The research team, led by Elahe Meftah and colleagues at Amir Oncology Teaching Hospital in Shiraz, combed through medical records of immunocompromised children under 18 who were screened for invasive pulmonary aspergillosis between April 2016 and December 2023. Their analysis focused on 141 children classified as having proven or probable disease according to established diagnostic criteria. The median age was just eight years, and nearly two thirds of the patients were male. Only a small fraction, 14.2 percent, had definitively proven infection confirmed by direct demonstration of the fungus, underscoring how difficult this diagnosis remains even in specialized centers. Cases labeled as possible aspergillosis were analyzed separately and descriptively, keeping the main cohort diagnostically rigorous.

One of the study’s central questions was what chest computed tomography actually reveals in children with this infection, and how those images relate to survival. Radiologists reviewed the available scans using predefined criteria, and a clear hierarchy of findings emerged. Pulmonary nodules, rounded shadows that mark where the fungus has invaded lung tissue, were by far the most common abnormality, present in 75 of the 141 patients. Consolidation, the dense opacification of lung tissue typically seen in pneumonia, came second at 44 patients. The famous halo sign, a nodule surrounded by a rim of ground-glass opacity that radiologists consider a hallmark of early invasive aspergillosis, appeared in 37 patients. Ground-glass opacities and pleural effusion, fluid around the lungs, each turned up in 16 patients.

The pattern of co-occurrence was equally informative. When children had nodules, those nodules most frequently appeared alongside the halo sign, with 33 patients showing both features simultaneously. This makes biological sense: the halo represents hemorrhage around a fungal lesion, and its frequent pairing with nodules reflects the angioinvasive nature of Aspergillus, which seeds blood vessels and starves surrounding tissue. For diagnostic purposes, the study confirms that CT remains a cornerstone of disease detection and characterization, giving clinicians a visual map of how far the infection has spread. What the scan could not do, however, was predict who would survive.

That was the study’s most striking twist. Among the 136 patients included in the survival analysis, 41 deaths occurred during follow-up. The researchers estimated survival at 96 percent at four weeks after diagnosis, but that figure fell to 66.3 percent by the end of follow-up, a sobering trajectory that illustrates the delayed toll the infection takes on fragile patients. When the team fed CT variables, including the presence of nodules, the total nodule burden, and nodule size, into multivariable Cox proportional hazards models alongside laboratory markers, none of the radiological features showed a significant association with survival. The pictures told doctors where the fungus was, but not where the patient was headed.

The blood tests told a different story. Higher serum galactomannan, a sugar molecule released by growing Aspergillus hyphae and detected through a widely used enzyme immunoassay, independently predicted mortality, with a hazard ratio of 1.06 and a 95 percent confidence interval of 1.02 to 1.10, statistically significant at p below 0.001. In practical terms, every incremental rise in galactomannan corresponded to a measurable increase in the risk of death, likely reflecting the sheer fungal load multiplying inside the lungs and spreading through the bloodstream. Because galactomannan is shed by viable fungus, serial measurements essentially track the living enemy in real time, a capability no static imaging study can match.

C-reactive protein, the classic inflammatory sentinel produced by the liver in response to systemic inflammation, proved to be an equally powerful prognostic marker. Each unit increase in CRP carried a hazard ratio of 1.02, with a confidence interval of 1.01 to 1.03 and p below 0.001. While a hazard ratio per single unit may sound modest, CRP values in sick children routinely range across hundreds of units, so the cumulative effect on risk is substantial. Elevated CRP in this setting signals an uncontrolled inflammatory storm accompanying the infection, a process known to drive tissue damage and organ failure independent of the pathogen itself. Together, the two biomarkers capture both sides of the lethal equation: how much fungus is present and how violently the body is responding.

The authors’ conclusion is carefully framed and clinically meaningful. Chest CT, they write, primarily supported disease detection and radiologic characterization, whereas serum galactomannan and CRP demonstrated greater prognostic value for mortality risk stratification within diagnosed invasive pulmonary aspergillosis. This distinction matters because diagnostic and prognostic tools serve different purposes at the bedside. A scan answers the question of whether the disease is present and what it looks like; biomarkers answer the question of how the patient is likely to fare. The study suggests that once a diagnosis is established, clinicians should look to repeated blood tests, not follow-up imaging, to gauge trajectory and intensity of therapy.

