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    MKSAP 18 Infectious Disease

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    ace |IMKSAP Medical Knowledge Self-Assessment Program” Infectious Disease 25 AMARA 9 Category 1 Credits™ available until American College of Physicians December 31,2021 aading beer ein npn iro Attention MKSAP 18 Complete subscribers: If you are receiving the MKSAP 18 print books as part af your MKSAP 18, Complete subscription, remember that you will receive regular content updates in your online account through MKSAP 18 Digital's New Info Updates. New Info Updates will fheuson practice: changing updates, includ Ing new guidelines. You wil also receive four sets of MKSAP 18 Extension Questions (formerly MKSAP Update Questions) that will alow you to earn, CME credits and MOC points through January 202, Not a MKSAP 18 Complete subscriber? IF you wish to add MICSAP 18 Digital to your peint subscription at any time, upgrade to MKSAP 18 Complete for the most value-packed, cost-eifieient combination of NKSAP products, Please callour ACP Member and Customer Service Department, and they will help you arrange easy access to MKSAP 18 Complete. As part of MKSAP 18 Complete, you will receive MKSAP 18 Digital, Including regular content updates through New Info Updates, and fou sets of MESAPI8 Extension Questions (formerly MKSAP Update Questions) that ‘will allow you to earn CME credits and MOC pomts through 2024. You will also recelve MKSAP 18 Flashcards, Virtual Dx. and Board Basics (print and book) at no extra charge. ACP Member and Customer Service 800-ACP-1915 Outside the US. call 215-351-2600 (Monday to Friday. 9 am pm ET) Disclaimer Regarding Direct Purchases from Online Retailers ‘CME and/or MOG for NKSAP 18 fs available only if you purchase the pro sgfam directly trom ACP. CME ereditsamd MOC points cannot beawarded to these purchasers who have purchased the program from non authorized sellers, such as Amazon, eBay, or any other such online retailer acp| MKSAP & Infectious Disease Welcome to the Infectious Disease Section of MKSAP 18! {In these pages, you Will nd updated formation on central nervous system Infecttons, skin and soft tissue infections, ‘community-acquired pneumonia. tick-borne diseases, urinary tract infections, Mycobacterium tuberculosis and nontuber~ ccalous mycobacterial infections, sexually transmitted infections, bioterrorism, travel medicine, infectious gastrointestinal wdromes, ransplant-assoclated infections, HIV and AIDS, lcalth care-assoclated Infections, and other clinical challenges. All of these topics are uniqutely focused on the needs of generalists and subspecialists outside of infectious disease. ‘Tac core content of MKSAP 18 has been developed as in previous editions all essential information that is newly researched and written in TI topic areas of internal medicine —created by dozens of leading generalisss and subspecialis's and guided by certification and recertification requirements, emerging knowledge in the field, and user feedback, NKSAP 18 also contains 1200 all-new peer-reviewed, psychometrically validated, mulliple-choice questions (MCQy) for self assessment and study, including 108 in Infectious Disease. MKSAP 18 continues to include High Value Care (HVC) recommendations, based on the concept arbalancing clinical benefit with ensts and harms, with associated MCQs illastraring these principles and HVC Key Points called out in the (ex. Internists practicing in dhe hospilal setting can easily find comprehensive Hospitalist focused content and MCQs, specially designated in blue and with the (0 symb. Ifyou purchased MKSAP 18 Complete, you also have access to MKSAP 18 Digital, with additional tools allowing you to ‘customize your learning experience, MKSAP Digital includes regular text updates with new, practice-changing information, 200) new self-assessment questions, and enhanced custom-quiz options. MKSAP Complete alsa includes more than 1200 ‘electronic, adaptive learning, enhanced flasheards for quick review of important concepts, as well asan updated and enhanced version of Virtual Dx, MKSAP's image-based self-assessment tool. As before, MKSAP 18 Digital is optimized for use (on your mobile devices, with iOS- and Android-based apps allowing you to syne between sour apps and online account and submit for CME credits and MOC points online. Please visit us at the MKSAP Resource Site [mksan.aeponiline.org) to find out how we can help you stu and MOC points, and stay upto date, arn CME credit (On behalf of the many internists who have offered theit time and expertise to create the content for MRSAP 18 and the editorial staff who work to bring this material to yau in the best possible way, we