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Abstract

Case summary

Toxoplasma gondii is a globally distributed apicomplexan protozoan infecting all warm-blooded animals. Cats are the definitive host, susceptible to clinical disease. In Spain, studies have shown the widespread presence of Toxoplasma IgG antibodies in cats but there are no published data on clinical toxoplasmosis in cats from Spain. We describe a case of fatal disseminated toxoplasmosis in a 7-year-old outdoor domestic shorthair cat. The cat, an active hunter, was presented with a 1-week history of malaise and acute deterioration over 24 h. Fever, tachypnoea and abdominal discomfort were detected on physical examination. No evidence of immunosuppressive disease or previous treatment could be found. A moderate increase in alanine aminotransferase (ALT) and aspartate aminotransferase (AST) was found on serum biochemistry. Radiography revealed hepatomegaly and a small patchy pulmonary alveolar pattern in the caudal lung lobes. In 48 h, the AST and ALT levels were severely increased and the cat’s respiratory signs worsened. Parenteral clindamycin administration (25 mg/kg IV q12h) and supportive treatment could not prevent progression to death. Cytology from the liver and lungs revealed organisms morphologically consistent with T gondii. Indirect immunofluorescence antibody test Toxoplasma titres were 1:100 IgM and 1:100 IgG. PCR performed on scraped material from glass cytology slides was positive for T gondii in both lung and liver aspirates.

Relevant and novel information

To the authors’ knowledge, this is the first case of fatal disseminated toxoplasmosis in a cat described in Spain, confirmed by PCR. Fine-needle aspirates from the liver could assist in the diagnosis of fatal disseminated toxoplasmosis when liver enzymes are increased.

Keywords

Fatal disseminated toxoplasmosis liver cytology Spain

Case description

A 7-year-old spayed female outdoor domestic shorthair cat was presented after 1 week of inappetence and malaise. Blood tests (Table 1) and ultrasonography performed by the local veterinarian 4 days before presentation were unremarkable. The cat was an active hunter. The day before presentation, its condition deteriorated severely. On physical examination, the cat was mentally depressed, very weak and there was moderate tachypnoea of 40 breaths/minute (bpm). The cat’s temperature was 40°C and abdominal palpation elicited diffuse abdominal pain. Body condition score was 6/9.

Table 1

Blood tests performed by the local veterinarian 4 days before presentation, in-house at presentation and 48 h after presentation

Parameter	4 days before presentation	At presentation	48 h after presentation	Reference interval
Erythrocytes (M/µl)	8.30	5.38	4.39	6.54–12.2
Haemoglobin (g/dl)	12.7	7.9	6.4	9.8–16.2
PCV (%)	38.8	22.9	17.6	30.3–52.3
MCV (fl)	46.7	42.6	40.1	35.9–53.1
Reticulocytes (K/µl)	9	8.1	8	3.0–50.0
Leukocytes (K/µl)	4.87	13.38	17.35	2.87–17.2
Neutrophils (K/µl)	4.09	10.76	13.93	2.30–10.29
Lymphocytes (K/µl)	0.37	1.41	2.76	0.92–6.88
Monocytes (K/µl)	0.37	1.09	0.60	0.05–0.67
Eosinophils (K/µl)	0.01	0.10	0.01	0.17–1.57
Platelets (K/µl)	220	165	62	151–600
Glucose (mg/dl)	118.2	162	125	74–159
Creatinine (mg/dl)	0.6	0.5	<0.4	0.8–2.4
Urea (mg/dl)	33	–	–	30–65
Total protein (g/dl)	9.35	7.5	–	5.7–8.9
Albumin (g/dl)	3.79	2.9	–	2.2–4.0
Globulins (g/dl)	5.56	4.6	–	2.8–5.1
A:G ratio	0.68	0.6	–	–
ALT (U/l)	98	651	1405	12–130
AST (U/l)	71	538	1642	0–48
ALP (U/l)	21	<10	–	14–111
GGT (U/l)	1	7	–	0–4
Total bilirubin (mg/dl)	0.17	0.6	8.6	0.0–0.9
Lactate (mmol/l)	–	1.76	–	0.6–2.5
Sodium (mmol/l)	–	154	134	150–165
Potassium (mmol/l)	–	3.6	2.2	3.5–5.8
Chloride (mmol/l)	–	116	89	112–129

