DOCSLIB.ORG

Role of Intraocular Leptospira Infections in the Pathogenesis Of

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Role of Intraocular Leptospira Infections in the Pathogenesis Of Louisiana State University LSU Digital Commons LSU Master's Theses Graduate School 2012 Role of Intraocular Leptospira Infections in the Pathogenesis of Equine Recurrent Uveitis in the Southern United States Florence Polle Louisiana State University and Agricultural and Mechanical College, [email protected] Follow this and additional works at: https://digitalcommons.lsu.edu/gradschool_theses Part of the Veterinary Medicine Commons Recommended Citation Polle, Florence, "Role of Intraocular Leptospira Infections in the Pathogenesis of Equine Recurrent Uveitis in the Southern United States" (2012). LSU Master's Theses. 3492. https://digitalcommons.lsu.edu/gradschool_theses/3492 This Thesis is brought to you for free and open access by the Graduate School at LSU Digital Commons. It has been accepted for inclusion in LSU Master's Theses by an authorized graduate school editor of LSU Digital Commons. For more information, please contact [email protected]. ROLE OF INTRAOCULAR LEPTOSPIRA INFECTIONS IN THE PATHOGENESIS OF EQUINE RECURRENT UVEITIS IN THE SOUTHERN UNITED STATES A Thesis Submitted to the Graduate Faculty of the Louisiana State University and Agricultural and Mechanical College in partial fulfillment of the requirements for the degree of Master of Science In The School of Veterinary Medicine Through The Department of Veterinary Clinical Sciences By Florence Polle DrMedVet, Ecole Nationale Vétérinaire de Toulouse, 2007 August 2012 To my parents, who always let me make my own choices. ii ACKNOWLEDGMENTS My deepest gratitude to the members of my committee, Drs. Renee Carter, Susan Eades and Rebecca McConnico, for their guidance and support during the realization of this study and the preparation of this manuscript. For performing statistical analysis, I would like to thank Drs. Hugues Beaufrere and Michael Kearney. For performing all the cultures and graciously proving the media, I would like to thank Drs. Richard Hornsby, David Alt and Richard Zuerner from the National Centers for Animal Health in Aimes, Iowa. I would also like to thank Mike Keowen and Tommy Stevens for their time and assistance with the horses, and for helping me getting donation for this project. Thank you to the Veterinary Clinical Science and the Equine Health and Study Program for funding this work. Last, I would like to thank Dr. Susan Eades for her invaluable guidance and mentorship during the past three years. iii TABLE OF CONTENTS DEDICATION ................................................................................................................................. ii ACKNOWLEDGMENTS ............................................................................................................... iii LIST OF TABLES .......................................................................................................................... vi LIST OF FIGURES ........................................................................................................................ vii ABSTRACT .................................................................................................................................. viii INTRODUCTION............................................................................................................................ 1 CHAPTER ONE. REVIEW OF THE LITERATURE .................................................................... 2 1.1. The normal equine eye ........................................................................................................ 2 1.1.1. The uvea ................................................................................................................... 2 1.1.2. Normal immunology ................................................................................................. 3 1.2. Epidemiology of Equine Recurrent Uveitis ....................................................................... 4 1.2.1. Prevalence ................................................................................................................. 4 1.2.2. Breed and genetic susceptibility ............................................................................... 4 1.2.3. Age and sex .............................................................................................................. 5 1.2.4. Etiology .................................................................................................................... 5 1.3. Diagnosis and clinical signs ............................................................................................... 6 1.3.1. Clinical presentation ................................................................................................. 6 1.3.2. Additional tests ......................................................................................................... 7 1.3.3. Pathology of ERU ..................................................................................................... 9 1.4. Treatment, prevention and prognosis of ERU ................................................................... 9 1.4.1. Medical treatment ................................................................................................... 10 1.4.1.1.Anti-inflammatory drugs ............................................................................... 10 1.4.1.2.Cycloplegics and mydriatics ......................................................................... 10 1.4.1.3.Antibiotics ..................................................................................................... 