Several secondary analyses enriched the picture. The researchers examined predictors of nodules and nodule burden, probing which factors drove the most characteristic radiologic manifestation of the disease. While the source data abstracts these details, their inclusion signals the team’s effort to understand the biology behind imaging findings rather than merely cataloging them. Kaplan-Meier survival estimates anchored the mortality analysis, providing clear time-to-event curves that clinicians can interpret intuitively, and the Cox models adjusted for multiple variables simultaneously to isolate the independent contribution of each marker.

The study carries the usual caveats of retrospective, single-center research. All patients came from one oncology hospital in Shiraz, and practice patterns, host populations, and diagnostic thresholds elsewhere may differ. Not every child had a CT scan available for review, and biomarker values were drawn from routine clinical testing rather than a standardized protocol. Still, the cohort size of 141 children with proven or probable disease is substantial for a condition that remains rare and hard to diagnose, and the consistency of the statistical findings lends weight to the conclusions. For a disease in which early risk stratification can mean the difference between aggressive antifungal therapy and a fatal outcome, the message is potent: in children with invasive pulmonary aspergillosis, what is in the blood may matter more than what is on the scan.

Subject of Research: Prognostic value of chest CT findings and serum biomarkers for mortality in pediatric invasive pulmonary aspergillosis

Article Title: Chest CT findings and biomarker predictors of mortality in pediatric invasive pulmonary aspergillosis: a retrospective cohort study

Article References: Meftah, E., Mirbagheri, S. S., Reihani, Y., Jafarian, H., Hamzavi, S. S., Abbasi, A., Khajeh, S., Naseri, A., Nazemosadat, S. M. A., Habibzadeh, A., Haghshenas, A., Abdipour Mehrian, S. R., & Amanati, A. (2026). Chest CT findings and biomarker predictors of mortality in pediatric invasive pulmonary aspergillosis: a retrospective cohort study. BMC Infectious Diseases. https://doi.org/10.1186/s12879-026-14512-y

Image Credits: AI Generated

DOI: 10.1186/s12879-026-14512-y

Keywords: invasive pulmonary aspergillosis, pediatric oncology, chest CT, galactomannan, C-reactive protein, mortality, fungal infection, immunocompromised children, halo sign, prognostic biomarkers, retrospective cohort, Aspergillus

The review, led by Kaweesi Calvin Nantalaga and Alice Nantege, followed the PRISMA extension for scoping reviews and searched PubMed/MEDLINE for records published between 1980 and 2026, supplementing the primary search with the Web of Science Core Collection, Scopus and hand-searching of reference lists. After screening 1322 records in PubMed/MEDLINE and a further 3949 unique records retrieved by the supplementary searches, the team identified 55 cases of invasive aspergillosis in which diabetes mellitus stood as the principal risk factor. Each case was assessed against the 2020 EORTC/MSGERC definitions, the internationally accepted standard for classifying invasive fungal disease, with a crucial modification: because diabetes is not a recognised EORTC/MSGERC host factor, probable cases had to be classified using modified criteria.

The demographic profile of the affected patients is striking. The median age was 63 years, with cases ranging from a child of six to adults as old as 84. Among patients whose sex was reported, 65.3 percent were male. Geographically, the literature is dominated by Asia, which accounted for 60 percent of all cases, a distribution the authors suggest may reflect both genuine epidemiological patterns, including the enormous and often underdiagnosed diabetic populations of South and East Asia, and publication practices that have concentrated case reporting in certain regions.

Perhaps the most clinically consequential finding concerns anatomy. Invasive aspergillosis in diabetic patients shows a marked predilection for the nose, paranasal sinuses and orbit: rhino-orbital and sinonasal disease accounted for 43.6 percent of cases, far ahead of pulmonary disease at 14.5 percent and central nervous system involvement at 12.7 percent. This pattern echoes what clinicians have observed for decades with another fungus, the mould Rhizopus, which causes mucormycosis, a feared complication of diabetic ketoacidosis. The new review suggests that Aspergillus behaves in a disturbingly similar fashion when it encounters the metabolic terrain of poorly controlled diabetes, ascending from the nasal mucosa along vessels and nerves toward the orbit and cranial cavity.

