Kitten Scratch Triggers Rare Deadly Immune Syndrome in Kidney Transplant Patient

A single scratch from a kitten, seemingly trivial at the time, set off a chain of events that nearly claimed the life of a 33-year-old kidney transplant recipient in China, according to a case report published in BMC Infectious Diseases. The patient developed hemophagocytic lymphohistiocytosis, a rare and frequently fatal hyperinflammatory syndrome, as a consequence of bloodstream infection with Bartonella henselae, the bacterium best known for causing cat scratch disease. The case, reported by clinicians at the Second Affiliated Hospital of Chongqing Medical University, is described as an extremely rare presentation of disseminated bartonellosis in a transplant recipient, and it highlights both the diagnostic blind spots that immunosuppressed patients create and the growing role of metagenomic next-generation sequencing in unmasking elusive pathogens.

The clinical story began three years after the patient’s renal transplantation, when she presented to hospital with headache and fever. On the surface, these are among the most nonspecific complaints in medicine, but in a patient taking immunosuppressive drugs to protect her transplanted kidney, fever is never a trivial finding. The transplant team initiated empirical therapy with a carbapenem, a broad-spectrum antibiotic class reserved for serious infections, expecting to cover the common bacterial culprits. The fever refused to resolve. That failure to respond was the first signal that something unusual was driving the illness, and it prompted a deeper diagnostic workup that would ultimately reveal a diagnosis few clinicians would have suspected at the bedside.

Laboratory testing painted an increasingly alarming picture. The patient had pancytopenia, meaning that all three of the major blood cell lineages—red cells, white cells, and platelets—were depleted simultaneously. Her ferritin, an acute-phase protein that can soar in states of profound immune activation, was significantly elevated, as was her soluble interleukin-2 receptor, a marker of T-cell activation that features prominently in the diagnostic criteria for hemophagocytic lymphohistiocytosis. A bone marrow biopsy provided the decisive morphological evidence: hemophagocytosis, the sight of macrophages engulfing other blood cells and their precursors within the marrow. Together, these findings confirmed the diagnosis of HLH, a syndrome in which the immune system, failing to shut down after activation, turns its full destructive arsenal against the body’s own tissues and blood-forming machinery.

HLH exists in two broad forms. The primary, or familial, form arises from inherited genetic defects in the cytotoxic pathways that lymphocytes use to kill infected cells. The secondary form is acquired, triggered by infections, malignancies, or autoimmune disease, and it is the form of greatest concern in transplant recipients, whose iatrogenically suppressed immune systems leave them vulnerable to an unusually wide range of opportunistic infections. Untreated, secondary HLH carries a grim prognosis, because the cytokine storm at its core damages the liver, spleen, bone marrow, and central nervous system. Identifying and treating the underlying trigger is therefore not an academic exercise but the single most important determinant of survival, which is precisely why the search for the causative organism in this patient became so urgent.

That search initially came up empty. Routine pathogen screening, which typically includes cultures, serological tests, and targeted molecular assays for the common opportunistic agents of transplant medicine—viruses such as Epstein-Barr virus and cytomegalovirus, herpes simplex virus type 1, and a panel of bacteria and fungi—yielded no causative organism. The clinicians then turned to metagenomic next-generation sequencing, or mNGS, a technique that sequences all of the nucleic acid present in a clinical sample without needing to guess in advance which organism might be there. Applied to the patient’s peripheral blood, the assay detected Bartonella henselae as the most probable causative pathogen, identifying genetic material from a slow-growing, fastidious bacterium that blood cultures routinely fail to recover even in immunocompetent patients.

The epidemiological clue, once sought, was disarmingly simple. On further inquiry, the patient recalled being scratched by a kitten approximately one month before the onset of her symptoms. Bartonella henselae is transmitted to humans chiefly through the scratches or bites of infected cats, particularly kittens, and in healthy hosts it usually produces nothing worse than regional lymphadenopathy—the self-limited lymph node swelling of classic cat scratch disease. In a kidney transplant recipient on chronic immunosuppression, however, the same organism can disseminate through the bloodstream, and this report documents one of the rarest consequences of that dissemination: bacteremia sufficient to ignite secondary HLH. The month-long interval between scratch and symptoms fits the incubation behavior of the organism and underscores how easily the exposure history can be overlooked unless clinicians ask specifically about animal contact.

