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Answer: Disseminated Acanthamoeba infection . The biopsy of the palate lesion revealed ulcerated and necrotic tissues with the presence of protozoan parasites around blood vessels on H&E staining (see Fig. 1E and F in the photo quiz). Amoebic trophozoites were identified based on the presence of

The patient was a 25-year-old woman with a medical history of bilateral lung transplantation in 2012 for end-stage lung disease secondary to cystic fibrosis, chronic renal insufficiency, diabetes mellitus, exocrine pancreatic insufficiency, and chronic sinusitis. Her immunosuppressive therapy

A mature male, black and white ruffed lemur (Varecia variegata variegata) died in a zoological garden after a 4-day history of lethargy and non-responsive convulsions. Necropsy and histopathological examinations revealed acute necrotizing and haemorrhagic meningoencephalitis with intralesional amoebas confirmed by immunohistochemistry. Acanthamoeba T4 genotype was identified as the causative agent of the brain lesion, based on amplification and sequencing of 18S ribosomal RNA genes. The presence of free-living amoebas in water and mud from the lemur's environment was investigated by morphological and molecular analyses. The two predominant genera, representing 80% of isolated amoebas, were Naegleria spp. and Acanthamoeba spp. All Acanthamoeba isolates belonged to the T4 genotype. To the author's knowledge, this is the first report of a meningoencephalitis due to Acanthamoeba T4 genotype in Lemuridae with concurrent analysis of pathological tissues and environment.

INTRODUCTION: In highly endemic areas, up to 20 % of human immunodeficiency virus (HIV)-infected persons will develop progressive disseminated histoplasmosis (PDH). Europe is not endemic to histoplasmosis, and the disease is mainly found in immigrants often co-infected with HIV.METHODS: We present a case of a patient with HIV and PDH highlighting the possible diagnostic difficulties that may arise in a non-endemic area and review the literature of histoplasmosis in the context of HIV infection with special focus on Europe.DISCUSSION: When cellular immunity wanes (usually at CD4 T-lymphocyte counts CONCLUSION: European infectious diseases physicians, microbiologists and pathologists must be aware of histoplasmosis, particularly when facing HIV-infected immigrants from endemic areas. This is increasingly important due to migration and travel activities from these areas.

Autosomal dominant loss of function mutation of signal transducer and activator of transcription 3 (STAT3) gene (STAT3-deficiency) predisposes to recurrent bacterial pneumonia that are complicated in 67% of patients with bronchiectasis, cavitations and Aspergillus infection or colonization in 22% of patients1. We aimed to report the prevalence, describe clinical, mycological, pathological and radiological presentation and both medical and surgical treatment of mold infections in the National French cohort. Methods Referent physicians of STAT3-deficient patients (n= 74 patients) were contacted to know if patients had evidence of colonization or infection with molds. Clinical and mycological information were collected and imaging was centralized. An expert committee reviewed all charts and classified the cases (EC, SP, CT, AD, FL, OL, MOC). Results Eighteen episodes of filamentous fungal infection in ten (13.5%) STAT3-deficient patients were identified. The median age at first episode was 12 years (IQR 10.2–25). Ninety percent of patients had underlying pulmonary disease, bronchiectasis and cavitations, usually multiple. Mold infections were classified as follow: three aspergillomas, six Chronic Pulmonary Aspergillosis (CPA), five Allergic BronchoPulmonary Aspergillosis (ABPA), two mixed forms ABPA and CPA, one Chronic Allergic Sinus Aspergillosis and one Rasamsonia invasive pulmonary infection. According to EORTC/MSG definitions, no cases of invasive aspergillosis were reported. Aspergillus fumigatus was isolated in 13 cases, Rasamsonia argillocea in one case. Aspergillus precipitins were detectable in 86% of cases (12/14). Two-thirds of fungal episodes (12/18) were breakthrough infections (itraconazole prophylaxis in most cases), and half of the cases (9/18) occurred while on immunoglobulin substitutive therapy. First line antifungal therapy was voriconazole only (8/18) or amphotericin B alone or in association (6/18). Five patients required surgery (4 CPA, 1 aspergilloma). One patient died from respiratory failure at 11 years old. Conclusion Mold infections occurred in 13.5% of STAT3-deficient patients from the French cohort, mostly on anatomical modification of the lung. Notably, patients developed aspergilloma, ABPA or CPA, but no invasive aspergillosis. Despite prolonged antifungal treatment and/or surgery half of the patients (5/10) relapsed.

International audience; A wild common dolphin was found stranded on the French Atlantic coast. At necropsy, an intracranial grey- to tan-coloured mass (7 × 5 × 4 cm) was found at the right cerebellopontine angle, compressing the right cerebellar hemisphere, the brainstem and the occipital lobe of the right cerebral hemisphere. Microscopically, the tumour was composed of small lobules of polygonal to elongated neoplastic cells with multifocal areas of stellate and vacuolated cells. Neoplastic cells strongly expressed vimentin, S-100 protein and neuron-specific enolase. They were rarely positive for cytokeratin. Ultrastructurally, the neoplastic cells displayed all the diagnostic features of meningiomas and in some areas showed long cytoplasmic processes delimiting extracellular spaces. The immunohistochemical and ultrastructural features were consistent with the histopathological diagnosis of a microcystic meningioma. This is the first report of a meningioma in dolphins or in any other cetacean species.

Autoimmune diabetes has never been described in a juvenile dog, whereas serological evidence has established its development in adult dogs. Diabetes mellitus was diagnosed in a 3-mo-old Donge de Bordeaux dog suffering from persistent hyperglycemia and concurrent insulinopenia. Histological analysis of the pancreas revealed inflammatory lesions in 40% of the islets of Langerhans, with infiltration predominantly by T lymphocytes (more than 90%), either at the edge (peri-insulitis: 10%) or in the islets (insulitis: 30%). The remaining 60% of the islets showed a marked atrophy due to massive beta cell loss with no loss of alpha cells. This pattern is quite similar to that observed in humans in which a characteristic insulitis containing high numbers of T lymphocytes is found in 20% of the islets at diabetes diagnosis. By contrast, in rodent models, nearly 70% of the islets of Langerhans show inflammation at diagnosis and macrophages and dendritic cells predominate in the inflammatory lesions. This is the first report of lymphocytic insulitis in a juvenile dog exhibiting diabetes mellitus. Our observations suggest an autoimmune origin for the disease in this dog that is similar to human type 1 diabetes mellitus, for which there is no accurate spontaneous large animal model.