A Case of Fatal Systemic Toxoplasmosis in a Cat Being Treated With Cyclosporin a for Feline Atopy (Pages 194–198)

Published on December 2016 | Categories: Documents | Downloads: 52 | Comments: 0 | Views: 191
of 5
Download PDF   Embed   Report

vet derm

Comments

Content

Veterinary Dermatology 2004, 15, 194– 198

Case report

Blackwell Publishing Ltd.

A case of fatal systemic toxoplasmosis in a cat being treated with
cyclosporin A for feline atopy
ROBERT D. LAST*, YASUHIRO SUZUKI†, THOMAS MANNING‡, DAVID LINDSAY†,
LAURA GALIPEAU§ and TREVOR J. WHITBREAD¶
*Vetdiagnostix – Veterinary Pathology Services, P.O. Box 13624, Cascades 3202, South Africa
†Centre for Molecular Medicine and Infectious Diseases, Department of Biomedical Sciences and
Pathobiology, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Polytechnic
Institute and State University, USA
‡Department of Small Animal Clinical Sciences, Virginia-Maryland Regional College of Veterinary Medicine,
Virginia Polytechnic Institute and State University, USA
§Brookmead Veterinary Surgery, Horsham Road, Cranleigh, UK
¶Abbey Vet Services, 89 Queen Street, Newton Abbot, UK
(Received 21 February 2003; accepted 12 September 2003)

Abstract Acute systemic toxoplasmosis was diagnosed in a 4–5-year-old, male, Domestic Short Hair cat, which
had been on cyclosporine A immunomodulatory therapy for feline atopy, over an 8-month period. Cyclosporin A
(CsA) has shown promising results as a immunosuppresive agent in the cat for the treatment of eosinophilic
plaque and granulomas, allergic cervico-facial pruritus, feline atopy and other immune-mediated dermatoses.
However, inhibition of T-lymphocyte function by CsA is believed to have predisposed this cat to the development
of a newly acquired, acute Toxoplasma gondii infection, as characterized by severe hepatic and pancreatic pathology in conjunction with the heavy parasite load demonstrated on immunohistochemical (IHC) stains for
T. gondii. Cats on CsA therapy appear to be at risk of developing fatal systemic toxoplasmosis.
Keywords: cyclosporin A, feline atopy, immunomodulatory therapy, Toxoplasma gondii, toxoplasmosis.

I NTRO D U CTI ON
Feline atopy is a multisystemic syndrome characterized by pruritic, frequently nonlesional dermatitis and/
or respiratory disease, with gastrointestinal symptoms
and ocular signs being less common.1–5 The basis for
the diagnosis of feline atopy currently relies on the
demonstration of a compatible history and clinical
signs, and ruling out other causes of pruritus including
flea-bite hypersensitivity and food hypersensitivity.5
Unlike other species, there is no well-documented
genetic component to atopy in the cat and interpretation of the results of either intradermal or serological
testing is controversial.2–6 Identifying allergens responsible for the clinical disease can be extremely difficult
and there are no controlled studies of the response to
immunotherapy, with some cats not responding well to
conventional therapies (ectoparasitic prophylaxis, control of secondary infections, glucocorticoids, antihistamines, essential fatty acids, restoring and maintaining
epidermal barrier function, dietary management).2,5,7

Correspondence: R. D. Last, Vetdiagnostix – Veterinary Pathology
Services, P.O. Box 13624, Cascades 3202, South Africa. E-mail:
[email protected]
194

This has led veterinary dermatologists to continually
investigate alternative therapies for these nonresponsive cases, with Cyclosporin A (CsA) showing promising results in many anecdotal reports.2,5,7
CsA, a cyclic lipophilic peptide, has been used extensively in human medicine, as an immunomodulating
agent in organ transplantation and atopic dermatitis,
and has recently shown promise in the treatment of
eosinophilic plaques and granulomas, allergic cervicofacial pruritus, feline atopy and other immune-mediated
dermatoses of the cat.2,4,5,7 The rationale for the use
of CsA in atopic dermatitis of man is based on its
mode of action, which includes rapidly reversible
immunosuppression, depression of skin mast cell
counts, inhibition of eosinophil survival, reduction in
the number of epidermal Langerhans cells and inhibition of immunoglobulin (Ig)E and mast cell-dependant
cellular infiltration at the sites of cutaneous inflammation, all of which are integral parts of the pathogenesis
of atopic dermatitis in man.4,5 Similar pathogenic
mechanisms are suspected in the cat, hence the interest
in using CsA as a therapeutic agent in feline atopy.1,2
Felines are the definitive hosts of Toxoplasma gondii,
with nonfeline hosts (mammals and birds), as well as
cats, serving as intermediate hosts.8–10 Cats are most
frequently infected by ingestion of tissue cysts in prey
© 2004 European Society of Veterinary Dermatology