are honored that you have chosen to ‘use MKSAP 18 and appreciate any feedback about the program you may have. Please feel ree to send any comments 10 mksap_editors@aeponline org, Sincerely Patrick C. Alguire, MD, FACP. Falior in Chief Senior Vice President Emeritus ‘Medical Education Division American College of Phystclans Infectious Disease Committee Patricia D. Brown, MD, FACP, Section Editor* Professor of Medicine ‘Wayne State University School of Medicine Assodate Chief of Staff for Medicine John D. Dingell VA Medical Center Detroit, Michigan Karen C Bloch, MD, MPH, FACP! Associate Professor Department of Medicine and Health Policy Division of Infectious Diseases Vanderbilt University Medical Center Dashvill, Tennessee Larry M. Bush, MD, FACP? Affiliated Professor of Biomedical Sciences Charles E. Schunidt College of Meateine Florida Atlantic University Boca Raton, Florida Adfillted Assoctate Professor of Medicine Unversity of Miami-Miller School of Medicine FFK Medical Center alm Beach County, Florida {Loulse M. Dembry, MD, MS, MBA, FACP® Professor of Medicine Infectious Diseases and Kpidemiology “ale University School of Meuicine New Haven, Connecticut Michael Frank, MD, FACP! Professor of Medicine hief, Division of Infectious Diseases ice Chair for Education Department of Medicine Medical Callege of Wisconsin Milwaukee, Wisconsin Rocirigo Hasbun, MD, MPH* Profescar af Medisine Department of Infectious Diseases UT Health-MeGovern Medical School Houston, Texas Fred A. Loper, MD, MACP* Richard Vial Professor Vice Chair for Education Department of Medicine {Louisiana State University Health Sciences Center New Orleans, Louisiana Jose A. Vazquez, MD, PACP? Chief. Division of Infectious Diseases Professor, Department of Medicine Medical College of Georgia at Augusta University Augusta, Georgi Editor-in-Chief Patriek C. Alguire, MD, EACP? Senor Vice President Emeritus, Medical Education American College of Physicians Philadelphia, Pennsyhania Deputy Editor Davoren Chick, MD, FACP* Senior Vice President, Medkcal Education American College of Physicians Philadelphia, Pennsyvanis Infectious Disease Reviewers Susan C. Bleasdale, MD, ACP? Reata C.Casanas, DO, FACP? Manjit S. Dhillon, MBBS, EXCP! Dimitri M. Drekonja, MD, FACP! Lisa A. Grobskopt, Mtn! Muhanumad Umar Khan, MBBS, EACP* Felicia M. Lewis, MD, FACP* Maricar E Malinis, MD, EACP2 Zavi Min, MD, FACE George Samuel, MD! Hospital Medicine Infectious Disease Reviewers J. Hoon Beang, MD, FACP? Jeana Benwill, MD! Infectious Disease ACP Editorial Staff Linnea Donnarumuna?, Staff Roltor Margaret Wells', Director, Self-Assessment and Fiducational Programs Becky Krumm’, Managing Fditor, Self Assessm¢ Educational Programs and ACP Principal Staff Davoren Chick, MD FACE Senior Vice President. Medical Education Patrick C. Alguire, MD, FACP* Senior Vice President Emeritus, Medical Education Sean Mckinney" Vice President, Medical Education Margaret Wells! Director, Self-Assessment and Educational Programs Becky Krummt Managing Fiitor Valerie Dangovetsky* Administrator Ellen Mefonald, PhD" Senior Staff Faitor Megan Zhorowshi Senior Staff Editor adkle Twomey" Senior Staff iditor Randy Hendrickson! Production Administrator/tditor Julia Nawrocki! Digital Content Associate /Hditor Linnea Donnarumma' Stal] Editor Chuck Feng suajf ator Joysa Winter* Staff Flitor Kimberly Kerns! Audmain'straive Coordinator Disclosure of Relationships with any entity producing, ‘marketing, reselling. or distributing health care goods or services consumed by, or used on, patients. Patrick C. Alguire, MD, FACP Royalties UpToDate Hoon Baang, MD, FACP Stock Options’Holdings Sarepta Therapenties Susan C. Bleasdale, MD, FACP Reseurch Grants/Contracts Rempex Pharmaceuticals, Theravance Biopharma Consultantship MedMined, Ine Larey M. Bush, MD, FAC. Homoraria Merck Manual Beata C. Casanas, DO, FACP Speakers Bureau Pfizer, Allergan Davoren Chick, MD, FAC Rowalties Wollers Kluwer Publishing, Consukariship EBSCO Health's DynaMed Plus, Other: Owner and sole proprietor of Coding 101 LIC: research consultant (spouse) for Vedanta Biosciences Ine Louise M. Dembry, MD, MS, MBA Roarel Member Seciely for Llealtheare fpidemiology of America ‘Stocks Options/Hloldings Advzneed Technical Sunport/Ready och Rodrigo Hasbun, MD, MPH Speakers Bureau Pfizer. Medicine's Company, Biofire Diagnostics, Merck Consultanship BioMerieus Fred A. Lopez, MD, MACP Royalties UpTobatc Maricar F. Malinis, MD, FXCP Other: primary investigator for clinical trials for Chimerix, Astellas Pharma US Ing, and Oxiord Immunotec ‘ose A. Vazquez, MD, BACP Research Grants/Contraets Astellas Pharma US Ine Speukers Bureau Allergan Acknowledgments ‘The American Collage of Physician (ACP) gratefully acknowledges the