The technical reason for this tropism lies in the interplay between fungal virulence and diabetic physiology. Aspergillus species, above all Aspergillus fumigatus, the most frequently identified organism in this review, invade tissue through angioinvasion, colonising and destroying blood vessels, which produces infarction, necrosis and rapid spread. Hyperglycaemia impairs neutrophil chemotaxis, phagocytosis and oxidative killing, the very cellular defences that normally hold inhaled conidia in check. Acidosis, which accompanies decompensated diabetes, further disables complement activity and iron sequestration. Where glycaemic status was documented in the reviewed cases, most patients had poorly controlled diabetes, reinforcing the association between metabolic derangement and fungal invasion.

Diagnostic practice across the 55 cases revealed a sobering gap between modern non-culture diagnostics and the realities of this population. Galactomannan testing and Aspergillus polymerase chain reaction, the assays that anchor mycological evidence in haematology patients, contribute little here, partly because diabetic patients with rhino-orbital disease often present with localised, tissue-destructive infection rather than the angioinvasive pulmonary disease in which these tests perform best. The authors conclude that tissue-based diagnosis, obtained by biopsy where it can be done safely, is likely to be of decisive value, since histopathological demonstration of septate hyphae with acute-angle branching, combined with culture or molecular identification, was the pathway by which the overwhelming majority of cases achieved diagnostic certainty.

That certainty is not trivial. In this review, 90.9 percent of cases were proven invasive aspergillosis under EORTC/MSGERC criteria, with the remaining 9.1 percent classified as probable using the modified framework. This unusually high proportion of proven diagnoses reflects the fact that most reported patients underwent surgical debridement or biopsy, procedures that simultaneously provide tissue for the laboratory and remove necrotic, infected material. The review thus implicitly outlines a standard of care for diabetic patients with suspected sinonasal fungal invasion: urgent imaging of the sinuses, orbits and brain, followed by prompt tissue acquisition and early antifungal therapy, typically with voriconazole, which remains the guideline-endorsed first-line agent against Aspergillus.

The outcome data carry a clear warning. All-cause mortality across the 51 cases with a known outcome was 33.3 percent, meaning one in three patients died. Death clustered in the most aggressive anatomical presentations: cardiovascular involvement, disseminated disease, and pulmonary aspergillosis carried the highest fatality. The numbers also illustrate a bias inherent to scoping reviews of published cases, since fatal and spectacular cases are more likely to be written up than routine recoveries. Even allowing for that bias, the mortality figure for an infection classically considered rare outside haematology units demands that emergency physicians, ophthalmologists, otolaryngologists and endocrinologists alike reconsider how quickly they entertain the diagnosis.

The clinical message distilled by the authors is a plea for suspicion. A diabetic patient, frequently one whose glucose control has slipped, presenting with invasive sinonasal, cerebral or pulmonary disease should be regarded as a potential aspergillosis case until proven otherwise. Warning signs include facial pain and numbness, proptosis, vision loss, cranial nerve palsies, black necrotic turbinate mucosa, and pulmonary infiltrates that fail to respond to antibacterial therapy. In such patients, delaying antifungal therapy while pursuing alternative explanations can be fatal, because angioinvasion converts every day of delay into additional irreversible tissue death.

The review also exposes gaps in the evidence base that only prospective research can fill. Fifty-five cases across four decades is a small and heterogeneous corpus, assembled largely from case reports and case series, and the authors deliberately excluded reviews, non-invasive fungal forms, COVID-19-associated aspergillosis and cases driven by competing immunosuppression such as neutropenia or transplantation. The absence of diabetes from the EORTC/MSGERC host-factor list means that probable cases in this population exist in a diagnostic grey zone, a limitation the modified criteria only partly resolve. Larger multinational registries, standardised reporting of glycaemic control and antifungal regimens, and outcome data free from publication bias would sharpen the picture considerably. Until then, this scoping review stands as the clearest account yet of a fungal threat that diabetes quietly unlocks, and as a reminder that in medicine the most dangerous infections are sometimes the ones appearing in patients no one thought to worry about.

Subject of Research: Invasive aspergillosis complicating diabetes mellitus, characterised by rhino-orbital predominance, tissue-based diagnosis and substantial mortality.