A:G = albumin:globulin; ALP = alkaline phosphatase; ALT = alanine aminotransferase; AST = aspartate aminotransferase; GGT = gamma-glutamyl transferase; MCV = mean cell volume; PCV = packed cell volume

In-house haematology and serum biochemistry tests revealed non-regenerative anaemia, leukocytosis and a moderate increase in alanine aminotransferase (ALT), aspartate aminotransferase (AST) and gamma-glutamyl transferase (Table 1). An in-house feline leukaemia virus (FeLV)/feline immunodeficiency virus (FIV) test (SNAP combo; IDEXX) was negative for both viruses. Radiography (Figure 1) revealed one small patchy pulmonary alveolar infiltrate in the caudal lung lobes and hepatomegaly. The cat was placed in an oxygen cage, fluid therapy was initiated and ampicillin 22 mg/kg IV q8h, clindamycin 16 mg/kg IV q12h, maropitant 1 mg/kg IV q24h and buprenorphine 0.02 mg/kg IV q8h were administered. After 24 h, there was clinical improvement, but the cat’s respiratory rate had worsened to 70 bpm and a gallop rhythm was detected. The patient’s temperature was 39.5°C. A second radiograph (Figure 2) revealed a ventral alveolar pattern with multiple focal pulmonary opacities. In-house B-type natriuretic peptide (BNP) test (SNAP feline proBNP; IDEXX) was performed as a functional cardiac biomarker of myocardial stress. The result was abnormal. Furosemide 1 mg/kg SC was administered and the clindamycin dosage was increased to 25 mg/kg IV q12h. The cat’s respiratory rate decreased to 40 bpm, and ultrasound-guided fine-needle aspiration (FNA) from the lung and liver under mild sedation were scheduled. Twelve hours later, the cat had acutely deteriorated. Severe icterus and an increased respiratory effort in spite of a stable respiratory rate were detected. The cat’s temperature was 38.9°C. In-house haematology and serum biochemistry tests (Table 1) revealed a three-fold increase in AST and ALT, severe hyponatraemia, hypokalaemia, hypochloraemia and moderate leukocytosis. A third radiograph (Figure 3) showed ventral lung consolidation and air bronchograms. Dexamethasone 0.1 mg/kg IV was administered. There was mild improvement in the cat’s respiration and stamina, but despite supportive therapy, it died 5 h later. Permission for a post-mortem examination was declined. However, the caregivers gave their consent to obtain post-mortem FNA from the lungs and liver. Cytology glass slides were stained with haematoxylin and eosin (H&E) and the presence of organisms morphologically consistent with Toxoplasma gondii was detected. Post-mortem review by an external pathologist described the presence of an ovated spherical structure 100 µm in diameter compatible with a T gondii tissue cyst and isolated crescent-shaped structures 4–6 µm in diameter compatible with T gondii tachyzoites-bradyzoites in the liver (Figures 4 –6) and lungs (Figures 7 and 8). The slides of cytological samples stained with H&E were scraped with a microtomy blade. The scraped material was collected in a 1.5 ml conical plastic tube. DNA was extracted using the DNA mini-Blood Kit (QIAGEN Gmbh) following the protocol for tissues provided by the manufacturer. PCR for T gondii was performed in two successive amplifications in a single tube using 18S-5.8S rRNA ITS1 targeted primers. A region of 227 bp of the ITS1 of T gondii was amplified. The PCR products were analysed by electrophoresis through 1.5% (w/v) agarose gels in Tris-borate-EDTA buffer with GelRed Nucleic Acid Stain and the DNA fragments stained were visualised under ultraviolet light on a transilluminator. The PCR result was positive for T gondii in both liver and lung samples.

Figure 1

Radiograph taken at presentation. There is an ill-defined increase in opacity in the caudal lung lobes and oesophagus (white arrow), flattening of the diaphragm, cardiac silhouette spacing from the diaphragm and hepatic parenchyma size increase, with rounded borders

Figure 2

Radiograph taken 24 h (without approximately) after presentation. There is increased lung opacity in multiple ventral areas, small and ill-defined, an increase in the cardiac silhouette compared with presentation and an increase in abdominal distension

Figure 3

Radiograph taken 48 h after presentation, showing the presence of multiple areas of increased pulmonary opacity, with air bronchograms and loss of pulmonary vessel detail, affecting the ventral half of the lung parenchyma

