Feline trypanosomosis in a male pseudohermaphrodite cat (Felis catus): A rare case

Introduction

Feline trypanosomosis

Trypanosomosis refers to an infection caused by protozoans of the genus Trypanosoma, mainly transmitted by hematophagous vectors like Stomoxys, Tabanus, and Triatomine bugs, with carcass ingestion from recently infected animals also suggested as a transmission route [14] . Reports of naturally occurring trypanosomosis in felines are scarce in the scientific literature, likely due to the higher resistance of cats compared to other vertebrate hosts. Consequently, trypanosomosis is infrequently observed and diagnosed in felids, making it a rare parasitic infection in this species [5] . Documented cases of feline trypanosomosis in domestic cats include two reports from India [6,7] , one from Canada [5] , three from Kuwait [8] , and seven from Iraq [9] . Causative organisms have been identified as Trypanosoma brucei and Trypanosoma evansi [2,5,[7][8][9] , both of which elicit the same clinical symptoms in cats, severity of which is directly proportional to the parasitaemia. Peripheral blood smear evaluation and immunological tests help in diagnosis. Treatment involves the use of trypanocidal or chemotherapeutic drugs such as Diminazene aceturate.

DSD in cats

Chromosomal composition, gonadal histology, reproductive tract morphology and external genital appearance are the necessary criteria for definitive sex identification [10] . Mammalian sexual development involves three crucial steps: Chromosomal sex differentiation, Gonadal sex differentiation and phenotypic sex differentiation [11] . Aberrations at any stage of these processes can result in abnormal sexual phenotypes, with disruptions at one level often affecting subsequent developmental stages [12] . This creates true hermaphrodites (presence of gonadal tissues of both sexes) or pseudohermaphrodites (gonads of one sex, and alterations in one or more criteria for sex identification) [10] .

Cats normally have 38 chromosomes, including sex chromosomes (Queens: 38, XX; Toms: 38, XY) [11] . Male pseudohermaphrodites have a normal male karyotype (38, XY) and testes, but have feminine external reproductive organs/phenotype. This case discusses alleged male pseudohermaphroditism in a cat infected with trypanosomosis, making it a special, rare occurrence.

Case Discussion

This case revolves around the presence of two uncommon conditions in the same patient, Raju, a phenotypically female, free-ranging, DSH cat, detected at two separate consultations, approximately one month apart. The case discussion is therefore divided into two parts.

Part I: Alopecia

She was presented for her first consultation on 18 th November 2024 with bilateral alopecia of the head and neck and swelling in the right premandibular region (Figure 1a). The patient had previously received treatment at multiple veterinary clinics with no resolution of alopecia. On clinical examination, the mucous membranes were pale pink, and submandibular lymphadenopathy was noted. Based on prior experience with similar cases, trypanosomosis was included in the differential diagnoses. To establish a definitive diagnosis, a complete blood panel (CBC, liver function test [LFT], kidney function test [KFT]), peripheral blood smear, lymph node fine needle aspiration (FNA), and skin tape smear were performed. The blood test reports showed mild microcytic hypochromic anaemia and thrombocytopoenia, alongside other normal parameters (Figure 2a,b). On 19 th November 2024, peripheral blood smear results confirmed the presence of Trypanosoma spp. (Figure 3). The skin tape smear revealed the presence of dermatophytes, indicative of concurrent dermatophytosis (Figure 4). The lymph node FNA showed presence of Trypanosoma spp. and lymphoproliferative disorder (likely owing to the trypanosomosis), (Figure 5,6). Her progress was recorded weekly (Figure 1b-1e). Following the final diminazene aceturate injection on 10 th December 2024, a post-treatment bloodwork panel, consisting of CBC, LFT, KFT, and peripheral blood smear was conducted. The peripheral smear tested negative for Trypanosoma spp.