Article Title: Invasive aspergillosis complicating diabetes mellitus: a scoping review

Article References: Nantalaga, K. C., & Nantege, A. (2026). Invasive aspergillosis complicating diabetes mellitus: a scoping review. BMC Infectious Diseases. https://doi.org/10.1186/s12879-026-14503-z

Image Credits: AI Generated

DOI: 10.1186/s12879-026-14503-z

Keywords: invasive aspergillosis, diabetes mellitus, rhino-orbital aspergillosis, Aspergillus fumigatus, scoping review, EORTC/MSGERC criteria, mortality, fungal infection, poorly controlled diabetes, tissue-based diagnosis, BMC Infectious Diseases, Invasive

Histoplasma capsulatum is a thermally dimorphic fungus that grows as a mold in soil enriched with bat or bird guano and converts to a yeast form at human body temperature. People acquire infection by inhaling microconidia—tiny airborne spores—released when contaminated soil is disturbed, whether in caves, poultry farms, or construction sites. In most immunologically healthy people, inhaled spores are contained by the lungs’ innate defenses and produce either no symptoms or a self-limited pulmonary illness. The fungus is endemic to the Mississippi and Ohio River valleys of North America, with additional foci across Central and South America, parts of Africa, and regions of Asia including the Indian subcontinent. In a subset of patients, however, the infection escapes pulmonary containment and spreads throughout the body as progressive disseminated histoplasmosis, a condition classically seen in people with defective cellular immunity such as those with HIV/AIDS, transplant recipients on immunosuppressive drugs, or patients receiving biologic agents.

That is precisely why this case is so unsettling. The young man had no history of corticosteroid use, diabetes, substance abuse, or high-risk sexual behavior. He denied fever, night sweats, and cough. When HIV serology came back negative, and when his morning cortisol and adrenocorticotropic hormone levels proved normal—ruling out the adrenal insufficiency that clinicians had considered given his persistent hyponatremia—he was, by all standard measures, immunocompetent. Disseminated histoplasmosis in such individuals is recognized but rare, generally attributed to overwhelming inoculum exposure or subtle, often undocumented, defects in innate immune signaling. The one telling detail in his history was a recent exploration of caves in hilly terrain. Bat guano accumulated in cave environments serves as the primary ecological niche for the fungus’s mycelial growth, and heavy exposure to cave aerosols can flood the lungs with organisms in quantities sufficient to overwhelm even intact immune defenses, seeding systemic dissemination.

The diagnostic odyssey began long before his hospital admission. An outside colonoscopy had already suggested either intestinal tuberculosis or inflammatory bowel disease, and given the region’s high tuberculosis burden and a strong family history of TB, his physicians had reasonably started empirical four-drug anti-tubercular therapy. He complied fully for 60 days and improved not at all. On admission, he was cachectic, pale, and profoundly ill, with bilateral digital clubbing, pitting pedal edema, a solitary ulcer on the hard palate, and firm, non-tender cervical lymph nodes. Laboratory work revealed microcytic hypochromic anemia with hemoglobin of 8.6 grams per deciliter, a C-reactive protein of 143.35 milligrams per liter, albumin of just 2 grams per deciliter, and serum sodium of 127 millimoles per liter. A chest radiograph showed mild bilateral pleural effusions.

Imaging then painted a deceptively clear picture. Magnetic resonance enterography demonstrated multi-segmental bowel wall thickening involving the distal jejunum and ileum without stricture formation, along with small reactive-appearing mesenteric lymph nodes, and the radiological impression favored Crohn’s disease. Fecal calprotectin—a protein released from neutrophils in inflamed intestinal mucosa—was markedly elevated at 1849.47 micrograms per gram, a level widely associated with active inflammatory bowel disease. Stool microscopy showed 8 to 12 pus cells per high-power field with mucus. Everything pointed toward a chronic inflammatory process of the gut. Yet as the case authors emphasize, fecal calprotectin is a marker of mucosal neutrophilic infiltration, not of any specific disease. It can be substantially elevated in infectious enteritis, including histoplasmosis, salmonellosis, and intestinal tuberculosis, and its dramatic rise should prompt a search for etiology rather than a reflexive diagnosis of IBD.

Endoscopic findings reinforced the mimicry. Upper endoscopy revealed a small benign-appearing duodenal ulcer, while colonoscopy demonstrated an ulcero-nodular lesion in the caecum studded with pseudopolyps distributed across the ascending, transverse, and descending colon. A repeat colonoscopy days later confirmed ulcero-nodular lesions with skip-pattern involvement of the distal ileum, ileocecal valve, and caecum—an appearance that overlaps almost perfectly with the colonoscopic spectrum of tuberculosis and Crohn’s disease. The ileocecal region is preferentially affected in all of these conditions, partly because the high density of Peyer’s patches in the terminal ileum facilitates reticuloendothelial seeding by pathogens, whether mycobacteria or fungi. GeneXpert MTB/RIF testing of tissue was negative for Mycobacterium tuberculosis, and a QuantiFERON-TB Gold Plus assay was non-reactive, a combination that carries a high negative predictive value for active mycobacterial disease.