Figure 4

Fine-needle aspiration of the liver, × 100. The hepatocellular population shows discrete to moderate degenerative changes. Some hepatocytes evidence vacuolated and foamy cytoplasm, with small accumulations of bile pigment granules (red arrow). There is a mixed cellular inflammatory component consisting of different maturation stages of lymphocytes and a small number of neutrophils (white arrowheads)

Figure 5

Fine-needle aspiration of the liver, × 100. Structures 4–6 µm in size, crescent-shaped, in a group of seven, compatible with Toxoplasma gondii (yellow arrow)

Figure 6

Fine-needle aspiration of the liver, ×100. Spherical ovated structure, 100 µm in size, filled with crescent-shaped structures, compatible with a Toxoplasma gondii tissue cyst (yellow arrow)

Figure 7

Fine-needle aspiration of the lung, × 100. Epithelial respiratory cells showing typical apical cilia (white arrow) can be observed. One crescent-shaped organism (yellow arrow) compatible with Toxoplasma gondii is present outside the cells

Figure 8

Fine-needle aspiration of the lung, × 100. Three to four crescent-shaped organisms (yellow arrow) compatible with Toxoplasma gondii can be found in the cytoplasm of the respiratory cells

The results of blood tests performed by an external laboratory arrived after the death of the cat (Table 2).

Table 2

Blood tests performed at an external laboratory at presentation; the results arrived post mortem

Parameter	At presentation	Reference interval
Creatine kinase (UI/l)	137	71–146
Preprandial bile acids (µmol/l)	3.2	0.1–6.0
Ultrasensitive cardiac troponin I (ng/ml)	0.51	<0.06
Feline proBNP (pmol/l)	24	<270
Leishmania IgG (IFAT)	Negative	<1/50
Toxoplasma IgG (IFAT)	1/100	<1/100
Toxoplasma IgM (IFAT)	1/100	<1/100
Albumin (g/dl)	2.6	2.86–5.32
Total globulin (g/dl)	3.7	2.5–5.1
Alpha-1 globulin (g/dl)	0.3	0.04–0.22
Alpha-2 globulin (g/dl)	1.5	0.6–1.58
Beta-globulin (g/dl)	1.1	0.48–1.1
Gamma-globulin (g/dl)	0.8	0.33–1.84
A:G ratio	0.7	–

A:G = albumin:globulin; BNP = B-type natriuretic peptide; IFAT = immunofluorescence antibody test

Discussion

T gondii is an apicomplexan coccidian protozoan with a global distribution. It can infect any nucleated cell and affect all warm-blooded animals.¹ Cats and other felids are the definitive hosts of its complex life cycle and release oocysts, the environmentally resistant form of the parasite, with all other warm-blooded animals acting as intermediate hosts.² Oocysts, which can be found in all environments, are ingested by intermediate hosts in which an asexual cycle is completed. Tachyzoites disseminate throughout the body and produce tissue cysts in which, probably for the life of the host, they persist as bradyzoites, mostly in neural and muscular tissues, but also in visceral organs, including the lungs, liver and kidneys.³ The main source of infection for cats is ingestion of intermediate hosts or their tissues, either by hunting small prey or eating raw meat fed by humans.^4,5 Other sources of infection are congenital^6,7 and, probably, galactophorous.^7,8 The parasite can either first undergo an asexual cycle, remaining in the cat as tissue cysts, or complete an enteroepithelial sexual cycle, producing oocysts that will again contaminate the environment. The relationship between T gondii and felids and their prey is ancient, meaning that evolutionary mechanisms have adapted both in a highly specialised relationship.⁹ This could play a role in the rare presentation of clinical disease in cats: in a large institution located in Boston (USA), 100 cases of confirmed clinical toxoplasmosis were described over 40 years.¹⁰ In Finland, 3% of a long series of cats positive for toxoplasma showed signs of clinical disease over 3.5 years.¹¹ The same rate was described in Denmark over a 2-year period.¹²

Feline toxoplasmosis was first reported in 1942.¹³ In 1954, the first clinically diagnosed case was published.¹⁴ Different presentations have been described since in many countries,^15
–45 as well as series of cases.^6,8,46
–50 In Spain, studies have detected the presence of T gondii antibodies in 24.2–84.7 % of domestic cats, free-roaming cats and wild felids in different regions.^51
–58 However, no cases of fatal disseminated toxoplasmosis in cats have been described in Spain.

