Extensive Vasculitis Research Articles

E025 From risk to reward: a case of systemic antineutrophilic cytoplasmic antibody associated vasculitis

Abstract Background/Aims The background and aims of this case involve a 70-year-old female patient with a history of complex medical conditions, including bronchiectasis and dementia, who initially presented with respiratory symptoms and fever. The primary aim was to understand the underlying cause of her deteriorating condition, which did not respond to initial antibiotic treatment for suspected pneumonia. Subsequent diagnostic efforts, including extensive vasculitis workup, were undertaken to identify the source of her symptoms, which led to the discovery of positive PR3 results and elevated inflammatory markers. The key goal was to determine the most effective treatment strategy, considering the patient’s unique medical history, balancing the need for immunosuppressive therapy against the potential risks of exacerbating underlying infections. The case ultimately aimed to demonstrate the successful management of the patient’s complex clinical presentation through a multidisciplinary approach, including immunosuppressive therapy and supportive care, resulting in significant improvements in her neurological and functional status. Methods We conducted a comprehensive assessment of a 70-year-old patient with ANCA-associated vasculitis (AAV) involving the central nervous system (CNS) and cutaneous manifestations. Lab tests targeted PR3-positive ANCA, and imaging assessed disease extent. A multidisciplinary team designed a tailored treatment plan with cyclophosphamide, closely monitoring progress. Ethical considerations were adhered to, and a literature review provided context. Data analysis evaluated treatment efficacy, leading to a discussion of lessons learned in managing complex AAV cases. Results We documented the remarkable trajectory of a 70-year-old patient with ANCA-associated vasculitis (AAV) presenting with central nervous system (CNS) involvement and cutaneous manifestations. With a meticulous and tailored treatment plan involving the judicious use of cyclophosphamide, we witnessed a profound recovery marked by significant improvements in both motor and cognitive function. This case underscores the importance of balancing potent immunosuppression with the imperative to curb disease progression and mitigate treatment-associated repercussions in complex AAV presentations. The patient’s restoration to baseline functioning serves as a compelling testament to the potential of precision medicine in managing intricate clinical scenarios of AAV. Our findings emphasize the need for continued awareness and consideration of individualized treatment approaches in similar cases, offering hope and insights for improved outcomes in challenging AAV presentations. Conclusion This case offers valuable lessons on the complexities and challenges involved in diagnosing and managing a multi-faceted condition like AAV. It emphasizes the urgent need for a timely and accurate diagnosis, especially when presented with atypical cases involving the central nervous system and cutaneous manifestations. Moreover, the case enriches our understanding of AAV and contributes insights into its nuanced management. It calls for a sophisticated, patient-centered approach, informed by cutting-edge research, to optimize patient outcomes in this challenging clinical scenario. Disclosure A.J. AlZeera: None. D. Gurdeep: None.

The innate immune receptor Nlrp12 suppresses autoimmunity to the retina

BackgroundNod-like receptors (NLRs) are critical to innate immune activation and induction of adaptive T cell responses. Yet, their role in autoinflammatory diseases of the central nervous system (CNS) remains incompletely defined. The NLR, Nlrp12, has been reported to both inhibit and promote neuroinflammation in an animal model of multiple sclerosis (experimental autoimmune encephalomyelitis, EAE), where its T cell-specific role has been investigated. Uveitis resulting from autoimmunity of the neuroretina, an extension of the CNS, involves a breach in immune privilege and entry of T cells into the eye. Here, we examined the contribution of Nlrp12 in a T cell-mediated model of uveitis, experimental autoimmune uveitis (EAU).MethodsMice were immunized with interphotoreceptor retinoid-binding protein peptide 1–20 (IRBP1–20) emulsified in Complete Freund’s adjuvant, CFA. Uveitis was evaluated by clinical and histopathological scoring, and comparisons were made in WT vs. Nlrp12−/− mice, lymphopenic Rag1−/− mice reconstituted with WT vs. Nlrp12−/− CD4+ T cells, or among bone marrow (BM) chimeric mice. Antigen-specific Th-effector responses were evaluated by ELISA and intracellular cytokine staining. Cellular composition of uveitic eyes from WT or Nlrp12−/− mice was compared using flow cytometry. Expression of Nlrp12 and of cytokines/chemokines within the neuroretina was evaluated by immunoblotting and quantitative PCR.ResultsNlrp12−/− mice developed exacerbated uveitis characterized by extensive vasculitis, chorioretinal infiltrates and photoreceptor damage. Nlrp12 was dispensable for T cell priming and differentiation of peripheral Th1 or Th17 cells, and uveitis in immunodeficient mice reconstituted with either Nlrp12−/− or WT T cells was similar. Collectively, this ruled out T cells as the source of Nlrp12-mediated protection to EAU. Uveitic Nlrp12−/− eyes had more pronounced myeloid cell accumulation than uveitic WT eyes. Transplantation of Nlrp12−/− BM resulted in increased susceptibility to EAU regardless of host genotype, but interestingly, a non-hematopoietic origin for Nlrp12 function was also observed. Indeed, Nlrp12 was found to be constitutively expressed in the neuroretina, where it suppressed chemokine/cytokine induction.ConclusionsOur data identify a combinatorial role for Nlrp12 in dampening autoimmunity of the neuroretina. These findings could provide a pathway for development of therapies for uveitis and potentially other autoinflammatory/autoimmune diseases of the CNS.