special contributions tothe develop ment and production of the ith ection ofthe Medical Knowledge Self Assessment Program’ (MKSAP" 18) made by the following people: Graphic Design Barry Moshinski (Dinecion Graphic Services), Michael Ripa (Graphics Tecnica Administrator. and Jenner Groner (Graphic Designer Proctuction Systems: Dan Tloffimann (Director, Information Technology), Scott Hur (Manager, Cntere Sysiems), Net! Kohl (Genior Architet), and Chris Faticrson (Senior Archie) MESAP 18 Digital: Under the direetion of Steven Spadt (Senior Viee President, Technology), the digital version of MKSAP 18 was developed within the ACP’s Digital Products and Services Department, led by Brian Sweigard (Diteetor, Digital Products and Services). Other members ofthe team, incuuded Dan Barron (Senior Web Application Developer Architect), Chris Forrest (Senior Software Developer/Liesign Lead), Kathleen Hoover (Senior Web Developer, Kara Regis (Manager, User interface Design and Development) Brad Lord (Senior Web Application Developer), ard John DicKnight (Senior Wed Developer). The College also wishes to acknowledge that many other petsons, (y0 numerous to mention, have contributed to the production of this program. Without their dedicated efforts, this program would not have been possible MKSAP Resource Site (mksap.acponline.org) ‘The MKSAP Resource Site (mksap.aeponline.ong) is 4 con lunually updated site that provides links to MKSAP 18 online answer sheets for print subseribers: access to MKSAP 18, Digital: Beard Basics e book access instructions; informa tuon cn antinuing Medical Fdacation (CME), Maintenance of Certification (MOC), and international Continuing Professional Development (CPD) and MOG errata; and ‘other new information. International MOC/CPD For information and instructions on submission of inter natlonal MOCICFD, please yo to the MKSAP Resource Site (mksapacponline org) Continuing Medical Education The American College of Physicians is accredited by the Acereditation Council for Continuing Medical Fauestion (ACCME) o provide continning medical education for physicians ss cesignates this endur SAP 18, for a maximum of 275 AMA PRA (Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of thelr participation inthe activity Up t0 25 ANA PRA Category 1 Credits! are available from, December al, 2018, to December 31, 2021, for the MKSAP 18, infectious Disease section. Learning Objectives The learning objectives of MKSAP 6 are + Close gaps hetween actual cate in your pructice and preferred standards of care, based on best evidence +» Diagnose disease states that are Tess common and sometimes overlooked andl confusing » Improve management of comorbid cunditions that can complicate patient care + Determine when to refer patients for surgery or care by subspevitises Pass the ABIM Certification Examination Pass the ABIM Maintenance of Certification Examination Target Audience + General internists and primary care physicians + Subspecislists wino need to remain wp to date in internal medicine + Residents preparing for the certifying examination in internal medicine + Plysiclans preparing for mannenance of eerification in ‘internal medicine (recertification) ABIM Maintenance of Certification (Check the MKSAP Resouve Site (rnksap.aepontine.org) for the latest information on how MKSAP tests ean be used fo apply to the Ameriean Board of Internal Medicine (ARIM) for Maintenance of Certification (MOC) points allowing completion of the CME activity Successful completion of the CME activity, witieh includes participation in the evaluation component, enables the pa ejpant to earn up to 275 medical knowledge MOC ports the ABIM'S MOC program. Itisthe CME activity provider's esponsibility o submit participant completion information 1O ACCME for the purpose of granting MOC ered Earn Instantaneous CME Credits or MOC Points Online Print subscribers can enter their answers online to eam instantaneous CME credits o MOC points. You can submit yourarswers using online answer sheets that are provided at mksap acoonline org. wherea record of your MKSAP 18 credits will be aallable, To earn CME credits or to apply for MOC points younced to answer allof the questions ina test and eam a score of at least 50% correct (number of comect answers divided by the total number of questions), Please ‘note that ifyou are applying for MOC points, you must also enter your birth date and ABIM candidate number, ‘Take either of the fol wing approaches: 1. Use the printed answer sheet at the back ofthis book to record your answers. Go to mksap.acponline.org, access ‘Ute appropriate online ansiver sheet, transcribe your ‘ansivers, and submit your test for instantaneous CME credits or MOC points. There is no additional