The first biopsies were inconclusive, yielding only granulation tissue with acute and chronic inflammatory infiltration—no definitive granulomas, no malignancy, and no organisms. This pattern is well documented in gastrointestinal histoplasmosis, where superficial sampling frequently misses the intracellular yeasts lurking within lamina propria histiocytes. The breakthrough came from two directions. A repeat deep biopsy targeting the caecum and ileocecal valve revealed dense inflammatory infiltration rich in eosinophils and, crucially, multiple encapsulated, uniform, small oval yeast forms exhibiting narrow-based budding and eccentric nuclei, both within and outside histiocytes—morphological features diagnostic of Histoplasma capsulatum. The following day, fine-needle aspiration cytology of a cervical lymph node showed granulomatous inflammation teeming with intracellular and extracellular Histoplasma organisms, confirming that the infection was disseminated. Periodic acid-Schiff and Gomori methenamine silver stains are widely advocated to enhance fungal detection in tissue sections, particularly when organism burden is low, and the case authors argue that clinicians should maintain a low threshold for requesting such stains in unresolved ileocecal pathology, especially after anti-tubercular therapy fails.

Treatment began immediately. Oral itraconazole at 200 milligrams twice daily was started on the day of diagnosis, and systemic therapy was escalated to liposomal amphotericin B at 3 milligrams per kilogram per day the following day. It was too late. After just two doses of amphotericin, the patient suffered a massive lower gastrointestinal hemorrhage with acute hemodynamic collapse—his blood pressure became unrecordable and his oxygen saturation fell to 85 percent on 15 liters per minute of supplemental oxygen. Despite transfusion, intravenous fluid resuscitation, and vasopressor support, he was transferred to the intensive care unit and died roughly six hours later of refractory cardiorespiratory failure. Extensive mucosal ulceration, vascular erosion by the fungal inflammatory process, and consumptive coagulopathy from disseminated infection all predispose to this most feared complication, and antifungal therapy initiated a mere 72 hours earlier could not reverse tissue destruction that had already progressed past the threshold of reversibility.

The broader lessons are sobering. Published mortality rates for disseminated gastrointestinal histoplasmosis range from 20 to 50 percent, rising substantially when diagnosis is delayed beyond four weeks; this patient’s diagnosis lagged more than three months after symptom onset. In high-tuberculosis-burden settings, anchoring bias favors mycobacterial explanations for ileocecal pathology, weight loss, and lymphadenopathy, and failure of empirical anti-tubercular therapy is often the first signal that a different diagnosis deserves consideration. Equally hazardous is the temptation to treat a compelling Crohn’s-like phenotype—bowel wall thickening on enterography, skip lesions, pseudopolyps, and sky-high fecal calprotectin—with immunosuppressive therapy before infection has been histopathologically excluded, a step that could accelerate fungal dissemination with catastrophic consequences. In this case, the decision to defer immunosuppression pending tissue confirmation likely bought valuable time. The authors note that fungal culture and urine or serum Histoplasma antigen testing, which might have accelerated diagnosis, were unavailable, and formal immunological evaluation for rare innate immune defects such as STAT3 or IL-12 pathway mutations was not feasible in the acute setting. Their conclusion is unambiguous: when anti-tubercular therapy fails in ileocecal disease, fungi belong on the differential, deep colonoscopic biopsies with fungal stains are essential and may need repeating, and no patient should receive empirical immunosuppression for presumed inflammatory bowel disease until infection has been ruled out under the microscope.

