Response to Penicillin for Presumed Neurosyphilis in a Patient with Human Immunodeficiency Virus (HIV), a Normal CD4 Count, and an Undetectable Viral Load: A Case Report.

BACKGROUND Neurosyphilis is a bacterial infection of the brain and the spinal cord, caused by Treponema pallidum. Its nonspecific clinical presentation includes cognitive impairment and motor and/or sensory function compromise. Neurosyphilis infections in patients with HIV have increased over the past few years and many cases of neurosyphilis manifest in patients with HIV who have low CD4 T-cell counts and high viral loads (VL). However, there is extremely limited acknowledgement in the literature about neurosyphilis presentations in patients with HIV who have normal CD4 counts. CASE REPORT We present a neurosyphilis and HIV coinfection in a patient with a normal CD4 count and an undetectable VL. A 69-year-old woman with a medical history of HIV was on a prescribed antiretroviral treatment regimen. She presented in the Emergency Room in an unresponsive state, although this had been preceded by a period of rapidly progressive cognitive decline. Her brain computed tomography scan without contrast was unremarkable. Laboratory test results were within normal limits, except for a positive result for the microhemagglutination assay for Treponema pallidum antibodies and rapid plasma regain (RPR) test, which was highly suggestive of neurosyphilis as a presumed diagnosis. She showed remarkable clinical improvement after the initiation of conventional treatment for neurosyphilis, which is a 14-day regimen of intravenous penicillin G. CONCLUSIONS Given the broad neurological manifestations of neurosyphilis and its increasing incidence in patients with HIV, it is important to consider neurosyphilis in the differential diagnosis after ruling out other causes of encephalopathy, especially in patients with an undetectable VL and a normal CD4 count.

Experiences of HIV-related discrimination and consequences for internalised stigma, depression and alcohol use.

Objective: HIV stigma undermines health and well-being of people living with HIV (PLWH). Conceptual work on stigma mechanisms suggests that experiences of stigma or discrimination increase internalised stigma. However, not all PLWH may internalise the HIV discrimination they experience. We aimed to investigate the role of stress associated with events of HIV-related discrimination on internalised HIV stigma, as well as the downstream effects on depressive symptoms and alcohol use severity. Design: 199 participants were recruited from an HIV clinic in the southeastern United States. Main study measures: HIV-related discrimination was assessed using items adapted from measures of enacted HIV stigma and discrimination. Participants rated perceived stress associated with each discrimination item. Internalised HIV stigma was assessed using the internalised stigma subscale of the HIV Stigma Mechanisms Scale. Depressive symptoms were assessed with the Centre for Epidemiological Studies-Depression Index. Alcohol use severity was assessed with the Alcohol Use Disorders Identification Test. Results: In serial mediation models, HIV-related discrimination was indirectly associated with both depressive symptoms and alcohol use severity through its associations with stress and internalised HIV stigma. Conclusions: Understanding the mechanisms through which PLWH internalise HIV stigma and lead to poor health outcomes can yield clinical foci for intervention.

Psychosocial complications of HIV/AIDS-metabolic disorder comorbidities among patients in a rural area of southeastern United States.

As people living with HIV experience longer life-expectancies resulting from antiretroviral therapy, comorbid conditions are increasing, particularly metabolic disorders. There is potential for psychosocial factors such as stigma experiences, depression, and alcohol use to complicate both HIV infection and metabolic disorders, including diabetes mellitus and hyperlipidemia. While the impact of these psychosocial factors on HIV infection alone are widely studied, their role in potentially complicating HIV co-morbid metabolic conditions has received little attention. This study examined the association between HIV-related stigma and depression, and the potential role of alcohol use as a mediating factor in a clinical sample of patients with comorbid HIV infection and metabolic conditions. Results demonstrated that HIV stigma is associated with depression and this relationship is in part accounted for by alcohol use. Our results indicate that interventions aiming to improve the health of people living with HIV and co-morbid metabolic disorders should prioritize addressing alcohol use as it is related to sources of stress, such as stigma, and depression.

Pneumatocele complicating acute hydrocarbon pneumonitis.

We present the radiological images and clinical summary of a patient with hydrocarbon ingestion and aspiration complicated by the development of a large pneumatocele.

Cytomegalovirus vasculitis and mucormycosis coinfection in late-stage HIV/AIDS.

