Microsoft word - 10 toxoplasma guideline web edition.rtf
Toxoplasma gondii infection Agent properties Toxoplasma (T.) gondii is an obligate intracellular coccidian parasite that can infect
virtually all species of warm-blooded animals, including people. Domestic cats and other
Felids are the definitive hosts. All non-feline hosts are intermediate hosts (Dubey, 2005;
There are three infectious stages: sporozoites in oocysts, tachyzoites (the actively
multiplying stage), and bradyzoites (the slowly multiplying stage) enclosed in tissue
cysts. Oocysts are excreted in faeces, whereas tachyzoites and bradyzoites are found in
tissues and milk (Dubey, 2005; Dubey & Lappin, 2006).
Entero-epithelial Life Cycle
This cycle is found only in the definitive feline host. Most cats are infected by ingesting
intermediate hosts infected with tissue cysts. Bradyzoites are released in the stomach
and intestine from the tissue cysts when their wall is dissolved by digestive enzymes.
Bradyzoites penetrate the epithelial cells of the small intestine and give rise to schizonts,
initiate five types of predetermined asexual stages, and merozoites released from
schizonts form male and female gamonts. After fertilization, a wall is formed around the
fertilized macrogamont to form an oocyst. Oocysts are round to oval, 10 x 12 µm in size,
and are unsporulated (uninfective) when passed in faeces. After exposure to air and
moisture for one to five days, they sporulate to contain two sporocysts, each with four
sporozoites (Dubey, 2005; Dubey & Lappin, 2006).
The enteroepithelial (coccidian) cycle is usually completed within three to ten days after
ingestion of tissue cysts and occurs in up to 97% of naive cats. However, after ingestion
of oocysts or tachyzoites, the formation of oocysts is delayed and shedding can occur up
to 18 days (rarely more), and only 20% of cats fed oocysts will shed (Dubey, 2005;
Extraintestinal Life Cycle
The extraintestinal development of T. gondii is the same for all hosts, including cats,
dogs, and people, and is not dependent on whether tissue cysts or oocysts are ingested.
After the ingestion of oocysts, sporozoites hatch in the lumen of the small intestine and
penetrate intestinal cells, including the cells in the lamina propria. Sporozoites divide into
two by an asexual process known as endodyogeny and thus become tachyzoites.
Tachyzoites are lunate in shape, approximately 6 x 2 µm, and multiply in almost any cell
of the body. If the cell ruptures, they infect new cells. Otherwise, tachyzoites multiply
intracellular for an undetermined period and eventually encyst. Tissue cysts vary in size
from 15 to 60 µm and usually conform to the shape of the parasitized cell. Tissue cysts
are formed mainly in the CNS, muscles, and visceral organs, and probably persist for the
life of the host (Dubey, 2005; Dubey & Lappin, 2006).
Parasitaemia during pregnancy of the host can cause placentitis followed by spread of
tachyzoites to the foetus. In people and sheep, congenital transmission occurs usually
when the woman or ewe becomes infected during pregnancy. Many kittens born to
queens infected with T. gondii during gestation become infected transplacentally or via
suckling. Clinical signs are common in these kittens, varying with the stage of gestation
at the time of infection, and some newborn kittens shed oocysts (Dubey, 2005; Dubey &
In cats, antibody prevalence to T. gondii varies geographically; in a study in Portugal,
24% of cats had antibodies (Duarte et al., 2010) and in the USA around 30% of cats
were antibody-positive, but this varies from 16% to 40% depending on the states
(Dubey & Lappin, 2006). Only 3 (0.9%) samples of faeces from 326 cats in the Morro
Bay area of California contained T. gondii-like oocysts and 1 among 252 in Switzerland
(Berger-Schoch, 2011). On the basis of the estimated tonnage of cat faeces deposited
outdoors in this area, the annual burden in the environment was estimated to be 94 to
4,671 oocysts/m2 (9 to 434 oocysts/ft2; Dabritz et al., 2007). The proportion of T. gondii-
positive samples collected between January and June was significantly lower than
between July and December. The age of cats shedding T. gondii oocysts was not
significantly different from the age of negative control cats (Herrmann et al., 2010).