Acute systemic toxoplasmosis is the result of overwhelming intracellular replication of tachyzoites. It mostly affects pulmonary, hepatic, central nervous system (CNS) and pancreatic tissues,^25,28,59 arising from primary infection or through reactivation of tissue cysts present in the cat. Our case was an outdoor hunting cat, showing vague illness with acute deterioration 24 h before presentation. In reported cases, an immunosuppressive predisposing cause can be found, such as a renal transplant, oclacitinib, cyclosporine or prednisolone treatment, concurrent FIV/FeLV infection or feline infectious peritonitis infection.^{15,21,29,30,38,40,42,48,49} However, in other cases,^18,22,27,44 including ours, a predisposing cause cannot be determined. It has been suggested that more pathogenic strains may be involved.^{15,23,25,35,59,60} As in other cases described, findings on physical examination included fever, tachypnoea, depression and diffuse abdominal discomfort on palpation. The detection of an increase in ALT, AST, leucocytosis and radiographic pulmonary patchy alveolar infiltrates, indicating hepatic and respiratory disease, has also been described in cases of fatal disseminated toxoplasmosis.^{10,18,21,22,27,40,44,46,48} Eliciting a pain response on abdominal palpation has been attributable to hepatitis, pancreatitis or discomfort from interference with respiration in those cats with advanced pneumonia.¹⁰ In our case, acute hepatic disease and early pneumonia would be the most likely causes, since hepatomegaly and some pulmonary alveolar infiltrates could be detected on radiographs at presentation. Pneumonia is a common finding in fatal disseminated toxoplasmosis,^22,28,46,61 being present in 97.7% of cats in a series of cases.¹⁰The most striking biochemical change was abnormal AST and ALT, which presented a massive increase over 48 h. We could not assess the presence of pancreatitis and there were no CNS clinical signs. Severe hypokalaemia, hypochloraemia, hyponatraemia were detected 48 h after presentation. That could reflect acute hepatic failure and severe respiratory disease.^{18,25,26,40,44,62} Acid-base disorders contributing to the electrolyte imbalances detected could not be determined. Furosemide administration²⁷ is an unlikely cause, since only a single low dose was administered. There was an acute fatal evolution despite treatment, similar to other cases described.^{10,18,21,27,38,40,44,50}

A diagnosis of fatal disseminated toxoplasmosis is based on the presence of compatible clinical signs and demonstration of the organism.⁵⁹ Nevertheless, it is rarely confirmed ante mortem. In our case, FNA from the lungs and liver were performed post mortem, enabling the detection of organisms consistent with T gondii. Although cytology has been described for the diagnosis of toxoplasmosis using bronchoalveolar lavage (BAL) and other body fluids and tissues,^{10,16,19,22,23,25,27,29,31,32,34
–38,40,42,43,48,50} its application in detecting T gondii in liver parenchyma FNA has not previously been reported. Acute Toxoplasma hepatitis has been described, but no liver cytology was performed.²² In one study, cytological observation of tachyzoites in BAL fluid proved more sensitive than histological examination of tissue samples.⁶³ It is important to distinguish T gondii from Neospora caninum^25,27 and to note that our area is endemic for Leishmania infantum.⁶⁴ PCR is a useful technique for confirming T gondii infection^59,65 and the use of fixed stained smears and scrape lysates as material for PCR has been described in the diagnosis of mycobacteria and pulmonary toxoplasmosis in cats.^37,38,66,67 In our case, PCR performed on samples of lung and liver scraped from cytology slides allowed confirmation of fatal disseminated T gondii infection.

One limitation of our case is that molecular characterisation was not possible. In Spain, one study in cats revealed type I and type II strains of T gondii.⁶⁸

Serology has been used in the diagnosis of T gondii with varying results. An IgM titre of 1:64 or higher is indicative of active infection, as seen in our case (Table 2). The interpretation of IgG is more complex, as single positive titres indicate only exposure rather than infection. For a tentative diagnosis, multiple requirements are needed.^{4,10,17,27,41,47,59} Some confirmed cases may present negative titres.^36,39,48 In acute cases, serology is of little use ante mortem as results often arrive after the cat has died, as occurred in our case.