The following treatment regimen was initiated

(Figure 7a,b). The doxycycline course was completed on 18 th December 2024 as prescribed. The alopecia, thrombocytopenia and anaemia had resolved by 20 th December 2024. The leucocytosis observed in the report was attributed to a secondary respiratory infection that she had contracted during the course of treatment from other cats in the cattery where she was housed, which had resolved one month post treatment (Figure 8) with the help of an herbal immunomodulator and phagocytosis enhancer (Immunol ® ; [The Himalaya Drug Company])-1 mL PO q12h for 4 weeks. Part II: Ovariohysterectomy Raju was scheduled for a routine ovariohysterectomy (OVH) on 24 th December 2024 prior to release into her original environment. Following standard preoperative preparation, a ventral midline celiotomy was performed with an incision placed one inch caudal to the umbilicus. However, no uterine horns were identified, even after extending the incision. Further abdominal exploration revealed a small, nodular, slightly oblong structure, morphologically resembling a testis, located at the expected anatomical position of the left ovary (Figure 9a). This structure was attached to a cord-like structure resembling the spermatic cord, which was ligated using chromic catgut (3-0 TRUGUT ® ; Healthium Medtech Limited) and excised. Further intra-abdominal and intra-pelvic exploration did not reveal any additional testicular or female reproductive structures. However, on palpation of the right lateral perivulvar region, a firm, nodular structure was identified. A small incision over the area exposed a second identical structure, which was subsequently ligated and excised (Figure 9b). The excised gonadal structures were fixed in 10% neutral buffered formalin (NBF) and submitted for histopathological evaluation. Histopathology results dated 26 th December 2024 confirmed the presence of azoospermic testicular tissue (Figure 10), supporting the diagnosis of male pseudohermaphroditism. In this case, due to financial constraints, additional diagnostics such as Trypanosoma spp. PCR, hormonal assays, and genotype sequencing were not performed.

Discussion

Feline trypanosomosis

Trypanosomosis, also known as Surra, is widespread throughout the tropical and subtropical regions of North America, Southeast Asia, as well as Central and South America [13,14] . It is primarily transmitted via hematophagous vectors such as Stomoxys, Tabanus, and Triatomine bugs. Ingestion of carcasses from recently infected animals has also been recently suggested as a mode of transmission [1][2][3][4] . Clinical manifestations include acute febrile episodes, hyperthermia, anorexia, anaemia, lethargy, chronic wasting, lymphadenopathy, and neurological signs such as encephalitis, seizures, and ataxia [8,[15][16][17][18] .

Trypanosomosis is found frequently in wild and domesticated animals such as deers, elephants, and domestic animals such as cattle and buffalo [19] . Amongst wild felids, few instances of deaths in tigers have been published in India 20,21 , however, amongst domestic felids, documented cases of naturally occurring feline trypanosomosis include a total of only 13 reports across the globe, out of which, two reports are from India [6,7] . To date, there is no definitive pathophysiological explanation for the infrequent occurrence of trypanosomosis in felids. It has however been hypothesized that their stronger immune systems aid in shielding them from the infection, however, no evidence has yet been published. Detection of trypanosomes in Giemsa-stained thick and thin peripheral blood smears (collected from the ear vein), PCR, ELISA, immunofluorescent tests, or cerebrospinal fluid (CSF) analysis for patients with central nervous system involvement aid in diagnosis [3,15] . The treatment protocol includes the use of trypanocidal or chemotherapeutic agents, such as dimidium bromide, potassium antimony tartrate, suramin, melarsamine, quinapyramine, homidium, diminazene aceturate, and isometamidium, with the latter six also exhibiting prophylactic potential [3,22,23] , usually administered intramuscularly to avoid injection site/vascular wall necrosis [3] . The zoonotic potential of Trypanosomosis has been reported in South Asian countries, including India, with signs ranging from lethargy, headache, chronic fever, to death [24][25][26] . Atypical human trypanosomosis (aHT) due to Trypanosoma evansi is a newly emerging disease in India. Card agglutination test for trypanosomosis (CATT) revealed that 5.2% (9/173) of the individuals tested positive in West Bengal, whereas 4.5% (81/1806) of individuals tested positive in Maharashtra [27] . It is hence a notifiable disease and needs to be documented as and when found, especially in improbable circumstances.

