Manual of the International Statistical Classification of Diseases, Injuries, and Causes of Death
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The Combined Effect of Sulfanilamide and Penicillin in Treatment Of
THE COMBINED EFFECT OF STJLFANILAMIDE AND PENICILLIN IN TREATMENT OF EXPERIMENTAL ERYSIPELOTHRIX RHUSIOPATHIAE INFECTION OF MICE* JOSEPH V. KLAUDER, M.D. AND ANNA M. RULE In a previous communication (1) we reported the results of determinations oi the therapeutic effect of sulfonamide compounds in mice inoculated with Er- ysipelothrix rhusiopathiae. A report was also made of the ineffective use of these compounds in treatment of patients with erysipeloid of Rosenbach and in treatment of one patient with the septicemic form of the infection (2). In our experimental study sulfanilamide, sulfapyridine, sulfathiazole and sul- fadiazine were separately administered to mice orally in doses of 0.2 Gm. per kilogram of body weight. To some the compounds were administered twice daily for two days before inoculation with a virulent strain of Erysipelothrix rhu- siopathiae and twice daily thereafter for six additional days. For others treat- ment was begun four hours after inoculation and then administered twice daily for six additional days; in still others, for eight additional days. It was observed that 12.5 per cent of mice treated before or after the admin- istration of these compounds survived. Additional evidence of some therapeutic effect was the greater percentage (50 per cent) of survival of the animals treated before inoculation and the longer time of survival of animals treated after inocu- lation compared with those of the untreated control group. The therapeutic effect of these compounds is therefore limited. Sulfanilamide and sulfapyridine appeared to give better results than sulfathiazole and sulfadiazine. The thera- peutic effect of these compounds was slightly enhanced when they were employed in conjunction with subcurative injections of immune serum. -
A Review of Outbreaks of Infectious Disease in Schools in England and Wales 1979-88 C
Epidemiol. Infect. (1990), 105, 419-434 419 Printed in Great Britain A review of outbreaks of infectious disease in schools in England and Wales 1979-88 C. JOSEPH1, N. NOAH2, J. WHITE1 AND T. HOSKINS3 'Public Health Laboratory Service, Communicable Disease Surveillance Centre, 61 Colindale Avenue, London NW9 5EQ 2Kings College School o Medicine and Dentistry, Bessemer Road, London SE5 9PJ 3 Christs Hospital, Horsham, Sussex (Accepted 20 May 1990) SUMMARY In this review of 66 outbreaks of infectious disease in schools in England and Wales between 1979-88, 27 were reported from independent and 39 from maintained schools. Altogether, over 8000 children and nearly 500 adults were affected. Most of the outbreaks investigated were due to gastrointestinal infections which affected about 5000 children; respiratory infections affected a further 2000 children. Fifty-two children and seven adults were admitted to hospital and one child with measles died. Vaccination policies and use of immunoglobulin for control and prevention of outbreaks in schools have been discussed. INTRODUCTION The prevention and control of infectious disease outbreaks in schools are important not only because of the number of children at risk but also because of the potential for spread of infection into families and the wider community. Moreover, outbreaks of infection in such communities may lead to serious disruption of children's education and the curtailment of school activities. Details made available of 66 school outbreaks to the Communicable Disease Surveillance Centre between 1979 and 1988 are analysed in this paper and policies for prophylaxis, for example immunoglobulin and vaccination are described. SOURCES OF INFORMATION Information on outbreaks in schools between 1979 and 1988 was obtained from reports of investigations in which the Public Health Laboratory Service (PHLS) Communicable Disease Surveillance Centre (CDSC) had been asked to assist [1] and Communicable Disease Report (CDR) inserts (Table 1). -
Benign Fibro-Osseous Lesions Plus…
