively to
the parasite and therefore he or she must be in the active phase of the infection (Acha and Szyfres,
2003).
Persons should be initially tested for the presence of Toxoplasma-specific IgG Abs to determine their
immune status. A positive IgG titer indicates infection with the organism at sometime. If more precise
knowledge of the time of infection is necessary, then an IgG positive person should have an IgM test
performed by a procedure with minimal none specific reactions, such as IgM-capture ELISA. A negative
IgM test essentially excludes recent infection, but a positive IgM test is difficult to interpret between
Toxoplasma specific IgM Abs may be detected by ELISA for as long as 18 months after acute acquired
infection (Jenkins, 2009). Antibodies to Toxoplasma gondii where determined by the modified direct
agglutination by using a commercially available kit and the test employs intact tachyzoites as antigen as,
hence antibodies IgG to surface antigens are detected. The advantage of MDAT is that it is easy to
perform, can be used on any species since specific conjugates are not used and the results obtained
strongly correlated with other serological test (Negash et al., 2008).
PCR is used to detect Toxoplasma gondii DNA in body fluids and tissues. It has been successfully used
to diagnose congenital, ocular, cerebral and disseminated toxoplasmosis. PCR performed on amniotic
fluid has revolutioned the diagnosis of fetal Toxoplasma gondii infection by enabling early diagnosis to be
made, thereby avoiding the use of more invasive procedure on the fetus (Montoya et al., 2011).
8
Afr. J. App. Microbiol. Res.
TREATMENT
Most healthy people recover from toxoplasmosis without treatment persons with ill can be treated with a
combination of drugs such Pyrimethamine and Sulfadiazine, plus Folinic acid. Pregnant women,
newborns and infants can be treated, although the parasite is not eliminated completely spiramycine is an
antibiotic used most for pregnant women to prevent the infection of their child. Persons with compromised
immune systems need to be treated until they are improvement in their condition. For AIDS patients,
continuation of medication for the rest of their life may be necessary, or for as long as they are immuno
suppressed (Jenkins, 2009). In people with latent toxoplasmosis, the cysts are immune to this treatment,
as the antibiotics do not reach the bradyzoites in sufficient concentration. Atovaquone is an antibiotic that
have been used to kill toxoplasma cysts inside AIDS patients. Clindamycin is an antibiotic which, in
combination with Atovaquone, seemed to optimally killed mice patients (Djurković-Djaković et al., 2002).
Monensin and Decoquinate have also been administered to ewes in mid pregnancy in attempt to control
abortion due to toxoplasmosis (Urquhart et al., 2001).
PREVENTION AND CONTROL
In Humans
To prevent infection of human beings with Toxoplasma gondii especially pregnant women, children, and
immuno compromised individuals, contact with cats, soil, and raw meat should be avoided and people
should be made aware of the dangers of toxoplasmosis. Toxoplasma gondii organism in meat can be
killed by exposure to extreme heat or cold. Tissue cysts in meat are killed by heating the meat through
o
o
out to 67 c or by cooling to -13 c (William, 2001). Pregnant women and immune deficient individuals
should not perform tasks that expose them potentially contaminated soil with the oocyst of Toxoplasma
unless they should use water proof gloves and wash their hands carefully afterward. Flies and
cockroaches should be controlled to prevent them from serving that transport hosts for the fecal oocysts
of cats. It would appear that an effective in means of infection in newborns is to identify pregnant women
with acute infection and treat them. At present there is no vaccine to prevent infection in humans (Acha
and Szyfres, 2003).
In Animals
Cats should be kept indoors and fed canned, cooked, or previously frozen food to keep them from hunting
and catching infected rodents and birds and thus becoming infected. It has been shown in the laboratory
that the addition of monensin to dry cat food can suppress the excretion of oocysts in feces (Acha and
Szyfres, 2003). For some years, work has been under way to develop vaccines against toxoplasmosis for
cats, sheep, and swine. So far, the only successfully effort has been a modified live parasite vaccine for
sheep, which is administered before impregnation to prevent congenital infections. This live vaccine
consisting of tachyzoites attenuated by repeated passage in mice (Urquhart et al., 2001).