fe for this 2. Go to inksapacponllinorg, access Uie appropriate online: answer sheet, cirectly enter your answers, and submit ‘your tes for instantaneons CME credits or MOC points, ‘There is no adlitional fe fbr this service Earn CME Credits or MOC Points by Mail or Fax Pay a $20 processing fee per answer sheet and submit the printed answer sheet at the back ofthis book by ‘mall or {x 28 instructed on the answer sheet. Make sure you calculate your score and enter your birth date and ABIM candidate number, and fax the answer sheet to 215-351-2799 or mail the answer sheet 'o Member an Cascomer Service. American College of Physicizins, 190 N. Independence Mall West, Philadelphia, PA 19196-1572, using the courtesy envelope provided in your MKSAP 18: slipcase, You will need your 10 digit order number and 8-digit ACP ID number, which are printed on your pack ing slip. Please allow 4 to 6 weeks for your score report to be emailed back to you, Be sure to include your email address for a response Ifyou do not havea 10 digit order number and @ digit ACP 1D number, or Ifyou neal help creating a user-name and password fo access the MKSAP 18 onlineanswer sheets, go to mksap.acponline.org or email custserv@acponline.org, Disclosure Policy Iis the policy of the American College of Physicians (ACP) to ensure balance, independence, objectivity, and scientific rigor in all ofits echicational activities. To this ‘end, and consistent with the policies of the ACP and the Accreditation Couneil for Continuing Medical Education (ACCME), contributors to all ACP continuing medical ‘education activities are required to diselose all relevant Ahanctal relationships with any entity producing. mar keting, re-selling. of distributing health care goods or ser vices consumed by, oF used on, patients. Contributors are required to use generic names in the discussion of ther peutic options and are required to identify any unap proved, off label, or investigative use af commercial prod ucts or devices. Where 2 trade name Is used, all available trade names for the same product type are also included. I trade-name products manufactured by companies with whom contribistors have relationships are discussed, con tributors are asked to provide evidence-based eltatlons in support ofthe discussion, The information is reviewed. by the committee responsible for producing this text. If necessary, adjustments to topics or contributors’ roles In content development are made to balance the discussion. Further, all readers of this text are asked to evaluate the: content for evidence of commercial bias and send any rel evant comments to mksap_editors@acpontine.org so that Future decisions about content and contributors can be ‘made in light of this information, Resolution of Conflicts To resolve all conflicts of Interestand influences of vested interests, ACP’s content planners used best evi dence and updated clinical care guidelines in developing content, when such evidence and guidelines were avait able. All content underwent review by peer reviewers not on the committee {0 ensure that the material was balanced and unblased. Contributors’ disclosure infor ‘mation can be found with the list of contributors’ names and those of ACP principal staff listed in the beginning, of this book, Hospital-Based Medicine Forthe canvenience of suseribers wi provide care in hospital settings, content that is specific to the hospital setting has beet highlighted in blue. Hapa eons ED) highlight where the hospital-only comtent begins, continues over more than one page. and ends High Value Care Key Points ey Points in the text that relate o High Value Care concepts (ahatis, concepts that aiseuss balancing clinical benefit with costs and harms) are designated by the HVC icon HVC] Educational Disclaimer ‘The editors and publisher of MRSAP 18 recognize that the development of new material offers many opportu- nities for error. Despite our best efforts, some errors may persist in print. Drug dosage schedules are, we believe, accurate and in accordance with current standards. Readers are advised, however, (o ensure that the recom- mended dosages in MKSAP 18 coner with the infor mation provided ia the product information material This s especially important in cases of new, infrequently used, or highly toxic drugs. Application of the informa ton in MKSAP 18 remains the professional responsibility, of the practitioner, The primary purpose of MKSAP 18 is educational Information presented, as well as publications, technol ‘gies, products, and/or services discussed, is intended to inform subscribers about the knowledge, techniques, and ‘experiences of the contributors. A diversity of professional ‘opinion exists, and the views of the contributors