The three major modes of transmission of T. gondii to all host species, including humans
and cats, are congenital infection, ingestion of infected tissues, and ingestion of oocyst-
contaminated food or water (Dubey & Lappin, 2006). Minor modes of transmission
include blood transfusion and organ transplantation (Dubey, 2005; Dubey & Lappin,
Tachyzoites of T. gondii have been found in the milk of sheep, goats, cows, and mice,
and infection by ingestion of raw goat milk has been documented in humans. Lactational
transmission from infected cats to their kittens is also suspected since the organism has
been detected in feline milk (Powell et al., 2001).
T. gondii blocks the innate aversion of rats for cat urine, instead makes them attracted
by the feline pheromone, which may increase the likelihood of a cat predating a rat. This
is thought to reflect adaptive, ”behavioural manipulation“ by T. gondii in that the parasite
reproduces only in the feline intestines. The "behavioural manipulation" hypothesis
postulates that a parasite will specifically manipulate host behaviours essential for
enhancing its own transmission. However, the neural circuits implicated in innate fear,
anxiety, and learned fear all overlap considerably, raising the possibility that T. gondii
may disrupt all of these non-specifically (Vyas et al., 2007). Some studies looking at
experimental infection of rodents (Flegr & Havlicec ,1999; Hrda et al., 2000; Havlicec et
al., 2001; Webster, 2001; Flegr et al., 2002; Flegr et al., 2003) found that T. gondii may
change chemical messages in the CNS that affect behaviour; the proposed mechanism is
that T. gondii infection may lead to cyst formation in the CNS with production of tyrosine
hydroxylase (which is needed for dopamine production), leading to a lack of dopamine.
Meat contaminated with T. gondii cysts has been the primary source of infection in
persons in Europe and the United States, but recent changes in animal management and
husbandry practices, and improved food handling and processing have significantly
reduced the prevalence of cysts in meat. Nonetheless, antibody prevalence in humans
remains relatively high, suggesting that exposure from oocyst contaminated soil or water
is likely. Indeed, waterborne outbreaks of toxoplasmosis have been reported worldwide
and support the theory that exposure to the environmental oocyst form poses a health
risk. Research on the prevalence of T. gondii oocysts in the water and environment is
limited due to the lack of tools to detect oocysts in the environment (Staggs et al.,
Clinical signs develop due to inflammation and tissue necrosis caused by intracellular
growth of tachyzoites (Dubey & Lappin, 2006). Congenital infection tends to be much
more serious than infection of the adult cat (Dubey & Lappin, 2006).
Approximately 10 to 20% of cats experimentally inoculated with T. gondii tissue cysts
develop self-limiting small bowel diarrhoea for one to two weeks; this is caused by local
replication of the organism during the intestinal phase of infection. However, detection of
oocysts in faeces is rarely reported in client-owned cats with diarrhoea, and T. gondii
infection therefore does not seem to be a major cause of diarrhoea.
In cats, toxoplasmosis can develop during dissemination and intracellular replication of
tachyzoites. Usually the disease develops from reactivation of latent infections rather
than after a newly acquired infection. If a cat with chronic T. gondii infection is
immunosuppressed, bradyzoites in tissue cysts can replicate rapidly and disseminate
again as tachyzoites. This is also common in humans with acquired immune deficiency
syndrome (AIDS). Clinical toxoplasmosis has also been documented in cats infected with
FIV or FeLV (Davidson et al., 1993). Commonly used doses of glucocorticoids do not
appear to predispose to activated toxoplasmosis (Lappin et al, 1992). However,
administration of cyclosporine to cats or dogs with renal transplantations or dermatologic
disease has been associated with clinically manifest disease (Beatty & Barrs, 2003; Last
Commonly, pulmonary and CNS tissues are involved; hepatic and pancreatic involvement
is less likely. Clinical signs in cats with toxoplasmosis include depression, anorexia, fever
followed by hypothermia, peritoneal effusion, icterus, and dyspnoea. T. gondii infection
also can cause anterior or posterior uveitis, fever, muscle hyperesthesia, weight loss,
anorexia, seizures, ataxia, diarrhoea, or pancreatitis. T. gondii is also a common cause of
uveitis in cats (Dubey & Lappin, 2006).
