Lacrimal Excretory System Sequelae in Patients Treated for Leishmaniasis
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Ocular Leishmaniasis Presenting As Chronic
perim Ex en l & ta a l ic O p in l h t C h f Journal of Clinical & Experimental a o l m l a o n l r o g u Ayele et al., J Clin Exp Ophthalmol 2015, 6:1 y o J Ophthalmology ISSN: 2155-9570 DOI: 10.4172/2155-9570.1000395 Case Report Open Access Ocular Leishmaniasis Presenting as Chronic Ulcerative Blepharoconjunctivitis: A Case Report Fisseha Admassu Ayele*, Yared Assefa Wolde, Tesfalem Hagos and Ermias Diro University of Gondar, Gondar, Amhara, Ethiopia *Corresponding author: Fisseha Admassu Ayele MD, University of Gondar, Gondar, Amhara 196, Ethiopia, Tel: 251911197786; E-mail: [email protected] Received date: Dec 01, 2014, Accepted date: Feb 02, 2015, Published date: Feb 05, 2015 Copyright: © 2015 Ayele FH, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract Leishmaniasis is caused by unicellular eukaryotic obligate intracellular protozoa of the genus Leishmania that is endemic in over 98 countries in the world-most of which are developing countries including Ethiopia. It is transmitted by phlebotomine sandflies. The eye may be affected in cutaneous, mucocutaneous and Post Kala-Azar Dermal Leishmaniasis. We report a case of ocular leishmaniasis with eyelid and conjunctival involvement that had simulated ulcerative blepharoconjunctivitis not responding to conventional antibiotics. The patient was diagnosed by microscopy of a sample obtained via direct smear from the lesions. He was treated with systemic sodium stibogluconate (20 mg/kg/day) for 45 days and was clinically cured with this treatment. -
Differentiate Red Eye Disorders
Introduction DIFFERENTIATE RED EYE DISORDERS • Needs immediate treatment • Needs treatment within a few days • Does not require treatment Introduction SUBJECTIVE EYE COMPLAINTS • Decreased vision • Pain • Redness Characterize the complaint through history and exam. Introduction TYPES OF RED EYE DISORDERS • Mechanical trauma • Chemical trauma • Inflammation/infection Introduction ETIOLOGIES OF RED EYE 1. Chemical injury 2. Angle-closure glaucoma 3. Ocular foreign body 4. Corneal abrasion 5. Uveitis 6. Conjunctivitis 7. Ocular surface disease 8. Subconjunctival hemorrhage Evaluation RED EYE: POSSIBLE CAUSES • Trauma • Chemicals • Infection • Allergy • Systemic conditions Evaluation RED EYE: CAUSE AND EFFECT Symptom Cause Itching Allergy Burning Lid disorders, dry eye Foreign body sensation Foreign body, corneal abrasion Localized lid tenderness Hordeolum, chalazion Evaluation RED EYE: CAUSE AND EFFECT (Continued) Symptom Cause Deep, intense pain Corneal abrasions, scleritis, iritis, acute glaucoma, sinusitis, etc. Photophobia Corneal abrasions, iritis, acute glaucoma Halo vision Corneal edema (acute glaucoma, uveitis) Evaluation Equipment needed to evaluate red eye Evaluation Refer red eye with vision loss to ophthalmologist for evaluation Evaluation RED EYE DISORDERS: AN ANATOMIC APPROACH • Face • Adnexa – Orbital area – Lids – Ocular movements • Globe – Conjunctiva, sclera – Anterior chamber (using slit lamp if possible) – Intraocular pressure Disorders of the Ocular Adnexa Disorders of the Ocular Adnexa Hordeolum Disorders of the Ocular -
Diagnostic Code Descriptions (ICD9)
INFECTIONS AND PARASITIC DISEASES INTESTINAL AND INFECTIOUS DISEASES (001 – 009.3) 001 CHOLERA 001.0 DUE TO VIBRIO CHOLERAE 001.1 DUE TO VIBRIO CHOLERAE EL TOR 001.9 UNSPECIFIED 002 TYPHOID AND PARATYPHOID FEVERS 002.0 TYPHOID FEVER 002.1 PARATYPHOID FEVER 'A' 002.2 PARATYPHOID FEVER 'B' 002.3 PARATYPHOID FEVER 'C' 002.9 PARATYPHOID FEVER, UNSPECIFIED 003 OTHER SALMONELLA INFECTIONS 003.0 SALMONELLA GASTROENTERITIS 003.1 SALMONELLA SEPTICAEMIA 003.2 LOCALIZED SALMONELLA INFECTIONS 003.8 OTHER 003.9 UNSPECIFIED 004 SHIGELLOSIS 004.0 SHIGELLA DYSENTERIAE 004.1 SHIGELLA FLEXNERI 004.2 SHIGELLA BOYDII 004.3 SHIGELLA SONNEI 004.8 OTHER 004.9 UNSPECIFIED 005 OTHER FOOD POISONING (BACTERIAL) 005.0 STAPHYLOCOCCAL FOOD POISONING 005.1 BOTULISM 005.2 FOOD POISONING DUE TO CLOSTRIDIUM PERFRINGENS (CL.WELCHII) 005.3 FOOD POISONING DUE TO OTHER CLOSTRIDIA 005.4 FOOD POISONING DUE TO VIBRIO PARAHAEMOLYTICUS 005.8 OTHER BACTERIAL FOOD POISONING 005.9 FOOD POISONING, UNSPECIFIED 006 AMOEBIASIS 006.0 ACUTE AMOEBIC DYSENTERY WITHOUT MENTION OF ABSCESS 006.1 CHRONIC INTESTINAL AMOEBIASIS WITHOUT MENTION OF ABSCESS 006.2 AMOEBIC NONDYSENTERIC COLITIS 006.3 AMOEBIC LIVER ABSCESS 006.4 AMOEBIC LUNG ABSCESS 006.5 AMOEBIC BRAIN ABSCESS 006.6 AMOEBIC SKIN ULCERATION 006.8 AMOEBIC INFECTION OF OTHER SITES 006.9 AMOEBIASIS, UNSPECIFIED 007 OTHER PROTOZOAL INTESTINAL DISEASES 007.0 BALANTIDIASIS 007.1 GIARDIASIS 007.2 COCCIDIOSIS 007.3 INTESTINAL TRICHOMONIASIS 007.8 OTHER PROTOZOAL INTESTINAL DISEASES 007.9 UNSPECIFIED 008 INTESTINAL INFECTIONS DUE TO OTHER ORGANISMS -