are their ‘own and not those of the ACP. Inclusion of any material in the program does not constitute endorsement or recom mendation ty the ACP. The ACP does not warrant the safety, reliability, accuracy, completeness, or usefulness of and dis- 50y orthore wth aktered cellars enmity ampicillin iors | covemgp ali W cafrinsne dreoloterine plusiV I moxifonacn insead of cephalospara NM vimetheprin suliamethowsssie hatesd of amprelin| Allergies to lactams Hosptakacquired bacterial W vancomycin plus ether V meningitis cotazdime,colepme, or mecopene'n Neurosurgical procedurse | Wencomycin plus ther V cefosidine,celepmne,cr | meropenem redhces morbidity and mortality in adults with pneumoceecal ‘meninytis and reduces the risk of neurologic sequclacin bacte tal meningitis in developed countries it should be gen «on comitanily with the first dose of antibiotic therapy: RRP INSamiatareste a ES *+ For diaghonis of hactesial meninglus, dhe cerebrospinal Mute Gram stain resltispesitve In 60% 10 90% of infections; latex aggatination esting for arterial antigens snot ree ‘ommended because low senstnity and specifiy Intravenous antibiotic therapy and dexamethasone should be started @s soon as possible when bacterial ‘meningitis s suspectec Selection of initial empiric ant bioties is based on age. local epidemiologic patterns of pneumococcal resistance, and the necessity for ampseil lin coverage for Lsterta monocytogenes, Adjunctive dexamethasone seduces morbidity and mor tality in adults with pneumococcal meningitis and reduces the risk of neurologic sequelie in bacterial ‘meningitis in developed countries. Central Nervous System Infectior Subacute and Chronic Meningitis, Subacute and chronie meningitis are defined by symptom duration between 5 and 30 days and more than 36 days, respectively. The most common infectious causes. are Mycobacterium tubereulesis and fang Tuberculous Meningitis: Mycobacterial tuberculesis meningitis classically presents as, basilar meningitis with cranial ncuropathies (particulary of era nial nerve), mental status changes. and the sendrome of nap propriate seeretion of anticuretic hormone. A history of tuber culosis exposure, an abnormal chest radiograph, 2 positwe tuberculin skin tes! result, and a positive interferon 7 release assay result are suggestive but can be absent, CSP examination, shows. lymphocytic pleocytosis (leukocyte eountof 100 500/41 100 50010). clevated protein evel, and hypeghcorrhachia. CSF acid. fst bacilli smenris insensitive, and culture results are Positive In only 38% to 88% OF patlents. Culture sensitivity Increases when lumbar punctures are performed serially for at least 3 days. Nuclet acid aruplifeation testing should be per formed when possible, espectally when the aeid-L! bacl stain result s negativeand suspicion & high, because it might increase diagnostic yield. Antituberculous therapy should be adminis tered for | year, and adjunctive glucocorticatds shoald be given. initially because oftheir assocation with improved outcomes. Fungal Meningitis Fungal pathogens, including Cryptococcus neoformans, Coccldloides immitis, Hisioplesma capsulatum, and endemic smyeoses, are a significant cause of subacute or chronie menin= agitis syndromes. Fungal meningitis is diseussed in the Fungal Infections chapter: Neurobrucellosis Neurobrucellosis cccurs in 4% £0 18 of patients wath bruce- losis, which is endemic to countries in the Mediterranean, Middle Fas, and Central America. It may present with menin itis, meningoencephaiitis,eranial neuropathies, myelopathy. radiculopathy; or strake or as 2 brain abscess. The diagnosis is made by a positive cullaze or serologic test result for brucel losis in the CSF or blood. Treatment consists of combination antimicrobial therapy (such as ceftriaxone, fampin, and doxy: ‘ycline) for atleast 6 months. Parasitic Meningit Acute primary amebie meningaencephallds caused by Naeger, Balamuthia, and Acanthamoeba species isi fatal infection that lnicaly resembles bacterial meningitis. Preshwater exposure is a key historical cle, Examination of a fesh SF sample can reveal motile trophovoltes, hut the Centers for Disease Control ‘and Presenton shold perform confirmatory testing by PCR Treatment shoud Include mitefosin: Helminth infections causing eosinophilic: meningitis inchide Angiastrongylus cantonensis, Raylisasearis procyonis. ‘Teentasoltum (neuroeysticercosts), Schisiosomaspecies schis osomiasis), and Gnathosioma, Neurceysticereesis is endemic inMexico, South Ameriea,and Asia. It most commonly presents with setzares or hydrocephalus, and CT sean of the head shows, ‘multiple cysts orcalified lesions. Noninfectious Causes MedicationssuchasNSAIDS, antibities,and intravenous immune lobalin can oceasiomally