Parenteral clindamycin treatment^4,20,47 was initiated in this case; however, there was no clinical response. This lack of response may be due to overwhelming infection, parasite drug resistance or an antibiotic-associated decrease in the antitoxoplasmic activity of phagocytic cells, which are responsible for the control of T gondii.⁶⁹ Parenteral trimethoprim-sulfonamide was unavailable; other similar cases treated with combination protocols have also not survived.^{22,40,46,48,49} Some chronic cases treated with clindamycin, even at doses lower than described, have survived.^18,33,22 Treatment with oral pyrimetamine or azithromycin was not an option in this case.

Dexamethasone was administered at a low anti-inflammatory dose to control parasite-related inflammation.²³ However, it is unlikely to have contributed to the poor outcome, as the cat’s condition had already deteriorated before administration. The use of prednisolone in the treatment of toxoplasmosis has been described without evidence of worsening disease or a predisposition to recrudescence.^16,24

A second limitation of our case is that no post-mortem examination was allowed, which hindered the description of all affected organs. However, it is possible that myocardial disease was present. Upon admission, feline cardiac proBNP was within the normal range, but 24 h later, the in-house test returned abnormal results and a gallop rhythm was detected. In addition, ultrasensitive cardiac troponin I levels were mildly elevated at presentation (Table 2). Unfortunately, it was not possible to perform an echocardiogram. In a series of 100 cases, myocarditis was detected post mortem in 62.7% of the cats.¹⁰ Another study on neonatal infections revealed myocardial lesions in 100% of kittens.⁷⁰

Conclusions

To the authors’ knowledge, this is the first reported case of fatal disseminated toxoplasmosis in a cat in Spain, confirmed using PCR. When suspecting fatal disseminated toxoplasmosis, FNA of the liver could assist in achieving an early diagnosis.

Footnotes

Acknowledgements

The authors would like to thank Histolab Veterinaria (Malaga, Spain) for the post-mortem review of the liver and lung FNA cytology samples.

Accepted: 24 October 2024

Conflict of interest

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The authors received no financial support for the research, authorship, and/or publication of this article.

Ethical approval

The work described in this manuscript involved the use of non-experimental (owned or unowned) animals. Established internationally recognised high standards (‘best practice’) of veterinary clinical care for the individual patient were always followed and/or this work involved the use of cadavers. Ethical approval from a committee was therefore not specifically required for publication in JFMS Open Reports. Although not required, where ethical approval was still obtained, it is stated in the manuscript.

Informed consent

Informed consent (verbal or written) was obtained from the owner or legal custodian of all animal(s) described in this work (experimental or non-experimental animals, including cadavers, tissues and samples) for all procedure(s) undertaken (prospective or retrospective studies). No animals or people are identifiable within this publication, and therefore additional informed consent for publication was not required.

ORCID iD

Llibertat Real

References

Dubey

Cerqueira-Cézar

Murata

FHA

, et al. All about toxoplasmosis in cats: the last decade. Vet Parasitol 2020; 283. DOI: 10.1016/j.vetpar.2020.109145.

Dubey

JP.

Advances in the life cycle of Toxoplasma gondii.

Int J Parasitol 1998; 28: 1019–1024.

Dubey

Lindsay

Speer

CA.

Structures of Toxoplasma gondii tachyzoites, bradyzoites, and sporozoites and biology and development of tissue cysts.

Clin Microbiol Rev 1998; 11: 267–299.

Dubey

Lappin

MR.

Toxoplasmosis and neosporosis. In: Greene

(ed). Infectious diseases of the dog and cat. 3rd ed. St Louis, MO: Saunders Elsevier, 2006, pp 754–775.

Lappin

George

Pedersen

, et al. Primary and secondary Toxoplasma gondii infection in normal and feline immunodeficiency virus-infected cats. J Parasitol 1996; 82: 733–742.

Dubey

Johnstone

Menrath

, et al. Congenital toxoplasmosis in Abyssinian cats. Vet Parasitol 1989; 32: 261–264.

Powell

Brewer

Lappin

MR.

Detection of Toxoplasma gondii in the milk of experimentally infected lactating cats.

J Vet Parasitol 2001; 102: 29–33.

Powell

Lappin

MR.

Clinical ocular toxoplasmosis in neonatal kittens.

Vet Ophthalmol 2001; 4: 87–92.