Case reports have previously been published describing various complications of cytomegalovirus (CMV) and mucormycosis in patients with HIV/AIDS. We describe the first case of CMV vasculitis and mucormycosis coinfection resulting in necrotizing myofascial cellulitis in an extremity in late stage HIV/AIDS. In AIDS patients, CMV reactivates when the CD4 count falls to less than 50 cells/microL (normal, 720-1440 cells/microL). Transient episodes of neutropenia in patients with HIV/AIDS who have low CD 4 cell counts are a predisposing factor for mucormycosis. These predisposing conditions were both present in our patient. Our case raises the question of CMV vasculitis leading to tissue ischemia as a possible contributing factor to the mucormycosis superinfection.

Pancreatic abscess secondary to Alcaligenes faecalis.

We report a patient with pancreatic abscesses and necrosis secondary to Alcaligenes faecalis infection. He initially presented with alcohol-induced acute pancreatitis. Twenty days after the initial presentation, he re-presented with increasing pain and was found to have pancreatic necrosis and abscesses. Treatment was initiated with meropenem. Because of persistent fevers, computed tomography-guided drainage was performed. The fluid grew A faecalis resistant to meropenem and the patient continued to be febrile. He recovered only after adequate surgical intervention and appropriate antibiotic coverage. Although this is the first case of A faecalis reported to cause pancreatic abscess, we believe selection of this organism occurred because surgical drainage was delayed while the patient was on the recommended treatment with meropenem. This case emphasizes the need for early surgical drainage of pancreatic abscesses to avoid the selection of such resistant pathogens.

A presumptive case of toxocariasis associated with eosinophilic pleural effusion: case report and literature review.

Human toxocariasis is a helminthozoonosis caused by Toxocara sp. Larval migration of the organism through the tissues can result in eosinophila associated with a broad spectrum of clinical manifestations. We report a case of eosinophilic pleural effusion and CD8 cell deficiency associated with Toxocara sp. The symptoms of this patient responded promptly to a nonsteroidal anti-inflammatory medication (naproxen). This is only the fourth reported case of a pleural effusion associated with Toxocara.

Open-label study of a twice-daily indinavir 800-mg/ritonavir 200-mg regimen in HIV-infected adults failing a protease inhibitor regimen.

There is no standard treatment of HIV-infected patients who fail protease inhibitor (PI)-containing antiretroviral therapy. This open-label, noncomparative 24-week study with a 24-week extension evaluated the efficacy, safety, and tolerability of twice-daily indinavir/ritonavir 800/200 mg plus 2 nucleoside reverse transcriptase inhibitors (NRTIs) in this population. Presented here are the results of the 24-week study. Patients were HIV-infected adults who had prior viral RNA (vRNA) suppression (<400 copies/mL), subsequent failure (> or =400 and < or =100,000 copies/mL) on antiretroviral therapy, and at least one new NRTI available for treatment. The proportions of patients achieving plasma vRNA <400 and <50 copies/mL were analyzed with data as observed (DAO) and intention-to-treat (ITT) models using generalized estimating equations (GEE) or counting noncompleters as failures (NC = F). Mean changes from baseline in vRNA and CD4 cell count were evaluated using DAO and an ITT mixed-model approach. Sixty-three patients (87% male) with a mean age of 42 years and mean baseline vRNA and CD4 cell counts of 3.8 log(10) copies/mL and 360 cells/mm(3), respectively, were enrolled. The proportion (95% confidence interval) of patients achieving vRNA <400 and <50 copies/mL at week 24 were 76% (61%, 87%) and 50% (35%, 65%) for DAO, 64% (50%, 75%) and 43% (30%, 56%) for GEE, and 56% (43%, 68%) and 37% (25%, 50%) for NC = F, respectively. At Week 24, baseline vRNA decreased by >1.0 log(10) copies/mL and CD4 cell counts increased by approximately 90 cells/mm(3). Three patients (5%) experienced serious drug-related adverse events. Seven patients (11%) discontinued treatment due to clinical or laboratory adverse events. In this study, the enhanced, twice-daily regimen of indinavir/ritonavir 800/200 mg plus 2 NRTIs provided suppression of HIV in many patients who had failed a PI-containing regimen and was generally well tolerated.