cans aseptic meningitis. Meningeal Iinovement of leukemia, lymphoma, and metasatic carcinoma cean ako present as aseptic meningtis, with the CSE cytology showsing atypical or irmmatore cells and severe hypelyeorrhnchi (10 my/dl-[0.6 mmol/L). Systemic lnpuserythematosas Behiet disease (recurrent cral and genital uleers with iidocyelts), Vogt Koyanagi ada syndireme (uwworeninggencenaits sarcoidosis can all present with asepric meningitis. Finally, chemical meningitis can be seen ater intrathecal injections, new resuugeal procedies, or spinal anesthesia, ‘+ Tubercalous meningitis classically presents as basilar ‘meningitis with crantal neuropatiies, menial status ‘changes, and the syndrome of inappropriate secretion, ofantidturesie hormene; i should be treated with antituberculous therapy for 1 year along with initial adjunctive glucocorticoids. neu Freshwater exposure is a key historical ciue in suspected cate primary amebie meningoencephalts. ‘Medications such 2s NSAIDS, antibiotics, and intrave- ‘nous immune globulin can occasionally cause aseptic meningits. Health Care-Associated Meningitis and Ventriculitis Health care associated meningitis and venteiculitis, of noo, ‘comial meningitis, canoccur after head trauma or aneurosur- gical procedure (craniotomy, lumbar puncture) or secondary to.2 device infection (for example, CSF shunt or drain, intra ‘thecal pamp, deep brain stimulatos)..Normal or abnormal CSF cell count, glucose level, and protein level do not reliably con: firm or rule out infection in these patients, Staphylococcus species and entere gram-negative becteria are the mest com: mon causes, but up (0 SO% of infections can have negative ‘aalture eaults, The use of -D-gluean and galaetomannan CSF assays may ald in the diagnosis of health care related fungal \entriculitis and meningitis. Empirie antimicrobial therapy i cautlined ia Table 2 and should be accompanied by device moval if present (Gi oc So # Staphylacoceusspecies and enteric gram-negative bacieria are the most common causes of health care associated meningitis and ventriculitis, but up to 50% of infections ean have negative cultare resus. Focal Central Nervous System Infections Brain Abscesses Brain abscesses can occur tn immunocompetent or immuno: suppressed persons and are most commonly seen in men. Predisposing conditions in immunocompetent patients can be ssc in Table 3, Brain abscesses are most commonly caused by sznacrobes, aerobic and microaerophilie streptococci, and Enterobacteriacene. Initial erupirie therapy is gnided by the kely predisposing condition and is outlined in Table 4. Aspiration of the brain absexss for culture is preferred for efinitive diagnosis: surgical or stereotactic drainage should be Condition Incidence Contguousioc ofinfectionsuchassinuitis 50% | (Frontal lobe) ard otis mecka (emporal lobe oF leerebolirn) Hematogenous sometimes th mutiple 25% abscesses odontogene resultng from vricans reprococti, endocarditis injection drug use) Cryptogenic most lively odontogeric} 19% | Neurosurcery oc nenetating head trauma 10% ntral Nervous System Infections performed if tne abscess is large (2.5 em), Antibiot therapy should be given for 4 (08 weeks with follow up emanial imag. ing to ensure resolution of the infection, Immunossppressed patients (those with HIV or AIDS, patients undergoing solid organ or bone marrow trangplemia tlon) are al risk for development of brain abscesses from sev eral oppoctuntstic mfections. See HIV/AIDS and Infeetions in Transplant Recipients for further discussion. + Drainabscesses in immunocompetent paltents are ‘treated empirically based on the likely predisposing fac tor with surgical or sereatactic drainage of abscesses greater than 2.5 em. Cranial Abscess (Cranial epidural and subdural abscesses can arise from under Iyingostcomyelitis complicating paranaeal sinusitis (Pott pully fumor) of otitis media or after neurosurgical procedures oF head trauma, Rarely they may arises a complication of bac terial meningitis. Cranial epidural abscesses are usually slow growing, presenting with subacute t chronic symptoms of headache, localized bone pain, and focal neurologie sign. In contrast, subdural empyema isa mpidly progressive infection Predisposing Condition Usual Causative Agents Empiric Antimierobial Therapy Ottis media ar mastoicits Streptococci (aerobic ar anaerobic), Metronidazole plus third-generation | Bucteroidesspecies, Pevotells species, cephalosporin’ i} Enterobacteriacsae’ Sinaetie Streptococs Bactersides species, Metronidazole pls «third-generation Enterobarteriscene, Saphylococeus aureus, cephalespora> Mhaemephiles species Dental sepsis Mixed Fusobacterium, Prevotlla and Bacteroides species; streptococci S.oureus