Retropharyngeal Abscess and Pott’s Disease Due to Tuberculosis: A Case Report

Introduction: Extrapulmonary mycobacterial infection can lead to vertebral spondylitis and osteomyelitis (Pott’s disease). Retropharyngeal abscess with concurrent spinal osteomyelitis is a rare presentation of tuberculosis in the US. Chart review on a patient was completed, and the relevant published literature was reviewed. Case Presentation: A previously healthy 34-year-old male originally from Sudan presented to an outside hospital with a 2-month history of neck pain, sore throat, odynophagia, fevers, and chills. MRI showed a retropharyngeal abscess and suspected cervical spine osteomyelitis. Acid-fast bacillus (AFB) smear was positive from a neck drain specimen, but sputum was negative. Chest imaging did not show findings consistent with pulmonary tuberculosis. He was treated with rifampin, isoniazid, pyrazinamide, and ethambutol (RIPE) along with moxifloxacin and linezolid due to concern for possible multidrug resistant tuberculosis and transferred to our center for further care. Culture isolated Mycobacterium tuberculosis. CT neck showed vertebral tuberculous osteomyelitis (Pott’s disease) of C1-C3 with a multiloculated retropharyngeal and prevertebral abscess (Figure 1). The patient was taken to the OR for posterior spinal fusion from occiput to C4 and transoral incision and drainage of the abscess. The post-operative course was uneventful, and moxifloxacin and linezolid were discontinued when Xpert MTB/RIF test revealed rifampin susceptibility. At follow-up the patient’s symptoms had resolved. Patient consent was obtained to utilize this case for educational purposes. Conclusions: This report presents the multidisciplinary treatment of this patient requiring infection control measures and antibiotic therapy by infectious disease, posterior spine fusion by orthopedic surgery, and retropharyngeal abscess drainage by otolaryngology

The CSF in neurosarcoidosis contains consistent clonal expansion of CD8 T cells, but not CD4 T cells

The tissue-specific drivers of neurosarcoidosis remain poorly defined. To identify cerebrospinal fluid (CSF) specific, antigen-driven T and B cell responses, we performed single-cell RNA sequencing of CSF and blood cells from neurosarcoid participants coupled to T and B cell receptor sequencing. In contrast to pulmonary sarcoidosis, which is driven by CD4 T cells, we found CD8 T cell clonal expansion enriched in the neurosarcoid CSF. These CSF-enriched CD8 T cells were composed of two subsets with differential expression of EBI2, CXCR3, and CXCR4. Lastly, our data suggest that IFNγ signaling may distinguish neurosarcoidosis from other neurological disorders

Human Herpesvirus 8 (HHV8) Sequentially Shapes the NK Cell Repertoire during the Course of Asymptomatic Infection and Kaposi Sarcoma

The contribution of innate immunity to immunosurveillance of the oncogenic Human Herpes Virus 8 (HHV8) has not been studied in depth. We investigated NK cell phenotype and function in 70 HHV8-infected subjects, either asymptomatic carriers or having developed Kaposi's sarcoma (KS). Our results revealed substantial alterations of the NK cell receptor repertoire in healthy HHV8 carriers, with reduced expression of NKp30, NKp46 and CD161 receptors. In addition, down-modulation of the activating NKG2D receptor, associated with impaired NK-cell lytic capacity, was observed in patients with active KS. Resolution of KS after treatment was accompanied with restoration of NKG2D levels and NK cell activity. HHV8-latently infected endothelial cells overexpressed ligands of several NK cell receptors, including NKG2D ligands. The strong expression of NKG2D ligands by tumor cells was confirmed in situ by immunohistochemical staining of KS biopsies. However, no tumor-infiltrating NK cells were detected, suggesting a defect in NK cell homing or survival in the KS microenvironment. Among the known KS-derived immunoregulatory factors, we identified prostaglandin E2 (PGE2) as a critical element responsible for the down-modulation of NKG2D expression on resting NK cells. Moreover, PGE2 prevented up-regulation of the NKG2D and NKp30 receptors on IL-15-activated NK cells, and inhibited the IL-15-induced proliferation and survival of NK cells. Altogether, our observations are consistent with distinct immunoevasion mechanisms that allow HHV8 to escape NK cell responses stepwise, first at early stages of infection to facilitate the maintenance of viral latency, and later to promote tumor cell growth through suppression of NKG2D-mediated functions. Importantly, our results provide additional support to the use of PGE2 inhibitors as an attractive approach to treat aggressive KS, as they could restore activation and survival of tumoricidal NK cells

Analysis of the spectrotypes of autoantibodies against thyroglobulin in two rat models of autoimmune thyroiditis.

We have studied the isoelectric focusing (IEF) spectrotypes of autoantibodies against thyroglobulin in two rat models of Hashimoto's thyroiditis: (1) AUG strain rats immunized with autologous thyroglobulin in Freund's complete adjuvant; (2) PVG/c strain rats which have been thymectomized and sublethally irradiated. The IEF spectrotypes revealed differences between the two models. The anti-thyroglobulin response in immunized AUG rats is mainly oligoclonal or polyclonal, often with dominant clones in the spectrotype, similar to about 90% of Hashimoto's patients, whereas the response in the PVG/c rat is highly restricted. There were pronounced changes in spectrotype with time in the PVG/c, but not AUG, rats with considerable variation in the lifespan of individual clones. The maximum lifespan of an anti-self secreting B-cell clone in the PVG/c rat, determined by persistence of its clonotype, was at least 16 weeks