The two sequencing approaches represent different philosophies for reading genetic material from a patient sample. Targeted next-generation sequencing, often abbreviated tNGS, uses panels of primers or probes to enrich and amplify DNA from a predefined list of pathogens, which concentrates sequencing capacity on organisms that clinicians already suspect. Metagenomic next-generation sequencing, or mNGS, takes the opposite approach: it sequences all nucleic acid in a sample without any preselection, allowing the laboratory to detect virtually any microbe present, including unexpected or fastidious organisms that no one thought to test for. That breadth comes at a cost, both financially and computationally, because vast amounts of background human and environmental DNA must be filtered out before a pathogen signal emerges. The question facing hospitals is whether mNGS’s unbounded scope translates into measurably better care for patients with suspected pulmonary tuberculosis.

To answer that question fairly, the researchers confronted a familiar obstacle in observational medicine: patients are not assigned to tests at random. In routine practice, physicians choose mNGS or tNGS based on how sick a patient appears, what previous tests have shown, and what the patient can afford, which means simple comparisons between the two groups can be badly skewed. The team therefore turned to propensity score matching, a statistical technique that pairs patients from each group who share similar baseline characteristics, effectively simulating the balance of a randomized trial. After this matching procedure, the analysis rested on 403 patients with confirmed pulmonary infections, of whom 304 had undergone tNGS and 99 had received mNGS.

The headline diagnostic finding was one of statistical equivalence. In the matched cohorts, the final rate of tuberculosis diagnosis was 17.4 percent in the tNGS group versus 23.2 percent in the mNGS group, a difference that did not reach statistical significance, with a p value of 0.257. Similarly, the proportion of samples in which the Mycobacterium tuberculosis complex was directly detected by sequencing was 20.4 percent for tNGS and 28.3 percent for mNGS, again without a significant difference at p equals 0.134. When the researchers plotted receiver operating characteristic curves to summarize overall diagnostic accuracy, the area under the curve came to 0.936 for tNGS, with a 95 percent confidence interval of 0.898 to 0.975, and 0.967 for mNGS, with a confidence interval of 0.939 to 0.995. The comparison between these two areas yielded a p value of 1.000, about as close to a tie as statistics allows.

Beneath that tie, however, lay one of the study’s most striking results. Within the matched mNGS cohort of 99 patients, metagenomic sequencing achieved 100 percent sensitivity and a 100 percent negative predictive value for tuberculosis, meaning that in this dataset a negative mNGS result reliably ruled the disease out. That figure deserves careful interpretation: in the larger unmatched full cohort of 104 patients who received mNGS, sensitivity slipped to 95.8 percent and the negative predictive value to 98.7 percent, a reminder that perfect performance in a small matched subset can be fragile. Even so, the authors argue that such a high negative predictive value, if confirmed in larger studies, could make mNGS a powerful tool for excluding tuberculosis in diagnostically challenging cases, where every additional day of uncertainty carries clinical and emotional weight.

The sequencing tests were also benchmarked against the established tuberculosis diagnostic arsenal. In subset-specific area-under-the-curve analyses performed after propensity score matching, sequencing targeting the Mycobacterium tuberculosis complex, referred to as MTBC-NGS, outperformed the interferon-gamma release assay, the tuberculosis DNA test, and acid-fast staining, three workhorses of mycobacterial diagnosis that respectively measure immune response, detect bacterial DNA by conventional amplification, and visualize acid-fast bacilli under the microscope. Notably, MTBC-NGS also showed an advantage over the Xpert MTB/RIF assay, the World Health Organization-endorsed rapid molecular test that has transformed tuberculosis detection worldwide, although that advantage was smaller and only became statistically significant after the researchers applied a Bonferroni correction to account for multiple comparisons. The pattern suggests that while newer sequencing platforms do not render existing tools obsolete, they can extract additional diagnostic signal in the right clinical subsets.