A Description of the Clinical Features of Brimonidine- Associated Uveitis Alyssa Louie Primary Care Resident, San Francisco VA
Drug-induced intraocular inflammation: A description of the clinical features of brimonidine- associated uveitis Alyssa Louie Primary Care Resident, San Francisco VA Abstract: A description of the clinical features, diagnostic work-up, and management of acute anterior uveitis caused by brimonidine, a widely used glaucoma medication. I. Case History a. Patient demographics: 74 year-old white male b. Chief complaint: eye pain, redness, irritation for last 2 weeks c. Ocular and medical history: i. Ocular history 1. Primary open angle glaucoma OU, diagnosed 8 years ago 2. Senile cataracts OU, not visually significant 3. Type 2 Diabetes without retinopathy OU 4. No prior history of uveitis ii. Medical history: Diabetes Mellitus Type 2 iii. No known drug allergies d. Medications i. Ocular: dorzolamide BID OU (1.5 years), brimonidine BID OU (11 months), travatan QHS OU (5.5 years) ii. Medical: metformin 500mg tab BID PO II. Pertinent Findings a. Clinical exam i. Visual acuities: OD 20/20-, OS 20/20- ii. Goldmann applanation tonometry: 13 mm Hg OD, 13 mm Hg OS iii. Anterior segment 1. OU: 3+ diffuse conjunctival injection 2. OU: central and inferior granulomatous keratic precipitates 3. OU: Grade 1+ cell, 1+ flare 4. OU: No synechiae or iris changes were present iv. Posterior segment 1. Optic Nerve a. OD: Cup-to-disc ratio 0.70H/V, distinct margins b. OS: Cup-to-disc ratio 0.75H/V, distinct margins 2. Posterior pole, periphery, vitreous: unremarkable OU b. Laboratory Studies i. ACE, Lysozyme, FTA-ABS, VDRL, HLA-B27, Rheumatoid Factor, ANA, PPD, Chest X- ray: all negative/unreactive III. -
2012 Case Definitions Infectious Disease
Arizona Department of Health Services Case Definitions for Reportable Communicable Morbidities 2012 TABLE OF CONTENTS Definition of Terms Used in Case Classification .......................................................................................................... 6 Definition of Bi-national Case ............................................................................................................................................. 7 ------------------------------------------------------------------------------------------------------- ............................................... 7 AMEBIASIS ............................................................................................................................................................................. 8 ANTHRAX (β) ......................................................................................................................................................................... 9 ASEPTIC MENINGITIS (viral) ......................................................................................................................................... 11 BASIDIOBOLOMYCOSIS ................................................................................................................................................. 12 BOTULISM, FOODBORNE (β) ....................................................................................................................................... 13 BOTULISM, INFANT (β) ................................................................................................................................................... -
Reiter's Syndrome