Transplacentally or lactationally infected kittens develop more severe signs and
frequently die of pulmonary or hepatic disease (Dubey et al., 1995). Chronic
toxoplasmosis is rare and appears with vague and recurrent clinical signs. Immune
complex formation (Lappin et al., 1993) and deposition in tissues and delayed
hypersensitivity reactions may be involved in chronic clinical toxoplasmosis. Since T. gondii is never cleared from the body, neither naturally, nor with drugs, recurrence of the
Immunity to T. gondii in the cat is poorly understood. More work has been done in the
mouse than in the cat. In the mouse and in people, immunity is highly dependent on cell-
mediated effector responses (Sanchez et al., 2010).
Only 80% of infected cats develop IgM antibodies, all develop IgG and IgA. IgG can take
four to six weeks to appear, and maximal antibody titres are achieved within two to three
weeks after antibody first appeared (Dubey & Lappin, 2006).
Diagnosis Antibody testing
Several antibody tests have been used in the diagnosis of toxoplasmosis. The indirect
fluorescence test can be adapted to detect IgM, IgG, or IgA antibodies, using whole or
immunoblotted antigens. For assessing human health risks, antibody test results from
healthy cats can be interpreted. An antibody-negative cat is potentially shedding oocysts
(early infection before antibodies have developed) and will likely shed oocysts if exposed
for the first time; this cat poses the greatest public health risk.
An antibody-positive cat is unlikely to currently shed oocysts (antibodies need two to
three weeks to develop, and by that time cats usually do not shed any more - and a cat
is only shedding once in its lifetime) and is also unlikely to shed oocysts if re-exposed or
Because antibodies occur in both healthy and sick cats, results of these tests do not
prove clinical toxoplasmosis. Also antibodies of the IgM class are commonly detected in
healthy cats, and thus are not diagnostically useful. T. gondii-specific IgM is detected in
cats with latent or reactivated infection and does not always correlate with clinical signs.
Thus, antemortem diagnosis of clinical toxoplasmosis ideally is based on the detection of
the organism in muscle biopsies or bronchoalveolar lavage, or by PCR in CSF or aqueous
humour. Tachyzoites may be detected in various tissues and body fluids by cytology
during acute illness. They are rarely found in blood, but occasionally in CSF, fine-needle
aspirates of organs (e.g., lymph nodes), transtracheal or bronchoalveolar washings, and
are common in the peritoneal and thoracic fluids of animals developing thoracic effusions
or ascites. Detection of tachyzoites leads to a definitive diagnosis.
If appropriate samples cannot be taken, a tentative diagnosis is sometimes based on the
presence of high or increasing IgM titers, exclusion of other causes for the clinical signs,
and beneficial clinical response to an anti-Toxoplasma drug (Dubey, 2005; Dubey &
Gross and microscopic changes may be found in any organ but are most common in
lungs, CNS, eyes, and mesenteric lymph nodes. Granulomas may be present in intestines
and mesenteric lymph nodes (Dubey, 2005). Cholangiohepatitis, found in cats infected
with T. gondii, has not been reported in any other host. The bile ducts are hyperplastic
and plugged with desquamated bile duct epithelium and exudate. T. gondii schizonts (not
tachyzoites) were seen in the biliary epithelium in both naturally occurring and
experimentally induced disease. (Dubey, 2005).