Fatal systemic toxoplasmosis in a cat
species, or less commonly by ingestion of oocysts.9–11
In immunocompetent cats, which have not previously
been exposed to T. gondii, the ingestion of infective
tissue cysts results in the typical coccidian enteroepithelial cycle in the intestinal epithelium, with oocysts
being shed in the faeces.11–13 The extra-intestinal cycle
with intestinal invasion and visceral dissemination, as
occurs in the intermediate hosts, also occurs in the cat,
usually simultaneously with the entero-epithelial cycle,
but rapid development of specific cell-mediated immunity usually prevents any further clinical complications
from arising.11,13 Acute systemic toxoplasmosis has
been described in neonates, young immunologically
immature kittens and immunocompromised cats.11–14
Recrudescent toxoplasmosis, where there is reactivation of dormant cysts, has been reported in adult cats
which have undergone an immunosuppressive incident, either through pharmacological immunosuppressive therapy or concurrent feline leukaemia virus
(FLV) or feline immunodeficiency virus (FIV) infection. This form of the disease, however, is considered
rare.9–11,13,15–21
In this particular case the immunosuppressive
effects of CsA are believed to have predisposed this cat
to the development of a newly acquired, acute T. gondii
infection.

CASE
The feline patient was a 4–5-year-old, neutered, male,
Domestic Short Hair, originating from a single-cat
household and fed a commercial diet. The cat lived predominantly indoors but was known to scavenge outdoors. In 1999, the cat had presented with alopecia,
erythema with some papules on the ventral abdomen,
associated with over-grooming. A full clinical examination had failed to reveal any abnormalities other
than these dermatological signs. Microscopic examination of skin scrapings did not reveal mites, mite eggs or
faecal pellets, and fungal cultures produced no fungal
growth. Haematology, serum chemistry and urinalysis
assays were all within normal parameters. There was
no response to an 8-week lamb-based elimination diet
trial (LB, Iams UK Ltd, Crawley, UK) or ectoparasitic
exclusion. A diagnosis of feline atopy was made and in
light of this, intradermal and serological tests were
advised to try and identify allergens to include in an
immunotherapy vaccine.
The cat was sedated with medetomidine (Domitor,
Pfizer Ltd, Sandwich, UK) and an intradermal test
performed using aqueous allergens (Greer Laboratories Inc, Lenoir, NC, USA). The intradermal test was
carried out according to recognized criteria with Dermatophagoides farinae and D. pteronyssinus allergens
at 1/10 000 w/v, flea at 1/1000 w/v, other allergens at
1000 PNU mL−1 and histamine at 1 in 100/000 w/v.
Other allergens included cat dander, mattress dust,
sheep epithelia, mixed feathers, kapok, birch, alder,
beech, sycamore, poplar, oak, willow, elm, privet,