Disorders of sexual development

Chromosomal sex is determined at the time of fertilization, when the zygote obtains a normal number of autosomal chromosomes and either two X chromosomes or an X and a Y chromosome [12] . Both XX and XY zygotes initially develop into sexually indifferent embryos. At this stage, the embryonic phenotype resembles the female form more closely.

Toward the end of this indifferent phase, the genital ridge (the precursor to the gonad) emerges. Removal of the genital ridge at this point results in the development of a female phenotype in both XX and XY embryos. This underscores the fact that while ovarian signals are not inherently required for female phenotypic development, testicular signals are required to drive male phenotypic development.

Gonadal sex development marks the conclusion of the embryonic indifferent stage, where the gonads become genetically committed to differentiating as either ovaries or testes [12] . Phenotypic sex development encompasses the formation of the remaining sexual characteristics and depends on the presence or absence of testicular secretions [12] . Changes in any of the steps of sexual development cause disorders of sexual development.

Male pseudohermaphrodites have a normal male karyotype (38, XY) and testes but have defects in either Mullerian duct regression or in androgen-dependent masculinization [12] , thereby falling under the category of phenotypic abnormalities. Androgen receptor defects causing failure of androgen dependent masculinization (also known as testicular feminization) has been documented in dogs [28] and cats, the degree of which depends on the degree of loss of function in the androgen receptors [11] .

Conclusion

Accurate diagnostics are essential in the clinical management of animals presenting with atypical or nonspecific signs. Establishing a definitive etiological diagnosis not only facilitates targeted and effective treatment for the affected individual(s), but also contributes to the broader scientific understanding of disease processes. This, in turn, enhances the collective veterinary knowledge base and supports the global advancement of evidence-based medical practices.

Acknowledgement

AcknowledgementsVetcore Laboratories and Unique Bio Diagnostics Enterprises for diagnostic tests.

