We report a rare survival case of anthrax meningoencephalitis in a 56-year-old male from a low-incidence region. The patient presented with nasal discharge, fever, headache, and rapid onset of coma following the slaughter of a diseased cow. Physical examination revealed a characteristic ulcerative eschar on the right index finger, while laboratory investigations showed significant leukocytosis and hemorrhagic cerebrospinal fluid (CSF) characterized by elevated protein and decreased glucose levels. Although initial microscopy misidentified the pathogen as Bacillus cereus, metagenomic next-generation sequencing (mNGS) of the CSF confirmed Bacillus anthracis within 48 hours. This rapid molecular diagnosis enabled a timely switch to a CDC-recommended combination regimen, initially with quadruple therapy (penicillin G, ciprofloxacin, amikacin, and linezolid) followed by optimization to triple therapy (penicillin G, levofloxacin, and linezolid) during the ICU stay, ultimately leading to the patient's full neurological recovery. This case underscores that the synergistic use of rapid mNGS-based diagnosis and appropriate combination therapy is critical for achieving survival in anthrax meningoencephalitis.

Tularemia is a zoonotic infection caused by Francisella tularensis (F. tularensis). Although tularemia has historically been considered rare in Denmark, increasing numbers of diagnosed cases and recent seroepidemiological data suggest that the infection is increasingly recognized and may be more widespread than previously appreciated. This paper describes two pediatric cases presenting with persistent fever, punched-out inoculation ulcer (eschar) and local (inguinal)lymphadenitis, initially misdiagnosed as a common bacterial soft tissue infection. Both cases highlight delayed diagnosis, lack of response to first line antibiotics (beta lactam antibiotic), and the importance of considering tularemia in local persistent lymphadenitis especially combined with an adjacent punched out skin ulcer.

Diabetic foot ulcers are predominantly attributed to bacterial aetiologies, but invasive fungal infections are an increasingly recognised opportunistic threat in immunocompromised patients. We present the case of a male farmer in his 30s with uncontrolled diabetes who developed a worsening necrotic ulcer on the left tibia following agricultural trauma. Despite treatment with broad-spectrum antibiotics, the wound deteriorated, exhibiting a central black eschar. Deep tissue biopsy revealed hyaline septate hyphae and fungal culture confirmed Fusarium oxysporum, identified by characteristic banana-shaped macroconidia. Management required a multimodal limb-salvage approach involving strict glycaemic control, dual antifungal therapy with liposomal amphotericin B and voriconazole and aggressive serial surgical debridement. Complete healing was achieved after 5 months without amputation. This case highlights the importance of suspecting fungal aetiology in antibiotic-refractory diabetic wounds, particularly in patients with occupational soil exposure.

Decubitus ulcers, also termed bedsores or pressure ulcers, are skin and soft tissue injuries that form as a result of constant or prolonged pressure exerted on the skin. These ulcers occur at bony areas of the body such as the ischium, greater trochanter, sacrum, heel, malleolus (lateral than medial), and occiput. These lesions mostly occur in people with conditions that decrease their mobility making postural change difficult. Jean-Martin Charcot was a French doctor in the 19th century who studied many diseases, including decubitus ulcers. He noticed that patients who developed eschar of the buttocks and sacrum died after some time. He named this lesion "decubitus ominous," which meant death was inevitable after developing this lesion.