stieprococe, Enterebacteraceae, Coowridiom species Ponevating trsume or aker newosurgery Lung abscess, empyema, bronchi Nocarcia spaces Endocerdis Hematogenousspread frem pelvic. ita abdominal ox gynecolaci infections Inmunecompromises patents, Hiv.infected patients acter Species Fuscbacterium, Actinomyces, Racteroides, ‘and Prevotolla spaces: steptococd: S.aureus, sueprococel Enteric gramnegativebactoria, anaerobic Listeria species, tungal organisms (Cryptococausneotormansy.o parasiicor os protozoal organisms (oxoplasmn gor Asporgilus, Cocodloides, anc Nocarcia Ponicilin plus metronidazole | | Vancorryen us a third-generation ephalesporn Pesiclin rue matronidazsle placa sulfonamide! | Vancomycin plus gentamicin Metronidasole plus third-genérstion cephalosporins Metronidazole plus thite-guneration halosporin’***; antifungal or amtiparastc agent “etme tain cued by reins Sap yaa Vue ceasidne or calepie finicton case by Prudomants runes asc Maropotem an supa aneamyen ea aa barons a wtitaphyacees lacmoxciin Central Nervous System Infections ‘with high mortality that represents'a neurosurgical emergency. ‘The CSF formula in both parsmeningeal infections shows newt tophilie pleaeytoss and a very high protein level, frequently ‘with negative Gram stain and culture results. Pathogen ident Fieation is best achieved by ealtare of theahscess obtained dir ing sangjealceainage. © Incranialepidural and suhelural abscess, pathogen -entifization fs best achieved ky culture of the abscess objained during surgical drainage. Spinal Epidural Abscess Spinal epidural abscess most commonly results from hemratoa ‘enous dissemination, with S. aureus accounting for approxi mately 50% of infections; streplocaceus and gram-negative bacillisuchas Escherichia coliarealsoimplicated, Predisposing factors fur bacteremia include endocarditis, injection drug use, Jong: term) intravenous catheters (hemodialysis catheters, cen ‘al Hines), and urinary tract infection. Spinal epidural abscess ‘ean abo occur after neurosutgieal procedures (spinal fasion, ‘epidural catheter placement) or paraspinal mjection. Patients usually develop localized pain atthe site of infection that later radiates down the spine. MEI i theimaging modality of chotce to identify location and extent of the abscess. All patients Should undergo 4 haseline laboratory evaluation, including, ‘exythrocyte sedimentation rate and C reactive protein. Blood caltures should be obtained before starting. antibiotics. ‘Although the duration of antibiotic therapy lacks robust sup ‘porting data and must be determined on a case-by case bess atleast 6 weeks of efective antimicrobial terapy is reasonebie, Surgical drainage i indicated in patients with neurologic sympioms or signs (ower extremity weakness, numbness, bladder and bowel dysfunction), Follow-up MRI is not ma cated unless the patient has persistent elevation of inflamma tory markers, lack of clinical response, or new neurologic symptoms or signs. Tubercalosis (Port disease) and brucelioxs should be considered in patients with negative culture results and appropriate travel history and risk factors. EL ‘= MRI is the imaging modality of choice t identify Ioca. tion and extent of a spinal epidural abseess, and blood Ccaltures should be obtained before staring amibiotic therapy. Encephalitis Encephalitis is Inflammation of the brain parenchyma Possible encephalitis is defined by the presence of one major {ateted consciousness formore than 24 hoats) and bw minor (fever, new onset seize, new onset focal neanslogic fil Ings, CSE pleocylosis, and abnormal MR orelectrocucephal raphie findings! cetera fom the Intemational Fncephalitis Consortium, probable or confined encephalts teqires one 6 major and at least three minor erliela, The causative agent is ‘unknown in 37% t070% of infections, depending on whether ‘viral PCR is used and autoimmune causesare investigated. The ‘most common Known causes are viral (hexpes simplex virus Iypes | and 6, varicella-zoster virus, and West Nile virus) and autoimmune diseases. Viral Encephalitis Herpes Simplex Encephalitis, HSV-1 is the most common cause of sporadic encephalitis in the United States. requiring prompt identification and treat ment with intravenous acyelovie. Factors associated with an adverse outcome include older age, abnormal Glasgow coma scale. and delay in starting antiviral therapy. HSY-1 encephalt lis presents with fever, seizures, altered mental status. and focal neurologe derieas with unilateral temporal lobe edema, hemorrhage, or enhancement on imaging, Bilateral temporal lobe findings in the insula or cingulate are less commonly seen. The CSF formula usually shows lymphocytic pleoeytoss, anclevated protein level, anda normal glucose level. The diag, nosis is