Case Report: Immune-Mediated Neutropenia in a French Bulldog

Clinical Course of a French Bulldog With Suspected Immune-Mediated Neutropenia Managed With Immunosuppressive Therapy and Adjunctive Huaier-Derived TPG-1 

A 4-year-old neutered male French Bulldog weighing 7.5 kg was evaluated for severe leukopenia.

At presentation, body temperature was 39.0°C, heart rate was 88 beats/min, and respiratory rate was 44 breaths/min.

Initial hematologic testing revealed marked leukopenia and severe neutropenia, with a white blood cell count of 2,240/µL and an absolute neutrophil count of 160/µL.

C-reactive protein (CRP) was >20 mg/dL, indicating marked systemic inflammatory activity.

Other hematologic findings included an erythrocyte count of 7.16 × 10⁶/µL, hemoglobin concentration of 17.2 g/dL, packed cell volume of 46.1%, platelet count of 314,000/µL, and reticulocyte count of 29,000/µL.

The absolute neutrophil count at initial presentation was markedly decreased to 160/µL, compared with the reported reference interval of 3,000–11,400/µL.

CRP was >20 mg/dL, indicating a marked inflammatory response.

Bone marrow cytology demonstrated hyperplasia of both the myeloid and erythroid lineages (Figure 1).

These findings suggested that bone marrow hematopoietic activity was preserved despite the severe peripheral neutropenia and were considered compatible with peripheral loss, destruction, or consumption of neutrophils rather than primary failure of granulopoiesis.

Based on the overall clinical findings, hematologic abnormalities, bone marrow findings, and exclusion of other clinically apparent causes, a presumptive clinical diagnosis of immune-mediated neutropenia (IMN) was made.

 Figure 1. Bone marrow cytology at initial evaluation.
Hyperplasia of the myeloid and erythroid lineages was observed. These findings indicated preserved marrow hematopoietic activity but were not, by themselves, specific for immune-mediated neutropenia. 

Immunosuppressive therapy constituted the principal treatment strategy.

The initial response was considered insufficient for stable long-term management, and continued adjustment of therapy was required.

Treatment Protocol

1. Initial treatment

Prednisolone was initiated at 0.5 mg/kg once daily (SID), together with minocycline.

2. Introduction of TPG-1 on Day 36

On Day 36, when the prednisolone dose was reduced to 0.25 mg/kg SID, Huaier-derived TPG-1 was introduced at twice the standard feeding amount as an adjunctive nutritional intervention.

3. Subsequent prednisolone tapering

During subsequent follow-up, neutrophil counts increased and no recurrence of the initial severe neutropenia was documented within the observation period shown.

From Day 64, prednisolone was further reduced to 0.15 mg/kg SID while adjunctive TPG-1 supplementation was continued.

The temporal relationship among leukocyte and neutrophil counts and administration of prednisolone, minocycline, and Huaier-derived TPG-1 is summarized in Figure 2.

Serial hematologic monitoring demonstrated increases in both total white blood cell and neutrophil counts over the course of treatment.

A transient marked increase was observed around Day 64. Thereafter, neutrophil counts remained approximately 2,000/µL or higher during the observation period shown.

Huaier-derived TPG-1 was introduced on Day 36 at the same time that the prednisolone dose was reduced from 0.5 to 0.25 mg/kg SID.

Prednisolone was subsequently reduced further to 0.15 mg/kg SID from Day 64 while TPG-1 supplementation was continued.

The dog therefore remained clinically and hematologically stable during a period in which the prednisolone dose was progressively reduced.

Because prednisolone tapering, minocycline treatment, the natural clinical course, and adjunctive TPG-1 administration occurred within the same treatment period, the relative contribution of each intervention to the observed hematologic changes cannot be determined from this case alone.

The reduction of prednisolone to 0.15 mg/kg SID decreased overall glucocorticoid exposure. This may have reduced the risk or severity of glucocorticoid-associated adverse effects, although a direct effect of TPG-1 on steroid-related adverse events cannot be established.

 Figure 2. Clinical course and treatment timeline.

Serial changes in white blood cell and neutrophil counts are shown together with treatment periods for prednisolone, minocycline, and adjunctive Huaier-derived TPG-1. TPG-1 was introduced on Day 36 concurrently with reduction of the prednisolone dose. Prednisolone was subsequently reduced further while TPG-1 supplementation was continued. The temporal relationship shown in the figure does not establish that TPG-1 caused the hematologic improvement or enabled glucocorticoid tapering. 

This case describes the clinical course of a dog with presumptive immune-mediated neutropenia managed with immunosuppressive therapy and adjunctive Huaier-derived TPG-1.

Severe neutropenia was present at the initial evaluation, while bone marrow cytology demonstrated preserved and hyperplastic hematopoietic lineages. These findings were considered compatible with peripheral neutrophil loss or destruction and contributed to the clinical diagnosis of IMN.

Following introduction of TPG-1, increases in neutrophil counts were observed while the prednisolone dose was progressively reduced. Severe neutropenia similar to that observed at initial presentation was not documented during the subsequent period shown.

This temporal sequence is clinically noteworthy. However, TPG-1 was introduced during ongoing immunosuppressive treatment and at the same time as a change in prednisolone dosage.

Accordingly, the independent contribution of TPG-1 to the increase or stabilization of neutrophil counts cannot be determined from this single uncontrolled case.

Similarly, the ability to reduce prednisolone to 0.15 mg/kg SID cannot be attributed specifically to TPG-1. The observed course may have reflected the effects of immunosuppressive therapy, the natural course of the disease, concurrent minocycline administration, individual variation, or a combination of these factors.

The case nevertheless provides a clinical observation in which hematologic stability was maintained during progressive glucocorticoid tapering while adjunctive TPG-1 supplementation was continued.

This observation may support further investigation of TPG-1 as a potential adjunctive approach in dogs with difficult-to-manage immune-mediated neutropenia.

However, immune function and the proposed biological mechanisms of TPG-1 were not directly evaluated in this dog. Therefore, any proposed immunomodulatory contribution remains hypothetical.

This case describes a French Bulldog with severe neutropenia and bone marrow findings compatible with preserved hematopoietic activity, leading to a presumptive clinical diagnosis of immune-mediated neutropenia.

Treatment consisted primarily of prednisolone-based immunosuppressive therapy with minocycline, followed by adjunctive introduction of Huaier-derived TPG-1 on Day 36.

During subsequent follow-up, neutrophil counts increased and prednisolone was progressively reduced to 0.15 mg/kg SID while clinical and hematologic stability was maintained.

However, because this was a single uncontrolled case involving concurrent and changing treatments, a causal relationship between TPG-1 supplementation and improvement in neutrophil counts or successful glucocorticoid tapering cannot be established.

The findings should therefore be interpreted as preliminary, hypothesis-generating clinical observations rather than evidence of therapeutic efficacy.

Additional cases and appropriately controlled studies would be required to determine whether adjunctive TPG-1 has a reproducible clinical role in dogs with immune-mediated neutropenia.