A 30-year-old man with recent diagnosis of HIV-infection was seen in the hospital, because of a 1-month history of swollen lips, painful oral mucosa ulcers, cervical lymph nodes and skin lesions. The medical history showed a previous patient contact with 10 subjects, with positivity for Monkeypox virus in 8 subjects. A week later, he began with lesions on the genitals, managed with acyclovir, and subsequent development of manifestations in the mouth and skin, with dissemination to the entire body. He was admitted to our clinic for increased volume in penis and scrotum, and a disseminated dermatosis affecting all body segments, characterized by polymorphic lesions reflecting various stages; the condition presents as infiltrated plaques with a central eschar and two halos at the periphery: one pale and another erythematous, of varying sizes, accompanied by significant edema (Figure 1A). In the mouth there was lip edema, with the presence of multiple superficial round ulcers and vesicles, with a hemorrhagic center and a white-yellowish border, that coalesce forming circinate plaques, with serohematic crusts on the upper vermilion and hematic and meliceric crusts on the lower one, as well as pale mucosa (Figure 1B). Intraorally, painful large shallow ulcers, covered with fibrin and hemorrhagic areas, with rounded and irregular edges, affected both labial mucous membranes, the hard palate and gums, with gingival enlargement and necrosis of the interdental papillae (Figure 1C); the tongue showed partial atrophy of filiform papillae with some isolated punctiform ulcers. A presumptive diagnosis of Monkeypox infection was suggested. Biopsies on lower labial mucosa and plantar skin were performed. Analysis of blood test revealed: hemoglobin 10.8 (13.1 - 18.1) g/dL, iron 22 µg/dL (50 - 212), ferritin 2362 (23 - 336,2) ng/mL, leukocytes 10.8 (3.9 - 10.1)/mm3, aspartate aminotransferase 47.3 (13 - 39) U/L, albumin 2.4 (3.5 - 5.7) g/dL, CD4 count 121 (500-1500) cells/mm3 and HIV-viral load 312,000 (<20-75) copies/mL, starting antiretroviral therapy with bictegravir/emtricitabine/tenofovir alafenamide (biktarvy) and management with antibacterials and antivirals. The histopathological study of lesions was compatible with monkeypox infection and PCR test for the monkeypox virus confirmed the diagnosis (1,2). The patient had increased difficulty in swallowing, first with solids then with liquids; and, given the risk of airway obstruction due to oropharyngeal edema, a tracheostomy was performed. Disease progression was observed, with kidney damage and pulmonary dysfunction, and he died a month later. Mucocutaneous and other clinical features such as fever, chills, headache, muscular pains, backaches, and weariness, are some of the first symptoms of a Monkeypox infection.(2-5) A gradual maculopapular rash with lesion diameters ranging from 0.2-1 cm appears after the prodrome stage; initially on the face and neck, and moving to the legs with involvement of the palms and soles, spreading throughout the body.(2, 5) These last characteristics favored the initial diagnosis of a Monkeypox infection in our patient. Differential diagnosis should include other pox-like viruses, such as varicella, herpes zoster, measles, and arboviruses (Dengue, Zika and chikungunya). (2) This case represents a rare situation where the host rapidly developed progressive worsening of Monkeypox manifestations in HIV-infection.

The most common skin cancer is basal cell carcinoma. The neoplasm is characterized by several different morphologic presentations; the most frequent morphologic variants are superficial and nodular. Each clinical presentation of the tumor has a corresponding histologic presentation. The biological behavior of a basal cell carcinoma depends not only on its histologic subtype but also on its location. Surgical excision is the treatment of choice for most basal cell carcinomas; this intervention is typically used for basal cell carcinomas that demonstrate aggressive behavior. Nonsurgical treatment, such as topical 5% imiquimod cream, may be considered for lower-risk tumors. After consultation with the dermatologist, I (a 65-year-old man) decided to treat my primary nodular basal cell carcinoma on my right periocular temple by applying 5% imiquimod cream daily to the neoplasm and the adjacent skin. The cancer was treated for a total of 45 days; during treatment, I had to discontinue the therapy twice because I developed severe, medication-related, local cutaneous adverse side effects, which included inflammation, eschar, and ulcers. I achieved complete clinical clearance of the carcinoma; the only residual finding at the previous tumor site was an atrophic patch. The management of basal cell carcinoma includes noninvasive and invasive modalities. Mohs micrographic surgery is the treatment of choice for most facial basal cell carcinomas and tumors of infiltrative histologic subtype. Mohs surgery is an invasive procedure; it can be associated with not only postoperative complications and scar but also possibly inferior cosmetic results. However, the advantages of Mohs surgery are not only its 97.5% cure rate for primary basal cell carcinomas but also the very low rate of tumor persistence following the procedure. Superficial basal cell carcinomas on the neck, trunk, or extremities can be treated with a daily topical application of 5% imiquimod cream, five times per week, for six weeks. In contrast to surgical excision, topical imiquimod has a lower cure rate; however, it is a noninvasive therapy and may result in cosmetically superior results. Nodular basal cell carcinomas, including periocular tumors, have also been successfully treated with topical 5% imiquimod cream. Treatment using topical 5% imiquimod cream for a basal cell carcinoma, compared to Mohs surgical excision, has several potential disadvantages. Some of these include a lower cure rate, a longer treatment duration (such as six weeks with five daily applications each week to treat a superficial basal cell carcinoma versus a single day of surgery), and the development of localized adverse cutaneous reactions that occur both on the tumor-containing epithelium and the skin surrounding the cancer. In conclusion, the management of basal cell carcinoma is an individualized decision for which several factors need to be evaluated. Although surgery is the gold standard of treatment, patients who do not want surgical intervention and possibly a better cosmetic result without a surgical scar may appropriately elect potentially effective noninvasive therapies, which have lower cure rates, longer treatment duration, and more frequently have associated adverse cutaneous reactions. This experience has taught me as a patient and as a physician that the topical management of a basal cell carcinoma with 5% imiquimod cream can result in more complicated adverse cutaneous effects than anticipated.