Detecting oocysts in faeces T. gondii oocysts are 10 µm in size and are best demonstrated by centrifugation using
Sheather’s sugar solution during the shedding period. T. gondii oocysts are
morphologically indistinguishable from oocysts of Hammondiahammondi, Besnoitiaorcytofelisi and Besnoitiadarlingi (Dubey & Lappin, 2006). A modified CsCl method that
easily purifies T. gondii oocysts from faeces of infected cats has also been described
Clindamycin is the treatment of choice (Davidson, 2000) and should be administered at
10 to 12 mg/kg orally q 12 h for four weeks (Table 1). Cats with systemic disease
combined with uveitis should be treated with clindamycin in combination with topical,
oral, or parenteral corticosteroids to avoid secondary glaucoma and lens luxations
(Lappin et al., 1998). Prednisolone acetate (1% solution) applied topically to the eye
three to four times daily is generally sufficient.
Clinical signs not involving the eyes or the CNS usually begin to resolve within the first
two to three days of clindamycin administration. Ocular and CNS toxoplasmosis respond
more slowly. In cases of pulmonary toxoplasmosis, total resolution of radiographic
abnormalities may not occur for several weeks. The prognosis is usually poor in
pulmonary or hepatic disease, particularly in immunocompromised animals (Dubey et al.,
Prevention Prevention of Cat Infections
The best way to avoid T. gondii infection in cats is not to feed any raw meat. It is
currently discussed whether there is benefit of testing cats for T. gondii infection and of
treating antibody-positive animals before administering cyclosporine therapy for other
Public Health Considerations
Because of pet ownership issues, it is important for all small animal practitioners to
familiarize themselves with the T. gondii infection. Discussions have come in focus,
partially because of the increasing number of immunocompromised persons (e.g., people
infected with the human immunodeficiency virus), and because of recent research linking
psychological and cognitive disorders (reduced IQ evidenced by psychomotor and verbal
intelligence tests) to T. gondii infection. Unfortunately, a recent survey on US
obstetrician-gynaecologists to determine their knowledge and practices about
toxoplasmosis prevention and testing found that most overestimated the risk of having
pets in a household, versus environmental risk factors (Jones at al., 2010). A systematic
review of risk factors for T. gondii infection in pregnant women is available (Leroy,
2005); it reports a relatively low risk of cat ownership. In addition to questions that arise
concerning risk for human health, veterinarians will be confronted with cases in which T. gondii has caused illness in cats and dogs.
These are possible routes in infection for humans:
Ingestion of meat containing tissue cysts is the most common route. Thorough
cooking or freezing for several days will kill tissue cysts (Lunden & Uggla., 1992;
Dubey, 1988; Dubey et al., 1990; Dubey, 1998).
Ingestion of sporulated oocysts, either from the environment, e.g., through contact
with soil containing sporulated oocysts (indirectly) or from contact with faeces of
cats that are shedding oocysts, is the second most common route. This can also
occur indirectly through eating unwashed fruit or vegetables. Contamination via the
environment is more common than via cats.
Other routes of human infection are less common:
Ingestion of sporulated oocysts through contact with contaminated water
Ingestion of raw (unpasteurised) goat milk
Inhalation of sporulated oocysts on dust particles is possible but extremely rare.
The Feline Advisory Bureau has collected research data, indicating that cats are a minor
risk for people to acquire toxoplasmosis
(http://www.fabcats.org/owners/toxoplasmosis/info.html). Contact with cats does not
increase the risk of T. gondii infection (Elmore et al., 2010). Studies have shown that:
Cats shedding oocysts in faeces are rarely identified. While 24% of 206 cats had
antibodies to T. gondii indicating prior infection, oocysts were not found in the
faeces of any of them (Hill et al., 2000). (Berger–Schoch, 2011: 1 cat among 252 -
mainly domestic cats - sheds oocysts in a Swiss study)
Veterinarians working with cats are not more likely to be infected than the general
population, including people without cat contacts (Behymer et al., 1973;
Sengbusch & Sengbusch, 1976; DiGiacomo et al., 1990).
