Neurobrucellosis presenting with mania

Akçay, Halil İbrahim; Kürtüncü, Murat; Celik, Senay Yidiz; Gündüz, Tuncay; Eraksoy, Mefküre

doi:10.1007/s13760-016-0648-8

Cited by 3 publications

(5 citation statements)

References 2 publications

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“…In this scenario, B. abortus-infected microglia would then cause a slow, progressive loss of neurons by primary phagocytosis in the CNS milieu. This damage could explain the neurological deficits observed during neurobrucellosis (Akcay, Kurtuncu, Celik, Gunduz, & Eraksoy, 2016;Giambartolomei et al, 2008;Nalini et al, 2012;Pappas et al, 2005). If, as we hypothesized, neuronal death is at the root of the neurocognitive symptoms observed in neurobrucellosis, then blocking microglial phagocytosis may be a significant therapeutic approach for the treatment of this form of the disease.…”

Section: Discussionmentioning

confidence: 72%

“…It has been postulated that phagoptosis may dominate in conditions in which TLRs are activated but pro-inflammatory cytokine levels are relatively low. This damage could explain the neurological deficits observed during neurobrucellosis (Akcay, Kurtuncu, Celik, Gunduz, & Eraksoy, 2016;Giambartolomei et al, 2008;Nalini et al, 2012;Pappas et al, 2005). Brucella organisms provoke chronic infections characterized by an inflammatory response.…”

Section: Discussionmentioning

confidence: 99%

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Brucella abortus‐activated microglia induce neuronal death through primary phagocytosis

Rodrı́guez

Delpino

Miraglia

et al. 2017

Glia

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Inflammation has long been implicated as a contributor to pathogenesis in neurobrucellosis. Many of the associated neurocognitive symptoms of neurobrucellosis may be the result of neuronal dysfunction resulting from the inflammatory response induced by Brucella abortus infection in the central nervous system. In this manuscript, we describe an immune mechanism for inflammatory activation of microglia that leads to neuronal death upon B. abortus infection. B. abortus was unable to infect or harm primary cultures of mouse neurons. However, when neurons were co-cultured with microglia and infected with B. abortus significant neuronal loss occurred. This phenomenon was dependent on TLR2 activation by Brucella lipoproteins. Neuronal death was not due to apoptosis, but it was dependent on the microglial release of nitric oxide (NO). B. abortus infection stimulated microglial proliferation, phagocytic activity and engulfment of neurons. NO secreted by B. abortus-activated microglia induced neuronal exposure of the "eat-me" signal phosphatidylserine (PS). Blocking of PS-binding to protein milk fat globule epidermal growth factor-8 (MFG-E8) or microglial vitronectin receptor-MFG-E8 interaction was sufficient to prevent neuronal loss by inhibiting microglial phagocytosis without affecting their activation. Taken together, our results indicate that B. abortus is not directly toxic to neurons; rather, these cells become distressed and are killed by phagocytosis in the inflammatory surroundings generated by infected microglia. Neuronal loss induced by B. abortus-activated microglia may explain, in part, the neurological deficits observed during neurobrucellosis.

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Section: Discussionmentioning

confidence: 72%

Section: Discussionmentioning

confidence: 99%

Brucella abortus‐activated microglia induce neuronal death through primary phagocytosis

Rodrı́guez

Delpino

Miraglia

et al. 2017

Glia

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“… 8 Furthermore, in another case study, the patient was diagnosed as a case of mania for a long period of time before reaching the diagnosis of neurobrucellosis. 9 …”

Section: Discussionmentioning

confidence: 99%

“…8 Furthermore, in another case study, the patient was diagnosed as a case of mania for a long period of time before reaching the diagnosis of neurobrucellosis. 9 Neurobrucellosis treatment plan should be fast and effective owing to the nature of the pathology. Treatment should include long-term antibiotics with adequate neuromeningeal diffusion, and it is typically based on a mixture of 2 or 3 antibiotics.…”

Section: Therapeutic Interventionmentioning

confidence: 99%

Unusual presentation of neurobrucellosis in Jeddah, Kingdom of Saudi Arabia

Kanjo

Ahmed

Alnahari

2021

NSJ

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A 35-year-old female without any history of medical or psychiatric illness. One month prior to presenting to our clinic, she had intermittent headaches, night sweats, and muscle pain that went unnoticed by her. A week later, the patient developed agitation and behavioral changes. The patient was admitted through emergency room (ER) to the psychiatry unit for 3 days. During a detailed interview in the Neurology Clinic 10 days post discharge, she described the previously mentioned symptoms. Her cerebrospinal fluid analysis revealed leukocytosis, with normal protein and glucose, and positive brucella titers in blood. She received antibiotics for neurobrucellosis with frequent follow ups. Repeated spinal tap was reported normal. Her symptoms gradually improved. Neuropsychiatric manifestations are an unusual presentation of brucellosis. This case emphasizes the importance of considering an organic cause, such as neurobrucellosis, as a differential diagnosis in patients with new onset of unexplained neuropsychiatric symptoms in endemic countries like Kingdom of Saudi Arabia.

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“…However, sputum and CSF microscopy along with the PCR test can help rule out tuberculosis 14 . Similarly, schizophrenia and affective disorder may be other common differentials 15,16 . However, if a detailed history is taken, these psychiatric illnesses can be easily ruled out.…”

Section: Discussionmentioning

confidence: 99%