Subject of Research: Disseminated gastrointestinal histoplasmosis mimicking intestinal tuberculosis and Crohn's disease in an immunocompetent host

Article Title: Gastrointestinal Histoplasmosis Mimicking Intestinal Tuberculosis and Crohn's Disease: Ileocecal Involvement in an Immunocompetent Host

Article References: Sazal, R. S., Esha, S. S., Faisal, A. A., Azad, M. A. K., Murshed, K. M., & Aftab, K. A. (2026). Gastrointestinal Histoplasmosis Mimicking Intestinal Tuberculosis and Crohn's Disease: Ileocecal Involvement in an Immunocompetent Host. Clinical Case Reports, 14(9), Article e73555. https://doi.org/10.1002/ccr3.73555

Image Credits: AI Generated

DOI: 10.1002/ccr3.73555

Keywords: histoplasmosis, Histoplasma capsulatum, gastrointestinal histoplasmosis, intestinal tuberculosis, Crohn's disease, ileocecal disease, fecal calprotectin, immunocompetent host, liposomal amphotericin B, diagnostic delay, colonoscopy biopsy, fungal infection

The dog was referred to the Veterinary Clinic of the Faculty of Veterinary Medicine at the University of Tehran with a striking dermatological picture. It lived outdoors under unsanitary conditions with regular exposure to vegetation and soil, and it presented with diffuse hair loss, marked redness, itching and scaling across the skin of its back. Crucially, there was no ulceration or open wound, no lethargy and no loss of appetite, so systemic illness seemed unlikely and a complete blood count was not performed. The owner declined a skin biopsy, which meant the team could not obtain histopathological evidence of fungal invasion, a detail that would later shape how carefully the conclusions had to be framed. Hair plucks and skin scrapings were collected from the affected areas under sterile conditions and sent to the laboratory for fungal examination.

The initial diagnostic workup followed the standard playbook for suspected dermatophytosis, the superficial fungal infection of keratinized skin that is usually caused by organisms such as Microsporum canis, Microsporum gypseum or Trichophyton mentagrophytes. A Wood’s lamp examination was negative, and a direct microscopic examination of material treated with 10 percent potassium hydroxide also failed to reveal fungal elements. But the story changed when the samples were cultured on Sabouraud Dextrose Agar. After incubation at 28 degrees Celsius, colonies emerged that were creamy-brown and powdery with a colorless reverse surface. Lactophenol cotton blue staining of the growth revealed thin, septate hyphae studded with large, round, warty conidia, a morphological signature that immediately suggested the team was not dealing with a routine dermatophyte.

Seeking to probe the organism’s thermal behavior, the researchers subcultured the colonies onto blood agar and incubated them at 37 degrees Celsius, close to mammalian body temperature, for five days. The fungus produced creamy, dome-shaped, mucoid colonies under these conditions, and Giemsa staining revealed round-to-oval yeast-like cells with budding and point attachments when viewed under oil immersion at 100 times magnification. This dimorphic tendency, the ability to alter its appearance under different growth conditions, added another layer of complexity to the identification. Morphology alone could not settle the question, particularly since members of the family Chaetomiaceae, to which Corynascus belongs, are notorious for overlapping phenotypic features among closely related species. The team therefore turned to the laboratory’s molecular arsenal.

Genomic DNA was extracted from the isolate using a commercial fungal DNA extraction kit, and the internal transcribed spacer region of ribosomal DNA, comprising the ITS1 spacer, the 5.8S rRNA gene and the ITS2 spacer, was amplified with the universal primers ITS1 and ITS4. The polymerase chain reaction protocol began with denaturation at 94 degrees Celsius for three minutes, followed by 37 cycles of denaturation for 30 seconds, annealing at 60 degrees Celsius for 30 seconds and extension at 72 degrees Celsius for 30 seconds, with a final extension of eight minutes. The roughly 600-base-pair amplicon was then sequenced, and the resulting sequence was deposited in GenBank under accession number PV082530, making it publicly available for future comparisons by researchers anywhere in the world.

The sequence told a clear story. BLAST analysis showed 99.36 percent nucleotide similarity to reference sequences of Corynascus verrucosus and 99.34 percent similarity to a reference sequence of Corynascus sepedonium, a closely related species whose ITS region differs only marginally. To resolve the placement further, the researchers aligned their sequence with reference data from GenBank and constructed a maximum likelihood phylogenetic tree in MEGA7 using the Kimura two-parameter model with 1000 bootstrap replicates. The Iranian isolate fell squarely within the broader Corynascus lineage and clustered tightly with C. verrucosus sequences from different geographic regions, while reference sequences annotated as Myceliophthora, including Myceliophthora sepedonium and Myceliophthora verrucosa, occupied the same larger assemblage. The tree was rooted with Amesia atrobrunnea as the outgroup, and the resulting topology was consistent with previously published taxonomic frameworks placing Corynascus within the family Chaetomiaceae.

