Search Results (71)

Multicentric reticulohistiocytosis (MRH) is a rare systemic histiocytic disorder of uncertain etiology characterized by papulonodular cutaneous lesions and potentially destructive polyarthritis, with variable multisystem involvement. Owing to its low prevalence, evidence for optimal management remains limited, and treatment responses are heterogeneous. Emerging reports suggest that Janus kinase (JAK) inhibition may provide benefit in refractory disease. We report a 60-year-old woman with MRH presenting with papulonodular skin lesions, symmetric polyarthritis, constitutional symptoms, and interstitial lung disease (nonspecific interstitial pneumonia pattern) in the context of co-existing primary biliary cholangitis and no evidence of malignancy. Prior therapies (glucocorticoids, methotrexate, leflunomide) achieved suboptimal control. Upadacitinib, a selective JAK1 inhibitor, induced rapid and complete remission of cutaneous and articular disease with improvement of pulmonary involvement. Secondary weight gain and incident diabetes were managed with tirzepatide. This case adds to the limited literature supporting JAK inhibition as a targeted option for refractory MRH, including multisystem disease with pulmonary involvement. Systematic evaluation of efficacy, durability, and safety is warranted. Full article

Rheumatoid arthritis (RA) is a chronic autoimmune rheumatic disease of unknown etiolgy, characterized by erosive polyarthritis that leads to joint destruction and systemic inflammatory lesions in internal organs. Pain is a primary symptom of RA and a major contributor to psychological disturbances, which influence patients’ subjective evaluation of their condition. These psychological issues may stem from disruptions in central pain regulation mechanisms, such as central sensitization (CS), which can also affect central metabolic processes. The objective was to investigate how the severity of central sensitization, measured by the Central Sensitization Inventory (CSI) questionnaire (Part 1), impacts clinical and neuropsychiatric parameters, as well as the expression of genes related to inflammation, tissue destruction, carbohydrate metabolism, and fatty acid metabolism in peripheral blood mononuclear cells (PBMCs) in patients with RA. Methods involved collecting blood samples from 59 RA patients (mean age 52.0 years). Clinical status was assessed using the DAS28 index and serum levels of CRP, ASPA, and RF. Neuropsychiatric parameters were evaluated through questionnaires measuring CS severity score (CSI), pain intensity (VAS, BPI), neuropathic pain (PainDETECT), anxiety and depression (HADS), fatigue (FSS, FACIT-F), fibromyalgia symptoms (FIRST), and pain catastrophizing. Protein expression in PBMCs was measured by ELISA, while gene expression was analyzed using quantitative real-time RT-PCR. All patients exhibited moderate to high disease activity. Participants were divided into four subgroups according to their CSI scores: subclinical (0–29 points), mild (30–39 points), moderate (40–49 points), and severe/extreme (50–100 points). Higher CSI scores correlated with significant increases in neuropsychiatric symptoms and a notable decrease in vitality. However, clinical parameters showed no significant differences among the subgroups. Gene expression analysis revealed upregulation of genes involved in the pentose phosphate pathway (G6PD), antioxidant defense (SOD1), fatty acid metabolism (FASN, CPT1B), apoptosis (CASP3), and tissue destruction and hypernociception (MMP-9) compared to healthy controls. The pro-inflammatory cytokine IL-1β expression was comparable to controls, while TNFα expression was elevated only in patients with severe/extreme CS scores. These findings suggest that CS-related disturbances may contribute to increased disease severity in RA, even in patients receiving active antirheumatic treatment. At the cellular level, disease severity appears linked to dysregulated expression of genes governing central metabolic processes, despite low expression of pro-inflammatory cytokine genes. Full article

Mycoplasma hyosynoviae is a significant pathogen in swine populations, contributing to polyarthritis and lameness in growing pigs. This study characterizes the clinical presentation, pathogen detection, immune response, and lesion development following experimental inoculation with two distinct M. hyosynoviae strains. Pigs were inoculated with either a low- or high-virulence strain and monitored for 18 days. Lameness was observed throughout the study, with affected pigs exhibiting mild to moderate clinical signs. M. hyosynoviae was often detected in the tonsils, while detection in oral fluids was transient. Serum IgG levels increased significantly in the inoculated groups. IL-1β, IL-6, and TNF-α cytokines were elevated only at 7 DPI, whereas IL-8, IL-10, and IFN-γ levels were unchanged in both inoculated groups. Notably, only pigs inoculated with the high-virulence strain developed lesions, and M. hyosynoviae was detected only in the synovial fluid by PCR from this group. These findings highlight strain-dependent differences in the pathogenesis of M. hyosynoviae. The pathological differences between these strains suggest variations in adherence factors, immune evasion capabilities, or metabolic adaptability. Further research is warranted to elucidate the genetic determinants of virulence and the protective role of humoral and cellular immune responses in M. hyosynoviae infection. Full article