Past COVID-19 infection and feasibility of transcatheter aortic valve replacement in a patient with severe aortic stenosis (a clinical case study)

A fatal case of severe stenosis of the aortic orifice in a patient with not diagnosed in time, long-term persistent covid infection is presented. The patient was hospitalized to resolve the issue of surgical correction of the aortic stenosis. On admission, there were symptoms of circulatory failure at the level of 3–4 functional class according to NYHA and angina pectoris clinic. A detailed collection of anamnesis about the epidemiological environment and symptoms of pneumonia suffered in the fall of 2020 raised suspicions of its covid genesis. Subsequently, this assumption was confirmed by the data of laboratory, instrumental studies, as well as the results of the pathological and anatomical autopsy. The study of microslides showed signs of extensive vasculitis with thrombosis of small branches of the pulmonary artery and foci of pneumofibrosis of various degrees of prescription, which also testified in favor of the transferred covid infection. Taking into account the severity of the patient’s condition upon admission, it was not possible to perform emergency intervention on the aortic valve. After stabilization of the state and regression of the phenomena of circulatory failure, it was planned to simultaneously perform endovascular revascularization of the coronary valve bed and transcatheter aortic valve replacement. The planned surgical intervention failed. The immunosuppressive effect of the SARS-CoV-2 virus, apparently, led to the activation of autoflora and an increase in inflammation for nosocomial infection. Bilateral polysegmental bacterial pneumonia that joined during hospitalization, against the background of postcoid changes in the lung parenchyma, contributed to the development of acute coronary syndrome with ventricular arrhythmias. The patient died from acute cardiopulmonary failure. The article also presents ideas about the operational tactics of managing patients with aortic stenosis in a pandemic.

