Diagnostic and therapeutic management of canine distemper

Introduction

Canine Distemper (CD) is a highly contagious and often fatal viral disease that affects domestic dogs and a variety of wild carnivores globally. The causative agent belongs to the genus Morbillivirus under the family Paramyxoviridae (Geetha & Selvaraju, 2021) [3] . CDV exhibits a broad host range, infecting not only domestic dogs but also wildlife species such as lions, tigers, leopards, and foxes. The disease is characterized by multi systemic disease development with highest mortality rate after rabies (Latha et al., 2007) [6] . Following infection through the upper respiratory tract, the virus primarily targets lymphoid tissues, resulting in marked immunosuppression, (Krakowka et al., 1980; Krakowka, 1985) [1,5] . As the disease progresses, virus disseminates systemically, affecting multiple organ systems including the respiratory, gastrointestinal, integumentary, and central nervous systems. Neurological complications are particularly severe and may persist as chronic sequelae even after the acute phase of infection (Summers et al., 1978) [9] . Despite the availability of effective vaccines, outbreaks of CDV continue to occur, particularly in inadequately vaccinated or stray dog populations. No specific antiviral therapy exists, and current treatment is largely based on symptomatic therapy.

Materials and Methods

A total of twelve dogs (n = 12) that were presented to Veterinary Clinical Complex, Rajendranagar were included in the present study, consisting of six clinically affected dogs (Group I) and six apparently healthy dogs (Group II, control group). All animals were of similar age (4-7 years), different breeds, and sex (male), and were maintained under comparable managemental and nutritional conditions.

Clinical Examination

The dogs of canine distemper that were presented to the Veterinary Clinical Complex, Rajendranagar with clinical signs such as temporal muscle twitching, inappetence, and pyrexia were selected in present study. A detailed clinical and physical examination was performed in all the animals. Approximately 5 mL of blood was collected aseptically from the cephalic vein of each dog.

• 2 mL was placed into EDTA-coated vials for hematological analysis. • 3 mL was placed into plain vials, allowed to clot, and centrifuged at 3,000 rpm for 10 minutes to obtain serum for biochemical and CD antigen testing. Given intramuscularly @ 20 mg/kg bwt once daily for one week to prevent or treat secondary bacterial infections. 2. Tab Pregamyl Forte 4mg (Pregabalin75mg and methylcobaiamin1500mcg) -Provided orally once daily to enhance appetite, improve digestion, and provide nutritional support. 3. Melonex (Meloxicam) -Given intramuscularly at 0.2 mg/kg once daily to reduce inflammation and alleviate pain or discomfort. 4. Histanil (Antihistamine) -Administered intramuscularly at 0.5 mg/kg once daily for three consecutive days to minimize histamine-mediated allergic and inflammatory responses. 5. Atropine Sulphate -Injected intramuscularly for one week @ 0.04 mg/kg e to control hypersalivation 6. Neurokind Injection -Administered intramuscularly at 1 mL per animal once daily for seven days to support neurological health and nerve regeneration.

After one week of therapy, clinical improvement in appetite was observed, although mild neurological manifestations such as temporal twitching and intermittent salivation persisted.

Then Cicuta virosa 30C homeopathic tablets were administered (five pills twice daily for one month) alongside continued Pregamyl Forte and Neurokind supplementation. Blood samples were collected from all animals (both affected and control groups) prior to treatment and again at the end of the therapy period. After one month, a follow-up PCR test for Canine Distemper was performed, yielding a negative result. All treated dogs exhibited complete clinical recovery, with resolution of neurological signs and restoration of normal behavior and appetite.

Results

Before treatment, all six affected dogs exhibited classical clinical signs of canine distemper, including inappetence, temporal muscle twitching, prolapse of the third eyelid (Fig. 1), and excessive froathy salivation (Fig. 2). Supportive therapy resulted in gradual improvement of appetite within one week; however, neurological manifestations persisted in all cases. After one month (Fig. 3) of administration of Cicuta virosa 30CC, all neurological symptoms resolved completely in the affected dogs. Post-treatment, the dogs regained normal appetite, activity levels, and behaviour. PCR testing for canine distemper performed after therapy yielded negative results, confirming recovery. Hematological analysis of affected dogs prior to treatment revealed leukopenia, lymphopenia, and mild anemia compared to healthy control dogs. Following recovery, hematological values returned to normal ranges, comparable to those of the healthy group. Biochemical evaluation before treatment showed elevated liver enzymes (ALT, AST) and reduced total protein and glucose levels in affected dogs relative to controls. After one month of therapy, biochemical parameters normalized, indicating restoration of hepatic function and metabolic status.