11 1.4.1.4.Other .............................................................................................................. 11 1.4.1.5.Limitations .................................................................................................... 12 1.4.2. Surgical treatment ................................................................................................... 12 1.4.2.1.Vitrectomy ..................................................................................................... 12 1.4.2.2.Cyclosporine implants ................................................................................... 13 1.4.2.3.Other .............................................................................................................. 14 1.4.3. Vaccination ............................................................................................................. 15 1.4.4. Prognosis ................................................................................................................ 15 1.5. Immunology of ERU ........................................................................................................ 16 1.5.1. Targeted autoantigens ............................................................................................. 17 1.5.2. Molecular mimicry ................................................................................................. 17 1.5.3. Differentially regulated candidates in uveitis target tissues ................................... 18 1.6. Leptospirosis and ERU ................................................................................................... 18 1.6.1. Leptospirosis ........................................................................................................... 18 1.6.1.1.Bacteriology .................................................................................................. 18 iv 1.6.1.2.Diagnostic testing .......................................................................................... 19 1.6.1.3.Leptospirosis in horses .................................................................................. 20 1.6.2. Leptospiral uveitis in human medicine ................................................................... 21 1.6.3. Evidence for leptospirosis as a cause of ERU ........................................................ 22 1.6.3.1.Europe ........................................................................................................... 23 1.6.3.2.North America ............................................................................................... 24 1.6.3.3.Other .............................................................................................................. 24 CHAPTER TWO. ROLE OF INTRAOCULAR LEPTOSPIRA INFECTIONS IN THE PATHOGENESIS OF EQUINE RECURRENT UVEITIS IN THE SOUTHERN UNITED STATES ......................................................................................................................................... 26 2.1. Materials and methods .................................................................................................... 26 2.2. Results ............................................................................................................................. 28 2.2.1. Horses ..................................................................................................................... 28 2.2.2. Ophthalmic examination ........................................................................................ 29 2.2.3. Histological findings .............................................................................................. 33 2.2.4. Serology ................................................................................................................. 36 2.2.5. Culture .................................................................................................................... 37 2.2.6. Real-Time PCR .....................................................................................................
Load more

Recommended publications
  • 12 Retina Gabriele K
    299 12 Retina Gabriele K. Lang and Gerhard K. Lang 12.1 Basic Knowledge The retina is the innermost of three successive layers of the globe. It comprises two parts: ❖ A photoreceptive part (pars optica retinae), comprising the first nine of the 10 layers listed below. ❖ A nonreceptive part (pars caeca retinae) forming the epithelium of the cil- iary body and iris. The pars optica retinae merges with the pars ceca retinae at the ora serrata. Embryology: The retina develops from a diverticulum of the forebrain (proen- cephalon). Optic vesicles develop which then invaginate to form a double- walled bowl, the optic cup. The outer wall becomes the pigment epithelium, and the inner wall later differentiates into the nine layers of the retina. The retina remains linked to the forebrain throughout life through a structure known as the retinohypothalamic tract. Thickness of the retina (Fig. 12.1) Layers of the retina: Moving inward along the path of incident light, the individual layers of the retina are as follows (Fig. 12.2): 1. Inner limiting membrane (glial cell fibers separating the retina from the vitreous body). 2. Layer of optic nerve fibers (axons of the third neuron). 3. Layer of ganglion cells (cell nuclei of the multipolar ganglion cells of the third neuron; “data acquisition system”). 4. Inner plexiform layer (synapses between the axons of the second neuron and dendrites of the third neuron). 5. Inner nuclear layer (cell nuclei of the bipolar nerve cells of the second neuron, horizontal cells, and amacrine cells). 6. Outer plexiform layer (synapses between the axons of the first neuron and dendrites of the second neuron).