195

fescue, Italian rye grass, timothy, couch grass, oat,
mugwort, Jerusalem oak, lambs quarter, daisy, plantain, sheep sorrel, yellow dock, dandelion, clover, nettle, mixed moulds, mixed smut/grain and mixed insect.
Skin test reactions were scored positive with a wheal
score of 4 equivalent to the positive histamine control
score of 4. Sedation was reversed with atipamezole
(Antisedan, Pfizer Ltd). Positive reactions were
obtained for flea antigen and house dust mites.
At the time of skin testing, serum was collected and
submitted for measurement of allergen-specific IgE
using the ALLERCEPT™ Definitive Allergen Panels
ELISA (Axiom Veterinary Laboratories, UK). Allergens tested included Aspergillus, Penicillium, Cladosporium, Alternaria, storage mite (Acarus sp.), storage
mite (Tyrophagus sp.), D. farinae, D. pteronyssinus,
feathers, cat dander, cockroach, flea saliva, timothy
grass, cocksfoot, meadow grass, rye grass, sheep sorrel,
English plantain, nettle, lambs quarter, mugwort,
alder, oak and birch. All were negative except for flea.
After a poor response to ectoparasite control, allergenspecific immunotherapy (based on house dust mite
allergens), dietary management (essential fatty acids),
antihistamines, antibiotics and low-dose glucocorticoids, cyclosporin A (ciclosporin, CsA, MIMMS and
BNF UK, Novartis Pharmaceuticals Ltd, Surrey, UK)
immunomodulatory therapy was instituted. Low-dose
glucocorticoids had last been used 3 months prior to
the implementation of CsA therapy. The initial dosage
of CsA was 5 mg kg−1 once daily orally with food, but
the cat became anorexic after a month. Serum chemistry performed at this stage revealed values within the
normal ranges. Dosage was then reduced to 5 mg kg−1
on alternate days, with good clinical control of the pruritus and alopecia for 6 months, after which some reappearance of clinical signs was noted and the dosage
was again increased to 5 mg kg−1 once daily. Three
weeks later the cat became severely depressed, dyspnoeic and developed acute hepatic failure with rapid
clinical deterioration and was euthanased. During this
period of clinical disease the cat had tested negative for
FLV and FIV.
At necropsy the liver had a mottled, bronze brown
appearance with multiple, small, pale foci of necrosis
and increased friability. The pancreas was swollen and
oedematous with suspected areas of interstitial necrosis. Mesenteric lymph nodes were large with an irregular surface and multiple pale necrotic foci scattered
through the parenchyma. Lungs had a diffuse reddish
brown coloration with firm consistency. Samples of liver,
pancreas, lung, mesenteric lymph node and intestine
were collected into 10% formalin for histopathology.
Histological examination of the liver, pancreas,
lymph node and lung revealed a severe multifocal
hepatic necrosis with nonsuppurative cholangiohepatitis, acute necrotizing interstitial pancreatitis, necrotizing granulomatous lymphadenitis and proliferative
nonsuppurative interstitial pneumonia. Immunohistochemical (IHC) staining of tissue sections for Toxoplasma gondii, revealed numerous T. gondii tachyzoites

© 2004 European Society of Veterinary Dermatology, Veterinary Dermatology, 15, 194–198

196

RD Last et al.

Figure 1. Multifocal areas of hepatic necrosis with positive
immunohistochemical staining of Toxoplasma gondii organisms,
within as well as at the periphery of these necrotic foci.
Bar = 100 µm. Avidin-biotin Complex (ABC) immunoperoxidase
stain (Toxoplasma gondii polyclonal anti-rabbit sera at 1:500).
Hematoxylin counterstain.

Figure 2. Strong positive immunohistochemical staining of
Toxoplasma gondii tachyzoites in the liver. Bar = 10 µm.
Avidin-biotin Complex (ABC) immunoperoxidase stain
(Toxoplasma gondii polyclonal anti-rabbit sera at 1:500).
Hematoxylin counterstain.

in the liver in association with areas of necrosis (Figs 1
and 2). Large numbers of tachyzoites were also detectable in the lung (data not shown). According to these
findings a diagnosis of acute systemic toxoplasmosis
was made.22,23

D ISCU SSIO N
The visceral distribution and severity of microscopic
lesions is somewhat different in acute systemic toxoplasmosis and recrudescent infections in adult
cats.10,23,24 In acute disease following ingestion of tissue
cysts or oocysts, lesions tend to be most prominent in
the mesenteric lymph nodes, liver, pancreas and lungs,

