Hidden tickborne coinfection emerges in patients evaluated for Crimean-Congo hemorrhagic fever
Turkey’s 2022 Crimean-Congo hemorrhagic fever outbreak became the setting for an unexpected microbiologic finding: Anaplasma capra DNA in adults hospitalized with suspected CCHF. The pathogen matters because its presentation overlaps with other tickborne febrile syndromes—fever, headache, myalgia, weakness, gastrointestinal complaints, and sometimes cytopenias—yet it is easy to miss when clinicians anchor on a more familiar regional diagnosis. In a hyperendemic setting where CCHF dominates diagnostic attention, a second tickborne bacterium can remain clinically silent until molecular testing brings it into view.
The investigation drew from 263 adults admitted during the outbreak to Sivas Cumhuriyet University Hospital, a tertiary referral center designated for CCHF care in Turkey’s Middle Anatolia region. All patients met a clinical case definition that required compatible symptoms and at least one epidemiologic or laboratory criterion, such as recent residence or travel in an endemic area, tick exposure, thrombocytopenia, or leukopenia. Each patient underwent routine laboratory assessment, CCHF confirmation testing, and parallel screening for A. capra using nested PCR directed at the gltA gene, followed by sequencing of gltA and groEL in positive samples.
Molecular confirmation places A. capra inside the CCHF differential
Six of the 263 patients, or 2.28%, were positive for A. capra. The result is small in absolute terms but clinically meaningful in a syndrome where delayed recognition can alter isolation decisions, antimicrobial treatment choices, and the interpretation of persistent fever or cytopenia. Molecular confirmation of CCHF and serologic confirmation were performed separately, so the study does not collapse these syndromes into one another; it instead shows that they can coexist in the same referral pathway and present with near-identical admission features.
The sequencing data strengthen the diagnosis. Partial gltA sequences showed 84.16%–100% similarity with GenBank entries, while partial groEL sequences showed 90.24%–100% similarity. Phylogenetic analysis placed all of the recovered gene sequences within genotype 1. In practical terms, this is not a vague molecular signal but a genetically characterized human infection with a defined lineage, adding to the evidence that A. capra is not confined to animals or isolated geographic niches.
Why a CCHF ward is a likely place to find A. capra
Turkey sits at a geographic and epidemiologic crossroads where zoonotic infections are common and tick exposure is routine in some regions. The clinical overlap between CCHF and anaplasmosis is exactly what makes A. capra easy to overlook. Both can begin with nonspecific systemic illness. Both can produce laboratory abnormalities that point clinicians toward severe tickborne disease. In a patient with fever, weakness, and thrombocytopenia after possible tick exposure, the diagnostic frame often narrows quickly to the most feared regional pathogen, especially in a ward built to manage CCHF.
Yet the biology argues for broader testing. Ticks transmit multiple bacterial and viral agents, and the same patient may be exposed to more than one. A. capra was first identified in goats in 2012 and later in humans in China in 2015; subsequent reports linked it to influenza-like illness and occasional liver enzyme elevation, with leukopenia and thrombocytopenia in a smaller subset of cases. That symptom pattern sits close enough to CCHF to blur bedside differentiation unless molecular methods are applied.
Routine testing for brucellosis, blood cultures, and standard supportive care were part of the clinical workflow in this cohort. The ward also used ribavirin at clinician discretion under a standard protocol for suspected CCHF, while patients received transfusions and cardiovascular or respiratory support as needed. Those details matter because they illustrate the real-world environment in which an unusual pathogen can be discovered: a high-acuity inpatient setting where clinicians must manage life-threatening hemorrhagic fever while still considering alternative etiologies.
Genotype 1 expands the clinical map of A. capra infection
The genotype finding carries direct epidemiologic value. Human A. capra infection had already been documented elsewhere, but genotype 1 in Turkish patients with suspected CCHF extends the organism’s recognized clinical territory. The sequences were robust enough to undergo phylogenetic analysis with maximum-likelihood methods, and bootstrap support was applied to assess tree stability. In other words, the diagnosis rested on more than a single amplification signal; it was supported by gene-specific sequence comparison and evolutionary placement.
This kind of molecular detail is useful at the bedside because it changes how clinicians think about syndrome-based care. Febrile patients in endemic areas do not always have one pathogen. Some will have CCHF; some will have another tickborne infection; some may have overlapping exposures that produce mixed or confusing presentations. If the working diagnosis is too narrow, the patient may be treated for the feared disease while the contributing bacterial infection goes unrecognized.
What this means for clinicians managing hemorrhagic-fever referrals
For clinicians in endemic areas, the message is straightforward: A. capra belongs in the differential diagnosis of CCHF-like illness. The strongest case for inclusion comes from the combination of epidemiology and presentation rather than any single symptom. Tick exposure, travel or residence in an endemic area, fever, diffuse pain, weakness, diarrhea, bleeding, thrombocytopenia, and leukopenia can all sit within the same diagnostic frame, but molecular testing is what separates the organisms.
The findings also reinforce a broader diagnostic principle in tickborne medicine. When one pathogen is common and dangerous, another can hide in plain sight. PCR-based workflows that examine patients suspected of CCHF for additional tickborne bacteria can reveal cases that routine serology and supportive care would miss. That approach becomes more important in regions where domestic ruminants and water buffalo harbor A. capra, because animal reservoirs and human exposure pathways may overlap.
The study was descriptive and retrospective, so it was not designed to estimate incidence beyond the tested hospitalized cohort or to test causation between symptoms and any single pathogen. Even so, the detection of genetically confirmed genotype 1 A. capra in adults with suspected CCHF provides concrete clinical evidence that more than one tickborne agent can circulate in the same outbreak setting. The unanswered question is not whether the bacterium can infect humans in Turkey; it can. The harder question is how often it is missed when clinicians stop after a positive or presumptive CCHF workup.