gondii is an intracellular coccidian parasite and is
one of the most common parasitic diseases of animals and man.
The definitive hosts for the parasite (the only animals in
which the organism reproduces sexually) are members of the
Felidae family (mainly domestic cats). T gondii is of primary importance since the range of intermediate hosts
which can become infected encompasses virtually all warm-blooded
animals, including man. Although infection with T gondii is extremely common, it is rarely a cause of significant
disease in any species.
life cycle of T gondii has been reviewed extensively.
Cats usually become infected with T gondii by ingestion
of encysted organisms present in the tissues of a chronically
infected intermediate host (see below). The cyst wall is digested
by the cat, releasing infectious organisms into the intestinal
lumen. The organisms penetrate through the intestinal wall
and replicate throughout the body as rapidly dividing tachyzoites
(extra-intestinal cycle). Simultaneously, the organisms invade
and replicate within the intestinal epithelial cells (entero-epithelial
cycle). This entero-epithelial cycle culminates in sexual
reproduction and the formation of oocysts (eggs) which are
excreted in the faeces. As the cat develops an immune response,
oocyst shedding is halted, and the development of tachyzoites
is also arrested with the resultant formation of bradyzoites
(slowly replicating forms of the organism) contained within
tissue cysts. Tissue cysts are present in a variety of sites
throughout the body of chronically infected animals, each
cyst containing large numbers of bradyzoites.
previously unexposed to T gondii usually begin shedding
oocysts between 3 and 10 days after ingestion of infected
tissue, and continue shedding for around 10-14 days, during
which time many millions of oocysts may be produced. Once
a cat has developed an immune response, further shedding of
oocysts is extremely rare.
oocysts have been passed in the faeces, they undergo sporulation
(formation of infection sporozoites within the oocyst). This
process takes 1-5 days depending on environmental conditions
and, prior to this, they are not infectious. Oocysts are very
resistant and may survive in the environment for well over
hosts (eg, rodents, birds, sheep, pigs, cattle) may become
infected by ingestion of sporulated oocysts. As in the cat,
an extra-intestinal cycle of infection occurs, and the subsequent
immune response results in the development of encysted bradyzoites.
The tissue cysts probably remain viable (contain infectious
organisms) for the life of the animal. Unlike infection in
the cat, an enteroepithelial cycle (with oocyst production)
does not occur in intermediate hosts. Encysted bradyzoites
are infectious to cats, and importantly, also to other intermediate
hosts, so that in man for example, infection may be acquired
either through the ingestion of oocysts, or through the ingestion
of cysts within infected meat.
addition to ingestion of sporulated oocysts or bradyzoites,
infection with T gondii may also be acquired by
a foetus in utero (transplacental infection). This
can only occur if the host acquires infection during pregnancy,
as it is only tachzoites (present during the acute stage of
infection) that are able to cross the placenta.
of feline toxoplasmosis
generally show a 20-60% prevalence of infection with T
gondii in cats. The prevalence will depend on many factors
but is primarily related to the availability and ingestion
of infected intermediate hosts (rodents, birds etc). Infection
is therefore more common in stray and feral cats than in pet
cats, and the prevalence also increases with age. Although
there is generally a high prevalence of infection in cats,
most surveys show a less than 1% incidence of oocyst shedding.
This is to be expected as infected cats generally do not re-shed
oocysts following their first exposure to T gondii.
the high prevalence of T gondii infection, significant
clinical disease in cats (and other species) appears to be
very rare. When disease does occur, it may develop either
following primary infection (where an inadequate immune response
fails to arrest the invasive tachyzoites), or as a result
of reactivated infection (where compromised immunity allows
the reactivation of infection from encysted bradyzoites with
the formation of invading, multiplying tachyzoites).
disease appears to be most common in young cats (less than
2 years of age), and this may be due, in part, to a poorly
developed immune response in these cats. Reactivation of infection
in older cats may be linked to co-infection with feline leukaemia
virus or feline immunodeficiency virus in some cats.
most commonly reported clinical signs associated with feline
toxoplasmosis are anorexia, weight loss, lethargy, dyspnoea
(due to pneumonia), ocular signs (iritis, chorioretinitis)
and pyrexia. Other less common features include gastrointestinal
signs (vomiting/diarrhoea), neurological signs, lymphadenopathy,
jaundice, myositis and abortion.
of feline toxoplasmosis
diagnosis of toxoplasmosis is problematic and a definitive
diagnosis rests on demonstration of the active form of the
organism in tissues taken at post mortem examination or in
biopsy samples. Laboratory tests may also be used as diagnostic
aids and these are outlined below:
samples may be examined for the presence of T gondii oocysts, although this test is both technically difficult
and requires experience to correctly identify the oocysts.