Introduction/Objectives: Restless legs syndrome (RLS), a chronic neurological disorder related to brain iron metabolism, has been linked to immune-mediated inflammatory conditions such as psoriatic arthritis (PsA). However, the role that inflammation plays in this association and the impact of RLS on PsA outcomes remain unclear. This study aims to investigate the association between RLS and inflammatory/clinical parameters in PsA patients. Materials and Methods: In this cross-sectional study, 230 PsA patients completed the International Restless Legs Syndrome Study Group (IRLSSG) screening questionnaire, with diagnoses confirmed by a neurologist. Data collected included clinical features, disease activity, and comorbidities (obesity, anxiety, depression, insomnia, and fibromyalgia). Results: In total, forty-six patients met the IRLSSG criteria (20%). Those with RLS more frequently had polyarthritis (27% vs. 6%; p < 0.001), more swollen joints (2.0 vs. 1.4; p = 0.04), greater psoriatic involvement (5.7 vs. 3.6; p < 0.001), greater fatigue (39.0 vs. 30.5; p < 0.001), and greater disease activity (14.5 vs. 10.5; p < 0.001). They also exhibited increased disease impact (4.7 vs. 2.9; p < 0.001), poorer functioning (0.7 vs. 0.5; p = 0.01), and higher levels of anxiety (8.0 vs. 5.5; p < 0.001), depression (6.5 vs. 3.9; p < 0.001), and sleep disturbance (13.9 vs. 8.7; p < 0.001). Skin lesions and polyarthritis explained nearly 40% of RLS cases (Odds Ratio (OR) 1.4; 95% Confidence Interval (CI) 1.03–2.0; p = 0.03 and OR 1.03; 95% CI 1.00–1.9; p = 0.04). Conclusions: Psoriatic activity and inflammation may contribute to RLS in PsA. The coexistence of RLS was associated with greater disease activity, greater disease impact, and more emotional and sleep-related comorbidities. Full article

Background: Primary Sjogren Disease (pSD) is a chronic autoimmune disease characterized by a classic triad of keratoconjunctivitis sicca, xerostomia, and polyarthritis. The primary pathological feature of pSD is lymphoplasmacytic infiltration in glandular epithelial tissue, often affecting the salivary and lacrimal glands, leading to classic sicca symptoms (ocular and oral dryness). Sjogren Disease (SD) can be categorized as “primary” when occurring independently or “secondary” when accompanying another autoimmune connective tissue disorder such as rheumatoid arthritis, systemic lupus erythematosus, or systemic sclerosis. Additionally, systemic disease is common in pSD and can manifest with kidney dysfunction resulting in nephrolithiasis and distal renal tubular acidosis (dRTA). Methods: This report details a case series drawing patients from the literature as well as patients from our institution which serves to demonstrate key points in clinical hallmarks. We utilize a literature search with key words Sjogren Disease, nephrolithiasis, renal tubular acidosis, and nephrocalcinosis in addition to pSD patients with concomitant nephrolithiasis at our institution to characterize clinical and serologic findings as well as treatment modalities. Results: We find well demonstrated clinical hallmarks such as female predominance and presence of dRTA amongst the cohort of pSD patients. We also find that further research on pSD serologies could prove beneficial in risk stratifying those most likely to develop renal disease and nephrolithiasis. Furthermore, we review signs, symptoms, pathophysiology, and management of SD with added emphasis on associated renal disease including nephrolithiasis and dRTA. Conclusion: Overall, pSD associated renal disease remains an area of ongoing research and further study on patient serologies may aid clinicians in better serving and surveilling patients at risk of systemic involvement. Full article