The taxonomy behind that placement is itself a story of scientific revision. The genus Corynascus comprises seven recognized species, and its boundaries have shifted repeatedly over decades of study, from early work by von Klopotek in 1974 and Stchigel and colleagues in 2000, who described three new thermotolerant species, to a 2015 re-evaluation of Myceliophthora using morphological and multilocus phylogenetic data that affirmed Corynascus as a distinct genus. More recent comprehensive studies have supported that distinction using multigene analyses incorporating ITS, LSU, rpb2, tub2 and tef sequences. Meanwhile, members of the Myceliophthora lineage have attracted industrial attention for their production of thermostable enzymes, and C. verrucosus itself made headlines in 2020 when researchers documented it as a mycoendophyte of Croton bonplandianus and a potential source of bioactive metabolites active against multidrug-resistant pathogens and cancer cells. None of this industrial or pharmacological relevance implies pathogenicity, a distinction the authors are careful to draw.

Where might a pet dog have encountered such a fungus? Environmental studies of composting offer a suggestive clue. Research on organic waste and manure composting has documented substantial shifts in fungal community composition as physicochemical conditions change, with thermophilic and thermotolerant fungi, exactly the ecological guild to which many Corynascus species belong, flourishing in these habitats. Composting environments and similar organic-material settings may therefore serve as reservoirs of environmentally adapted fungal taxa. The Tehran patient’s outdoor lifestyle, unsanitary surroundings and regular contact with soil and vegetation provided ample opportunity for exposure. Still, the authors emphasize that phylogenetic relatedness does not imply shared biological function or pathogenic potential, and that genetic similarity alone should never be read as evidence of a shared disease-causing role.

The clinical narrative, however, lends weight to a genuine association rather than a chance contaminant. The same fungal species was recovered on three independent cultures from the lesion, no bacterial growth was detected, and mite infestation was excluded. The dog was treated with oral ketoconazole combined with ketoconazole shampoo, receiving four weekly medicated baths. The itching and redness resolved within about a month, hair regrowth followed, and a uniform coat had returned approximately six months after treatment began. Over a nine-month follow-up period, the original cutaneous signs never recurred. The combination of repeated isolation, exclusion of other pathogens, molecular identification and clinical improvement following antifungal therapy supports, though it does not prove, a causal link.

That caution about proof is the intellectual heart of the report. Because histopathological examination was never performed, tissue invasion by the fungus could not be demonstrated directly, and the authors explicitly frame the finding as an association rather than definitive evidence of causality. Their broader message concerns method: for uncommon environmental fungi recovered from veterinary specimens, accurate identification demands a polyphasic approach that integrates morphology, ITS sequencing and phylogenetic placement rather than relying on any single line of evidence. Molecular methods can rescue isolates that fail to produce characteristic reproductive structures in culture, but they carry their own biases and limited discriminatory power, as the near-identical ITS sequences of C. verrucosus and C. sepedonium illustrate. By expanding the documented occurrence of C. verrucosus to a canine cutaneous lesion, the case adds a small but genuinely novel data point to veterinary mycology and a reminder that the fungal world’s opportunists may be more numerous, and better camouflaged, than current diagnostics routinely reveal.

Subject of Research: A rare case of cutaneous infection by the environmental fungus Corynascus verrucosus in a Shih Tzu dog, identified through molecular and phylogenetic analysis.

Article Title: A Rare Case of Cutaneous Infection by Corynascus verrucosus in a Shih Tzu Dog: Molecular Identification and Phylogenetic Analysis

Article References: Ghahremani, M., Sharifzadeh, A., Ashrafi Tamai, I., & Faridfar, G. (2026). A Rare Case of Cutaneous Infection by Corynascus verrucosus in a Shih Tzu Dog: Molecular Identification and Phylogenetic Analysis. Veterinary Medicine and Science, 12(5), Article e71205. https://doi.org/10.1002/vms3.71205

Image Credits: AI Generated

DOI: 10.1002/vms3.71205

Keywords: Corynascus verrucosus, veterinary mycology, canine dermatology, fungal infection, ITS sequencing, phylogenetic analysis, Chaetomiaceae, dermatophytosis, Shih Tzu, molecular identification, environmental fungi, ketoconazole treatment