Fatal granulomatous amoebic encephalitis caused by Acanthamoeba in a newly diagnosed patient with systemic lupus erythematosus

Thamtam, Vamshi Krishna; Uppin, Megha S; Pyal, Anjan; Kaul, Subhash; Rani, Jyostna Y; Challa, Sundaram

doi:10.4103/0028-3886.173662

Cited by 13 publications

(1 citation statement)

References 3 publications

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“…Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease with various symptoms and a constantly changing clinical course. Skin, joints, kidneys, lungs, and the neurological system are just a few organs that might be affected (Fava & Petri, 2019; Thamtam et al, 2016). Immune‐mediated inflammation and tissue damage induced by immune system dysregulation cause certain autoimmune rheumatic diseases, such as SLE (Zhong et al, 2020).…”

Section: Autoimmunity Post‐covid‐19 Infectionmentioning

confidence: 99%

COVID‐19: A trigger of autoimmune diseases

Zebardast

Hasanzadeh

Shiadeh

et al. 2023

Cell Biology International

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The SARS‐coronavirus‐2 (SARS‐CoV‐2) that causes coronavirus disease 2019 (COVID‐19), has spread worldwide and caused a global health emergency. SARS‐CoV‐2 is a coronaviridae virus that infects target cells by interacting with the plasma membrane‐expressed angiotensin‐converting enzyme 2 (ACE2) via the S1 component of the S protein. Effective host immune response to SARS‐CoV‐2 infection, which includes both innate and adaptive immunity, is critical for virus management and elimination. The intensity and outcome of COVID‐19 may be related to an overabundance of pro‐inflammatory cytokines, which results in a “cytokine storm” and acute respiratory distress syndrome. After SARS‐CoV‐2 infection, the immune system's hyperactivity and production of autoantibodies may result in autoimmune diseases such as autoimmune hemolytic anemia, autoimmune thrombocytopenia, Guillain‐Barré syndrome, vasculitis, multiple sclerosis, pro‐thrombotic state, and diffuse coagulopathy, as well as certain autoinflammatory conditions such as Kawasaki disease in children. We have reviewed the association between COVID‐19 and autoimmune disorders in this article.

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Section: Autoimmunity Post‐covid‐19 Infectionmentioning

confidence: 99%

COVID‐19: A trigger of autoimmune diseases

Zebardast

Hasanzadeh

Shiadeh

et al. 2023

Cell Biology International

View full text Add to dashboard Cite

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In vivo CNS infection model of Acanthamoeba genotype T4: the early stages of infection lack presence of host inflammatory response and are a slow and contact-dependent process

et al. 2016

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This study was developed in order to describe the early morphological events observed during the invasion of two pathogenic strains of Acanthamoeba (genotype T4); A. castellanii and A. culbertsoni, at the olfactory meatus and cerebral, pulmonary, renal, hepatic and splenic tissues levels, an in vivo invasion study. Histological and immunohistochemical description of the events at 24, 48, 72, and 96 h postintranasal inoculations of BALB/c mice was performed. A. castellanii showed a higher invasion rate than A. culbertsoni, which was only able to reach lung and brain tissue in the in vivo model. The current study supports previous evidence of lack of inflammatory response during the early stages of infection. Acanthamoeba invasion of the CNS and other organs is a slow and contact-dependent process. The early morphological events during the invasion of amoebae include the penetration of trophozoites into different epithelia: olfactory, respiratory, alveolar space, and renal tubule, which resemble the process of amoebae invasion described in corneal tissue. The data suggest that after reaching the nasal epithelium, trophozoites continued invasion, separating and lifting the most superficial cells, then migrating and penetrating between the cell junctions without causing a cytolytic effect on adjacent cells. These results reaffirm the idea that contact-dependent mechanisms are relevant for amoebae of Acanthamoeba genus regardless of the invasion site.

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Various brain-eating amoebae: the protozoa, the pathogenesis, and the disease

Zhang

Cheng

2021

Front. Med.

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Among various genera of free-living amoebae prevalent in nature, some members are identified as causative agents of human encephalitis, in which Naegleria fowleri followed by Acanthamoeba spp. and Balamuthia mandrillaris have been successively discovered. As the three dominant genera responsible for infections, Acanthamoeba and Balamuthia work as opportunistic pathogens of granulomatous amoebic encephalitis in immunocompetent and immunocompromised individuals, whereas Naegleria induces primary amoebic meningoencephalitis mostly in healthy children and young adults as a more violent and deadly disease. Due to the lack of typical symptoms and laboratory findings, all these amoebic encephalitic diseases are difficult to diagnose. Considering that subsequent therapies are also affected, all these brain infections cause significant mortality worldwide, with more than 90% of the cases being fatal. Along with global warming and population explosion, expanding areas of human and amoebae activity in some regions lead to increased contact, resulting in more serious infections and drawing increased public attention. In this review, we summarize the present information of these pathogenic free-living amoebae, including their phylogeny, classification, biology, and ecology. The mechanisms of pathogenesis, immunology, pathophysiology, clinical manifestations, epidemiology, diagnosis, and therapies are also discussed.

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Fatal granulomatous amoebic encephalitis caused by Acanthamoeba in a newly diagnosed patient with systemic lupus erythematosus

Cited by 13 publications

References 3 publications

COVID‐19: A trigger of autoimmune diseases

COVID‐19: A trigger of autoimmune diseases

In vivo CNS infection model of Acanthamoeba genotype T4: the early stages of infection lack presence of host inflammatory response and are a slow and contact-dependent process

Various brain-eating amoebae: the protozoa, the pathogenesis, and the disease

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