iMedPub JOURNALS ARCHIVES OF MEDICINE | 2009 | Vol. 1 | No. 1:1 | doi: 10.3823/032 Review Reiter's Syndrome Digna Llorente Molina, Susandra Cedeño Facultad de Ciencias Médicas 10 de Octubre. Ciudad Habana, Cuba. E-mail: [email protected] Reiter’s syndrome is a systemic disorder characterized by ocular conjunctivitis or uveitis, reactive arthritis, and urethritis manifestations. The exact cause of reactive arthritis is unknown. It occurs most commonly in men before the age of 40. It may follow an infection with Chlamydia, Campylobacter, Salmonella or Yersinia. Certain genes may make you more prone to the syndrome. The diagnosis is based on symptoms. The goal of treatment is to relieve symptoms and treat any underlying infection. Reactive arthritis may go away in 3 - 4 months, but symptoms may return over a period of several years in up to a half of those affected. The condition may become chronic. Preventing sexually transmitted diseases and gastrointestinal infection may help prevent this disease. Wash your hands and surface areas thoroughly before and after preparing food. © Archives of Medicine: Accepted after external review ■ The first description of Reiter’s syndrome was attributed in occasionally, cutaneous-mucosal lesions such as keratodermia 1916 to the re-known German physician Hans Reiter, linked to blennorrhagica and balanitis circinata; yellow papule lesions Nazi powers, and to his experiments in the concentration on the soles, palms and with less frequency on the nails, camps. In 1918, Junghanns described the first case in a young scrotum, scalp and trunk, amongst others (3), (4), (5).. The patient (1), (2). earliest manifestation of joint disorder is entesitis, normally in the Achilles tendon and in the plantar fascia of the calcaneus, Due to the syndrome’s abnormal immunological reactivity to causing shortening or lengthening of fingers and toes certain pathogens as a result of the interaction between resembling "sausage fingers and toes". -
Idiopathic Interstitial Keratitis in a Child 35
Summer 2021 • Vol 16 | No 1 Case report SA Ophthalmology Journal Idiopathic interstitial keratitis in a child 35 Idiopathic interstitial keratitis in a child DA Erasmus MBBCh, MMed, Dip Ophth (SA); Registrar, Department of Neurosciences, Division of Ophthalmology, University of the Witwatersrand, Johannesburg, South Africa ORCID: https://orcid.org/0000-0002-8395-7080 R Höllhumer MBChB, MMed, FC Ophth(SA); Consultant ophthalmologist, Department of Neurosciences, Division of Ophthalmology, University of the Witwatersrand, Johannesburg, South Africa ORCID: https://orcid.org/0000-0002-4375-2224 Corresponding author: Dr DA Erasmus, 40 2nd Avenue, Parktown North, 2193; tel.: +27 76 462 3355; email: [email protected] Abstract Interstitial keratitis represents inflammation and new vessel investigations can help to establish the underlying cause of formation in the middle layers of the cornea without tissue interstitial keratitis. loss. The most important infective aetiologies include herpes viruses, tuberculosis and syphilis. Keywords: interstitial, keratitis, inflammation, cornea, stroma Non-infectious causes such as Cogan’s syndrome should be considered in those cases with associated neurosensory Funding: No external funding was received. hearing loss. The pattern and laterality of inflammation together with the Conflict of interest: The authors have no conflicts of interest presence or absence of systemic features as well as relevant to declare. Severe Mild Moderate Moderate/Mild A * Dry Eye range like NEVER BEFORE Introduction systemic features provides a clue to the a tuberculosis (TB) endemic area such as Interstitial keratitis is a non-ulcerative underlying cause of interstitial keratitis. South Africa. Parasitic infections causing inflammation and subsequent Interstitial keratitis can be broadly interstitial keratitis are very uncommonly vascularisation of the corneal stroma divided into infectious and non-infectious encountered in South Africa but imported which does not primarily involve the aetiologies. -
The Uveo-Meningeal Syndromes