frequently associated with numerous tachyzoites.
Recrudescent infections, however, tend to have lesions
in the central nervous system, skeletal muscle and
myocardium, as these are the main locations for the
bradyzoite-containing tissue cysts.10,11,13,23,24 In the
feline patient described here, in light of the severe hepatic
and pancreatic pathology and heavy parasite load
demonstrated on IHC stains, acute systemic disease was
considered far more likely than recrudescent infection.
Reactivation of dormant T. gondii cysts with subsequent
clinical disease as a result of immunosuppression in an
adult cat is extremely rare. Immunosuppressive doses
of corticosteroids (10–80 mg kg−1 methylprednisalone
acetate intramuscularly weekly or 10–80 mg kg−1
prednisone orally daily), may cause some chronically
infected cats to re-excrete T. gondii oocysts.25 However,
commonly used therapeutic doses (5–20 mg kg−1
weekly for 4 weeks or 5 mg kg−1 daily for 7 days), failed
to induce recrudescence in recently or chronically
infected cats.15,26 Some chronically infected cats which
have undergone a primary FIV infection show an
increase in T. gondii antibody titres, suggesting some
reactivation of encysted stages, but experimental studies failed to substantiate this, indicating that there is no
reactivation of cysts or development of active clinical
disease.16 Experimental feline leukaemia virus infection prior to T. gondii challenge did not appear to predispose cats to clinical infection and had no effect on
oocyst excretion.21 The negative FLV and FIV status of
this cat and use of only therapeutic doses of corticosteroids (some months earlier), would be further supporting evidence of acute systemic disease rather than
recrudescent disease.
In relation to our findings in this case, fatal toxoplasmosis has been reported in three cats with renal transplantation that received treatment with CsA alone or
CsA plus prednisolone.24 In these cases, it is most likely
that the seronegative recipient animals had received
kidneys from seropositive donors and those kidneys
had contained T. gondii cysts, resulting in acute
acquired infection. Thus, it appears that CsA treatment
significantly increases the susceptibility of cats to acute
acquired infection with T. gondii.
Various experimental studies have shown that the
immunosuppressive effects of CsA, which involves
inhibition of T-lymphocyte activation and impairing
proliferation of activated T-helper and T-cytotoxic
lymphocytes, may alter the natural course of T. gondii
infection with increased severity of lesions, persistence
of parasites in visceral locations and down-regulation
of the host–parasite interaction all being reported.7,27–31
Predisposition to recrudescent flare-ups of chronic
T. gondii infection, in addition to the development of
acute systemic disease following acquired infection,
might occur in cats on CsA therapy, however, this point
needs to be clarified.
Precautions to consider during immunomodulatory
therapy would include feeding only commercial cat
food or other cooked foods, avoiding feeding of raw
meat, poultry, viscera or bones and preventing hunting

© 2004 European Society of Veterinary Dermatology, Veterinary Dermatology, 15, 194– 198

Fatal systemic toxoplasmosis in a cat
and scavenging.8,31 Monitoring of serological antibody
status, for both IgG and IgM class antibodies to T.
gondii, both prior to initiation of immunomodulatory
therapy, as well as during immunosuppressive therapy,
might be helpful to detect seroconversion.24,31,32
When seroconversion occurs, or significant rises in
toxoplasma antibody titres are observed in association with developing clinical illness in cats which were
seropositive prior to initiation of immunosuppresive treatment, antitoxoplasma chemotherapy should
be applied immediately to prevent acute systemic
toxoplasmosis.24,31
In our case, it is suspected that the immunosuppresive effects of CsA predisposed this cat to the development of acute systemic toxoplasmosis, due to acute
acquired infection, rather than reactivating dormant
tissue cysts. To our knowledge, this is the first report of
acute fatal toxoplasmosis in cats associated with CsA
treatment for feline atopy.

ACKN OWLEDGE ME NT S
We are grateful to Aiden Foster for all the assistance
with this case and preparation of the manuscript. This
study is supported in part by a National Institute of
Health Grant (A147730 to Yasuhiro Suzuki).

REFEREN C E S
1. Roosje PJ, Thepen TH, Rutten VPMG et al. Feline
atopic dermatitis: a review (Abstract). Veterinary Dermatology 2000; 11 (Suppl. 1): 12.
2. Foster A. Diagnosing and treating feline atopy. Veterinary Medicine 2002; 97: 226 – 40.
3. Power H. A practitioner’s approach to allergic skin disease in cats. Proceedings of the 17th Annual Meeting of
the European Society of Veterinary Dermatology/European College of Veterinary Dermatology. Copenhagen,
2001: 79 –86.
4. Prelaud P, Gilbert S. Atopic dermatitis. In: A Practical
Guide to Feline Dermatology. France: Merial, 1999.
5. Scott DW, Miller WH, Griffin CE, eds. Small Animal
Dermatology, 6th edn. Philadelphia: W.B. Saunders,
2001; 601– 8.
6. Wassom DL, Grieve RB. In vitro measurement of canine
and feline IgE. A review of Fc epsilon R1 alpha-based
assays for detection of allergen-reactive IgE. Veterinary
Dermatology 1998; 9: 173 – 8.
7. Guaguere E. Cyclosporin A a new drug in the field of
veterinary dermatology. In: Proceedings of the Spring
Meeting of the British Veterinary Dermatology Study
Group 2001: 23 –34.
8. Center SA. Acute hepatic injury: hepatic necrosis and
fulminant hepatic failure. In: Gulford WG, Center SA,
Strombeck DR. et al. eds. Small Animal Gastroenterology, 3rd edn. Philadelphia: W.B. Saunders, 1996:
683.
9. Jones TJ, Hunt RD, King NW, eds. Veterinary Pathology, 6th edn. Baltimore: Williams & Wilkins, 1996:
555 – 61.

