Medycyna Weterynaryjna - Summary Medycyna Wet. 66 (11), 784-786, 2010

Medycyna Wet. 2010, 66 (11) 784

Opis przypadku Case report

Toxoplasmosis is caused by the obligate intracellular

protozoan parasite Toxoplasma gondii. Even though

the protozoan is capable of infecting almost all

spe-cies of warm-blooded animals and humans, sexual

reproduction takes place only during enteroepithelial

cycle in the gut of domestic and wild Felidae, which

therefore comprise a definitive host for T. gondii. The

infection is widespread among cats and seroprevalence

ranges between from 30 to 60% (9, 13).

Extraintesti-nal development concerns all animals infected with

the parasite – both definitive and intermediate hosts.

There are three major routes of the transmission of

toxoplasmosis: congenital infection, ingestion of

in-fected tissues and ingestion of food or water

contami-nated with sporulated oocysts. Although cats usually

become infected by ingesting intermediate hosts

bearing dormant cysts in their tissues, kittens can also

contract an infection either transplacentally or via

suckling. Regardless of the infection route, clinical

disease is rare in Felidae. Immunosupression, for

instance caused by retroviral infection, is the main

fac-tor known to predispose to the reactivation of dormant,

asymptomatic infection and the development of

clini-cal toxoplasmosis (6, 11, 14). Cliniclini-cal signs result from

the spread of invasive forms of the parasite from tissue

cysts, subsequent parasitemia and damage to vital

organs, from which lungs, central nervous system,

liver, pancreas, heart and eyes are the most common.

Cerebral toxoplasmosis is associated with the

occur-rence of various and unspecific neurologic signs such

as ataxia, circling, behavioral changes, anisocoria,

torticollis, seizures, twitching and tremors (4, 11).

The treatment of choice for cats with clinical

toxo-plasmosis is clindamycin hydrochloride. Alternatively,

although considered inferior to the aforementioned

therapy, the combination of pirymetamine or

thrimeto-prim with sulphonamide can be administered.

Regard-less of the treatment applied, the prognosis for cats

with cerebral toxoplasmosis is poor (11).

Case description

A 5-year-old, intact, male cat was presented to the vete-rinary clinic because of a sudden onset of general seizures. The cat was semi-stray, spending most of the time outdoors. The cat was vaccinated against feline herpesvirus, feline calicivirus and panleucopaenia virus as well as against rabies. Anamnesis also revealed that at the age of approxi-mately 6 months it was checked for feline leucaemia virus (FeLV) and feline immunodeficiency virus (FIV) infection with the use of in-clinic speed-tests and the result of the latter test turned out to be positive. Despite the diagnosis, the cat did well until two weeks earlier, when the owner noticed temporal left-hand head tilt. As there were no other alarming symptoms, medical consultation was not conside-red necessary. The condition deteriorated suddenly: in the morning the cat was found in the state of general seizures

Cerebral toxoplasmosis in a cat

MICHA£ CZOPOWICZ, OLGA SZALUŒ-JORDANOW*, TADEUSZ FRYMUS*

Department of Large Animal Diseases with the Clinic, *Department of Small Animal Diseases with the Clinic, Faculty of Veterinary Medicine, Warsaw University of Life Sciences – SGGW,

Nowoursynowska 159c, 02-776 Warsaw, Poland

Czopowicz M., Szaluœ-Jordanow O., Frymus T.

Cerebral toxoplasmosis in a cat

A five year-old semi-stray intact tom cat with acute multifocal neurological signs, including seizures, opisthotonus and horizontal nystagmus was presented to the veterinary clinic. The onset of severe neurological signs was sudden but preceded by a mild left-hand head tilt, which had been observed for the previous two weeks. Results of in-house tests for both FeLV antigen and FIV antibody were negative although the owner claimed that the cat had been diagnosed as seropositive to FIV infection in the first year of life. Despite antibacterial and symptomatic treatment the state of the cat tended to deteriorate and eventually euthanasia was performed. The examination of the cerebrospinal fluid (CSF) using polymerase chain reaction (PCR) revealed the presence of T. gondii DNA. No bacteria, fungi or feline coronavirus RNA were detected in the microbiological and molecular examination of CSF. Thus, cerebral toxoplasmosis was recognized.

Medycyna Wet. 2010, 66 (11) 785 with accompanying profuse salivation. The cat arrived at