Diagnostic performance, however, is only half the story, because healthcare systems must also weigh what each test costs and how it shapes the patient’s journey through the hospital. Here the study delivered a clear verdict: the mNGS group incurred substantially higher healthcare costs than the tNGS group. Metagenomic sequencing’s untargeted design requires deeper sequencing, more intensive bioinformatics, and greater laboratory infrastructure, expenses that are inevitably passed on to patients and payers. Targeted sequencing, by focusing resources on a curated panel of pathogens, achieves comparable diagnostic accuracy for tuberculosis at a lower price point, a distinction that matters enormously in the high-burden settings where tuberculosis testing decisions are made most often.

One widely held assumption did not survive the study’s statistical scrutiny. Earlier comparisons had suggested that patients who received mNGS experienced longer hospital stays, an observation that seemed intuitive given the turnaround time and complexity of untargeted sequencing. But when the researchers adjusted their analysis for the calendar period in which patients were tested, that difference in length of stay lost its statistical significance. The authors conclude that the apparent prolongation of hospitalization may have been attributable in part to temporal changes in clinical practice over the course of the study rather than to the test modality itself. It is a subtle but important methodological lesson: in fast-evolving fields like clinical genomics, when a test was ordered can matter as much as which test was ordered.

The study, led by Xinle Liang and colleagues in the Department of Respiratory and Critical Care Medicine at Yan’an University Affiliated Hospital, was approved by the hospital’s ethics committee and conducted in accordance with the Declaration of Helsinki. The team acknowledged the Xi’an Regional Medical Laboratory Center, which provided both tNGS and mNGS testing services, and the hospital’s clinical laboratory for supporting the work. As a retrospective, single-center analysis, the investigation carries inherent limitations that the authors themselves flag, most notably the modest size of the mNGS group even after matching, and the possibility that unmeasured differences between patients influenced both test selection and outcomes. The 100 percent sensitivity and negative predictive value observed in the matched mNGS cohort, in particular, is explicitly presented as a finding that requires validation in larger studies before it can guide practice.

For clinicians wrestling with suspected pulmonary tuberculosis, the practical message is one of complementarity rather than replacement. Metagenomic sequencing offers unmatched breadth and, in this cohort, an exceptional ability to rule tuberculosis out when results are negative, making it attractive for critically ill or diagnostically perplexing patients in whom the causative pathogen could be almost anything. Targeted sequencing delivers essentially equivalent accuracy for tuberculosis at lower cost, positioning it as the rational first-line genomic option when the clinical question is narrower. As sequencing costs continue to fall and bioinformatics pipelines mature, studies like this one, grounded in real-world propensity-matched cohorts rather than idealized trial conditions, will be essential for deciding which patients truly benefit from the most expensive diagnostic technology and which can be served just as well by its leaner cousin.

Subject of Research: Comparative diagnostic performance of targeted and metagenomic next-generation sequencing for pulmonary tuberculosis

Article Title: Clinical value of targeted next-generation sequencing and metagenomic next-generation sequencing in the diagnosis of pulmonary tuberculosis: a real-world propensity score matching study

Article References: Liang, X., Sun, Y., Sun, J., Zhao, J., He, F., & Bai, Z. (2026). Clinical value of targeted next-generation sequencing and metagenomic next-generation sequencing in the diagnosis of pulmonary tuberculosis: a real-world propensity score matching study. BMC Infectious Diseases. https://doi.org/10.1186/s12879-026-14537-3

Image Credits: AI Generated

DOI: 10.1186/s12879-026-14537-3

Keywords: pulmonary tuberculosis, targeted next-generation sequencing, metagenomic next-generation sequencing, propensity score matching, Mycobacterium tuberculosis complex, Xpert MTB/RIF, diagnostic accuracy, negative predictive value, healthcare costs, BMC Infectious Diseases, molecular diagnostics, retrospective study

The research team, led by Parasmal Suresh and Aiswarya R. Nath of the Amrita School of Nanosciences and Molecular Medicine and Lalitha Biswas, with microbiologists at the Amrita Institute of Medical Sciences and Research Centre in Kochi, undertook a retrospective analysis of 239 archived MTBC clinical isolates collected between 2017 and 2024. Kerala had a conspicuous gap in the literature: despite its strong health infrastructure and active tuberculosis control programme, no published data existed on which MTBC species circulate in the state. The study was designed to close that gap using molecular tools that can resolve differences invisible to routine phenotypic testing, and it was supported by funding from the Kerala Biotechnology Commission under the Kerala State Council for Science, Technology and Environment.