CONCLUSION
The socio-economic impact of toxoplasmosis in humans suffering and the cost care of sick children,
especially those with mental retardation and blindness are enormous. The clinical disease usually occurs
sporadically and has low levels of incidence. However, occasionally there are small epidemics attributed
to the consumption of infected meat or contaminated water among human beings and animals.
Keskes and Muhie
9
Authors' contributions
Both authors contributed equally in making critical reviewing of this manuscript.
Table 1: Prevalence of T. gondii in Ethiopia
Study area
Prevalence (%) of different study Test
subjects
References
used
Cattl
Shee
Goa
Cat
Human
e
p
t
Central Ethiopia
6.6
11.9
22.9
-
-
MDAT
Bekele and Kasali (1989)
Debre Birhan
-
35
34
-
-
MDAT
Tilaye
and
Getachew
(2002)
Nazareth
52.6
East and West
24
-
19.7
MDAT
Negash et al. (2004)
ELISA
Zewdu et al. (2012)
Shewa Zones
Nazareth
60
Addis Ababa
90
South
Omo,
Negash et al. (2008)
ELISA
Teshale et al. (2009)
Teshale et al. (2007)
74.9
North Omo and
East
Shewa
Zones
Jimma town
83.6
ELISA
Zemene et al. (2012)
Centeral Ethiopia
81.4
ELISA
Gebremedhin et al. (2013)
10
Afr. J. App. Microbiol. Res.
Figure 1: Life cycle and mode of transmission of Toxoplasma gondii in different
species of animals
Source: Keith, 2010
REFERENCES
1. Acha PN, Szyfres B (2003). Zoonoses and communicable diseases common to man and animals,
rd
parasitoses, volume III, 3 ed., Washington D.C, U.S.A., Pp 76-84.
2. Bekele T, Kasali OB (1989). Toxoplasmosis in sheep, goats and cattle in central Ethiopia,
Veterinary Research Communications, 13(5):371-375.
3. Blood DC, Radostits OM (1989). Veterinary medicine, a text book of the disease of cattle, sheep,
th
pigs and horses, volume I, 7 ed., W.B. Saunders, London, Pp; 896-900.
4. Clementino MM, Souza MF, Andrade NV (2007). Seroprevalence and Toxoplasma gondii- IgG
avidity in sheep from Lajes, Brazil, Veterinary parasitology, 146:199-203
5. Djurković-Djaković O, Milenković V, Nikolić A, Bobić B, Grujić J (2002). Efficacy of atovaquone
combined with clindamycin against murine infection with a cystogenic (Me49) strain of
Toxoplasma gondii. J Antimicrob Chemother, 50 (6): 981–7.
6. Dubey JP, Darrington C, Tiao N, Ferreira, LR, Choudhary S, Molla B, Saville W JA, Tilahun G,
Kwok OCH, Gebreyes WA (2013a). Isolation of Viable Toxoplasma gondii from Tissues and
Feces of Cats from Addis Ababa, Ethiopia. J. Parasitol., 99(1): 56-58.
7. Dubey JP, Darrington C, Tiao N, Ferreira, LR, Choudhary S, Molla B, Saville W JA, Tilahun G,
Kwok OCH, Gebreyes WA (2013b). Genetic diversity of Toxoplasma gondii isolates from
Ethiopian feral cats. Vet. Parasitol., http://dx.doi.org/10.1016/j.vetpar.2013.01.015
Keskes and Muhie
11
8. Elwing S (2013). Zoonotic Pathogens at the Interface between Humans and Animals in
Cambodia, a Rural Approach., Uppsala, Sveriges lantbruksuniversitet.
9. Gebremedhin EZ, Abebe AH, Tessema TS, Tullu KD, Medhin G, Vitale M, Di Marco V, Cox E,
Dorny P (2013). Seroepidemiology of Toxoplasma gondii infection in women of child-bearing age
in central Ethiopia. BMC Infectious Diseases, 13:101.
10. Hakeen L (2010). The life cycle of toxoplasmosis, Ondokuz mayis university medical school
Turkey, 50603 Kuala Lumpur, P412.
11. Jenkins W (2009). Public Health Laboratories: Analysis, Operations, and Management. Jones &
Bartlett Learning. Amazon.com. pp. 1-283.