Introduction: In hemoglobinopathies, the amount of globin synthesis in hemoglobin (Hb) or its structure is altered. Clinical features are related to the rate and kind of structural aberrations. The heterozygous form of the Lepore syndrome resembles minor thalassemia both clinically and hematologically. On electrophoresis, abnormal Hb Lepore fractions are found at a rate of 5–15%, with a mildly higher percentage of HbF and lower HbA. In general, Hb Lepore heterozygotes are asymptomatic. Case presentation: A 32-year-old male was admitted to our hospital with complaints of pain and swelling in multiple large joints and high-grade fever for 11 days. His past history was unremarkable; one of his sisters had the β-thalassemia trait. On physical examination, he was moderately anemic, with mild hepatomegaly and normal spleen; both knees and ankles were tender and swollen. Laboratory showed mild microcytic hypochromic anemia with variables similar to the thalassemia trait and signs of inflammation with very high CRP, serum ferritin, and leukocytosis. Blood sugars were increased. Hb electrophoresis showed an abnormal pattern with mild elevation in HbS, normal Hb F, mild reduction in HbA, and high HbA2, compatible with heterozygosity for the Hb Lepore beta chain variant. He was initially diagnosed with diabetes (treated with insulin) and sepsis from unknown origin, but fever and joint pains did not respond to NSAIDs or antibiotics. He had very good response on high-dose methylprednisolone. Undifferentiated arthritis was diagnosed in the patient with Hb Lepore, and he was treated with oral prednisolone and sulfasalazine (SSZ). At follow up, the patient was doing well. He refused further investigations and did not allow testing on his family members. In summary: Hb Lepore is a rare hemoglobinopathy linked to thalassemia, which may manifest with musculoskeletal problems. Our patient with the Hb Lepore trait presented with undifferentiated polyarthritis and fever, but in our case, a causal relationship remains unclear. This is one of the first adult cases of Hb Lepore in Bangladesh and the first with arthritis of unknown origin. The prevalence of Hb Lepore in Bangladesh is unknown. Full article

Background and Aim: Rheumatoid arthritis (RA) is a chronic inflammatory polyarthritis of unknown etiology that symmetrically involves the synovial joints and leads to erosive arthritis. However, when inflammation remains uncontrolled, it not only affects the joints but also increases the risk of various systemic complications, particularly cardiovascular diseases, osteoporosis, and malignancies such as lymphoma. Early initiation of disease-modifying antirheumatic drugs (DMARDs) has been shown to yield superior outcomes in terms of both clinical response and the prevention of joint damage. Nevertheless, the development of hepatotoxicity during treatment may necessitate dose adjustments or even modifications of the therapeutic protocol. Our aim in this study was to retrospectively evaluate the changes in liver enzyme levels in RA patients before and during treatment, especially in MTX and combination therapies using MTX, and to evaluate how these abnormalities affect treatment strategies. Materials and Methods/Results: Among the 33 patients included in this study, 15 exhibited elevated liver enzymes prior to treatment, whereas 18 developed hepatic enzyme abnormalities during therapy. Of the 12 patients receiving methotrexate (MTX) monotherapy and the 15 patients using MTX within a combination regimen, a total of 7 patients (21%) continued to present with elevated liver enzymes during follow-up. Among these, 5 patients (19%) were managed successfully by reducing the MTX dose, while MTX therapy had to be completely discontinued in 2 patients (7%). Notably, all 7 patients who required treatment modification due to persistent enzyme elevation belonged to the group with pre-existing liver enzyme abnormalities and were receiving MTX as part of a combination therapy regimen. Conclusions: These findings indicate that hepatotoxicity risk in RA patients can be effectively managed through close laboratory monitoring and timely dose reduction, with treatment discontinuation being required only in rare cases. Full article