197

10. Lappin MR. Protozoal and miscellaneous infections. In:
Ettinger SJ, Feldman EC. eds. Textbook of Veterinary
Internal Medicine, 5th edn. Philadelphia: W.B. Saunders,
2000: 410–13.
11. Barker IK, Van Dreumel AA, Palmer N. The alimentary system. In: Jubb KVF, Kennedy PC, Palmer N. eds.
Pathology of Domestic Animals, 4th edn. San Dieago:
Academic Press, 1993: 308–10.
12. Bowman DD, Hendrix CM, Lindsay DS et al. Feline
Clinical Parasitology. Ames: Iowa State University
Press, 469.
13. Summers BA, Cummings JF, de Lahunta A, ed. Veterinary Neuropathology. St. Louis, MO: Mosby, 1995:
163–9.
14. Dubey JP, Mattix ME, Lipscomb TP. Lesions of neonatally induced toxoplasmosis in cats. Veterinary Pathology 1996; 33: 290–5.
15. Lappin MR, Dawe DL, Lindl PA et al. The effect of glucocorticoid administration on oocyst shedding, serology
and cell mediated immune responses of cats with recent
or chronic toxoplasmosis. Journal of the American
Animal Hospital Association 1991; 27: 625–32.
16. Lappin MR, Gasper PW, Rose BJ et al. Effect of primary
phase feline immunodeficiency virus on cats with chronic
toxoplasmosis. Veterinary Immunology and Immunopathology 1992; 35: 121–31.
17. Lappin MR, Marks A, Greene CE et al. Effect of
feline immunodeficiency virus on Toxoplasma gondiispecific humoral and cell mediated immune responses
of cats with serological evidence of toxoplasmosis.
Journal of Veterinary International Medicine 1993; 7:
95–100.
18. Lappin MR, George JW, Pedersen NC et al. Primary
and secondary Toxoplasma gondii infections in normal
and feline immunodeficiency virus infected cats. Journal
of Parasitology 1996; 82: 733–42.
19. Lin DS, Bowman DD. Macrophage functions in cats
experimentally infected with feline immunodeficiency
virus and Toxoplasma gondii. Veterinary Immunology
and Immunopathology 1992; 33: 69–78.
20. Lin DS, Bowman DD, Jacobson RH. Immunological
changes in cats with concurrent Toxoplasma gondii and
feline immunodeficiency virus infections. Journal of
Clinical Microbiology 1992; 30: 17–24.
21. Patton S, Legendre AM, McGavin MD et al. Concurrent
infection with Toxoplasma gondii and feline leukemia
virus. Journal of Veterinary International Medicine
1991; 5: 199–201.
22. Lindsay DH, Dubey JP. Immunohistochemical diagnosis of Neospora caninum in tissue sections. American
Journal of Veterinary Research 1989; 50: 1981–3.
23. Dubey JP, Carpenter JL. Histologically confirmed clinical toxoplasmosis in cats: 100 cases (1952–90). Journal of
the American Veterinary Medical Association 1993; 203:
1556–66.
24. Bernsteen L, Gregory CR, Aronson LR et al. Acute toxoplasmosis following renal transplantation in three cats
and a dog. Journal of the American Veterinary Medical
Association 1999; 215: 1123–6.
25. Dubey JP, Frenkel JK. Immunity to feline toxoplasmosis: modification by administration of corticosteroids.
Veterinary Pathology 1974; 11: 350–79.
26. Hagiwara T, Katsube Y, Muto T et al. Experimental
feline toxoplasmosis. Japanese Journal of Veterinary Science 1981; 43: 329–36.

© 2004 European Society of Veterinary Dermatology, Veterinary Dermatology, 15, 194–198

198

RD Last et al.