the clinic at least 3 hours after the seizures started. Apart from the epileptic state, detailed clinical examination reve-aled high body temperature (40.2°C), opisthotonus, dilata-tion and stiffness of pupils with accompanying horizontal left-hand nystagmus; the cat was unconscious and only spinal reflexes were maintained. In the left auricular canal small amount of discharge resembling pus was discovered. The cat was admitted to the hospital with a tentative diagnosis of bacterial meningoencephalitis due to chronic outer ear infection which had expanded to middle and inner ear as a consequence of immunosupresion resulting from FIV infection. As a differential diagnosis neuropathy associated with the final stage of FIV infection was consi-dered although no other clinical signs typical of the feline acquired immunodeficiency syndrome (FAIDS), such as general lymphadenopathy or gingivitis, were found. Blood for morphological and biochemical tests as well as smears from both ears for bacteriological examination were collected. Diazepam (Relanium, 5 mg in one intravenous bolus) was given immediately, but only a temporal control of seizures was achieved so general anesthesia with pento-barbital (Vetbutal, 5 mg/kg i.v. repeated every 3-4 hours) was performed. Then a protocol for bacterial meningo-encephalitis treatment was applied: an anti-inflammatory dose of dexamethazone (Dexaven, 0.2 mg/kg i.v.) 15 minu-tes prior to broad spectrum antibiotics – cefriaxone (Bio-trakson, 50 mg/kg i.v. s.i.d.) and enrofloxacine (Baytril, 5 mg/kg i.v. s.i.d.). Continuous intravenous infusion of saline with 2.5% glucose was also started. Blood check results, which arrived after a few hours, revealed an elevated total serum protein concentration (113 g/l) due to hyper-globulinemia (75 g/l) with a normal level of albumins (38 g/l) as well as an increase in creatine kinase (999 U/l) and aspartate aminotransferaze (82 U/l). Since no leukocytosis was found, the cerebrospinal fluid (CSF) was collected to verify the tentative diagnosis. The CSF was clear and color-less. Its laboratory analysis revealed a markedly elevated total protein concentration (6.0 g/l, albumins – 2.1 g/l) accompanied by mononuclear pleocytosis, which ruled out bacterial meningoencephalitis as a cause of clinical signs. The CSF was sent for microbiological culture and PCR since a low serum albumin:globulin ratio (0.5) and features of myositis made a neurological form of both feline infectious peritonitis and toxoplasmosis essential to be taken into con-sideration. In-house tests for FeLV antigen and FIV anti-body were conducted as the cat had roamed freely, but both proved negative. Since there was no improvement in the condition of the cat within 24 hours and each attempt to wake it up from general anesthesia ended up with relapse of seizures, euthanasia was conducted. Unfortunately, it was not possible to perform an autopsy. Results of the micro-bial culture arrived 3 days later and revealed no growth of bacteria either from CSF or ear swabs. Moderate number of yeast cells was found in the slide of material from the left ear. No yeasts were present in CSF. The final diagnosis was made post-mortally on the basis of the results of PCR of CSF: while Real-Time PCR ruled out the presence of feline coronavirus RNA in the central nervous system, clas-sical PCR detected T. gondii DNA.

Discussion

The sudden onset and long duration of seizures in

a free-roaming cat accompanied by fever and

opistho-tonus, and preceded by clinical signs of vestibular

syndrome strongly suggest infectious

meningoence-phalitis secondary to an inner ear infection (12).

Although bacterial causes are most plausible, in the

case of immunosuppression less prevalent causes such

as cryptococcosis or toxoplasmosis should be

suspec-ted. Feline infectious peritonitis, which is a very

im-portant cause of neurological signs including seizures

in cats, should also be ruled out (12, 16, 21).

The situation of our patient was unclear as regards

FIV infection. Serological tests can yield false

nega-tive results during advanced stages of the disease (19).

On the other hand, the cat did not seem to suffer from

any chronic disease. FIV is a neurotropic agent but

is capable of producing clinical signs of the CNS

disease only in the final stage of infection, when more

typical signs are already evident (5). Such signs were

lacking in this patient. The owner reported that FIV

antibody had been found in this cat many years ago,

but false positive serological results are relatively

com-mon, especially in healthy cats from low-prevalence

populations (10). Thus, the predictive value of a

nega-tive result is much higher than that of a posinega-tive one. It

also seems that this cat was not infected with FIV. Our

laboratory tests excluded also FCoV infection as well

as fungal or bacterial background of the disease.

There is no single test to confirm cerebral

toxo-plasmosis ante mortem (13). The final diagnosis of

the disease requires demonstration of non-suppurative

encephalitis and the presence of tachyzoits in cerebral

tissue (11). This can be performed either postmortem

or in brain biopsy, which is certainly unavailable in

common veterinary practice. Under such

circumstan-ces demonstration of either the parasite itself or its

DNA in CSF seems to be a reasonable choice, which

enables verification of the diagnosis of cerebral

toxo-plasmosis with very high probability, especially when

more common causes have already been excluded (2,

15, 18, 20).

Cerebral toxoplasmosis is believed to be a rare

con-dition in cats. There have only been few case reports

on this condition published so far (8, 17, 22). Henriksen

at al. (7) revealed cerebral toxoplasmosis in 2 of 155

necropsied cats (1.3%) but the overall number of

toxo-plasmosis cases was five so cerebral toxotoxo-plasmosis

constituted 40% of all cases of the disease. Dubey and

Carpenter (3) diagnosed cerebral infection in 7 of 100

cats with confirmed toxoplasmosis (7%). Cerebral

toxoplasmosis was found in 8 of 286 cats with

neuro-logical disorders, which is 2.8% (1).

Cerebral toxoplasmosis appears to be a forgotten

feline disease – diagnosed occasionally, mainly during

postmortem examination and seldom taken into

con-sideration during a differential diagnosis. This case

Medycyna Wet. 2010, 66 (11) 786

report shows that it is a mistake. Even though the

overall prognosis in cerebral toxoplasmosis is poor,

it is always better in treated than untreated animals.

Therefore, anti-T. gondii chemotherapeutics should be

included in a treatment protocol of any cat with severe

signs of meningoencephalitis of unknown origin.

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