“Vision is the art of seeing things invisible.” Jonathan Swift 1667 - 1745 Benign Fibro-osseous Lesions Plus… Steven R. Singer, DDS [email protected] 212.305.5674 Benign Fibro-osseous Lesions Fibrous Dysplasia A group of lesions in which normal bone is Localized change in bone metabolism replaced initially by fibrous connective tissue Normal cancellous bone is replaced by Over time, the lesion is infiltrated by osteoid fibrous connective tissue and cementoid tissue The connective tissue contains varying amounts of abnormal bone with irregular This is a benign and idiopathic process trabeculae Trabeculae are randomly oriented. (Remember that normal trabeculae are aligned to respond to stress) Fibrous Dysplasia Fibrous Dysplasia Lesions may be solitary (monostotic) or Fibrous dysplasia is non-hereditary involve more than one bone (polyostotic) Caused by a mutation in a somatic cell. Monostotic form accounts for 70% of all Extent of lesions depends on the timing of cases the mutation. Polyostotic form is more common in the first If the mutation occurs earlier, the disease decade will be more widespread throughout the M=F except in McCune-Albright syndrome, body. An example is McCune-Albright which is almost exclusively found in females Syndrome 1 Fibrous Dysplasia Fibrous Dysplasia McCune-Albright Syndrome • Monostotic and polyostotic forms usually -Almost exclusively begins in the second decade of life females -Polyostotic fibrous • Slow, painless expansion of the jaws dysplasia • Patients may complain of swelling or have -
WO 2014/134709 Al 12 September 2014 (12.09.2014) P O P C T
(12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) (19) World Intellectual Property Organization International Bureau (10) International Publication Number (43) International Publication Date WO 2014/134709 Al 12 September 2014 (12.09.2014) P O P C T (51) International Patent Classification: (81) Designated States (unless otherwise indicated, for every A61K 31/05 (2006.01) A61P 31/02 (2006.01) kind of national protection available): AE, AG, AL, AM, AO, AT, AU, AZ, BA, BB, BG, BH, BN, BR, BW, BY, (21) International Application Number: BZ, CA, CH, CL, CN, CO, CR, CU, CZ, DE, DK, DM, PCT/CA20 14/000 174 DO, DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, (22) International Filing Date: HN, HR, HU, ID, IL, IN, IR, IS, JP, KE, KG, KN, KP, KR, 4 March 2014 (04.03.2014) KZ, LA, LC, LK, LR, LS, LT, LU, LY, MA, MD, ME, MG, MK, MN, MW, MX, MY, MZ, NA, NG, NI, NO, NZ, (25) Filing Language: English OM, PA, PE, PG, PH, PL, PT, QA, RO, RS, RU, RW, SA, (26) Publication Language: English SC, SD, SE, SG, SK, SL, SM, ST, SV, SY, TH, TJ, TM, TN, TR, TT, TZ, UA, UG, US, UZ, VC, VN, ZA, ZM, (30) Priority Data: ZW. 13/790,91 1 8 March 2013 (08.03.2013) US (84) Designated States (unless otherwise indicated, for every (71) Applicant: LABORATOIRE M2 [CA/CA]; 4005-A, rue kind of regional protection available): ARIPO (BW, GH, de la Garlock, Sherbrooke, Quebec J1L 1W9 (CA). GM, KE, LR, LS, MW, MZ, NA, RW, SD, SL, SZ, TZ, UG, ZM, ZW), Eurasian (AM, AZ, BY, KG, KZ, RU, TJ, (72) Inventors: LEMIRE, Gaetan; 6505, rue de la fougere, TM), European (AL, AT, BE, BG, CH, CY, CZ, DE, DK, Sherbrooke, Quebec JIN 3W3 (CA). -
Phenotypic and Genotypic Characterisation of Noonan-Like
1of5 ELECTRONIC LETTER J Med Genet: first published as 10.1136/jmg.2004.024091 on 2 February 2005. Downloaded from Phenotypic and genotypic characterisation of Noonan-like/ multiple giant cell lesion syndrome J S Lee, M Tartaglia, B D Gelb, K Fridrich, S Sachs, C A Stratakis, M Muenke, P G Robey, M T Collins, A Slavotinek ............................................................................................................................... J Med Genet 2005;42:e11 (http://www.jmedgenet.com/cgi/content/full/42/2/e11). doi: 10.1136/jmg.2004.024091 oonan-like/multiple giant cell lesion syndrome (NL/ MGCLS; OMIM 163955) is a rare condition1–3 with Key points Nphenotypic overlap with Noonan’s syndrome (OMIM 163950) and cherubism (OMIM 118400) (table 1). N Noonan-like/multiple giant cell lesion syndrome (NL/ Recently, missense mutations in the PTPN11 gene on MGCLS) has clinical similarities with Noonan’s syn- chromosome 12q24.1 have been identified as the cause of drome and cherubism. It is unclear whether it is a Noonan’s syndrome in 45% of familial and sporadic cases,45 distinct entity or a variant of Noonan’s syndrome or indicating genetic heterogeneity within the syndrome. In the cherubism. 5 study by Tartaglia et al, there was a family in which three N Three unrelated patients with NL/MGCLS were char- members had features of Noonan’s syndrome; two of these acterised, two of whom were found to have mutations had incidental mandibular giant cell lesions.3 All three in the PTPN11 gene, the mutation found in 45% of members were found to have a PTPN11 mutation known to patients with Noonan’s syndrome. -