27. Chappell LH, Wastling JM. Cyclosporin A. Antiparasitic drug, modulator of the host parasite relationship
and immunosuppressant. Parasitology 1992; 105 (Suppl.):
S25 – 40.
28. Garon CLG, Scott MA, Selting KA et al. Idiopathic
thrombocytopaenic purpura in a cat. Journal of the
American Animal Hospital Association 1999; 35: 464–
70.
29. Silverman JA, Hayes ML, Luft BJ et al. Characterization of anti-toxoplasma activity of SDZ 215 –918, a
cyclosporin derivative lacking immunosuppressive and
peptidyl-prolyl-isomerases inhibiting activity: possible
role of a P glycoprotein in toxoplasma physiology. Anti-

microbial Agents and Chemotherapy 1997; 41 (9): 1859–
66.
30. Sumyuen MH, Gavin YJ, Derouin F. Effect of immunosuppresive drug regimens on acute and chronic murine
toxoplasmosis. Parasitology Research 1996; 82: 681–6.
31. Groves MG, Harrington KS, Taboada J. Frequently
asked questions about soonoses. In: Ettinger SJ,
Feldman EC. eds. Textbook of Veterinary Internal Medicine, 5th edn. Philadelphia: W.B. Saunders, 2000: 388–9.
32. DeFeo ML, Dubey JP, Mather TN et al. Epidemiologic
investigation of seroprevalence of antibodies to Toxoplasma gondii in cats and rodents. American Journal of
Veterinary Research 2002; 63: 1714–17.

Résumé Une toxoplasmose aigüe généralisée a été diagnostiquée chez un chat européen, mâle âgé de 4–5 ans,
qui était en traitement pour une atopie avec la cyclosporine A depuis 8 mois. La cyclosporine A (CsA) est un
agent immunomodulateur qui a donné des résultats encourageants dans le traitement des plaques et des granulomes éosinophiliques du chat, du prurit cervico-facial et d’autres dermatoses immunologiques. Cependant,
l’inhibition des lymphocytes T par la CsA est probablement responsable du développement de l’infection généralisée par Toxoplasma gondii chez ce chat, avec une hépatite et une pancréatite sévère, associée à la présence de nombreux parasites, démontrée par des marquages immunohistochimiques spécifiques. Les chats recevant de la CsA
semblent être à risque pour le développement d’une toxoplasmose systémique.
Resumen Se diagnosticó una toxoplasmosis sistémica aguda en un gato macho europeo de pelo corto de 4–5
años, que había recibido durante 8 meses una terapia inmunomoduladora con ciclosporina A para la atopia
felina. La ciclosporina A (CsA) ha mostrado resultados prometedores como agente immunosupresor en el gato
para el tratamiento de la placa y granuloma eosinofílicos, prurito alérgico cérvico-facial, atopia felina y otras
dermatosis inmunomediadas. Sin embargo, se cree que la inhibición de la función de linfocitos T por CsA puede
haber predispuesto este gato al desarrollo de una nueva infección aguda por Toxoplasma gondii, caracterizada
por una grave lesión hepática y pancreática, junto a una elevada carga parasitaria mostrada con tinciones
inmunohistoquímicas (IHC) para T. gondii. Los gatos sometidos a terapia con CsA parecen encontrarse predispuestos al desarrollo de una toxoplasmosis sistémica fatal.
Zusammenfassung Bei einer 4 –5 Jahre alten, männlichen Europäisch Kurzhaar Katze, die immunmodulatorische Therapie mit Cyclosporin A zur Behandlung feliner Atopie über einen Zeitraum von 6 Monaten erhielt,
wurde akute systemische Toxoplasmose diagnostiziert. Cyclosporin A (CsA) hat vielversprechende Resultate als
immunsuppressives Medikament zur Behandlung von eosinophilen Plaques und Garnulomata, allergischem
cervico-facialem Juckreiz, feliner Atopie und anderen immun-mediierten Hauterkrankungen gezeigt. Man
nimmt jedoch an, dass die Hemmung der T-Lymphozyten-Funktion durch CsA diese Katze für die Entwicklung
einer neu erworbenen, akuten Toxoplasma gondii- Infektion prädisponiert hat. Diese Toxoplasma gondiiInfektion wurde durch schwere Leber- und Pankreasveränderungen in Verbindung mit einer starken Parasitenlast,
die durch immunhistochemische (IHC) Färbungen für T. gondii nachgewiesen wurde, gekennzeichnet. Katzen,
die mit CsA behandelt werden, scheinen Gefahr zu laufen, fatale systemische Toxoplasmose zu entwickeln.

© 2004 European Society of Veterinary Dermatology, Veterinary Dermatology, 15, 194– 198

Sponsor Documents

Or use your account on DocShare.tips

Hide

Forgot your password?

Or register your new account on DocShare.tips

Hide

Lost your password? Please enter your email address. You will receive a link to create a new password.

Back to log-in

Close