Non-oliguric acute kidney injury with haemorrhagic signs in a dog with canine distemper and concurrent anaplasmosis

Introduction

Canine distemper is a globally distributed, highly contagious viral disease caused by canine distemper virus (CDV), belonging to the genus Morbillivirus. The infection produces multisystemic illness affecting the respiratory, gastrointestinal and nervous systems. CDVinduced immunosuppression, mediated through lymphoid depletion and impairment of cellmediated immunity, predisposes affected dogs to secondary opportunistic infections (Beineke et al., 2019; Rendon-Marin et al., 2021) [2,11] . Anaplasmosis in dogs is primarily caused by Anaplasma platys transmitted by ixodid ticks. The A. platys specifically infects platelets and is associated with infectious cyclic thrombocytopenia, which may manifest clinically as petechiae, ecchymoses and bleeding tendencies (Dumler et al., 2021; Kohn et al., 2023) [4,6] . Currently, tick-borne coinfections are increasingly recognized in tropical regions due to high vector burden. Viral immunosuppression may enhance susceptibility to other bacterial and parasitic infections, leading to a fatal outcome. However, reports describing hemorrhagic manifestations due to Anaplasma infection and co-infection with CDV remain limited in the literature. The present report describes a case of acute kidney injury with bleeding signs in a non-descript dog with canine distemper and co-infection with anaplasmosis. This case underscores the importance of early screening for subclinical vector-borne infections in immunosuppressive distemper-cases and need for specific treatment. Case History and Observations An unvaccinated male non-descript dog of two year old was presented to the Teaching Veterinary Hospital, Veterinary College and Research Institute, Namakkal, with signs of tick infestation, hyporexia, pyrexia, congested conjunctival mucosae, enlarged popliteal lymphnode, vomiting, diarrhoea, serous ocular and nasal discharge, sunken eyeball, melena and hyperkeratosis of nasal planum and foot pads. The clinical signs were suggestive of systemic form of canine distemper. Ecchymoses were observed on ventral abdomen, inguinal region, inner thigh, periorbital region and scrotal sac (Figure 1a, 1b and1c). The serum sample was subjected to sandwich lateral flow assay based immunochromatography test (Pet X®, J & B Biotech Ltd, UK) to detect antibodies to Anaplasma spp. and the test proved positive (Figure 2). Faecal examination revealed no helminthic egg or ova and peripheral blood smear examination performed to rule out the blood parasites that may cause bleeding signs such as Ehrichia, Babesia or Anaplasma, proved negative. Whole blood and serum samples were collected for haemato-biochemical analysis (Table 1). On day-1 before treatment, a reduction in WBC, platelets, lymphocyte count and calcium level with an increase in phosphorus level was observed. On day-4 post treatment, hematological analysis revealed an increase in packed cell volume (PCV) and lymphocyte count. Whereas, serum biochemical analysis revealed an increase in alanine aminotransferase (ALT), blood urea nitrogen (BUN), creatinine, bilirubin (direct and indirect) and phosphorus levels, with a reduction in calcium level. On day-11 post treatment, a reduction platelet count and an increase in BUN, creatinine and phosphorus levels was observed.

Treatment and Discussion

The case was administered with doxycycline @ 10 mg/kg b.wt., IV, once daily to treat anaplasmosis, dextrose normal saline @ 10 mL/kg b.wt., IV, chlorpheniramine maleate @ 0.5 g/kg bwt and furosemide as diuretic @2 mg/kg bwt, IV for 7 days. Prednisolone @ 1.0 mg/kg was administered as an immunosuppressant for 3 days to treat the thrombocytopenia. The case was then treated with oral doxycycline @ 10.0 mg/kg, once daily for 21 days. Oral supplements such as hepatic stimulant (Tefrolipet®), neurine stimulant (Neurobind®) and renal probiotics (Renodis®) were recommended until the hepatic and renal parameters return to normal range. On day-5 post treatment, the bleeding signs start to subside (Figure 3a and3b). The clinical signs observed on day-1 were similar to the findings stated by Greene (2012) [5] . Although, myoclonus is one of the most common clinical manifestations, 50% of the infected dogs were not known to show this clinical sign (Menezes et al., 2023) [9] . The antibody based test detected the infection by Anaplasma spp. though microscopic examination of Giemsa stained blood smears mostly fails to detect the inclusion bodies inside the platelets, owing to the low level of parasitaemia (Lima et al., 2010) [8] . Lymphopenia and the resultant leukopenia observed on day-1 before treatment could be associated with the infection of lymphoid tissues caused by the CDV (Palomino., et al.,2022) [10] . The thrombocytopenia could be due to direct destruction of platelets and also the immune mediated thrombopathy caused by the intracellular bacterium, Anaplasma platys (Dyachenko et al., 2012) [3] . The changes in calcium and phosphorus levels, without any changes in renal markers, may be indicative of an early stage of azotemia. The normal platelet count observed on day-4 post treatment could be due to the specific treatment initiated or associated with the cyclic pattern of the A. platys, with alternating periods of thrombocytopenia corresponding to waves of parasitaemia. The haemorrhagic signs such as melena and ecchymotic haemorrhages observed in this study were similar to the findings observed by Venugopal et al. (2025) [13] . Recurrence of thrombocytopenia observed on day-11 might be due to the recrudescence of the A. platys owing to it's cyclical pattern (Atif et al., 2021) [1] . Renal azotemia could be due to the interstitial nephritis and acute tubular necrosis caused by deposition of IgM complex in CDV infections (Silva et al., 2022) [12] . The elevated liver enzymes and total bilirubin levels were similar to the findings of Kumar and Sirisha (2025) [7] in CDV infections. However, on day-18 post treatment, the case recovered completely with the absence of bleeding signs and all the haemato-biochemical values were within normal range. In conclusion, dogs affected with the immunosuppressive canine distemper could become vulnerable to the inapparant or subclinical vector borne infections such as anaplasmosis and such a complication might lead to a fatal outcome with poor prognosis. Hence an early detection of anaplasmosis by an antibody based test owing to the poor sensitivity of microscopy and specific treatment would help preventing fatal complications.

Acknowledgement

AcknowledgementThe authors thank the Dean, Veterinary College and Research Institute, Namakkal, and Director of Clinics, Tamil Nadu Veterinary and Animal Sciences University for the support rendered to carry out this study.

References

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