    [Show full text]
  • Equine Uveitis Lauren Hughes, DVM
    New England Equine Medical & Surgical Center 15 Members Way · Dover NH 03820 · www.newenglandequine.com · 603.749.9111 Understanding Equine Uveitis Lauren Hughes, DVM One of the most common ocular diseases affecting the horse is a condition known as uveitis. This occurs when inflammation affects the uveal tract of the eye that is composed of the iris, ciliary body and choroid. This inflammation can be caused by a variety of conditions including ocular, systemic or immune mediated disease. Fig 1. Equine Eye Cross-Sectional Anatomy Understanding Uveitis In order to better understand uveitis we need to take a closer look at the causes of this relatively common disease. 1-Ocular- Any condition that affects the eye can lead to uveitis as a secondary complication. This includes trauma, corneal ulcers, intraocular tumors, and cataracts (which cause lens-induced uveitis). 2-Systemic- Many infectious diseases can also predispose a horse to development of uveitis. These diseases can be bacterial, viral, parasitic, or neoplastic, with one of the most recognized being the bacterial disease Leptospirosis. 3-Immune Mediated- The most commonly seen presentation of uveitis is an immune mediated form known as equine recurrent uveitis (ERU) or moon blindness. This disease consists of recurrent episodes of inflammation in which the immune system targets the tissues of the eye. This can be an ongoing and frustrating condition for owners as treatment is not curative and lifelong management is often necessary. This condition has been reported to affect upwards of 25% of the horse population with increased prevalence in certain breeds including Appaloosas, draft horses, and warmbloods.1 It can affect one or both eyes, with chronicity potentially leading to permanent vision deficits or blindness.
    [Show full text]
  • Hypotony Following Intravitreal Silicone Oil Removal in a Patient with a Complex Retinal Detachment with Giant Retinal Tear
    Open Access Case Report DOI: 10.7759/cureus.16387 Hypotony Following Intravitreal Silicone Oil Removal in a Patient With a Complex Retinal Detachment With Giant Retinal Tear Ilias Gkizis 1 , Christina Garnavou-Xirou 1 , Georgios Bontzos 1 , Georgios Smoustopoulos 1 , Tina Xirou 1 1. Ophthalmology, Korgialenio-Benakio General Hospital, Athens, GRC Corresponding author: Georgios Smoustopoulos, [email protected] Abstract Postoperative ocular hypotony after silicone oil removal in complex cases of retinal detachment is a complication that can occur in about 20% of cases and can prevent the successful management of retinal detachments. Thus, it is critical to understand the mechanisms of hypotony and the potential interventions that can be done in order to avoid irreversible tissue damage. We present a case of a 35-year-old man who underwent intraocular surgery for removal of silicone oil tamponade following a combined scleral buckling and pars plana vitrectomy (PPV) surgery for a rhegmatogenous retinal detachment associated with a giant retinal tear. On Day 1 after the operation, the patient was found to have hypotony with optic disc edema, chorioretinal folds, and visual acuity of ‘hand movement’ perception. Two weeks postop, the patient’s condition stabilized, with a visual acuity of 0.38 logMAR, an intraocular pressure (IOP) of 12 mmHg, and the absence of macular edema. Categories: Ophthalmology Keywords: hypotony, silicone oil removal, retinal detachment, vitrectomy, giant retinal tear Introduction Ocular hypotony is defined as intraocular pressure (IOP) of 5 mmHg or less. Depending on the duration and time of onset, it can be classified as acute, chronic, transient, or permanent. Whilst acute hypotony is not an uncommon phenomenon following intraocular surgery, it is generally reversible after 10-15 days [1].