Rheumatoid arthritis (RA) is the most common inflammatory polyarthritis. In addition, 60–80% of patients express anti-citrullinated protein antibodies (ACPAs), which serve as a diagnostic marker for RA. The effector functions of these autoantibodies can be heavily affected by the N-glycosylation of their Fc region. Here we present a comparison of the Fc N-glycosylation of ACPA IgG to that of non-ACPA IgG from the same patients, and of healthy controls, in an IgG isoform-specific manner. We isolated ACPA and normal serum IgG, digested by trypsin, and separated the resulting peptide mixture by a reversed-phase nanoLC coupled to a Bruker Maxis II Q-TOF, and determined the relative abundance of glycoforms. The paired analysis of galactosylation and sialylation of the IgG subclasses of ACPA and non-ACPA IgG has shown a significant, moderate negative correlation with the inflammatory markers, the level of C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR), as well as with rheuma-factor (RF), but not with the disease activity score (DAS) or cyclic citrullinated peptide specific antibodies (anti-CCP). However, we detected a significant negative correlation between glycosylation and DAS in the non-ACPA IgG fractions. Furthermore, the isoform-specific analysis revealed additional insight into the changes of the glycosylation features of IgG in RA: changes in the frequencies of the bisecting GlcNAc unit between sample groups could be explained by only the IgG1 isoform; while invariance in fucosylation is the result of the superposition of two isoforms with opposite changes. These results highlight the importance of analyzing immunoglobulin glycosylation in an isoform-specific manner. Full article

Background/Objectives: Infection with the Chikungunya virus (CHIKV) results in acute febrile diseases with severe polyarthritis, which can be followed by chronic rheumatic disease and long-term disability. To evaluate cytokine profiles in acute and chronic CHIKV infection and examine the relationship with clinical outcomes, including persistent musculoskeletal symptoms. Methods: Literature search was carried out systematically using electronic databases (PubMed, Embase, Scopus, and Google Scholar). Studies that met eligibility criteria were observational or intervention cohorts that measured levels of cytokines/chemokines in laboratory-confirmed CHIKV patients in acute (<3 months) or chronic (>3 months) phases. Data was extracted on the study design, population, biomarkers, and clinical outcomes. As the assays were not homogeneous in terms of timing, outcome, and definitions, the findings were synthesized in narrative form using tabular representation. Results: A total of 21 studies, including 4216 participants, were incorporated. In acute CHIKV, interleukin-6 (IL-6) (reported to be elevated in 81% of studies), IL-8 (77%), TNF-α (65%), and IFN-γ (60%) were most consistently increased, alongside interferon-inducible chemokines CXCL10/IP-10 and MCP-1. Chronic-phase cohorts showed persistent elevation of IL-6 (69%), IL-8 (63%), TNF-α (58%), and IL-17 (41%), especially among patients with prolonged arthralgia or arthritis. Chronic musculoskeletal symptoms were reported in 25–65% of cases, with some persisting beyond five years. A high degree of heterogeneity was observed in assay procedures and time of sampling. Conclusions: CHIKV infection is characterized by acute inflammatory surges and, in some cases, persistent cytokine dysregulation linked to chronic arthritis. These results showed the importance of prognostic biomarkers and targeted therapy. Full article

The aim of the paper was to characterize rheumatoid factor IgA, IgG, and IgM isotypes in patients with Sjögren’s syndrome (SS) subsets, based on the absence or presence of joint complaints of different etiologies. In total, 164 SS patients were grouped based on whether they had polyarthritis as an extraglandular manifestation (n = 73, SS+pa), rheumatoid arthritis as an associated autoimmune disorder (n = 46, SS+RA), or Sjögren’s syndrome without inflammatory joint pain (n = 45, SS). The highest IgA rheumatoid factor isotype levels were detected in SS patients, whereas the lowest levels were found in the SS+RA group, without a significant difference. Neither IgG nor IgM RF differed significantly between the patient subclasses. In addition to other disease-specific markers, seropositive patients who were seropositive for any RF isotype were significantly more frequently anti-Ro/SS-A and anti-La/SS-B positive and had higher ESSDAI levels. In SS and SS+pa patients, a strong negative correlation was observed between IgA RF and age, whereas a strong positive correlation was found between IgA RF and ESSDAI, RF, IgA, IgG, anti-Ro/SS-A, and anti-La/SS-B levels. High total IgG levels together with high IgA RF levels occurred most frequently in SS patients (p = 0.05), whereas the combination of normal IgG and high IgM RF was significantly more frequent in the SS+RA group. The co-occurrence of high total IgG and normal IgM RF did not differ significantly between the patient subsets; however, this was the combination with the highest sensitivity (94.5%) for SS+pa patients. Based on our findings, rheumatoid factor isotypes have an additive value in the differentiation of non-erosive polyarthritis and erosive rheumatoid arthritis during the disease course of patients with Sjögren’s syndrome. All rheumatoid factor isotypes predict a more severe disease course, but IgA RF may serve as a candidate for being an early, poor prognostic factor for SS patients. Full article