33. A case of ocular ischaemic syndrome caused by severe giant cell arteritis

IntroductionThis case describes a very aggressive form of giant cell arteritis (GCA) complicated by ocular ischaemic syndrome (OIS), complete bilateral visual loss and bilateral scalp muscle necrosis, despite treatment with high dose intravenous steroids. OIS, defined as ischaemia of all intraorbital and intraocular structures, is rare, estimated at 7.5 cases per million. This case also highlights the use of PET CT in management of complex cases of GCA.Case descriptionA 79-year-old lady presented with sudden onset pain above her right eye. A month earlier she had undergone curative surgery for infiltrating adenocarcinoma of the colon. 6 months earlier she had complained of bilateral shoulder pain. A month earlier she had developed pain on chewing and was unable to fully open her mouth. The next day she was reviewed in the eye hospital due to 24hrs of intermittent blurred vision. CT head was normal. Fundoscopy was normal and she was diagnosed with ocular migraine. Later that evening she lost vision in the right eye. Bloods showed CRP 58 and ESR 43. She was given 5 days of IV methylprednisolone (5x1g). Despite this she developed a right 6th nerve palsy. 2 days later her left eye developed visual loss, complete ptosis and loss of eye movements in all directions. MRI head with gadolinium showed temporoparietal juxtacortical diffuse white matter signal abnormalities.She underwent extensive investigation. ANCA was negative, lumbar puncture normal and temporal artery biopsy showed extensive fibrinoid necrosis of the vessel wall, with possible granulomata but no eosinophilia. Oral cyclophosphamide (2mg/kg) was started. 5 days later she developed severe bi-temporal pain and a rash which progressed to severe scalp necrosis. There were no vesicles to suggest shingles. Ten days later she suffered an upper gastro-intestinal bleed requiring a 4 unit transfusion. Gastroscopy showed mild gastritis. After this, cyclophosphamide was withheld, following discharge on steroids alone. Bilateral scalp necrosis remained a problem, complicated by pseudomonas infections. When a decreased left radial pulse was noted a PET CT was arranged. This showed active extensive vasculitis of the aorta. At this point methotrexate 15mg per week was added. The scalp lesions rapidly healed and the radial pulse returned to normal. The CRP has remained consistently below 5. DiscussionAn antiplatelet agent, clopidogrel was started due to the ischaemic cerebral findings on MRI, but it probably contributed, along with steroids, to her upper GI bleed. Antiplatelet therapy is no longer recommended routinely in the management of GCA. However in this case the diagnosis was still uncertain. None of us had ever seen orbital infarction syndrome as a complication of GCA. Perhaps a PET CT earlier on in the course of this lady’s disease would have made us more secure in the diagnosis. It could be argued that given the severity of her disease, methotrexate or even tocilizumab should have been commenced earlier. In fact, cyclophosphamide was used initially as it wasn’t clear if this was a medium vessel vasculitis. This was withheld when she had a large upper GI bleed (Hb dropped to 76). Once recovering, her CRP was down to 10. By this time the temporal artery biopsy was available, the ANCA was negative and GCA was felt to be the most likely diagnosis. It was also felt that given the bilateral visual loss, the most feared complication of GCA had already occurred so what was there to gain by using such strong immunosuppression? Hence cyclophosphamide was discontinued, and she was discharged on steroids alone. The addition of methotrexate had an impressive effect in terms of healing her weeping, secondarily infected scalp necrosis. Methotrexate was added in light of the PET CT which showed active large vessel vasculitis. The scalp necrosis, on reflection was due to an ongoing vasculitis that was being undertreated.There were missed opportunities for starting steroids earlier in the course of the disease: polymyalgic symptoms 6 months earlier, jaw claudication a month earlier. However it remains uncertain whether or not earlier treatment would have altered the course of this aggressive, severe disease. Key learning pointsScalp necrosis, which very easily can be mistaken for shingles or infections complicating steroid treatment, can be a feature of GCA. Orbital infarction syndrome can be a feature of GCA. Early PET CT might have clarified the diagnosis. Methotrexate should probably have been started once the limited response to IV steroids was apparent. Antiplatelet agents are no longer recommended in the updated BSR guidelines for managing GCA.Conflicts of interestThe authors have declared no conflicts of interest.

Weil’s disease in a 36 years old female: a case report

Leptospirosis is an acute zoonotic infection, itis caused by spirochetes of the genus Leptospira, has extensive vasculitis characterizes, can usually be transmitted indirectly, per contaminated water, rarely directly, and through contact with infected animals. Leptospira bacteria commonly enter the body through the damaged skin or mucous membranes. The clinical syndromes may vary from a subclinical infection and mild febrile condition to severe clinical symptoms with jaundice and renal failure. It is the case report from a woman 36 years old with leptospirosis (Weil’s disease) whose clinical manifestations included: icterus, renal failure, hemorrhagic syndrome and disturbances of consciousness. After the use of antibiotics, symptomatic and substitution therapy, all symptoms resolved completely.