    [Show full text]
  • Penetration of Synthetic Corticosteroids Into Human Aqueous Humour
    Eye (1990) 4, 526--530 Penetration of Synthetic Corticosteroids into Human Aqueous Humour C. N. 1. McGHEE,1.3 D. G. WATSON, 3 1. M. MIDGLEY, 3 M. 1. NOBLE, 2 G. N. DUTTON, z A. I. FERNl Glasgow Summary The penetration of prednisolone acetate (1%) and fluorometholone alcohol (0.1%) into human aqueous humour following topical application was determined using the very sensitive and specific technique of Gas Chromatography with Mass Spec­ trometry (GCMS). Prednisolone acetate afforded peak mean concentrations of 669.9 ng/ml within two hours and levels of 28.6 ng/ml in aqueous humour were detected almost 24 hours post application. The peak aqueous humour level of flu­ orometholone was S.lng/ml. The results are compared and contrasted with the absorption of dexamethasone alcohol (0.1%), betamethasone sodium phosphate (0.1 %) and prednisolone sodium phosphate (0.5%) into human aqueous humour. Topical corticosteroid preparations have been prednisolone acetate (1.0%) and fluorometh­ used widely in ophthalmology since the early alone alcohol (0.1 %) (preliminary results) 1960s and over the last 10 years the choice of into the aqueous humour of patients under­ preparations has become larger and more going elective cataract surgery. varied. Unfortunately, data on the intraocular penetration of these steroids in humans has SUbjects and Methods not paralleled the expansion in the number of Patients who were scheduled to undergo rou­ available preparations; indeed until recently, tine cataract surgery were recruited to the estimation of intraocular penetration has study and informed consent was obtained in been reliant upon extrapolation of data from all cases (n=88), Patients with corneal disease animal models (see Watson et ai., 1988, for or inflammatory ocular conditions which bibliography).
    [Show full text]
  • Onchocerciasis
    11 ONCHOCERCIASIS ADRIAN HOPKINS AND BOAKYE A. BOATIN 11.1 INTRODUCTION the infection is actually much reduced and elimination of transmission in some areas has been achieved. Differences Onchocerciasis (or river blindness) is a parasitic disease in the vectors in different regions of Africa, and differences in cause by the filarial worm, Onchocerca volvulus. Man is the the parasite between its savannah and forest forms led to only known animal reservoir. The vector is a small black fly different presentations of the disease in different areas. of the Simulium species. The black fly breeds in well- It is probable that the disease in the Americas was brought oxygenated water and is therefore mostly associated with across from Africa by infected people during the slave trade rivers where there is fast-flowing water, broken up by catar- and found different Simulium flies, but ones still able to acts or vegetation. All populations are exposed if they live transmit the disease (3). Around 500,000 people were at risk near the breeding sites and the clinical signs of the disease in the Americas in 13 different foci, although the disease has are related to the amount of exposure and the length of time recently been eliminated from some of these foci, and there is the population is exposed. In areas of high prevalence first an ambitious target of eliminating the transmission of the signs are in the skin, with chronic itching leading to infection disease in the Americas by 2012. and chronic skin changes. Blindness begins slowly with Host factors may also play a major role in the severe skin increasingly impaired vision often leading to total loss of form of the disease called Sowda, which is found mostly in vision in young adults, in their early thirties, when they northern Sudan and in Yemen.
    [Show full text]
  • [email protected]
    SAFETY DATA SHEET Revision Date 13-Jul-2016 Version 1 1. IDENTIFICATION OF THE SUBSTANCE/PREPARATION AND OF THE COMPANY/UNDERTAKING Product identifier Product Name Pred Forte Other means of identification Product Code FP61 Synonyms Prednisolone Acetate Recommended use of the chemical and restrictions on use Recommended Use Corticosteroid This safety data sheet is written to provide health, safety and environmental information for people handling this formulated product in the workplace. It is not intended to provide information relevant to medicinal use of the product. In this instance patients should consult prescribing information/package insert/product label or consult