ORIGINAL ARTICLE The Uveo-Meningeal Syndromes Paul W. Brazis, MD,* Michael Stewart, MD,* and Andrew G. Lee, MD† main clinical features being a meningitis or meningoenceph- Background: The uveo-meningeal syndromes are a group of disorders that share involvement of the uvea, retina, and meninges. alitis associated with uveitis. The meningeal involvement is Review Summary: We review the clinical manifestations of uveitis often chronic and may cause cranial neuropathies, polyra- and describe the infectious, inflammatory, and neoplastic conditions diculopathies, and hydrocephalus. In this review we define associated with the uveo-meningeal syndrome. and describe the clinical manifestations of different types of Conclusions: Inflammatory or autoimmune diseases are probably uveitis and discuss the individual entities most often associ- the most common clinically recognized causes of true uveo-menin- ated with the uveo-meningeal syndrome. We review the geal syndromes. These entities often cause inflammation of various distinctive signs in specific causes for uveo-meningeal dis- tissues in the body, including ocular structures and the meninges (eg, ease and discuss our evaluation of these patients. Wegener granulomatosis, sarcoidosis, Behc¸et disease, Vogt-Koy- anagi-Harada syndrome, and acute posterior multifocal placoid pig- ment epitheliopathy). The association of an infectious uveitis with an acute or chronic meningoencephalitis is unusual but occasionally the eye examination may suggest an infectious etiology or even a The uveo-meningeal syndromes are a specific organism responsible for a meningeal syndrome. One should consider the diagnosis of primary ocular-CNS lymphoma in heterogeneous group of disorders that share patients 40 years of age or older with bilateral uveitis, especially involvement of the uvea, retina, and meninges. -
Management of Chronic Anterior Uveitis Relapses: Efficacy of Oral Phospholipidic Curcumin Treatment. Long-Term Follow-Up
Clinical Ophthalmology Dovepress open access to scientific and medical research Open Access Full Text Article ORIGINAL RESEARCH Management of chronic anterior uveitis relapses: efficacy of oral phospholipidic curcumin treatment. Long-term follow-up Pia Allegri1 Abstract: Curcumin has been successfully applied to treat inflammatory conditions in Antonio Mastromarino1 experimental research and in clinical trials. The purpose of our study is to evaluate the efficacy Piergiorgio Neri2 of an adjunctive-to-traditional treatment with Norflo tablets (curcumin-phosphatidylcholine complex; Meriva) administered twice a day in recurrent anterior uveitis of different etiologies. The 1Uveitis Center, Ophthalmological Department of Lavagna Hospital, study group consisted of 106 patients who completed a 12-month follow-up therapeutic period. Genova, Italy; 2Uveitis Unit, The We divided the patients into three main groups of different uveitis origin: group 1 (autoimmune Eye Clinic, Azienda Ospedaliero- uveitis), group 2 (herpetic uveitis), and group 3 (different etiologies of uveitis). The primary Universitaria, Ospedali Riuniti di Ancona, Ancona, Italy end point of our work was the evaluation of relapse frequency in all treated patients, before and after Norflo treatment, followed by the number of relapses in the three etiological groups. Wilcoxon signed-rank test showed a P , 0.001 in all groups. The secondary end points were the evaluation of relapse severity and of the overall quality of life. The results showed that Norflo was well tolerated and could reduce eye discomfort symptoms and signs after a few weeks of treatment in more than 80% of patients. In conclusion, our study is the first to report the potential therapeutic role of curcumin and its efficacy in eye relapsing diseases, such as anterior uveitis, and points out other promising curcumin-related benefits in eye inflammatory and degenerative conditions, such as dry eye, maculopathy, glaucoma, and diabetic retinopathy. -
Immune Defense at the Ocular Surface
Eye (2003) 17, 949–956 & 2003 Nature Publishing Group All rights reserved 0950-222X/03 $25.00 www.nature.com/eye Immune defense at EK Akpek and JD Gottsch CAMBRIDGE OPHTHALMOLOGICAL SYMPOSIUM the ocular surface Abstract vertebrates. Improved visual acuity would have increased the fitness of these animals and would The ocular surface is constantly exposed to a have outweighed the disadvantage of having wide array of microorganisms. The ability of local immune cells and blood vessels at a the outer ocular system to recognize pathogens distance where a time delay in addressing a as foreign and eliminate them is critical to central corneal infection could lead to blindness. retain corneal transparency, hence The first vertebrates were jawless fish that preservation of sight. Therefore, a were believed to have evolved some 470 million combination of mechanical, anatomical, and years ago.1 These creatures had frontal eyes and immunological defense mechanisms has inhabited the