References

1. Nwoha RIO. A review on trypanosomosis in dogs and cats. African Journal of Biotechnology. 2013;12(26): 6432-6433. DOI: 10.5897/AJB2013.12093.
2. Desquesnes M, Holzmuller P, Lai D, Dargantes A, Lun Z, Jittaplapong S. Trypanosoma evansi and surra: a review and perspectives on origin, history, distribution, taxonomy, morphology, hosts, and pathogenic effects. BioMed Research International. 2013;2013:194176. DOI: 10.1155/2013/194176.
3. Uilenberg G. A field guide for the diagnosis, treatment and prevention of African animal trypanosomosis. Rome: Food and Agriculture Organization of the United Nations; 1998.
4. Raina AK, Kumar R, Rajora VS, Sridhar, Singh RP. Oral transmission of Trypanosoma evansi infection in dogs and mice. Veterinary Parasitology. 1985;18(1):67-69.
5. Hill DH. Trypanosoma brucei in the cat. British Veterinary Journal. 1955;1112:77-80.
6. Ganjwala H, Latkar R. Feline trypanosomosis in a freeranging domestic shorthair cat (Felis catus). International Journal of Veterinary Science and Animal Husbandry. 2025;10(3):75-79. DOI: 10.22271/veterinary.2025.v10.i3b.2109.
7. Shivajothi S, Reddy BS. Trypanosoma evansi infection in cat-a rare case. Comparative Clinical Pathology. 2018;27(1):115-116. DOI: 10.1007/s00580-017-2560-x.
8. Tarello W. Trypanosoma evansi infection in three cats. Revue de Médecine Vétérinaire. 2015;156(3):133-134.
9. Mohammed NH, Moosa DA, Altaliby MAM. Diagnostic study of trypanosomiasis of cats in Mosul, Iraq. Open Veterinary Journal. 2022;12(5):688-692. DOI: 10.5455/OVJ.2022.v12.i5.13.
10. Bredal WP, Thoresen SI, Kvellestad A, Lindblad K. Male pseudo hermaphroditism in a cat. Journal of Small Animal Practice. 1997;38(1):21-24. DOI: 10.1111/j.1748-5827.1997.tb02981.x.
11. Christensen BW. Disorders of sexual development in dogs and cats. Veterinary Clinics of North America: Small Animal Practice. 2012;42(3):515-525. DOI: 10.1016/j.cvsm.2012.01.008.
12. Meyers-Wallen VN. Inherited disorders of sexual development in dogs and cats. Tufts' Canine and Feline Breeding and Genetics Conference. New York: Baker Institute for Animal Health, Cornell University; 2007. Available from: https://www.vin.com/members/cms/project/defaultadv1.a spx?pId=11243&meta=Generic&catId=31943&id=38612 54
13. Desquesnes M, Gonzatti M, Sazmand A, Tevenon S, Bossard G, Thevenon S, et al. A review on the diagnosis of animal trypanosomoses. Parasites and Vectors. 2022;15:64.
14. Sánchez ET, Perrone G, Recchimuzzi I, Cardozo N, Biteau PA, Mijares A, et al. Molecular characterization and classification of Trypanosoma spp. Venezuelan isolates based on microsatellite markers and kinetoplast maxicircle genes. Parasites and Vectors. 2015;8:536.
15. Desquesnes M. Surra in all species (Trypanosoma evansi infection). In: Terrestrial Manual 2021. Paris: World Organisation for Animal Health (WOAH); 2021.
16. Dakshinkar NP, Dhoot VM, Uphadhye SV, Bhojne GR, Sarode DB, Kolte SW. Trypanosomiasis in a jungle cat. Indian Veterinary Journal. 2002;79(1):66-67.
17. Thirunavukkarasu PS, George RRS, Nambi AP, Ramesh S, Vasu K. Trypanosomiosis in a cat-a clinical report. Indian Veterinary Journal. 2000;77:428-429.
18. Paikne DL, Dhake PD. Trypanosomiasis in a domestic cat (Felis catus). Indian Veterinary Journal;1974.
19. Choudury A, Misra KK. Experimental infection of Trypanosoma evansi in the cat. Transactions of the Royal Society of Tropical Medicine and Hygiene. 1972;66(3):231-239.
20. Sengupta MR. A preliminary report on diseases and parasites of zoo animals, birds and reptiles. Indian Journal of Animal Science. 1974;13:15-24.
21. Dasgupta B, Pal N, Ghosh BN. Trypanosomiasis in tigers and leopards in Darjeeling. Journal of Parasitic Diseases. 1979;3(1):61-62.
22. Giordani F, Morrison LJ, Rowan TG, Koning HP, Barrett MP. The animal trypanosomiases and their chemotherapy: A review. Parasitology. 2016;143(14):1862-1889.
23. DaSilva AS, Zanette RA, Wolkmer P, Costa MM, Garcia HA, Lopes ST, et al. Diminazene aceturate in the control of Trypanosoma evansi infection in cats. Veterinary Parasitology. 2009;165(1-2):47-50.
24. Dakshinkar NP, Powar RM, Shegaokar VR, Dani VS, Kolte SW, Khan WA. Aberrant trypanosomiasis in human. Indian Journal of Veterinary Research. 2007;3:67.
25. Joshi PP, Shegokar VR, Powar RM, Herder S, Katti R, Salkar HR, et al. Human trypanosomiasis caused by Trypanosoma evansi in India: The first case report. American Journal of Tropical Medicine and Hygiene. 2005;73(3):491-495.
26. Powar RM, Shegokar VR, Joshi PP, Dani VS, Tankhiwale NS, Truc P, et al. A rare case of human trypanosomiasis caused by Trypanosoma evansi. Indian Journal of Medical Microbiology. 2006;24:72-74.
27. Sengupta PP, Jacob SS, Chandu AGS, Das S. Silent Trypanosoma evansi infection in humans from India revealed by serological and molecular surveys, and characterized by variable surface glycoprotein gene sequences. Acta Tropica. 2022;229:106369.
28. Peter AT, Markwelder D, Asem EK. Phenotypic feminization in a genetic male dog caused by nonfunctional androgen receptors. Theriogenology. 1993;40(5):1093-1105. DOI: 10.1016/0093691x(93)90377-h.