Overall, the group treated with Cicuta virosa 30C demonstrated complete clinical and laboratory recovery, comparable to the healthy control group.

Discussion

Canine distemper in dogs is characterized by temporal twitching, high temperature, in appetence, jaw champing, and hind limb paralysis. In our study and other researchers have reported similar clinical progressions of canine distemper in dogs (Martella et al., 2008; Amude et al., 2010) [7,2] The initial improvement in appetite and general health following supportive therapy aligns with the symptomatic management in CD, which aims to stabilize the animal while its immune system combats the virus.: Persistent neurological signs after the acute phase of CD are well documented. These are believed to result from demyelination and neuronal degeneration caused by viral persistence in the central nervous system (Summers et al., 1979) [8] . Age, immunity, viral strain and environmental impact of secondary pathogens determines the severity of Canine distemper infection. Oral administration of homeopathic medicine Cicuta virosa (Drops. Cicuta-30 C) was followed in all affected dogs showed remarkable clinical recovery. In this case, gradual improvement of neurological signs after its administration suggests a potential supportive role in neuronal recovery. The combination of conventional supportive care with complementary therapies may offer a more comprehensive approach for managing chronic CD cases, particularly those with neurological involvement. The negative PCR result following treatment indicates viral clearance and supports the clinical recovery observed.

Conclusion

This study demonstrates that Cicuta virosa 30C, when administered alongside conventional supportive therapy, may contribute to the improvement of neurological symptoms associated with Canine Distemper infection in dogs. The infected animals treated with Cicuta virosa 30C, revealed notable variations in hematological and biochemical parameters. Treated groups showed a normalization of key hematological indices, including hemoglobin concentration, total leukocyte count, and differential leukocyte profiles, compared to untreated infected controls. Similarly, biochemical parameters such as liver and kidney function markers (ALT, AST, ALP, creatinine, and BUN) indicated improved organ function in Cicuta virosa treated animals.

When compared with healthy animals, the Cicuta virosatreated group demonstrated partial restoration of physiological parameters toward normal reference ranges, suggesting a potential modulatory role of the remedy in mitigating systemic effects of CDV infection.

References

1. Krakowka S, Higgins RJ, Koestner A. Canine distemper virus: review of structural and functional modulations in lymphoid tissues. American Journal of Veterinary Research. 1980 Feb 1;41(2):284-92.
2. Amude AM, Alfieri AF, Alfieri AA. Non-conventional neuro-pathological manifestations of canine distemper virus infection in dogs. Current research, technology and education topics in applied microbiology and microbial biotechnology. Sao Paulo: Formatex. 2010:729-35.
3. Geetha M, Selvaraju G. Therapeutic management of canine distemper in dogs with alternate medicinal (homeopathy-Cicuta 30 C) approaches. 2021.
4. Krakowka, S., 1982. Mechanisms of in vitro immunosuppression in canine distemper virus infection, J. Clin. Lab. Immunol., 8: 187-196
5. Latha D, Srinivasan SR, Thirunavukkarasu PS, Gunaselan L, Ramadass P, Narayanan RB. Assessment of canine distemper virus infection in vaccinated and unvaccinated dogs. Indian Journal of Biotechnology. 2007 Jan;6(1):35.
6. Martella V, Elia G, Buonavoglia C. Canine distemper virus. Veterinary Clinics of North America: Small Animal Practice. 2008 Jul 1;38(4):787-97.
7. Summers BA, Greisen HA, Appel MJ. Early events in canine distemper demyelinating encephalomyelitis. Acta neuropathologica. 1979 Jan;46(1):1-0.
8. Summers BA, Greisen HA, Appel MJ. Possible initiation of viral encephalomyelitis in dogs by migrating lymphocytes infected with distemper virus. The Lancet. 1978 Jul 22;312(8082):187-9.