# Pneumocystis jirovecii pneumonia in a human caused by long-term use of veterinary drug oclacitinib: A case report

**Authors:** Keisuke Oshima, Ryo Koyama, Takashi Akimoto, Toshihiko Nishioki, Tomohito Takeshige, Junko Watanabe, Daisuke Usuda, Kazuhisa Takahashi

PMC · DOI: 10.1016/j.idcr.2025.e02459 · IDCases · 2025-12-11

## TL;DR

A man developed a rare fungal lung infection after long-term use of a dog medication, highlighting the risk of using veterinary drugs in humans.

## Contribution

First reported case of Pneumocystis jirovecii pneumonia linked to oclacitinib use in a human.

## Key findings

- A 53-year-old HIV-negative man developed PJP after using oclacitinib for 2 years.
- Diagnosis was confirmed via PCR and GMS staining of lung samples.
- The patient recovered after treatment with atovaquone following initial therapy.

## Abstract

Pneumocystis jirovecii pneumonia (PJP), an opportunistic fungal infection, typically occurs in immunocompromised patients, such as those with human immunodeficiency virus (HIV) infection or those receiving prolonged immunosuppressive therapy. Recently, PJP in non-HIV patients treated with novel immunomodulatory agents, including Janus kinase (JAK) inhibitors, has been increasingly reported. Here, we report a case of PJP in a 53-year-old HIV-negative Japanese man with no recognized immunosuppressive comorbidities. The patient, a veterinarian, had been self-administering oclacitinib (16–64 mg/day), a selective JAK1 inhibitor approved for the treatment of atopic dermatitis in dogs, daily for approximately 2 years to manage atopic dermatitis. He presented with progressive exertional dyspnea and fever. Chest computed tomography revealed bilateral ground-glass opacities with patchy consolidations. The diagnosis of PJP was confirmed by polymerase chain reaction of bronchoalveolar lavage fluid and Grocott’s methenamine silver staining of transbronchial lung biopsy specimens. He was initially treated with trimethoprim-sulfamethoxazole and corticosteroids; however, the regimen was switched to atovaquone owing to hepatotoxicity. The patient recovered fully and remained recurrence-free at 1-year follow-up. No other causes of immunosuppression were identified, and oclacitinib use was considered the likely precipitating factor. To our knowledge, this is the first reported case of PJP associated with oclacitinib use in humans. As JAK inhibitors are increasingly being used, clinicians should be aware of their potential to cause opportunistic infections, even with veterinary formulations without approved human indications.

•First known case of oclacitinib-associated Pneumocystis jirovecii pneumonia (PJP).•Oclacitinib is a Janus kinase inhibitor approved for veterinary, but not human use.•53-year-old HIV-negative Japanese man presented with exertional dyspnea and fever.•Diagnosed using PCR (bronchoalveolar lavage) and GMS staining (lung biopsy specimen).•Treatment: trimethoprim-sulfamethoxazole, corticosteroids, followed by atovaquone.

First known case of oclacitinib-associated Pneumocystis jirovecii pneumonia (PJP).

Oclacitinib is a Janus kinase inhibitor approved for veterinary, but not human use.

53-year-old HIV-negative Japanese man presented with exertional dyspnea and fever.

Diagnosed using PCR (bronchoalveolar lavage) and GMS staining (lung biopsy specimen).

Treatment: trimethoprim-sulfamethoxazole, corticosteroids, followed by atovaquone.

## Linked entities

- **Chemicals:** oclacitinib (PubChem CID 44631938), trimethoprim-sulfamethoxazole (PubChem CID 358641), atovaquone (PubChem CID 74989)
- **Diseases:** Pneumocystis jirovecii pneumonia (MONDO:0019121), atopic dermatitis (MONDO:0004980)
- **Species:** Homo sapiens (taxon 9606), Canis lupus familiaris (taxon 9615)

## Full-text entities

- **Genes:** JAK1 (Janus kinase 1) [NCBI Gene 3716] {aka AIIDE, JAK1A, JAK1B, JTK3}
- **Diseases:** opportunistic fungal infection (MESH:D009181), dyspnea (MESH:D004417), human immunodeficiency virus (HIV) infection (MESH:D015658), PJP (MESH:D011020), atopic dermatitis (MESH:D003876), fever (MESH:D005334), opportunistic infections (MESH:D009894)
- **Chemicals:** atovaquone (MESH:D053626), oclacitinib (MESH:C588062), trimethoprim-sulfamethoxazole (MESH:D015662)
- **Species:** Homo sapiens (human, species) [taxon 9606], Canis lupus familiaris (dog, subspecies) [taxon 9615]

## Full text

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## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12769418/full.md

## References

18 references — full list in the complete paper: https://tomesphere.com/paper/PMC12769418/full.md

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Source: https://tomesphere.com/paper/PMC12769418