Cherubism As a Systemic Skeletal Disease
Morice et al. BMC Musculoskeletal Disorders (2020) 21:564 https://doi.org/10.1186/s12891-020-03580-z CASE REPORT Open Access Cherubism as a systemic skeletal disease: evidence from an aggressive case Anne Morice1,2,3,4*, Aline Joly3,4, Manon Ricquebourg5,6, Gérard Maruani2,7,8, Emmanuel Durand9, Louise Galmiche2,10, Jeanne Amiel2,11, Yoann Vial12,13, Hélène Cavé12,13, Kahina Belhous14, Marie Piketty15, Martine Cohen-Solal6, Ariane Berdal1,16, Corinne Collet5,6, Arnaud Picard1,2,3,4, Amelie E. Coudert1,6,16† and Natacha Kadlub1,2,3,4† Abstract Background: Cherubism is a rare autosomal dominant genetic condition caused by mutations in the SH3BP2 gene. This disease is characterized by osteolysis of the jaws, with the bone replaced by soft tissue rich in fibroblasts and multinuclear giant cells. SH3BP2 is a ubiquitous adaptor protein yet the consequences of SH3BP2 mutation have so far been described as impacting only face. Cherubism mouse models have been generated and unlike human patients, the knock-in mice exhibit systemic bone loss together with a systemic inflammation. Case presentation: In light of these observations, we decided to search for a systemic cherubism phenotype in a 6-year-old girl with an aggressive cherubism. We report here the first case of cherubism with systemic manifestations. Bone densitometry showed low overall bone density (total body Z-score = − 4.6 SD). Several markers of bone remodelling (CTx,BALP,P1NP)aswellasinflammation(TNFα and IL-1) were elevated. A causative second-site mutation in other genes known to influence bone density was ruled out by sequencing a panel of such genes. -
Rat Bite Fever Due to Streptobacillus Moniliformis a CASE TREATED by PENICILLIN by F
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by PubMed Central Rat Bite Fever Due to Streptobacillus Moniliformis A CASE TREATED BY PENICILLIN By F. F. KANE, M.D., M.R.C.P.I., D.P.H. Medical Superintendent, Purdysburn Fever Hospital, Belfast IT is unlikely that rat-bite fever will rver become a public health problem in this country, so the justification for publishing the following case lies rather in its rarity, its interesting course and investigation, and in the response to Penicillin. PRESENT CASE. The patient, D. G., born on 1st January, 1929, is the second child in a family of three sons and one daughter of well-to-do parents. There is nothing of import- ance in the family history or the previous history of the boy. Before his present illness he was in good health, was about 5 feet 9j inches in height, and weighed, in his clothes, about 101 stone. The family are city dwellers. On the afternoon of 18th March, 1944, whilst hiking in a party along a country lane about fifteen miles from Belfast city centre, he was bitten over the terminal phalanx of his right index finger by a rat, which held on until pulled off and killed. The rat was described as looking old and sickly. The wound bled slightly at the time, but with ordinary domestic dressings it healed within a few days. Without missing a day from school and feeling normally well in the interval, the boy became sharply ill at lunch-time on 31st March, i.e., thirteen days after the bite. -
Prevalence and Incidence of Rare Diseases: Bibliographic Data
Number 1 | January 2019 Prevalence and incidence of rare diseases: Bibliographic data Prevalence, incidence or number of published cases listed by diseases (in alphabetical order) www.orpha.net www.orphadata.org If a range of national data is available, the average is Methodology calculated to estimate the worldwide or European prevalence or incidence. When a range of data sources is available, the most Orphanet carries out a systematic survey of literature in recent data source that meets a certain number of quality order to estimate the prevalence and incidence of rare criteria is favoured (registries, meta-analyses, diseases. This study aims to collect new data regarding population-based studies, large cohorts