Furthermore, clinical signs usually do not develop until after
oocyst shedding has ceased. For these reasons, oocyst detection
is rarely helpful.
gondii serology in cats has been based on the detection
of IgG-class immunoglobulins (antibodies). Recent work has
shown that following infection with T gondii , IgG
seroconversion typically occurs around 2-4 weeks after infection,
with peak titres being achieved at 4-6 weeks after infection.
Titres are then maintained at high levels for many months
or years. To diagnose recent infection it is therefore necessary
to demonstrate a fourfold rise in antibody titres over a 2-4
week period. However, in many cases clinical signs will develop
either before seroconversion occurs, or not until after peak
titres have developed. IgG serology is therefore often difficult
to interpret and a single antibody titre is rarely of any
IgM serology test for feline T gondii specific antibodies
has been developed in the USA . This appears to have many
benefits over IgG serology as IgM titres rise more rapidly
following infection and are normally maintained for only a
limited period of time. Therefore, a single high IgM titre
is usually adequate to demonstrate recent infection with T
gondii . It also appears that IgM titres may rise again
with reactivated infections. In the future, IgM serology will
hopefully become available in the UK .
should be remembered that oocyst shedding and seroconversion
occur in both clinical cases and cats with asymptomatic infection.
Consequently, these tests may give results which indicate
recent infection with T gondii , but they do not
provide a definitive diagnosis of clinical toxoplasmosis.
of feline toxoplasmosis
the past, treatment for toxoplasmosis has been based on a
combination of sulphadiazine and pyrimethamine. However, recently,
clindamycin used at doses of 25-50mg/kg/day (divided into
two or four doses) has been suggested as the treatment of
choice in feline toxoplasmosis. Although it has been proposed
that the use of clindamycin obviates the need for concurrent
pyrimethamine therapy, studies in man suggest dual therapy
is still required to maintain efficacy. The situation in cats
is unclear, but combining clindamycin with pyrimethamine (at
1mg/kg/day) may provide more effective therapy. Pyrimethamine
therapy is often associated with myleosuppression and, to
avoid this, cats may be given folic acid at 5mg/day for the
duration of treatment.
zoonotic potential of T gondii
is an important zoonotic disease. Around 30% of the adult
population in the UK have serological evidence of infection
but, as with cats, the vast majority of these human infections
are either asymptomatic or result in only mild clinical disease.
Of major concern however, is congenitally acquired toxoplasmosis.
As noted above, this can only occur when a previously unexposed
(non-immune) woman acquires toxoplasmosis during pregnancy.
In this situation there is approximately a 40% chance that
the foetus will acquire the infection, and in around 10% of
these cases, severe neurological or ocular disease is present
surveys show that owning a cat, or having direct contact with
a cat does not constitute an increased risk of acquiring
toxoplasmosis. Although cats are crucial in the life-cycle
of T gondii , and are the only known source of oocysts
present in the environment, it is stray and feral cats more
than pet cats that are implicated in this. In the UK and other
industrialised countries, it is mainly adolescent and adult
humans who acquire infection with T gondii , and
this is primarily correlated with the acquired habits of eating
undercooked meat, and of poor meat hygiene. Ingestion of infected
meat therefore appears to be the major source of human infection
in the UK .
a few sensible environmental and meat hygiene measures can
greatly reduce the risk of human infection.
all meat thoroughly to at least 70 degrees C
hands, utensils and surfaces carefully after handling
all vegetables carefully
gloves when gardening in soil potentially contaminated
by cat faeces
cat litter trays daily, dispose of litter
carefully and disinfect tray with boiling water. If this
is done every day, even if a cat is
excreting oocysts, they will not have sporulated and therefore
will not be infectious by the time the litter is changed
pet cats from hunting and avoid feeding raw/undercooked
any children's sandpits/boxes to prevent cats using them
as a litter tray.