The central technique of the study was polymerase chain reaction followed by restriction fragment length polymorphism analysis, or PCR-RFLP, targeting the gyrB gene. The logic is elegant. The gyrB gene, which encodes the B subunit of DNA gyrase, accumulates small sequence differences among MTBC members while remaining conserved enough within each species to serve as a reliable marker. When the amplified gyrB fragment is cut with restriction enzymes, each species produces a characteristic pattern of fragment sizes on a gel, a molecular fingerprint that allows speciation without the need for expensive whole genome sequencing. This approach has become a workhorse in reference laboratories because it is rapid, inexpensive and applicable directly to cultured isolates grown in liquid media such as the Mycobacterial Growth Indicator Tube.

To complement the gyrB analysis, the researchers deployed PCR assays targeting regions of difference, genomic segments that have been deleted from particular lineages during the evolution of the complex. Two of these segments were central to the work. Region of difference 1, or RD1, is absent from M. bovis BCG but present in wild-type M. bovis and M. tuberculosis, and it encodes key virulence factors including the ESAT-6 and CFP-10 proteins. Region of difference 4, or RD4, is likewise deleted in BCG but retained in wild-type M. bovis. By combining RD1 and RD4 PCR results, the team could distinguish the vaccine strain from its wild, disease-causing relatives, a distinction with direct clinical consequences because BCG infections are treated differently and carry different epidemiological implications.

The headline result was unambiguous. Of the 239 isolates, 232, or 97.1 percent, were identified as M. tuberculosis, the classic human-adapted pathogen. The remaining seven isolates, 2.9 percent, were M. bovis BCG. Notably, no wild-type M. bovis and no M. orygis were detected anywhere in the cohort. This absence of zoonotic species is itself informative. In many parts of the world, particularly where cattle husbandry and unpasteurized dairy consumption are common, M. bovis accounts for a meaningful share of human tuberculosis, and M. orygis, first described in antelopes but increasingly recognized in human patients across South Asia, has emerged as a zoonotic concern. Kerala’s data suggest that, at least among patients presenting to this tertiary centre, human-to-human transmission of M. tuberculosis overwhelmingly dominates the local tuberculosis landscape.

The seven BCG isolates, however, tell a more surprising and clinically urgent story. Four were recovered from children who had received BCG vaccination, including three infants and one four-year-old child. The remaining three came from adult patients who had received intravesical BCG therapy, a standard immunotherapy in which the live attenuated vaccine strain is instilled directly into the bladder to treat non-muscle-invasive bladder carcinoma. In both settings, the very organism intended to protect or to heal had instead caused disease. Among the paediatric cases, some infections were disseminated, spreading beyond the site of vaccination, a rare but well-documented complication in infants with undiagnosed immunodeficiencies and one that demands prompt recognition.

Why does this matter for treatment? The answer lies in drug susceptibility. M. bovis BCG, like wild-type M. bovis, is naturally resistant to pyrazinamide, the enzyme target of which is defective in these lineages. A patient with BCG disease who is treated with a standard four-drug regimen that includes pyrazinamide is effectively receiving an inactive drug, prolonging therapy and risking failure. When a laboratory identifies an isolate only as an MTBC member, or relies on commercial tests that do not distinguish species, this intrinsic resistance can be mistaken for acquired drug resistance, triggering unnecessary regimen changes and misclassification of the patient. Species-level identification therefore directly guides clinicians toward appropriate, pyrazinamide-sparing combinations for BCG and M. bovis infections.