studies). point prevalence, birth prevalence and incidence, and to update already published data according to new For congenital diseases, the prevalence is estimated, so scientific studies or other available data. that: Prevalence = birth prevalence x (patient life This data is presented in the following reports published expectancy/general population life expectancy). biannually: When only incidence data is documented, the prevalence is estimated when possible, so that : • Prevalence, incidence or number of published cases listed by diseases (in alphabetical order); Prevalence = incidence x disease mean duration. • Diseases listed by decreasing prevalence, incidence When neither prevalence nor incidence data is available, or number of published cases; which is the case for very rare diseases, the number of cases or families documented in the medical literature is Data collection provided. A number of different sources are used : Limitations of the study • Registries (RARECARE, EUROCAT, etc) ; The prevalence and incidence data presented in this report are only estimations and cannot be considered to • National/international health institutes and agencies be absolutely correct. -
Prioritization of Health Services
PRIORITIZATION OF HEALTH SERVICES A Report to the Governor and the 74th Oregon Legislative Assembly Oregon Health Services Commission Office for Oregon Health Policy and Research Department of Administrative Services 2007 TABLE OF CONTENTS List of Figures . iii Health Services Commission and Staff . .v Acknowledgments . .vii Executive Summary . ix CHAPTER ONE: A HISTORY OF HEALTH SERVICES PRIORITIZATION UNDER THE OREGON HEALTH PLAN Enabling Legislatiion . 3 Early Prioritization Efforts . 3 Gaining Waiver Approval . 5 Impact . 6 CHAPTER TWO: PRIORITIZATION OF HEALTH SERVICES FOR 2008-09 Charge to the Health Services Commission . .. 25 Biennial Review of the Prioritized List . 26 A New Prioritization Methodology . 26 Public Input . 36 Next Steps . 36 Interim Modifications to the Prioritized List . 37 Technical Changes . 38 Advancements in Medical Technology . .42 CHAPTER THREE: CLARIFICATIONS TO THE PRIORITIZED LIST OF HEALTH SERVICES Practice Guidelines . 47 Age-Related Macular Degeneration (AMD) . 47 Chronic Anal Fissure . 48 Comfort Care . 48 Complicated Hernias . 49 Diagnostic Services Not Appearing on the Prioritized List . 49 Non-Prenatal Genetic Testing . 49 Tuberculosis Blood Test . 51 Early Childhood Mental Health . 52 Adjustment Reactions In Early Childhood . 52 Attention Deficit and Hyperactivity Disorders in Early Childhood . 53 Disruptive Behavior Disorders In Early Childhood . 54 Mental Health Problems In Early Childhood Related To Neglect Or Abuse . 54 Mood Disorders in Early Childhood . 55 Erythropoietin . 55 Mastocytosis . 56 Obesity . 56 Bariatric Surgery . 56 Non-Surgical Management of Obesity . 58 PET Scans . 58 Prenatal Screening for Down Syndrome . 59 Prophylactic Breast Removal . 59 Psoriasis . 59 Reabilitative Therapies . 60 i TABLE OF CONTENTS (Cont’d) CHAPTER THREE: CLARIFICATIONS TO THE PRIORITIZED LIST OF HEALTH SERVICES (CONT’D) Practice Guidelines (Cont’d) Sinus Surgery . -
Wildlife Diseases and Humans
Robert G. McLean Chief, Vertebrate Ecology Section Medical Entomology & Ecology Branch WILDLIFE DISEASES Division of Vector-borne Infectious Diseases National Center for Infectious Diseases AND HUMANS Centers for Disease Control and Prevention Fort Collins, Colorado 80522 INTRODUCTION GENERAL PRECAUTIONS Precautions against acquiring fungal diseases, especially histoplasmosis, Diseases of wildlife can cause signifi- Use extreme caution when approach- should be taken when working in cant illness and death to individual ing or handling a wild animal that high-risk sites that contain contami- animals and can significantly affect looks sick or abnormal to guard nated soil or accumulations of animal wildlife populations. Wildlife species against those diseases contracted feces; for example, under large bird can also serve as natural hosts for cer- directly from wildlife. Procedures for roosts or in buildings or caves contain- tain diseases that affect humans (zoo- basic personal hygiene and cleanliness ing bat colonies. Wear protective noses). The disease agents or parasites of equipment are important for any masks to reduce or prevent the inhala- that