their pharmacist or physician. For health and safety information for individual ingredients used during manufacturing, refer to the appropriate safety data sheet for each ingredient. Details of the supplier of the safety data sheet Manufacturer ALLERGAN 400 Interpace Parkway, Morris Corporate Center III Parsippany, NJ 07054, USA +1-800-272-5525 E-mail address [email protected] Emergency telephone number Emergency Telephone Call CHEMTREC Day or Night Within USA or Canada: 1-800-424-9300 Outside USA and Canada: +1-703-741-5970 (collect calls accepted) 2. HAZARDS IDENTIFICATION Classification OSHA Regulatory Status This chemical is considered hazardous by the 2012 OSHA Hazard Communication Standard (29 CFR 1910.1200) Reproductive toxicity Category 2 Effects on or via lactation Yes Label elements Emergency Overview Danger Hazard statements H362 - May cause harm to breast-fed
    [Show full text]
  • BLINDNESS in MONGOLISM (DOWN's SYNDROME)*T by J
    Br J Ophthalmol: first published as 10.1136/bjo.47.6.331 on 1 June 1963. Downloaded from Brit. J. Ophthal. (1963) 47, 331. BLINDNESS IN MONGOLISM (DOWN'S SYNDROME)*t BY J. F. CULLENt The Wilmer Institute, Johns Hopkins University and Hospital, Baltimore, Maryland IN a previous communication (Cullen and Butler, 1963), the ocular abnor- malities encountered in a survey of 143 mongoloids at the Rosewood State Hospital in Maryland were enumerated, and particular attention was drawn to the occurrence of keratoconus in over 5 per cent. of these patients. The purpose of this paper is to elaborate the incidence and causes of blindness in this same group. In the earlier paper no mention was made of the fact that several blind mongoloids were discovered among those examined, and, as the cause of blindness was in all but one instance associated with cataract or keratoconus, they were classified under these aetiological headings. Earlier surveys of the ocular abnormalities in mongoloids by Ormond (1912), Lowe (1949), Skeller and Oster (1951), and Woillez and Dansaut (1960) do not list any patient as being blind. More recently Eissler and Longenecker (1962) reviewed the ocular findings in 396 mongoloids and, though they made no attempt to compile uncommon ocular conditions, they did not state whether any of this very large number of patients were blind. When one considers that serious ocular conditions occur so com- monly in mongoloids, and that the eyes of such patients might be expected to respond unfavourably to trauma or to surgical insult, it is surprising that http://bjo.bmj.com/ no reference has hitherto been made to the not unexpected occurrence of blindness, particularly if they survive for more than 30 years.
    [Show full text]
  • NINDS Custom Collection II
    ACACETIN ACEBUTOLOL HYDROCHLORIDE ACECLIDINE HYDROCHLORIDE ACEMETACIN ACETAMINOPHEN ACETAMINOSALOL ACETANILIDE ACETARSOL ACETAZOLAMIDE ACETOHYDROXAMIC ACID ACETRIAZOIC ACID ACETYL TYROSINE ETHYL ESTER ACETYLCARNITINE ACETYLCHOLINE ACETYLCYSTEINE ACETYLGLUCOSAMINE ACETYLGLUTAMIC ACID ACETYL-L-LEUCINE ACETYLPHENYLALANINE ACETYLSEROTONIN ACETYLTRYPTOPHAN ACEXAMIC ACID ACIVICIN ACLACINOMYCIN A1 ACONITINE ACRIFLAVINIUM HYDROCHLORIDE ACRISORCIN ACTINONIN ACYCLOVIR ADENOSINE PHOSPHATE ADENOSINE ADRENALINE BITARTRATE AESCULIN AJMALINE AKLAVINE HYDROCHLORIDE ALANYL-dl-LEUCINE ALANYL-dl-PHENYLALANINE ALAPROCLATE ALBENDAZOLE ALBUTEROL ALEXIDINE HYDROCHLORIDE ALLANTOIN ALLOPURINOL ALMOTRIPTAN ALOIN ALPRENOLOL ALTRETAMINE ALVERINE CITRATE AMANTADINE HYDROCHLORIDE AMBROXOL HYDROCHLORIDE AMCINONIDE AMIKACIN SULFATE AMILORIDE HYDROCHLORIDE 3-AMINOBENZAMIDE gamma-AMINOBUTYRIC ACID AMINOCAPROIC ACID N- (2-AMINOETHYL)-4-CHLOROBENZAMIDE (RO-16-6491) AMINOGLUTETHIMIDE AMINOHIPPURIC ACID AMINOHYDROXYBUTYRIC ACID AMINOLEVULINIC ACID HYDROCHLORIDE AMINOPHENAZONE 3-AMINOPROPANESULPHONIC ACID AMINOPYRIDINE 9-AMINO-1,2,3,4-TETRAHYDROACRIDINE HYDROCHLORIDE AMINOTHIAZOLE AMIODARONE HYDROCHLORIDE AMIPRILOSE AMITRIPTYLINE HYDROCHLORIDE AMLODIPINE BESYLATE AMODIAQUINE DIHYDROCHLORIDE AMOXEPINE AMOXICILLIN AMPICILLIN SODIUM AMPROLIUM AMRINONE AMYGDALIN ANABASAMINE HYDROCHLORIDE ANABASINE HYDROCHLORIDE ANCITABINE HYDROCHLORIDE ANDROSTERONE SODIUM SULFATE ANIRACETAM ANISINDIONE ANISODAMINE ANISOMYCIN ANTAZOLINE PHOSPHATE ANTHRALIN ANTIMYCIN A (A1 shown) ANTIPYRINE APHYLLIC
    [Show full text]
  • Leptospirosis Associated Equine Recurrent Uveitis Answers to Your Important Questions What Is Leptospirosis Associated Equine Recurrent Uveitis (LAERU)?