The study also looked forward. In a parallel in silico analysis, the team examined published gyrB sequences to identify a single nucleotide polymorphism that could enable specific detection of M. orygis, the zoonotic species that has been increasingly reported from human cases in the region and that standard commercial identification probes often miss. Although no M. orygis was found in this cohort, developing a targeted molecular assay based on such a SNP would allow laboratories across South Asia to screen their collections cheaply and determine whether this emerging pathogen is circulating undetected. The authors frame this as groundwork for future surveillance, an acknowledgment that absence of evidence in one cohort does not establish absence of the organism in the wider population.

Methodologically, the study illustrates the value of archiving clinical isolates. Because the team could revisit seven years of stored cultures, they were able to apply molecular techniques retrospectively and generate a dataset that no single prospective study could have assembled quickly. The work was approved by the Institutional Ethics Committee of Amrita Institute of Medical Sciences, and because only archived, de-identified isolates and clinical data were used, the requirement for individual informed consent was waived. The isolates had been cultured from a range of specimen types, including respiratory samples such as bronchoalveolar lavage fluid, cerebrospinal fluid and other extrapulmonary sources, reflecting the broad spectrum of tuberculosis presentations seen at a tertiary referral centre.

The broader message of the Kerala study resonates with a growing international consensus that tuberculosis diagnostics must move beyond a one-size-fits-all identification of the complex. Molecular epidemiology has repeatedly shown that the members of MTBC differ in host preference, virulence, drug susceptibility and public health significance, and that these differences are best captured by genotyping methods ranging from PCR-RFLP and region-of-difference PCR to whole genome sequencing. For a state like Kerala, with a large cattle-owning rural population and high BCG vaccine coverage at birth, the finding that human M. tuberculosis accounts for nearly all disease is reassuring, while the detection of BCG disease in vaccinated infants and bladder cancer patients is a reminder that even the attenuated vaccine strain can become a pathogen. Species-level molecular diagnosis, the authors conclude, is not a luxury but a necessity, one that guides correct treatment, recognizes vaccine-associated and iatrogenic disease, and builds the surveillance foundation needed to detect zoonotic tuberculosis should it emerge in the region.

Subject of Research: Molecular species identification of Mycobacterium tuberculosis complex clinical isolates in Kerala, India

Article Title: Molecular characterization of Mycobacterium tuberculosis complex isolates at a tertiary care centre in Kerala, India

Article References: Suresh, P., Nath, A. R., Kumar, A., Cletus, H., Venugopal, A., Biswas, R., Varghese, L., Bhaskaran, P. N., & Biswas, L. (2026). Molecular characterization of Mycobacterium tuberculosis complex isolates at a tertiary care centre in Kerala, India. BMC Infectious Diseases. https://doi.org/10.1186/s12879-026-14527-5

Image Credits: AI Generated

DOI: 10.1186/s12879-026-14527-5

Keywords: Mycobacterium tuberculosis complex, M. bovis BCG, tuberculosis, PCR-RFLP, gyrB, zoonotic tuberculosis, Kerala, India, pyrazinamide resistance, region of difference, molecular diagnostics, tertiary care

The scale of the dataset is what gives the study its power. Whole genome sequencing was performed on nearly every culture-confirmed tuberculosis case in Hamburg across 25 years, allowing the researchers to compare the full genetic blueprints of bacterial strains rather than relying on older, lower-resolution fingerprinting methods. The team analyzed population structure and transmission dynamics in relation to patients’ self-reported geographical origins, combining genomic data with demographic and epidemiological information gathered through mandatory public health surveillance under Germany’s infectious diseases law. This integration of pathogen genetics with host demographics is precisely what earlier molecular epidemiological studies lacked, and it allowed the investigators to distinguish between bacteria that had merely been imported with their hosts and bacteria that were genuinely transmitting from person to person within the city.