Levamisole-Adulterated Cocaine Leading to Fatal Vasculitis: A Case Report

Cocaine is often "cut" with various additives to increase the profitability of the drug. One of the most common additives on today's market is levamisole, an anthelmintic medication used to destroy and expel parasitic worms in animals. The use of levamisole-contaminated cocaine can result in agranulocytosis and vasculitis (inflammation and constriction of small blood vessels). The resulting clotting and decrease in peripheral blood flow lead to cutaneous lesions, particularly on the ears, face, hands, and feet, and in severe cases can cause generalized tissue necrosis throughout the entire body. Treatment is generally supportive, and symptoms typically abate with complete cessation of cocaine use. However, symptoms may recur with subsequent cocaine use and, as this case illustrates, severe neutropenia and extensive vasculitis may lead to overwhelming sepsis and death.

Primary Central Nervous System Vasculitis Mimicking Brain Tumor

Primary central nervous system vasculitis (PCNSV) is a rare disease with a nonspecific and expansive spectrum of clinical manifestations. A 40-year-old woman presented with acute onset of severe headache associated with nausea. Computed tomography of the brain showed 1 solitary hypodense parenchymal lesion over the left temporal lobe with an internal fluid level. A brain magnetic resonance imaging showed the presence of 1 isointense parenchymal lesion on T1-weighted and T2-weighed images, with surrounding brain edema. The patient accepted craniotomy for excision of lesion under the preoperative impression of brain tumor with hemorrhagic transformation. The pathologic report was extensive vasculitis with hemorrhagic infarction. The diagnosis of PCNSV was made after exclusion of secondary causes–related vasculitis and hereditary hypercoagulant status. This report highlights that PCNSV could appear as a hemorrhagic tumor-like lesion on neuroimaging. Considering PCNSV in the differential diagnosis is important in patients suspected with cerebral hemorrhage, cerebral thrombosis, or brain tumor.

Central retinal vein occlusion in a patient with retinal vasculitis and Crohn's disease.

The authors report a rare case of a 47-year-old woman with Crohn's disease (CD) who presented with retinal vasculitis and central retinal vein occlusion (CRVO) during remission. The patient complained of sudden painless visual loss in her left eye (OS). Ophthalmologic evaluation revealed a best corrected visual acuity (BCVA) of 20/20 in the right eye and hand movements in OS. Ophthalmoscopy and fluorescein angiography of OS showed signs of nonischemic CRVO and extensive vasculitis. She was treated with oral prednisolone, mercaptopurine, and intravitreal bevacizumab in OS. After 1 month of treatment, VA of OS improved to 5/10 and after 1 year it was 10/10 with complete resolution of retinal vasculitis and nonischemic CRVO.

The clinical characteristics of retinal vasculitis in HLA-B27-positive patients

Purpose: To investigate the ocular and systemic manifestations of retinal vasculitis in HLA-B27-positive patients.Methods: Retrospective noncomparative case series of 9 HLA-B27-positive patients with uveitis and retinal vasculitis. Main outcome measures consisted of ocular and angiographic findings and assessment of any additional systemic disorders.Results: Three male and 6 female HLA-B27-positive patients with a median age of 32 years were diagnosed with retinal vasculitis. Concurrent intraocular inflammation was noted in all patients. All patients suffered from extensive vasculitis of the large retinal veins. Five patients developed retinal vasculitis at the onset of uveitis and the remaining 4 exhibited retinal vasculitis 1–15 years after the onset of uveitis. Vascular occlusions occurred in 4 patients and subsequent neovascularizations developed in 3. Three patients were diagnosed with an HLA-B27-associated systemic disease.Conclusion: Retinal vasculitis may develop in the wake of HLA-B27-associated uveitis and might represent a rare manifestation of HLA-B27-associated disease.

Univ. Méd. ISSN 0041-9095. Bogotá (Colombia), 55 (1): 93-100, enero-marzo, 2014 REPORTES DE CASO Reporte de catorce casos de leptospirosis en un hospital universitario de IV nivel entre 2010 y 2012

La leptospirosis es una enfermedad infecciosa aguda generalizada, provocada por espiroquetas del género Leptospira, caracterizada por una extensa vasculitis. Siempre debe considerarse entre los diagnósticos diferenciales de síndrome febril en nuestra población. Se reporta una serie de catorce casos con clínica indicativa de leptospirosis, que presentó resultado positivo de serología para Leptospira spp., lo cual confirma el diagnóstico. Se describen las características demográficas en la población estudiada: fue más frecuente en población entre 20 y 35 años de edad. En el 35,7 % existía un antecedente de desplazamiento reciente a municipios del norte del departamento del Tolima y en el 14,2 %, a municipios del sur de Cundinamarca. El 71,4 % de los pacientes tuvo factores de riesgo para adquirir la infección. La mayoría de las consultas a urgencias se presentó siete días de iniciados los síntomas. En todos los pacientes hubo fiebre, cefalea, mialgias y artralgias, y en menor proporción, dolor abdominal y diarreas.