Bertranpetit

Jombart

Paradis

, et al. Phylogeography of Toxoplasma gondii points to a South American origin. Infect Genet Evol 2017; 48: 150–155.

10.

Dubey

Carpenter

JL.

Confirmed clinical toxoplasmosis in cats: 100 cases (1952–1990).

J Am Vet Med Assoc 1993; 203: 1556–1566.

11.

Jokelainen

Simola

Rantanen

, et al. Feline toxoplasmosis in Finland: cross-sectional epidemiological study and case series study. J Vet Diagn Invest 2012; 24: 1115–1124.

12.

Henriksen

Dietz

Henriksen

SA.

Fatal toxoplasmosis in five cats.

Vet Parasitol 1994; 55: 15–20.

13.

Olafson

Monlux

WS.

Toxoplasmosis in animals.

Cornell Vet 1942; 32: 176–190.

14.

Holzworth

Encephalitic toxoplasmosis in a cat.

J Am Vet Med Assoc 1954; 124: 313–316.

15.

Pena

HFJ

Evangelista

Casagrande

, et al. Fatal toxoplasmosis in an immunosuppressed domestic cat from Brazil caused by Toxoplasma gondii clonal type I. Rev Bras Parasitol Vet 2017; 26: 177–184.

16.

McConnell

Sparkes

Blunden

, et al. Eosinophilic fibrosing gastritis and toxoplasmosis in a cat. J Feline Med Surg 2007; 9: 82–88.

17.

Simpson

Devine

Gunn-Moore

Suspected toxoplasma-associated myocarditis in a cat.

J Feline Med Surg 2005; 7: 203–208.

18.

Cohen

Blois

Vince

AR.

Fatal extraintestinal toxoplasmosis in a young male cat with enlarged mesenteric lymph nodes.

Can Vet J 2016; 57: 483–486.

19.

Evans

Walker

Manchester

AC.

Acute respiratory distress syndrome and septic shock in a cat with disseminated toxoplasmosis.

J Vet Emerg Crit Care (San Antonio) 2017; 27: 472–478.

20.

Wagner

Cooper

JJ.

What is your neurologic diagnosis? Toxoplasmosis causing right facial nerve paralysis in a cat.

J Am Vet Med Assoc 2018; 253: 163–165.

21.

Last

Suzuki

Manning

, et al. A case of fatal systemic toxoplasmosis in a cat being treated with cyclosporin A for feline atopy. Vet Dermatol 2004; 15: 194–198.

22.

Dubey

Zajac

Osofsky

, et al. Acute primary toxoplasmic hepatitis in an adult cat shedding Toxoplasma gondii oocysts. J Am Vet Med Assoc 1990; 197: 1616–1618.

23.

Jeffery

Donnelly

, et al. What is your neurologic diagnosis? Toxoplasmosis with CNS involvement in a cat. J Am Vet Med Assoc 2016; 249: 1007–1010.

24.

Pfohl

Dewey

CW.

Intracranial Toxoplasma gondii granuloma in a cat.

J Feline Med Surg 2005; 7: 369–374.

25.

Little

Shokek

Dubey

, et al. Toxoplasma gondii-like organisms in skin aspirates from a cat with disseminated protozoal infection. Vet Clin Pathol 2005; 34: 156–160.

26.

Heidel

Dubey

Blythe

, et al. Myelitis in a cat infected with Toxoplasma gondii and feline immunodeficiency virus. J Am Vet Med Assoc 1990; 196: 316–318.

27.

Poitout

Weiss

Dubey

JP.

Lung aspirate from a cat with respiratory distress.

Vet Clin Pathol 1998; 27: 10. DOI: 10.1111/j.1939-165x.1998.tb01072.x.

28.

Duncan

Lindsay

Chickering

, et al. Acute primary toxoplasmic pancreatitis in a cat. Feline Pract 2000; 28: 6–8.

29.

Anfray

Bonetti

Fabbrini

, et al. Feline cutaneous toxoplasmosis: a case report. Vet Dermatol 2005; 16: 131–136.

30.

Zandonà

Brunetta

Zanardello

Cerebral toxoplasmosis in a cat with feline leukemia and feline infectious peritonitis viral infections.

Can Vet J 2018; 59: 860–862.

31.