The first major finding concerns lineage diversity. The Mycobacterium tuberculosis complex comprises several major lineages with distinct geographic footprints: Lineage 2 and Lineage 4 are highly transmissible, globally distributed generalists, while Lineages 1, 3 and 5 through 9 are geographically restricted specialists adapted to particular regions. In Hamburg, the researchers detected strains from lineages L1 through L6 as well as Mycobacterium bovis, the cattle-adapted member of the complex. Lineage 4 dominated throughout, accounting for 74.6 percent of all strains, or 2,337 isolates. But the composition of the bacterial population shifted markedly over time. In the first five years of the study, L4 strains made up 83.5 percent of isolates; in the final five years, that share had fallen to 63.0 percent. Over the same period, strains of Lineage 3, a specialist lineage classically associated with the Horn of Africa and South Asia, rose from 4.8 percent to 18.1 percent of the population.

That shift might seem to suggest that newly arrived lineages were outcompeting established ones, or that changing bacterial properties were driving the epidemiology. The genomic evidence says otherwise. When the researchers examined transmission clusters, groups of patients infected with nearly identical strains that indicate recent person-to-person spread, they found that the changing lineage distribution correlated with the increasing number of foreign-born patients rather than with enhanced transmission of any particular lineage. In other words, the diversification of Hamburg’s tuberculosis population was a demographic phenomenon, not a microbiological one. New strains arrived with new residents, but they did not, for the most part, go on to spread widely within the local population.

The cluster analysis drives this point home. Of the 269 transmission clusters identified across the 25-year period, 81 percent, or 218, were composed of Lineage 4 strains. This dominance was far out of proportion even to L4’s overall prevalence, indicating that sustained local transmission in Hamburg remained overwhelmingly the province of long-established bacterial lineages. Strains of specialist lineages such as L3, despite becoming numerically more common as imports increased, contributed relatively little to ongoing chains of transmission. The bacteria that thrive in Hamburg are, in an evolutionary sense, the bacteria that were already there.

Delving deeper into Lineage 4 revealed another layer of complexity: heterogeneity in transmission potential among its sublineages. Not all L4 strains are equal. The researchers found that sublineages L4.1.2.1, L4.8 and L4.3 were each detected in patients born in more than 15 different world regions, with more than 57 percent of those cases occurring in people from Europe. This pattern supports what evolutionary biologists call the generalist-specialist hypothesis at a finer resolution than ever before. Certain sublineages behave as globally successful generalists, capable of infecting and transmitting among host populations of vastly different genetic backgrounds and geographic origins, while others remain confined to specific regions. The importance of this sublineage-level resolution is a methodological lesson for the field: analyses that stop at the major-lineage level would miss the heterogeneity in transmissibility that the Hamburg data expose.

The technical machinery behind these conclusions deserves attention. Whole genome sequencing of more than 3,000 isolates allowed the team to apply a five-allele distance threshold, a conservative criterion under which strains sharing nearly identical core genomes are considered part of the same recent transmission chain. Core genome multilocus sequence typing and single nucleotide polymorphism analyses provided complementary views of population structure, and maximum likelihood phylogenetic methods placed the Hamburg strains within the global diversity of the tuberculosis complex. By combining these genomic tools with the patients’ self-reported regions and countries of birth, grouped according to United Nations statistical divisions, the researchers could ask, for any given cluster, whether it represented a single introduction with limited onward spread or sustained transmission across the community.

The public health implications are significant. In low-incidence settings, the central strategic question is whether each tuberculosis case is an isolated importation or part of an active local transmission network, because the two scenarios demand different responses. Imported cases call for ensuring that arriving populations have access to screening and care, while clustered cases call for contact investigation and outbreak response. The Hamburg study shows that genomic surveillance can make this distinction reliably at scale, and that the answer may not follow intuition. A rising share of foreign-born cases and a diversifying bacterial population did not translate into altered transmission dynamics; the city’s transmission landscape remained anchored in its established L4 sublineages. Policymakers worried that migration inherently fuels tuberculosis spread can point to this evidence that pathogen characteristics and local adaptation matter as much as host demographics.