We used the Queensland acute rheumatic fever (ARF) and rheumatic heart disease (RHD) register to describe the clinical phenotype and the characteristics of individuals diagnosed with ARF in Far North Queensland, Australia, between January 2012 and December 2023. There were 830 episodes of ARF in 740 individuals during the study period; 785/830 (95%) episodes occurred in First Nations Australians and 696/824 occurred in areas of socioeconomic disadvantage. There was no significant change in the overall incidence of ARF during the study period (Spearman’s rho = 0.51, p = 0.09). The median (interquartile range) age of the cohort was 15 (10–23) years, although 276/830 (33%) episodes of ARF occurred in individuals ≥ 20 years. Individuals with carditis, polyarthritis, an abnormal electrocardiogram, fever and elevated inflammatory markers were more likely to have confirmed ARF. The presence of polyarthralgia, monoarthritis or skin manifestations was not associated with a diagnosis of confirmed ARF. Individuals with monoarthralgia were less likely to have confirmed ARF. At the end of the study period, 264/706 (37%) individuals who had access to echocardiography had confirmed RHD. Individuals who did not have echocardiography documented as a component of their initial episode of care were more likely to have severe RHD at the end of the study (25/339 (7%) versus 7/401 (2%), p < 0.0001). ARF and RHD continue to be diagnosed in First Nations Australians in tropical Australia. It seems unlikely that Australia will achieve its stated aim of eliminating RHD by 2031. Full article

Rheumatoid arthritis (RA) is a chronic, common autoimmune disease. It is characterized by inflammatory polyarthritis, which can lead to permanent disability in patients. Current treatment is mainly symptom-related, aiming to reduce pain and inflammation, but does not lead to a full recovery. This treatment includes non-steroidal anti-inflammatory drugs (NSAIDs) and disease-modifying anti-rheumatic drugs (DMARDs). It has been shown that, due to chronic inflammation, reduced glucose levels and hypoxia, endoplasmic reticulum (ER) stress is induced in RA patients, leading to the activation of multiple signaling pathways, including the ER-dependent adaptation of the unfolded protein response (UPR) pathway. The aim of this study was to assess the level of apoptosis in patients diagnosed with RA. The study sought to investigate whether UPR response correlated with apoptosis induction could serve as a potential diagnostic marker or therapeutic target. In vitro studies have shown that UPR pathway activity can be observed in patients diagnosed with RA. The study group consisted of PBMC cells from 61 individuals, including a total of 31 rheumatoid arthritis patients and 30 healthy controls. In order to validate UPR activation, we estimated molecular markers of ER stress via RT-qPCR expression analysis. GAPDH expression was used as a standard control. Elevated levels of mRNA for the eIF2α (p-value = 0.001903), the BBC3 (PUMA) (p-value = 0.007457 × 10⁻⁷) and the TP53 (p-value = 0.002212) were confirmed in a group of RA patients. Further analysis showed that after the induction of apoptosis the percentage of DNA contained in the tail was 37.78% higher in RA patients than in the control group (p-value = 0.0003) measured by comet assay. The exogenous damage caused by hydrogen peroxide was found to be statistically elevated in RA patients and the caspase-3 level was calculated of 40.17% higher than in controls (p-value = 0.0028). It was also found that PBMC cells from RA patients were more sensitive to apoptotic induction. Our results were confirmed by flow cytometry. The most important finding from our data was the confirmation of elevated sensitivity to apoptosis induction in RA patients; the results showed a 40.23% higher percentage of cells in early apoptosis than in the control group (p-value = 0.0105). Our results may help to assess the feasibility of the application of early diagnosis and targeted therapy in the treatment of RA patients, including the ER signaling pathway via selected UPR-dependent molecular inhibitors. Full article