Treatment required a delicate two-front strategy. First, the team discontinued the patient’s oral immunosuppressants, a decision that carries inherent risk in a transplant recipient because it threatens the viability of the allograft, but one that was judged necessary to allow her immune system to regain control of the infection and the runaway inflammatory response. Second, she received short-course antimicrobial therapy with doxycycline and rifampin, a combination chosen for its activity against intracellular pathogens like Bartonella, with the duration and intensity guided by repeated mNGS monitoring of her blood. This dynamic sequencing approach allowed the clinicians to track the declining burden of bacterial DNA in real time and to individualize the length of therapy rather than committing to a fixed, prolonged course. Notably, the patient had bacteremia as her primary manifestation without disseminated multi-organ lesions, which the authors suggest is the scenario in which such short-course, mNGS-guided therapy is most appropriate.

In parallel, the HLH itself was treated with dexamethasone, a potent corticosteroid that dampens the cytokine storm, and intravenous immunoglobulin, which provides passive immune modulation and broad anti-infective support. The response was rapid. The patient’s symptoms improved quickly, and her blood counts gradually recovered as the combined anti-infective and immunomodulatory therapy took hold. At six-month follow-up, there had been no recurrence of the disease, and, critically, her renal allograft function remained stable despite the temporary withdrawal of immunosuppression. That outcome is far from guaranteed in such cases, since both the infection and the immunosuppressive withdrawal place the transplanted kidney in jeopardy, and it represents one of the most reassuring elements of the report.

The technical lessons of the case extend beyond a single patient. Bartonella henselae is notoriously difficult to culture because it is slow-growing and fastidious, and serological tests can be insensitive or nonspecific in immunocompromised hosts whose antibody responses are blunted. Metagenomic next-generation sequencing sidesteps both obstacles by detecting organism-specific nucleic acid directly, and this case adds to a growing literature demonstrating its value in transplant medicine, where the differential diagnosis of fever is extraordinarily broad and includes bacteria, viruses, fungi, and parasites. The authors also emphasize a practical point about antimicrobial stewardship: when mNGS can be repeated serially, it can serve not only as a diagnostic tool but as a therapeutic monitor, allowing clinicians to shorten courses of antibiotics that might otherwise be given for weeks on end, with all the attendant risks of toxicity, resistance, and cost.

For the transplant community, the message is one of heightened vigilance. Bartonella henselae should be considered a rare but probable infectious trigger of secondary HLH following renal transplantation, particularly when fever and pancytopenia fail to respond to empirical broad-spectrum antibiotics and routine screening is unrevealing. A careful exposure history—including questions about cats, kittens, scratches, and flea contact, since fleas transmit the bacterium among cats—can be as diagnostically valuable as any laboratory assay. And for patients whose presentation is dominated by bacteremia rather than focal organ involvement, the case suggests that short-course, individualized anti-infective therapy conducted under the guidance of dynamic mNGS can achieve cure while sparing patients unnecessarily prolonged treatment. What began with a kitten’s scratch ended in full recovery, but only after a diagnostic journey that illustrates how modern genomic tools, applied thoughtfully, can catch what conventional methods miss.

Subject of Research: Bartonella henselae bacteremia triggering secondary hemophagocytic lymphohistiocytosis in a renal transplant recipient, diagnosed by metagenomic next-generation sequencing

Article Title: Case report: hemophagocytic lymphohistiocytosis secondary to bartonella henselae bacteremia in a renal transplant recipient

Article References: Hu, B., Zhang, Z., Xiao, H., Li, D., Tang, M., Qiu, S., Ling, Q., & Peng, Q. (2026). Case report: hemophagocytic lymphohistiocytosis secondary to bartonella henselae bacteremia in a renal transplant recipient. BMC Infectious Diseases. https://doi.org/10.1186/s12879-026-14581-z

Image Credits: AI Generated

DOI: 10.1186/s12879-026-14581-z

Keywords: Bartonella henselae, hemophagocytic lymphohistiocytosis, renal transplantation, bacteremia, metagenomic next-generation sequencing, cat scratch disease, immunosuppression, doxycycline, rifampin, pancytopenia, opportunistic infection, case report