The study also underscores the interplay between pathogen evolution and human population structure. Successful transmission, the authors conclude, is mediated by locally adapted sublineages, and the predominance of L4.1.2.1 and L4.8 among patients from a wide range of countries demonstrates that these sublineages have achieved a breadth of host adaptation that specialist lineages lack. Migration substantially increased the genetic diversity of the bacterial population in Hamburg but did not fundamentally alter how tuberculosis transmits there. As genomic sequencing becomes cheaper and more routine, the Hamburg experience offers a template for other low-incidence cities: maintain long-term, systematic sequencing integrated with demographic data, analyze at sublineage resolution, and interpret lineage shifts in light of migration patterns before attributing them to changes in bacterial fitness. Twenty-five years of genomes have turned a single German city into a natural laboratory for understanding how one of the world’s deadliest pathogens responds to the movement of its human hosts, and the answer, reassuringly, is that established local strains still hold the ground.

Subject of Research: Molecular epidemiology of Mycobacterium tuberculosis complex transmission and lineage diversity in relation to migration in Hamburg, Germany, over 25 years

Article Title: Migration and tuberculosis transmission in Hamburg, Germany: insights from 25 years of molecular epidemiology

Article References: Ullrich, N., Diel, R., Meywald-Walter, K., Schwarzbach, C., Gröschel, M. I., Kuhns, M., Friesen, I., Niemann, S., & Dreyer, V. (2026). Migration and tuberculosis transmission in Hamburg, Germany: insights from 25 years of molecular epidemiology. Genome Medicine. https://doi.org/10.1186/s13073-026-01750-7

Image Credits: AI Generated

DOI: 10.1186/s13073-026-01750-7

Keywords: tuberculosis, Mycobacterium tuberculosis complex, whole genome sequencing, molecular epidemiology, migration, lineage 4, transmission clusters, generalist-specialist hypothesis, genomic surveillance, Hamburg, low-incidence settings, sublineages

The first patient was a four-year-old neutered male Savannah cat from Inverness, Scotland, who was presented to his general practice veterinarian with an intermittent cough and mild weight loss lasting three weeks. The cat was strictly indoor-only and had been fed a commercially available raw meat-based diet containing poultry and supplemental beef offal. Initial treatment with the anti-inflammatory drug meloxicam produced no response, and over the following two weeks the cough became more persistent while the cat grew increasingly lethargic with a reduced appetite.

Thoracic radiographs revealed a marked broncho-interstitial lung pattern, and a blind bronchoalveolar lavage performed under anaesthesia showed moderate neutrophilic inflammation but was negative on routine bacterial culture. An empirical course of the antibiotic marbofloxacin also failed to help. By the time the cat was referred to a specialist institution, he had lost 30 percent of his body weight. A computed tomography scan showed severe, diffuse nodular to confluent soft tissue lesions affecting all lung lobes, together with enlarged mediastinal lymph nodes. Fine-needle aspirates of consolidated lung tissue revealed severe pyogranulomatous inflammation, and Ziehl-Neelsen staining identified small numbers of acid-fast bacilli with the slender, curved morphology typical of mycobacteria. Culture subsequently confirmed Mycobacterium caprae.

Treatment began with a triple antibiotic protocol comprising pradofloxacin at 5 mg/kg, rifampicin at 10 mg/kg and azithromycin at 15 mg/kg, each given orally once daily in liquid formulations. An oesophagostomy tube was placed to help the owners administer the prolonged medication with minimal stress. The cat was hospitalised in isolation for eight days with strict infection control precautions, including personal protective equipment for staff. Public health officials were notified once the diagnosis was confirmed, but no further testing of in-contact people was deemed necessary. Clinically, the cat improved rapidly, gaining weight within a month and coughing far less frequently. Although repeat radiographs at three-monthly intervals showed only mild improvement, treatment was stopped after eleven months when lung changes had remained static for more than two months. The cat remains clinically normal a year after therapy ended.