Cutaneous leukocytoclastic vasculitis in the presence of methimazole therapy

Treatment with antithyroid drugs may be accompanied by side effects. We present a patient diagnosed with Grave's Disease who developed extensive vasculitis in the lower limbs during methimazole use. After suspension of the methimazole and the introduction of prednisone in immunesupressor doses the cutaneous lesions started to involute.

Immune Complex-Mediated Damage Is Under Complement Pathway Control

IgG receptors (FcγR) are critical in immune complex (IC)-mediated tissue damage. We performed reverse passive Arthus reactions, a model of IC-mediated cutaneous vasculitis, in normal C57Bl/6 mice and mice genetically deficient in C1q, C4, C3, and Factor B. We hypothesized classical complement pathway (CP) down-regulates while alternative complement pathway (AP) promotes IC binding to activating FcγR; therefore, CP deficiency (C1q-/-, C4-/-, C3-/-) would enhance the IC-induced cutaneous vasculitis, while AP deficiency (FB-/-) would diminish it. Sedated, shaved mice were injected intradermally with 20μl PBS on one side and rabbit anti-BSA IgG 5μg on the opposite. BSA 100μg and 125Iodine-labeled BSA 1.25μg with 1% Evans blue was then injected intravenously. After 4 hours, skin sections were weighed, radioactivity was measured (cpm/gm of tissue), and an Arthus index (AI) was calculated for each mouse (cpm/gm treated skin/control skin cpm/gm). Significant differences in AIs were analyzed by Kruskal-Wallis test, followed by Mann-Whitney tests. Complement absence strongly influenced degree of cutaneous vasculitis (p<0.001). Compared to normal mice (mean 2.5±1.2), C1q-/- (mean 3.6±0.8, p<0.05) and C4-/- (mean 4.7±2.3, p<0.05) exhibited more extensive vasculitis, and C3-/- (mean 3.5±0.5, p=0.05) trended towards greater vasculitis. FB-/- (mean 1.4±0.4, p<0.05) mice exhibited reduced vasculitis. Cutaneous vasculitis is significantly greater in CP-deficient mice and reduced in AP-deficient mice. Our results are first to provide in vivo evidence that complement critically influences IC and FcγR-mediated inflammation. They also refute previous data suggesting complement possesses no role in Arthus-induced vasculitis and may further understanding of why CP-deficient individuals are susceptible to autoimmunity.

A young woman with systemic lupus erythematosus and extensive mesenteric vasculitis involving small and medium vessels

