Acute Disseminated Paracoccidioidomycosis Septic Shock

Azulay, Rubem David; Velloso, M.; Suguimoto, Sueli Yuriko; Ishida, Cleide Eiko; Pereira, Antônio Carlos

doi:10.1111/j.1365-4362.1988.tb00934.x

Cited by 6 publications

(5 citation statements)

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“…In this study, we describe a novel model for the regulation of ACE2, which others have found is essential for the host cell entry of SARS-CoV-2. 6 In contrast to reports of patient susceptibility to SARS-CoV-2 owing to age, gender, smoking history, or thoracic malignancies, 4,5,90,91 we were unable to identify consistent differences in ACE2 expression on the basis of these variables. Our data suggest that ACE2 expression is restricted in both normal and malignant aerodigestive and respiratory tissues almost exclusively to epithelial cells, including highly specialized POU2F3-positive tuft cells, and that this restriction reflects regulatory mechanisms shared with EMT.…”

Section: Discussioncontrasting

confidence: 96%

Lung Cancer Models Reveal Severe Acute Respiratory Syndrome Coronavirus 2–Induced Epithelial-to-Mesenchymal Transition Contributes to Coronavirus Disease 2019 Pathophysiology

Stewart

Ramkumar

Cargill

et al. 2021

Journal of Thoracic Oncology

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COVID-19 is an infectious disease caused by SARS-CoV-2, which enters host cells via the cell surface proteins ACE2 and TMPRSS2. Using a variety of normal and malignant models and tissues from the aerodigestive and respiratory tracts, we investigated the expression and regulation of ACE2 and TMPRSS2 . We find that ACE2 expression is restricted to a select population of epithelial cells. Notably, infection with SARS-CoV-2 in cancer cell lines, bronchial organoids, and patient nasal epithelium, induces metabolic and transcriptional changes consistent with epithelial to mesenchymal transition (EMT), including upregulation of ZEB1 and AXL , resulting in an increased EMT score. Additionally, a transcriptional loss of genes associated with tight junction function occurs with SARS-CoV-2 infection. The SARS-CoV-2 receptor, ACE2, is repressed by EMT via TGFbeta, ZEB1 overexpression and onset of EGFR TKI inhibitor resistance. This suggests a novel model of SARS-CoV-2 pathogenesis in which infected cells shift toward an increasingly mesenchymal state, associated with a loss of tight junction components with acute respiratory distress syndrome-protective effects. AXL-inhibition and ZEB1-reduction, as with bemcentinib, offers a potential strategy to reverse this effect. These observations highlight the utility of aerodigestive and, especially, lung cancer model systems in exploring the pathogenesis of SARS-CoV-2 and other respiratory viruses, and offer important insights into the potential mechanisms underlying the morbidity and mortality of COVID-19 in healthy patients and cancer patients alike.

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Section: Discussioncontrasting

confidence: 96%

Lung Cancer Models Reveal Severe Acute Respiratory Syndrome Coronavirus 2–Induced Epithelial-to-Mesenchymal Transition Contributes to Coronavirus Disease 2019 Pathophysiology

Stewart

Ramkumar

Cargill

et al. 2021

Journal of Thoracic Oncology

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“…Younger children are likely to present a more frequent liver and spleen involvement 2,4,7,8,10,11 . Gastrointestinal tract, bone marrow, adrenal gland, testis, brain, kidney and heart are occasionally involved 1,14,19 . According to the greatest pediatric clinical series of PCM retrospectively reviewed (N = 52, 1944-1974), the lethality rate was 7.7% 14 .…”

Section: Discussionmentioning

confidence: 99%

“…On the other hand, it has been accepted that PCM results from and/or triggers a decrease of the cellular defense mechanisms, increasing the risk of severe systemic infections 1,3,6 . However, in this case, it is reasonable to suppose that the septic syndrome was directly related to P. brasiliensis infection, as already described elsewhere 1,3 . This inference is supported by the negative findings of bacterial pathogens on the blood cultures (two samples) and the autopsy findings of disseminated fungal yeast forms.…”

Section: Discussionmentioning

confidence: 99%

Fatal disseminated paracoccidioidomycosis in a two-year-old child

Pereira

Tresoldi

Silva

et al. 2004

Rev. Inst. Med. trop. S. Paulo

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A two year-old female child was admitted at the Pediatric Intensive Care Unit in a septic shock associated with a lymphoproliferative syndrome, with history of fever, adynamia and weight loss during the last two months. On admission, the main clinical and laboratory manifestations were: pallor, jaundice, disseminated enlarged lymph nodes, hepatosplenomegaly, crusted warts on face, anemia, eosinophilia, thrombocytopenia, increased direct and indirect bilirubin, alkaline phosphatase, and gammaglutamyl transpeptidase. A parenteral administration of fluids, dobutamine and mechanical ventilation was started, without improvement of the clinical conditions. A direct examination of exsudate collected from cervical lymph node revealed numerous oval-to-around cells with multiple budding, like a "pilot wheel" cell, suggesting Paracoccidioides brasiliensis. Even though treatment with intravenous sulfamethoxazole-trimethoprine was soon started, the child died 36 hours after hospital admission. Disseminated paracoccidioidomycosis was confirmed in the autopsy. This is the youngest case of paracoccidioidomycosis in children reported in the literature.

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“…Mesenteric lymph-nodal involvement may cause bowel obstruction and symptoms of an acute abdominal emergency. 62,78 Untreated PM also can be fatal owing to extensive pulmonary fibrosis, central nervous system dissemination, 80,81 or addisonian syndrome. 78,79,81 Unapparent subclinical infection and minor lung changes are, however, common in affected areas and in Europeans and Americans who lived in these areas.…”

Section: Rhinosporidiosismentioning

confidence: 99%

“…Other lymphoid tissue sites, such as axillary, inguinal, and mesenteric lymph nodes, also can be affected. 78 The cutaneous lesions of PM can vary from crusted papules to ulcers, nodules, plaques, and verrucous lesions. Centrofacial localization is typical of PM, and most of the lesions occur through dissemination of the oral and gingival lesions.…”

Section: Rhinosporidiosismentioning

confidence: 99%