The second patient was a three-year-old neutered female British Shorthair from Hampshire, England, who was fed the same raw meat-based diet product and presented with a one-month history of cough, weight loss and fever. Radiographs revealed a cavitating mass in the caudal left lung field, a large nodule in the left cranial lung and multifocal areas of dense consolidation throughout the remaining lung fields. Cytology of a bronchoalveolar lavage sample showed marked neutrophilic and macrophagic inflammation with epithelioid macrophages containing non-staining ghost bacilli, and Ziehl-Neelsen staining again revealed intracellular acid-fast organisms. Polymerase chain reaction testing at a mycobacterial reference laboratory detected DNA of the Mycobacterium tuberculosis complex, and sequencing confirmed M. caprae.

The same triple antibiotic regimen was prescribed, again using liquid formulations to support long-term daily compliance. The cat improved rapidly, gaining weight within a month, with coughing notably reduced by four months of therapy. Radiographs after five months showed significant improvement without complete normalisation, and after a further three months the findings were unchanged. Given the patient was clinically well and had completed nine months of treatment, therapy was discontinued. She remains clinically normal ten months after cessation.

The clinical significance of these cases extends beyond the rarity of the pathogen. In the United Kingdom, feline infections with the M. tuberculosis complex are usually caused by Mycobacterium bovis or Mycobacterium microti, and M. caprae has only recently been identified in domestic cats, previously documented in detail in a single post-mortem case. The treatment protocol used in both cats was adapted from human tuberculosis guidelines and consists of rifampicin, a fluoroquinolone and a macrolide continued for at least three months and for two months beyond resolution of clinical signs. Earlier retrospective work found that only 42 percent of treated cats achieved complete remission, often despite inappropriate therapy, whereas the updated multidrug approach has produced remission rates of approximately 80 percent.

Notably, neither cat achieved radiographic resolution despite extended therapy, yet both remained free of relapse. The authors draw an analogy with post-tuberculosis lung disease in humans, an increasingly recognised spectrum of structural and functional pulmonary abnormalities that persists after successful anti-mycobacterial therapy in 18 to 80 percent of treated patients. They suggest that stable radiographic changes could serve as a reasonable therapeutic endpoint in feline mycobacterial infections where initial lung damage is too severe to be expected to normalise.

The report also underscores the practical demands of treatment. Both cats required prolonged daily multidrug therapy with frequent follow-up visits, demanding substantial financial and emotional investment from their owners alongside excellent patient compliance. The authors caution that where such commitment is not feasible, euthanasia should be considered for severely affected animals, both for welfare reasons and to reduce the risk of antimicrobial resistance developing from inconsistent dosing. They further note that empirical treatment choices early in the diagnostic process, such as anti-inflammatory drugs, can complicate or worsen the clinical course and should be weighed carefully with owners.

Zoonotic considerations shaped the management of both cases. Transmission of M. bovis from cats to humans has been documented previously, although the risk is considered very low, and M. caprae transmission to humans has only been identified in proximity to infected goats, its reservoir host, never from cats. Because no in-contact humans had risk factors for zoonotic transmission, treatment of both cats was judged reasonable. The authors hope that raising awareness of this first reported successful treatment of M. caprae infection in UK domestic cats will aid patient management while mitigating zoonotic risks, and they highlight the oesophagostomy tube used in the first case as a practical aid that reduces stress and supports the owner-caregiver relationship throughout months of therapy.

Subject of Research: Successful treatment of Mycobacterium caprae tuberculosis infection in two domestic cats in the United Kingdom

Article Title: Successful Treatment of Mycobacterium caprae Infection in Two UK Cats

Article References: Clark, E., Gunn‐Moore, D., & O'Halloran, C. (2026). Successful Treatment of Mycobacterium caprae Infection in Two UK Cats. Veterinary Medicine and Science, 12(5), Article e71180. https://doi.org/10.1002/vms3.71180

Image Credits: AI Generated

DOI: 10.1002/vms3.71180

Keywords: Mycobacterium caprae, feline tuberculosis, zoonotic disease, veterinary medicine, triple antibiotic therapy, rifampicin, pradofloxacin, azithromycin, raw meat-based diet, post-tuberculosis lung disease, Mycobacterium tuberculosis complex, UK cats