History of the present illness The patient had 2 recent hospital admissions. Two months prior to her current presentation, she presented to the emergency department with a tooth abscess for which she underwent incision and drainage, and received a 1-week course of penicillin. One week later, she was admitted with a fever of 40.8°C and was noted to have tooth decay on panoramic radiographs without evidence of an abscess. She was treated with intravenous vancomycin and piperacillin tazobactam for 48 hours and then switched to oral clindamycin. Because of her elevated international normalized ratio (INR), she was unable to undergo tooth extraction prior to discharge. Two weeks later, she was readmitted with 4 days of recurrent fevers, malaise, diffuse arthralgias, and increased dyspnea with minimal exertion. Previous lupus exacerbations were characterized by arthralgias, rash, and hemolytic anemia. On this admission, laboratory evaluation revealed leukocytosis, worsening anemia and thrombocytopenia, creatinine of 0.7 mg/dl, alkaline phosphatase of 127 units/liter (normal value 111), spot urine proteinto-creatinine ratio of 1.47 (prior 1.1), low C3 and C4, and an increase in her double-stranded DNA by enzyme immunoassay from 120 to 768 IU/ml (normal value 30). She was empirically treated with vancomycin and piperacillin tazobactam given her recent tooth infection. The elevated alkaline phosphatase level prompted an abdominal ultrasound that showed multiple small hypoechoic areas in the spleen. An extensive infectious evaluation, including blood cultures, fungal serologies, knee arthrocentesis, magnetic resonance imaging of the lumbar spine, transthoracic and transesophageal echocardiograms, and computed tomography of the chest, abdomen, and pelvis, was negative. Her viral serologies were also unremarkable, other than evidence of IgG seropositivity for cytomegalovirus (CMV) with a negative viral load, consistent with prior exposure. Despite broad-spectrum antibiotics, she remained febrile. Her baseline prednisone dose of 12.5 mg was increased to 60 mg daily for possible lupus flare, after which she defervesced within 48 hours. Her thrombocytopenia was thought to be secondary to SLE-related idiopathic thrombocytopenic purpura because it resolved with high-dose steroids and intravenous immunoglobulin. She was discharged home 11 days after admission. The patient remained afebrile for 1 week at home. During this period she developed new-onset progressive upper abdominal pain with meals lasting 20–30 minutes. She denied associated constitutional symptoms, diarrhea, hematochezia, or melena.

Atteinte vasculaire et syndrome de Cogan. Une observation

Vascular manifestations of Cogan's syndrome are rarely reported. We report the case of a young woman followed for typical Cogan's disease. Serious vascular involvement was found only during work-up for arterial hypertension. This case highlights potentially asymptomatic nature of extensive vasculitis affecting large and medium-sized vessels in Cogan's disease. Careful screening is required to prevent life-threatening complications.

A patient with systemic lupus erythematosus and lupus nephritis: A 12-year follow-up

Systemic lupus erythematosus (SLE) is a chronic immunological disease causing a significant morbidity and mortality in younger women and involving several organs and systems, most often the kidneys, being consequently the incidence of lupus nephritis (LN) about 60%. We reported a 57 year-old patient with the diagnosed SLE in 1995. Pathohistological analysis of kidney biopsy revealed LN type V. The patient was treated with corticosteroid pulses and azathioprine during one year. A remission was achieved and maintained with prednisone, 15 mg daily. Nephrotic relapse was diagnosed in 2006 and the second kidney biopsy revealed recent kidney infarction due to extensive vasculitis. Soon, a cerebrovascul insult developed and CT-scan revealed endocranial infarctus. The patient was treated with corticosteroids and cyclophosphamide pulses (totally VI monthly pulses), and also with low-molecular heparine, anticoagulants and salicylates because of the right leg phlebothrombosis. After the pulses, the patient was adviced to take prednisone 20 mg daily and azothioprine 100 mg daily, and 6 months later mycophenolate mofetil because of persistent active serological immunological findings (ANA 1:320) and nephrotic syndrome. Mycophenolate mofetil was efficient in inducing and maintaining remission of nephrotic syndrome. The aim of LN treatment is to achieve and maintain remission, improve patients' outcome, reduce the toxicity of immunosuppressive drugs and the incidence of relapses.Mycophenolate mofetil was shown to be efficient in inducing and maintaining remission of nephrotic syndrome in the frame of LN.

Clinical characteristics, interdisciplinary treatment and follow-up of 14 children with Takayasu arteritis

Pediatric patients with Takayasu arteritis were studied by analyzing clinical presentation, diagnostic images, response to multimodal therapy, and long-term outcome. Fourteen consecutive children and adolescents (mean age: 10 years) were diagnosed with Takayasu arteritis at our institution between 1995 and 2007. They were subjected to clinical and diagnostic studies including color ultrasonography, MRI and angiography, and received interdisciplinary treatment. The median time lag between the first onset of symptoms and diagnosis was 7.7 weeks. The majority of patients presented with acute severe clinical symptoms and extensive vascular lesions. Hypertension was the most common finding on first presentation (93%), followed by headache (64%), nausea (64%) and palpitation (50%). Ten patients (71%) had reduced or absent carotid, brachial or femoral pulses in one or more locations. C-reactive protein was elevated in 79% of the patients and erythrocyte sedimentation rate in 64%. Cardiovascular imaging showed extensive vasculitis of both sides of the diaphragm in 86%. Complications included renal artery stenosis (n=7), aortic dissection, thoracic aortic aneurysm and infrarenal aneurysm (all n=1). Conservative drug treatment was effective in 50%. Interventional dilatation of stenosis and surgical therapy, including aortic bypass, resection of aneurysms and nephrectomy, were necessary in the remaining patients. Follow-up for 25 months to 12 years showed that all children are well without disease-related mortality. Takayasu arteritis is a rare and potentially life-threatening disease in children, likely with a prolonged subclinical course. Rapid diagnosis and interdisciplinary management help to prevent life-threatening complications.