    Lisa Dauten, DVM Tri-State Veterinary Services LLC " Leptospirosis Associated Equine Recurrent Uveitis Answers to your Important Questions! What is Leptospirosis Associated Equine Recurrent Uveitis (LAERU)? Let’s start by breaking down some terminology.! Uveitis- inflammation of the uvea. Resulting in cloudiness of the eye, pain, and potential blindness. Also know as “Moon Blindness”. Caused by trauma, infection, or corneal disease.! Uvea- part of the eye containing the iris, ciliary body, and choroid. It keeps the lens of the eye in place, maintains fluid in the eye, and keeps things in the blood from entering the inside of the eye (blood-ocular barrier). ! Recurrent Uveitis- inflammation of the uvea that sporadically reoccurs through out a horses life time. Each time there is a reoccurring episode, the damage to the eye is made worse, eventually leading to permanent damage and potential blindness. ! Leptospirosis- bacteria found in the environment shed in the urine of wildlife and livestock. Horses usually are exposed when grazing pastures or drinking from natural water sources.! LAERU- Recurrent Uveitis in horses caused by Leptospirosis.! What are the clinical signs of Uveitis? Uveitis can come on very suddenly. A lot of times horses present with severe pain in the eye, tearing, squinting, and rubbing face. The eye itself is cloudy, white or blue in color. Sometimes the signs are not as dramatic. The color change of the eye may progress slowly. In these cases, horse owners may mistake the changes for cataracts.! What do I do if I think my horse has Uveitis? Call your veterinarian to request an appointment.
    [Show full text]
  • Equine Recurrent Uveitis Slowly Releases Medication Over a Period of (ERU) Several Years
    Treatment ABOUT THE COLLEGE OF VETERINARY MEDICINE Treatment for uveitis in general depends upon the underlying cause as well as Ranked third in the nation among the severity of the symptoms. In most colleges of veterinary medicine by cases, the eye is treated with topical anti- U.S. News & World Report, NC State’s inflammatories and a pupil-dilating agent to College of Veterinary Medicine is a decrease the pain and inflammation. Oral driving force in veterinary innovation. anti-inflammatories such as Banamine® From our leadership in understanding (Flunixin meglumine) are also instituted, and and defining the interconnections in select cases bodily injections of steroids between animal and human health, to may be necessary. While these treatments groundbreaking research in areas like are helpful in subsiding the inflammation equine health, and our commitment to and pain - they’re not ideal for long-term training the next generation of veterinary use. If infectious disease is suspected to health professionals, we are dedicated be the cause, laboratory tests should be to advancing animal and human health performed followed by medical treatment if from the cellular level through entire recommended. ecosystems. If a horse responds favorably to medical therapy, Cyclosporine Implants may be an option for long-term management. This is the surgical implantation of a small Cyclosporine medicated disc that’s placed deep within the pink tissue surrounding the eye (sclera), it Equine Recurrent Uveitis slowly releases medication over a period of (ERU) several years. This medication modifies the reaction to the immune system and reduces NC State Veterinary Hospital Moon Blindness; Periodic Ophthalamia inflammation.