Falzone

Baroni

De Lorenzi

, et al. Toxoplasma gondii brain granuloma in a cat: diagnosis using cytology from an intraoperative sample and sequential magnetic resonance imaging. J Small Anim Pract 2008; 49: 95–99.

32.

Caporali

Albanese

Vicari

, et al. Pathology in practice. Cutaneous toxoplasmosis manifesting as nodules in a cat. J Am Vet Med Assoc 2018; 252: 57–60.

33.

McKenna

Augusto

Suárez-Bonnet

, et al. Pulmonary mass-like lesion caused by Toxoplasma gondii in a domestic shorthair cat. J Vet Intern Med 2021; 35: 1547–1550.

34.

Alves

Gorgas

Vandevelde

, et al. Segmental meningomyelitis in 2 cats caused by Toxoplasma gondii. J Vet Intern Med 2011; 25: 148–152.

35.

Spycher

Geigy

Howard

, et al. Isolation and genotyping of Toxoplasma gondiicausing fatal systemic toxoplasmosis in an immunocompetent 10-year-old cat. J Vet Diagn Invest 2011; 23: 104–108.

36.

Park

Ikadai

Yoshida

, et al. Cutaneous toxoplasmosis in a female Japanese cat. Vet Pathol 2007; 44: 683–687.

37.

Murakami

Mori

Takashima

, et al. A case of pulmonary toxoplasmosis resembling multiple lung metastases of nasal lymphoma in a cat receiving chemotherapy. J Vet Med Sci 2018; 80: 1881–1886.

38.

Salant

Klainbart

Kelmer

, et al. Systemic toxoplasmosis in a cat under cyclosporine therapy. Vet Parasitol Reg Stud Reports 2021; 23. DOI: 10.1016/j.vprsr.2021.100542.

39.

Lindsay

Barrs

Child

, et al. Myelitis due to reactivated spinal toxoplasmosis in a cat. J Feline Med Surg 2010; 12: 818–821.

40.

Moore

Burrows

Malik

, et al. Fatal disseminated toxoplasmosis in a feline immunodeficiency virus-positive cat receiving oclacitinib for feline atopic skin syndrome. Vet Dermatol 2022; 33: 435–439.

41.

Hughes

Hill

Feline ocular toxoplasmosis: a case study and literature review.

Aust Vet Pract 2008; 38: 2–8.

42.

Barrs

Martin

Beatty

JA.

Antemortem diagnosis and treatment of toxoplasmosis in two cats on cyclosporin therapy.

Aust Vet J 2006; 84: 30–35.

43.

Lo Piccolo

Busch

Palić

, et al. Toxoplasma gondii-assoziierte Cholezystitis bei einer Katze unter immunsuppressiver Therapie [article in German]. Tierarztl Prax Ausg K Kleintiere Heimtiere 2019; 47: 453–457.

44.

Nagel

Williams

Schoeman

JP.

Fatal disseminated toxoplasmosis in an immunocompetent cat.

J S Afr Vet Assoc 2013; 84: E1–E6.

45.

Kul

Atmaca

Deniz

, et al. Clinicopathologic diagnosis of cutaneous toxoplasmosis in an Angora cat [article in German]. Berl Munch Tierarztl Wochenschr 2011; 124: 386–389.

46.

Meier

Holzworth

Griffiths

RC.

Toxoplasmosis in the cat – fourteen cases.

J Am Vet Med Assoc 1957; 131: 195–201.

47.

Lappin

Greene

Winston

, et al. Clinical feline toxoplasmosis. Serologic diagnosis and therapeutic management of 15 cases. J Vet Intern Med 1989; 3: 139–143.

48.

Bernsteen

Gregory

Aronson

, et al. Acute toxoplasmosis following renal transplantation in three cats and a dog. J Am Vet Med Assoc 1999; 215: 1123–1126.

49.

Ludwig

Schlicksup

Beale

, et al. Toxoplasma gondii infection in feline renal transplant recipients: 24 cases (1998–2018). J Am Vet Med Assoc 2021; 258: 870–876.

50.

Lingard

O’Brien

Barrs

, et al. Concurrent feline infectious peritonitis and toxoplasmosis in three cases. Aust Vet Pract 2010; 40: 9–16.

51.

Millán

Cabezón

Pabón

, et al. Seroprevalence of Toxoplasma gondii and Neospora caninum in feral cats (Felis silvestris catus) in Majorca, Balearic Islands, Spain. Vet Parasitol 2009; 165: 323–326.