Anaplastic large cell lymphoma (ALCL) is part of the spectrum of CD30-positive lymphoproliferative disorders within cutaneous T-cell lymphomas. These disorders account for approximately 25%-30% of all primary cutaneous lymphomas (PCLs). Primary cutaneous ALCL (pcALCL) is an uncommon entity with heterogeneous clinical and histopathologic features, often posing a diagnostic challenge. We report a 79-year-old man who presented with a three-month history of a non-healing ulcer on the right lower limb following minor trauma. The lesion measured 6.7 × 9.8 × 0.3 cm and showed irregular erythematoviolaceous borders with areas of eschar. Histopathologic evaluation revealed a dense infiltrate of large atypical mononuclear cells with pleomorphic nuclei, prominent nucleoli, and atypical mitoses, accompanied by angiocentric and angiodestructive features. Immunohistochemistry demonstrated CD30 positivity in more than 75% of atypical cells and negative anaplastic lymphoma kinase (ALK) expression, confirming pcALCL. The patient responded favorably to electron beam radiotherapy. This case underscores the importance of early biopsy in atypical or treatment-refractory ulcers and highlights the diagnostic relevance of recognizing rare variants such as the angiocentric subtype.

BACKGROUND: Rhino-orbito-cerebral mucormycosis, caused by pathogens such as Rhizopus delemar, is a life-threatening opportunistic infection primarily affecting immunosuppressed individuals. Anti-melanoma differentiation-associated protein 5-positive dermatomyositis (MDA5+ DM) is a distinct subtype of DM associated with interstitial lung disease (ILD) and high mortality. Fungal co-infections in anti-MDA5+ DM, particularly mucormycosis, are rarely reported. CASE PRESENTATION: We report a case of rhino-orbito-cerebral mucormycosis caused by Rhizopus delemar in a patient with anti-MDA5+ DM. The patient was receiving high-dose glucocorticoids and immunosuppressive therapy for rapidly progressive ILD, and later she developed progressive neurological symptoms, palatal ulceration with black eschar, and periorbital swelling. Metagenomic next-generation sequencing (mNGS) of blood subsequently identified Rhizopus delemar, and the diagnosis was further supported by cerebrospinal fluid mNGS. Antifungal therapy was adjusted promptly after pathogen identification. Despite aggressive treatment, the infection progressed rapidly with central nervous system involvement. CONCLUSIONS: This case highlights the heightened susceptibility to invasive mucormycosis in patients with anti-MDA5+ DM, likely exacerbated by immunosuppressive therapy. Early diagnosis using mNGS and prompt initiation of targeted antifungal therapy are critical in managing such co-infections. Clinicians should maintain a high index of suspicion for invasive fungal infections in immunosuppressed anti-MDA5+ DM patients presenting with non-specific neurological or sinus symptoms.

Ecthyma gangrenosum (EG) is a necrotizing skin lesion that typically begins as an erythematous or hemorrhagic area and progresses to a necrotic ulcer with a black eschar. EG is most commonly associated with Pseudomonas aeruginosa infections in immunocompromised individuals, though other pathogens have been implicated in rare cases. We present an unusual case of EG originating in the oral cavity of an immunosuppressed patient, accompanied by extensive ecchymoses and polymicrobial infection, notably without P. aeruginosa involvement. This report highlights the atypical clinical and pathologic features of the case and reviews the broader spectrum of microorganisms associated with EG.