Management Dilemmas of Atypical Ocular Toxoplasmosis Aided by Wide-Field Fluorescein Angiography

Purpose: To report an atypical presentation of ocular toxoplasmosis and to demonstrate the utility of wide-field angiography in delineating peripheral retinal pathology.Methods: Case Report.Results: A 17-year-old male presented with acute unilateral papillitis and retinochoroiditis. Laboratory testing supported reactivation of congenitally acquired Toxoplasma gondii infection. Wide-field fluorescein angiography showed extensive retinal vasculitis. The patient was treated with sulfamethoxazole/trimethoprim. Ocular inflammation resolved over a two-week period. There was no documented visual loss.Conclusion: Wide-field fluorescein angiography details ocular pathology otherwise unnoticed on traditional posterior pole fluorescein angiography. Documentation of extensive vasculitis associated with ocular toxoplasmosis can assist with management decisions.

Third‐Degree Atrioventricular Block in a Horse Secondary to Rattlesnake Envenomation

Third‐Degree Atrioventricular Block in a Horse Secondary to Rattlesnake Envenomation

Extensive Medium-Vessel Vasculitis With SLE

Systemic lupus erythematosus (SLE) is a multisystem disease of autoimmune origin. Vasculitis is often seen with SLE, but is usually limited to small vessels alone. The primary pathology in SLE-related vasculitis is leukocytoclastic vasculitis. Medium- and large-vessel vasculitis in association with SLE is distinctly uncommon and is limited to occasional case reports only. In addition, reports of medium-vessel vasculitis with SLE generally describe involvement of a single vessel bed. We report a rare case of extensive vasculitis involving medium-sized vessels in a patient with SLE. Our patient presented with classic signs and symptoms of SLE and satisfied a majority of the American College of Rheumatology criteria for SLE. She also had toe gangrene at presentation and developed paraplegia during the hospital stay. Radiologic studies showed evidence of diffuse medium-sized vessel vasculitis. The patient was treated with monthly pulse cyclophosphamide and high-dose prednisolone. Follow-up showed no new features of vasculitis and improvement in the signs and symptoms of SLE. Her paraplegia showed no response to treatment. This case stresses that medium-sized vessel occlusion anywhere in the body can occasionally occur due to vasculitis in a patient with SLE.

Weil’s syndrome (Leptospiral infection): A case report

Leptospirosis is an acute zoonotic infection, caused by spirochetes of the genus Leptospira. It is characterized by extensive vasculitis. It is usually transmitted indirectly, per contaminated water, rarely directly, through contact with infected animals. Leptospira bacteria commonly enter the body through damaged skin or mucous membranes. The clinical syndromes may vary from a subclinical infection and mild febrile condition to severe clinical symptoms with jaundice and renal failure. This is a case report of a patient with leptospirosis (Weil's disease) whose clinical manifestations included: icterus, renal failure, hemorrhagic syndrome and disturbances of consciousness. After the use of antibiotics, symptomatic and substitution therapy, all symptoms resolved completely. However, in our patient, hemodialysis was necessary due to renal failure, as a palliative measure. Weil's syndrome is a severe form of leptospirosis, which can be fatal. Early clinical diagnosis of the disease, as well as serologic verification of infection, are very important prerequisites, followed by antibiotic and other symptomatic therapy, as soon as possible. This is a case report of a patient with rare clinical manifestations of leptosirosis. Although presenting with severe symptoms, thanks to palliative therapeutic measures, complete and fast recovery was achieved. We especially point out the role of.