12. Keith A (2010). Toxoplasmosis/ Adapted from Centers for Disease Control and
Prevention. National Center for for Zoonotic, Vector-Borne, and Enteric Diseases: Division of
Parasitic Diseases. http://www.dpd.cdc.gov/dpdx/ Toxoplasmosis.
13. Lappin MR (2000). Protozoal and miscellaneous infections, text book of veterinary
internal
th
medicine. 5 ed., W.B. Saunders, Philadelphia, Pp 1135-1137.
14. Lawley R, Curtis L, Davis J (2006). The Food Safety Hazard Guide book. RSC Publishing, http://
www.ars,usda.gov.
st
15. Mandal SC (2006). Veterinary parasitology at a glance, 1 ed., chaman studio building charbash,
India, Pp 267-272.
16. Molawi NA, Abumadi M, Behanke JM (2008). Seroprevalence and epidemiological correlates of
Toxoplasma gondii infection in Doha, Qatar. Parasites & vectors, 48(4): 1121-1128.
17. Montoya JG, Remigton J, Contopoulo SD (2011). Laboratory tests for the diagnosis of
toxoplasmosis, Palo Alto medical foundation, 1600 Clifton Rd. Atlanta, Pp 423-427.
th
18. Morgan, R.V., Bright, R.M. and Swartor, M.S. (2003). Hand book of small animal practice, 4 ed.,
Pp 1127-1130.
19. Negash T, Tilahun G, Medhin G (2008). Seroprevalence toxoplasma gondii in Nazareth town,
Ethiopia, East African journal of public health, 5:123-126.
20. Negash T, Tilahun G, Patton S, Prevot F, Dorchies PH (2004). Serological survey on
toxoplasmosis in sheep and goats in Nazareth, Ethiopia, Revue. Med. Vet., 155(10): 486-487.
21. Radostits OM, Blood DC, Gay CC (1994). A text book of disease of cattle, sheep, pigs, goats and
th
horses, 8 ed., W. B. Saunders, London, Pp 1201-1206.
nd
22. Schwarble CW. (1969). Veterinary medicine and human health, 2 ed., Pp 767-774.
23. Teshale S, Dumetre A, Darde ML, Merga B, Dorchies PH (2007). Serological survey of caprine
toxoplasmosis in Ethiopia, Parasite, 14:155-159.
24. Teshale S, Mekashew T, Endale T, Belete T, Ashenafi T (2009). Seroprevalence of latent
Toxoplasma gondii infection among HIV infected and HIV uninfected people in Addis Ababa,
Ethiopia. BMC research notes, 213:1186-1189.
nd
25. Urquhart G M, Armour J, Duncan JL, Dunn AM, Jennings FM (2001). Veterinary parasitology 2
ed. Black well science Ltd. UK, Pp 234-238.
26. Weese S (2008). Pets and immunocompromised people.Worms & Germs Blog, Ontario
Veterinary College’s Centre for Public Health and Zoonoses.
27. Zemene E, Yewhalaw D, Abera S, Belay T, Samuel A, Zeynudin A (2012). Seroprevalence of
Toxoplasma gondii and associated risk factors among pregnant women in Jimma town,
Southwestern Ethiopia. BMC Infectious Diseases, 12:337
28. Zewdu E, Agonafir A, Tessema TS, Tilahun G, Medhin G, Vitale M, Di Marco V, Cox E,
Vercruysse J, Dorny P (2013). Seroepidemiological study of caprine toxoplasmosis in East and
West Shewa Zones, Oromia Regional State, Central Ethiopia. Res. Vet. Sci.,
http://dx.doi.org/10.1016/j.rvsc.2012.07.020
29. Zowghi E (2008). Emerging and re-emerging zoonoses. Iranian Journal of Clinical Infectious
Diseases, 3(2):109-115.
Cite this article as:
Keskes and Muhie (2014). TOXOPLASMOSIS: EMERGING AND REEMERGING ZOONOSIS
. Afr. J. App.
Microbiol. Res. 3(1): 1-11
Submit your manuscript at
http://www.scienceparkjournals.org/AJAMR/submit