Rheumatoid arthritis (RA) is an immune-mediated disease characterized by polyarthritis that affects the small joints of the bilateral upper and lower extremities. RA shares several common clinical symptoms with Sjögren’s syndrome (SS), another rheumatic disease caused by the lymphocytic infiltration of exocrine glands, with dry eye and dry mouth being the two most common symptoms. Anti-Ro/SS-A antibodies, a diagnostic biomarker of SS, are positive in patients with RA at a certain rate. The coexistence of SS and/or positivity for anti-Ro/SS-A antibodies in patients with RA influences disease activity and the effectiveness of several classes of disease-modifying antirheumatic drugs (DMARDs). Furthermore, RA, SS, and certain DMARDs, including methotrexate, are associated with the onset of lymphoproliferative disorders (LPD). In contrast, several biological DMARDs, such as tocilizumab and rituximab, are plausible options without the risk of LPD relapse. Considering the results of the studies introduced in this article, RA with SS and/or positivity for anti-Ro/SS-A antibodies could be considered a phenotype different from isolated RA from the perspective of refractoriness to DMARD therapy and LPD risk. Hence, rheumatologists should observe caution when choosing DMARDs. Further studies are needed to establish the appropriate treatment for patients with RA, SS, and/or the presence of anti-Ro/SS-A antibodies. Full article

Background: Native knee joint infections, while uncommon, present a serious condition predominantly instigated by bacteria such as Staphylococcus aureus. Without timely intervention, they can result in joint destruction or sepsis, with risk factors encompassing preexisting medical conditions and iatrogenic procedures. The diagnostic process includes a comprehensive patient history, clinical evaluation, laboratory testing, imaging studies, and microbiological investigations. Treatment typically involves joint aspiration and arthroscopy. This study aims to examine and establish correlations between diagnostic criteria and treatment modalities, enhancing the speed and specificity of future therapeutic strategies. Materials and methods: The present study is a retrospective cohort study conducted at a 1200-bed university clinic between 2007 and 2017, with an in-depth examination of patient details, symptoms, treatments, and outcomes. A scoring system was developed to classify the severity of knee joint impairment, categorizing patients on the basis of hospital stay duration, surgeries, and postoperative factors such as recurring symptoms, pain, and range of motion. Results: This study of 116 patients with knee joint infections revealed that clinical symptoms such as pain, swelling, and effusion are common but not definitive for diagnosis. Laboratory analysis revealed no significant differences in CRP or leukocyte counts between cultures positive or negative for pathogens. Hospital stay and disease severity are influenced by factors such as age, sex, presence of polyarthritis, neutrophil count, and type of pathogen, with higher weight and cortisone treatment associated with poorer outcomes. Conclusions: This study highlights the diagnostic challenges in native knee joint infections, revealing the need for comprehensive approaches given the nonspecificity of clinical symptoms and laboratory findings. This underscores the importance of advancing research through standardized methodologies and prospective studies to increase the accuracy of diagnosis and the effectiveness of treatment in this field. Full article

The black skimmer (Rynchops niger) is a state-threatened, colonially nesting seabird in Florida, USA. Conservation threats include habitat alteration, human disturbances, severe weather, and predation. During nest monitoring (May–September, 2020–2022), black skimmer juveniles at colonies on Fort Myers Beach and Marco Island, Florida, had polyarthritis and died or were euthanized due to severe illness. Similarly-aged skimmers from geographically distant (considered unaffected) colonies were evaluated for comparison (2021–2023). We documented field, clinical, radiographical, and pathological findings to characterize disease and purported pathogenesis. The majority were lame and lethargic, in poor nutritional condition, and dehydrated. Additionally, 8/23 of the skimmers with dermatitis and arthritis from affected colonies also had penetrating sandspurs associated with skin ulceration, scabbing, and/or hemorrhage. The affected joints were often in limbs (interphalangeal and hock; less commonly stifle, elbow, carpus). A postmortem evaluation and bacteriology revealed Staphylococcal aureus-associated dermatitis, arthritis, tenosynovitis, and/or osteomyelitis in 21/22 of the juvenile skimmers from southwestern nest colonies. Staphylococcus aureus dissemination to internal organs occurred in 10/13 of the skimmers tested. Among skimmers evaluated from distant colonies, 5/10 that were examined histologically had skin crusting and inflammation but lacked arthritis. Occasional coinfections were documented (e.g., West Nile virus, Gram-negative bacilli). The results suggest that staphylococcal joint disease originated from sandspur-induced skin damage, followed by hematogenous dissemination to the joints and, occasionally, the internal organs. Additional nest sites should be tested to evaluate disease risk and potentially contributing environmental factors. We recommend that site managers employ techniques that reduce the risk of skimmer interactions with sandspurs. Full article