cause these zoonotic diseases can activity but become a matter of major tion of fungal spores. be contracted from wildlife directly by health concern when handling animals Protection from vector-borne diseases bites or contamination, or indirectly or their products that could be infected in high-risk areas involves personal through the bite of arthropod vectors with disease agents. Some of the measures such as using mosquito or such as mosquitoes, ticks, fleas, and important precautions are: tick repellents, wearing special cloth- mites that have previously fed on an 1. Wear protective clothing, particu- ing, or simply tucking pant cuffs into infected animal. -
Practice Parameter for the Diagnosis and Management of Primary Immunodeficiency
Practice parameter Practice parameter for the diagnosis and management of primary immunodeficiency Francisco A. Bonilla, MD, PhD, David A. Khan, MD, Zuhair K. Ballas, MD, Javier Chinen, MD, PhD, Michael M. Frank, MD, Joyce T. Hsu, MD, Michael Keller, MD, Lisa J. Kobrynski, MD, Hirsh D. Komarow, MD, Bruce Mazer, MD, Robert P. Nelson, Jr, MD, Jordan S. Orange, MD, PhD, John M. Routes, MD, William T. Shearer, MD, PhD, Ricardo U. Sorensen, MD, James W. Verbsky, MD, PhD, David I. Bernstein, MD, Joann Blessing-Moore, MD, David Lang, MD, Richard A. Nicklas, MD, John Oppenheimer, MD, Jay M. Portnoy, MD, Christopher R. Randolph, MD, Diane Schuller, MD, Sheldon L. Spector, MD, Stephen Tilles, MD, Dana Wallace, MD Chief Editor: Francisco A. Bonilla, MD, PhD Co-Editor: David A. Khan, MD Members of the Joint Task Force on Practice Parameters: David I. Bernstein, MD, Joann Blessing-Moore, MD, David Khan, MD, David Lang, MD, Richard A. Nicklas, MD, John Oppenheimer, MD, Jay M. Portnoy, MD, Christopher R. Randolph, MD, Diane Schuller, MD, Sheldon L. Spector, MD, Stephen Tilles, MD, Dana Wallace, MD Primary Immunodeficiency Workgroup: Chairman: Francisco A. Bonilla, MD, PhD Members: Zuhair K. Ballas, MD, Javier Chinen, MD, PhD, Michael M. Frank, MD, Joyce T. Hsu, MD, Michael Keller, MD, Lisa J. Kobrynski, MD, Hirsh D. Komarow, MD, Bruce Mazer, MD, Robert P. Nelson, Jr, MD, Jordan S. Orange, MD, PhD, John M. Routes, MD, William T. Shearer, MD, PhD, Ricardo U. Sorensen, MD, James W. Verbsky, MD, PhD GlaxoSmithKline, Merck, and Aerocrine; has received payment for lectures from Genentech/ These parameters were developed by the Joint Task Force on Practice Parameters, representing Novartis, GlaxoSmithKline, and Merck; and has received research support from Genentech/ the American Academy of Allergy, Asthma & Immunology; the American College of Novartis and Merck. -
THE INTERDEPENDENCE of TROPICAL MEDICINE and GENERAL MEDICINE by GEORGE CHEEVER SIIATTUCK, M.D.Fl INTRODUCTION Water Fever, Cholera, Dysentery, Plague and Lep- Rosy
TheMassachusettsMedicalSociety THE ANNUAL DISCOURSE* THE INTERDEPENDENCE OF TROPICAL MEDICINE AND GENERAL MEDICINE BY GEORGE CHEEVER SIIATTUCK, M.D.fl INTRODUCTION water fever, cholera, dysentery, plague and lep- rosy. Among them are other names which President and Fellows the Massachusetts may Mr. of appear new or such as Medical strange, oroya fever, Society: sodoku, or tsutsugamushi disease. It may be a you so kindly asked me to address surprise to find nearly two pages of references WHENyou on this occasion I assumed that you to rabies, and a few, respectively, to pneumonia, would wish to hear about the subject which has small-pox, tuberculosis, and typhus fever. absorbed most of my attention during the past As interpreted by the "Bulletin" the term seven years, namely, tropical medicine. Suppos- "tropical disease" is inclusive. It covers dis- ing that you might like to know something of eases of limited but not tropical distribution the background of this address I venture to say such as Rocky Mountain fever, as well as mal- that my first, contact with the subject was made adies like smallpox, typhus fever and rabies twenty years ago on a trip to the Par East. which modern hygiene knows how to banish and Later, in 1915, I saw much typhus fever, malaria, which, in consequence, are more likely to be relapsing fever, and papataci fever in Serbia.t found today in backward communities in the In 1921 I joined the Department of Tropical tropics than in highly civilized parts of the Medicine at Harvard, started a Service for Trop- temperate zone.