shorelines of ancient oceans. With evolved to protect the outer eye. These host better vision, these creatures were likely more defense mechanisms are classified as either a active and predatory. This advantage along with native, nonspecific defense or a specifically the later development of jaws enabled bony fish acquired immunological defense requiring to flourish and establish other habitats. One previous exposure to an antigen and the such habitat was shallow waters where lunged development of specific immunity. Sight- fish made the transition to land several hundred threatening immunopathology with thousand years later.2 To become established in autologous cell damage also can take place this terrestrial environment, the new vertebrates after these reactions. -
UVEITIS Eye74 (1)
UVEITIS Eye74 (1) Uveitis Last updated: May 9, 2019 Classification .................................................................................................................................... 1 Etiologic categories .......................................................................................................................... 2 Treatment ......................................................................................................................................... 2 Complications ................................................................................................................................... 2 COMMON UVEITIC SYNDROMES ............................................................................................................. 2 Masquerade Syndromes ................................................................................................................... 3 UVEITIS - heterogenous ocular diseases - inflammation of any component of uveal tract (iris, ciliary body, choroid). CLASSIFICATION ANTERIOR UVEITIS (most common uveitis) - localized to anterior segment - iritis and iridocyclitis. IRITIS - white cells confined solely to anterior chamber. IRIDOCYCLITIS - cellular activity also involves retrolental vitreous. etiology (most do not have underlying systemic disease): 1) idiopathic postviral syndrome (most commonly 38-60%) 2) HLA-B27 syndromes, many arthritic syndromes (≈ 17%) 3) trauma (5.7%) 4) herpes simplex, herpes zoster disease (1.9-12.4%) 5) iatrogenic (postoperative). tends to -
Results of Penetrating Keratoplasty in Syphilitic Interstitial Keratitis
RESULTS OF PENETRATING KERATOPLASTY IN SYPHILITIC INTERSTITIAL KERATITIS GOEGEBUER A.*, ***, AJAY LOHIYA**, ***, CLAERHOUT I.*, KESTELYN PH.* ABSTRACT ratite interstitielle (KI) syphilitique avec ceux dé- crits dans la litérature. Purpose: To compare the results in our patient se- Méthode: Analyse rétrospective des cas, avec acui- ries after penetrating keratoplasty (PKP) for syphi- té visuelle, clarté du greffon, épisodes de rejet, pres- litic interstitial keratitis (IK) with those described in sion intraoculaire et comptage postopératoire des the literature. cellules endothéliales. Methods: Retrospective case series in which visual Résultats: L’acuité visuelle s’est améliorée dans tous acuity (VA), graft clarity,rejection episodes, intraocu- les cas. Il n’y avait pas de signes de déhiscence du lar pressure and endothelial cell density (ECD) were greffon, ni d’ occurrence d’une membrane rétrocor- examined postoperatively. néenne. L’inflammation postopératoire n’était pas Results: Postoperative VA improved in all cases. plus prononcée chez nos patients avec une kératite There was no evidence of wound dehiscense or oc- interstitielle comparée aux patients opérés pour currence of retrocorneal membrane formation in any d’autres raisons. Un déclin normal du comptage des case. Postoperative inflammation was not more se- cellules endothéliales prouvait qu’il n’y avait pas d’in- vere in our patients with syphilitic IK compared to flammation infraclinique. patients undergoing PKP for other reasons. A nor- Conclusion: Une kératoplastie transfixiante pour KI mal decline in ECD proved that there was no sub- syphilitique a un bon pronostic en ce qui concerne clinical inflammation as well. la clarté du greffon. Tous les patients bénéficiaient Conclusion: PKP for syphilitic IK has a good prog- d’ une amélioration de l’acuité visuelle, bien que par- nosis in our case series as far as graft survival is con- fois limitée.