52.

Gauss

CBL

Almería

Ortuño

Seroprevalence of Toxoplasma gondii antibodies in domestic cats from Barcelona, Spain.

J Parasitol 2003; 89: 1067–1068.

53.

Miró

Montoya

Jiménez

, et al. Prevalence of antibodies to Toxoplasma gondii and intestinal parasites in stray, farm and household cats in Spain. Vet Parasitol 2004; 126: 249–255.

54.

Candela

Fanelli

Carvalho

, et al. Urban landscape and infection risk in free-roaming cats. Zoonoses Public Health 2022; 69: 295–311.

55.

Montoya

Garcia

Galvez

, et al. Implications of zoonotic and vector-borne parasites to free-roaming cats in central Spain. Vet Parasitol 2018; 251: 125–130.

56.

Miró

Rupérez

Checa

, et al. Current status of L. infantum infection in stray cats in the Madrid region (Spain): implications for the recent outbreak of human leishmaniosis? Parasit Vectors 2014; 7. DOI: 10.1186/1756-3305-7-112.

57.

Sherry

Miró

Trotta

, et al. A serological and molecular study of Leishmania infantum infection in cats from the island of Ibiza (Spain). Vector Borne Zoonotic Dis 2011; 11: 239–245.

58.

Matas Méndez

Fuentes Corripio

Montoya Matute

, et al. Prevalence of Toxoplasma gondii in endangered wild felines (Felis silvestris and Lynx pardinus) in Spain. Animals (Basel) 2023; 13. DOI: 10.3390/ani13152488.

59.

Lappin

MR.

Update on the diagnosis and management of Toxoplasma gondiiinfection in cats.

Top Companion Anim Med 2010; 25: 136–141.

60.

Crouch

EEV

Mittel

Southard

TL.

Littermate cats rescued from a shelter succumbed to acute, primary toxoplasmosis associated with TOXO DB genotype #4, generally circulating in wildlife.

Parasitol Int 2019; 72. DOI: 10.1016/j.parint.2019.101942.

61.

Parker

Langloss

Dubey

, et al. Pathogenesis of acute toxoplasmosis in specific-pathogen-free cats. Vet Pathol 1981; 18: 786–803.

62.

Ueda

Hopper

Epstein

SE.

Incidence, severity and prognosis associated with hyponatremia in dogs and cats.

J Vet Intern Med 2015; 29: 801–807.

63.

Hawkins

Davidson

Meuten

, et al. Cytologic identification of Toxoplasma gondii in bronchoalveolar lavage fluid of experimentally infected cats. J Am Vet Med Assoc 1997; 210: 648–650.

64.

Baxarias

Mateu

Miró

, et al. Serological survey of Leishmania infantum in apparently healthy dogs in different areas of Spain. Vet Med Sci 2023; 9: 1980–1988.

65.

Boothroyd

JC.

Toxoplasma gondii: 25 years and 25 major advances for the field.

Int J Parasitol 2009; 39: 935–946.

66.

Reppas

Fyfe

Foster

, et al. Detection and identification of mycobacteria in fixed stained smears and formalin-fixed paraffin-embedded tissues using PCR. J Small Anim Pract 2013; 54: 638–646.

67.

Burgess

Lockerbie

Marshall

TR.

Use of slide scrape lysates for polymerase chain reaction confirmation of disseminated Mycobacterium avium infection in a cat.

Can Vet J 2019; 60: 179–182.

68.

Montoya

Miró

Mateo

Molecular characterization of Toxoplasma gondii isolates from cats in Spain.

J Parasitol 2008; 94: 1044–1046.

69.

Davidson

Lappin

Rottman

, et al. Paradoxical effect of clindamycin in experimental, acute toxoplasmosis in cats. Antimicrob Agents Chemother 1996; 40: 1352–1359.

70.

Dubey

Mattix

Lipscomb

TP.

Lesions of neonatally induced toxoplasmosis in cats.

Vet Pathol 1996; 33: 290–295.

Fatal disseminated Toxoplasma gondii infection in a cat from Madrid,Spain

Abstract

Case summary

Relevant and novel information

Keywords

Case description

Discussion

Conclusions

Footnotes

Acknowledgements

Conflict of interest

Funding

Ethical approval

Informed consent

ORCID iD

References