    [Show full text]
  • Approach to the Patient with Presumed Cellulitis Daniela Kroshinsky, MD,* Marc E
    Approach to the Patient With Presumed Cellulitis Daniela Kroshinsky, MD,* Marc E. Grossman, MD, FACP,† and Lindy P. Fox, MD‡ Dermatologists frequently are consulted in the evaluation and management of the patient with cellulitic-appearing skin. For routine cellulitis, the clinical presentation and patient symptoms are usually sufficient for an accurate diagnosis. However, when the clinical presentation is somewhat atypical, or if the patient fails to respond to appropriate therapy for cellulitis because of routine bacterial pathogens, the differential diagnosis should be rapidly expanded. We discuss the approach to the patient with presumed cellulitis, with an emphasis on the differential diagnosis of cellulitis in both the immunocompetent and immunucompromised patient. Semin Cutan Med Surg 26:168-178 © 2007 Elsevier Inc. All rights reserved. KEYWORDS cellulitis, erysipelas 53-year-old woman with a history of recurrent breast of cellulitis, and telangiectasia and scattered enlarged mes- Acancer diagnosed 2 years before presentation and treated enchymal cells, characteristic of radiation changes. with radiation and chemotherapy (docetaxel, anastrozole, exemestane, gemcitabine) most recently 6 months before presentation was admitted for 3 weeks of worsening chest Clinical Problem wall pain and a rash over her mastectomy scar. Despite 5 days Dermatologists frequently are consulted in the evaluation of empiric antibiotic therapy with doxycycline and vancomy- and management of the patient with cellulitic-appearing cin, the chest wall erythema and pain were increasing. A dermatology consultation was called. An ulceration and sur- skin. Although the dermatologist may be consulted early on rounding erythematous papules were concentrated over the in the patient’s course, more often a dermatology consult is mastectomy scar with ill-defined erythematous patches that requested when a patient fails to respond to treatment.
    [Show full text]
  • Prednisolone Also Binds to Transcortin • Other Synthetic GS Only Bind to Albumin
    PK/PD considerations for corticosteroids P L Toutain, National Veterinary School, Toulouse, France Wuhan October 2015 1 Anti-inflammatory drugs Corticosteroids NSAIDs 2 Glucocorticoids: main properties • Glucocorticosteroids (GCS) are broad and potent anti- inflammatory drugs. • They are extensively used to mitigate or suppress inflammation associated with a variety of conditions especially joint and respiratory system inflammation. • GCs are not curative: • GCs are only palliative symptomatic treatments and chronic use of GCs can be, in fine , detrimental • GCs possess many other pharmacological properties (not reviewed in this presentation) 3 The cortisol or hydrocortisone 4 Cortisol : An endogenous hormone and a surrogate endpoint of the duration of the GCS effects; it physiology should be understood to use properly GCS 5 Cortisol synthesis • All GCs used in therapeutics are synthetic derivatives of cortisol. • Cortisol (hydrocortisone) is synthesized in the adrenal cortex and it is the main corticosteroid hormone in most species. 6 Steroids synthesis by the adrenal gland Aldosterone Cortisol Androgens Epinephrine (adrenalin) 7 Cortisol ou Hydrocortisone structure – activity relationship Three structural properties are required for a GC activity (i.e. for cortisol to bind to GC receptor) 8 Cortisol (hydrocortisone) • Minimal information on cortisol physiology (secretion, distribution & elimination ) needs to be known to understand the clinical pharmacology of GCS 9 Plasma cortisol • Cortisol levels are very different in domestic species • Pattern of secretion – Circadian rhythm (h) – Pulsatilty (minute) 10 Plasma cortisol level Plasma concentration (ng/mL) 600 500 400 300 Series1 200 100 0 1 2 3 4 5 11 Plasma cortisol levels: circadian rhythm & pulsatility Toutain et al. Domestic.Anim.Endocrinol.
    [Show full text]