Contact with cats has no influence on the probability of people having antibodies to
T. gondii, whereas consuming raw meat significantly increases the risk of acquiring
Stroking a cat will not spread infection from cats to people. Even when cats are
shedding oocysts in their faeces, oocysts cannot be found on their coat (Dubey
1995). Studies performed in dogs have shown that oocysts do not sporulate on
their fur and the same is probably true for cats (Lindsay et al., 1997).
Cat ownership does not increase the risk of toxoplasmosis in people suffering from
AIDS. Although they are generally at an increased health risk, this results from
reactivation of a previous infection rather than from acquiring a new infection.
The risk of infection from cats is low, except for young children playing in soil
contaminated with sporulated oocysts. Most people are infected through ingestion
of undercooked meat, especially goat, mutton, and pork (Wallace et al., 1993).
Infection is not transmitted by bites or scratches from an infected cat.
Infected cats under treatment with immunosuppressive drugs at standard doses do
not start shedding oocysts in their faeces (Lappin et al., 1992).
Infected cats do not re-shed oocysts in their faeces if they become
immunosuppressed due to infection with FIV or FeLV (Lappin 2001).
Cats infected with FIV or FeLV that are subsequently infected with T. gondii do not
shed oocysts for any longer or in any greater numbers than other cats (Lappin et
Newly identified strains of T. gondii are highly infectious for species other than
cats; some scientists think that cats are becoming less important in the spread of
Although the risk of parasite transmission from a cat to its owner is low, it can be further
reduced and its consequences minimised by adopting the following recommendations:
Litter trays should be emptied daily so that oocysts do not have sufficient time (24
Gloves should be used when handling cat litter, and hands should be washed
thoroughly after cleaning the litter tray.
Litter tray liners should be used if possible, and the litter tray should be cleaned
regularly with detergent and scalding water.
Cat litter should be disposed in sealed plastic bags.
Children's sandpits should be covered when not in use to prevent cats using them
Only properly cooked food or commercial cat food should be fed to cats.
Hands should be washed after contact with a cat (especially before eating).
Veterinary surgeons may get questions from clients whether or not to remove their cat.
If the above hygiene recommendations are followed, the risk of transmission is minimal,
and the ABCD does not recommend removing the cat.
Toxoplasmosis is particularly severe in immunosuppressed people, and infection is
problematic in pregnant women. In households with immunosuppressed people or
pregnant women the following additional advice can be given:
Immunosuppressed persons and pregnant women should avoid contact with cat
Cats should be kept indoors to prevent hunting and access to intermediate hosts
Cats should not be fed raw or partially cooked meat.
If avoidable, cats should not eat insects (e.g., cockroaches).
Cats should be tested for T. gondii antibodies; their presence indicates an infection
in the past. These cats will not be a source of infection as they have completed
their period of oocyst shedding. Cats without antibody have not been infected with
T. gondii in the past and are likely to shed oocysts in their faeces for a short time if
they become infected in the future. These cats should stay indoors during the
phase of immunosuppression or pregnancy of the owner.
Disease control in specific situations
Preventing toxoplasmosis in dogs and cats involves measures intended to reduce the
incidence of infections and subsequent shedding of oocysts into the environment. Kittens
raised outdoors usually become infected shortly after they are weaned and begin to hunt.
Cats should preferably be fed only dry or canned, commercially processed cat food. The
prevalence of canine and feline T. gondii infection has been higher in countries where raw
meat products are fed to pets. Freezing or X-ray irradiation can kill tissue cysts without
affecting meat quality. Household pets should be prevented from hunting and eating
potential intermediate hosts or mechanical vectors, such as cockroaches, earthworms,
and rodents. If meat is provided, it should always be thoroughly cooked before feeding,
even if frozen. Cats should be prevented from entering buildings where food-producing
animals are housed or where feed storage areas are located (Dubey, 2005).
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