confirmed by HSV PCR of the CSE (08% sensitivity 94% specificity). However, false-negative results have been reportedif HSV is suspected. a repent PCR should he obtained within 1 week while continuing acyelovie therapy. Therapy uration for HSV encephalitis should be M4 10 21 days. lectrocnceohalography can be helpful in identifying the Joral dysfunction and specific area of the brain involved and in deieeting subclinical seizure activity. Human herpesvirus 6 can cause severe encephalitis in transplant reefpients, Cytomegalovirus can cause encephalitis, with perwentricular enhancement on imaging in immano suppressed patients (hose with AIDS or ater transplantation) Dingnesis isby PCR of the CSE for eytomegalovinas. and treat ‘ment is parenteral ganciclovi, Cytomegalovirus and Epstein Barr virus can cause meningoencephalits in young. immuno ‘competent patients presenting with infectious menonucleasis syndromes, agree of ce Varicella-Zoster Virus Encephalitis, Vorieella zoster virus (VZV) is a commonly umderdiagnnsed. treatable cause of encephalitis in adulis. VZV ean present with vvasculopathy with a stroke, encephalitis, meningitis, raticw lopathy, or nyelitis, Patients can present without a vesicular ish, 9 a PCR of the CSF of a serum-to-CSF anti VZV IgG ‘shemle be ordered in all patients with encephalitis. Ireatment ‘with intravenous acyclovir for 10 to 1¢ days is recommended, Arboviruses Arboviral CNS infections in the United States are most com ‘monly seen in summer or fall and! include West Nile (WNV), Easier and Western equine encephalitis, St Louis encepha tis, Powsassan. and La Crosse viruses. WNV is the most com ‘ion cause of epidemic viral encephalitis in the United States. WAY can cause meningtis, encephalitis, acute accid paraly sis (Similar (© polionivelitis), neuropathy, and retinopathy. Older patients. andl those who have undergone trarsplantation rare immunosuppressed have a higher risk of death. WNV affects the thalamus and the basal gunglia patients present ‘with facial or atm tremors, parkinsonism, and myoclonts, Hypadense lesions orenhancements may be seen in the thal ims, basil ganglia, and midbrain on MRI of the brain. Diagnosis is confirmed by a positive WNY feM tn the CSF or Serum: treatment is suppoctive. IV encephalitsis the ease oF HIV-associated dementia in later stagss of the untreated illness; IL Gun abo present as CUS encephalitis, consisting of perivascular inflammation resulting frum infiltration of CDs” lymphocytes, which may oceur as part of an immune reconstituiion syndrome, in some easesassociated with viral escape (low levels of detectable HIV RNA in CSP). ED ‘+ Herpes simplex virus 11s the most common ease of sporadic encephalitis in the United States, presenting ‘with fever, seizures, altered mental status, and focal neurologe defieits; prompt dentitication and treatment ‘with intravenous acyclovir improves outcomes. Varicella zoster virus (V2¥) isa treatable form ot encephalitis and may present without vesicular rash, so polymerase chain reaction of the cerebrospinal Maid (CSP) ora serum. to CSF antt-VZ¥ igG should be ‘ondered in all patients with encephalitis. West Nile virus isthe most commun eause of epidemic Viral encephalitis in the United Slates Autoimmune Encephalitis Auioimmune neurologic diseuses can manifestas encephalitis, ‘cerebelils, dystonta, status epilepticus, cranial neuropathies, and myoclonus. Anti N-methyl D aspartate recepiorenceph slits is most common; i was intially described a8. paminee plastic syndrome:afecting young women with ovarian terato ‘mas, but it can be associated with other tumors (sex com seromal (umors, small cell hung cancer) or occur without a ‘tumor. Young women (<35 years) often present after viral Hike lulness with behavioral changes, headaches, and fever followed by altered mental status, scares, abnormal movements, and autonomic Instabiliy. Treaument includes intravenows gluco comticoids, intravenous immune globulin, tumor removal (if present), and, in some cases, plasmapheresis and ritaximeb. Prion Diseases of the Central Nervous System Prions cause rare but refentlessly progressive and rapidly fatal neurodegeneralive disezses characterized by dementia and ataxia. The cause of diseases an abnormally folded prion pro {cin, In humans, prion diseases ovcur by three mechanisins sporadic (spontaneous), familial (genetic), and acquired Prion Diseases of the Central Nervous System (infectious or ransmissbe). In patients of any age presenting ‘with otherwise unexplained mpidly progressive dementia and ataxia, diagnosis ofa prion dissase should be considered (TableS): the infectious forms aze now Tare (Table 6), Prion diseases have no known therapy Sporadic Creutzfeldt-Jakob Disease Spontaneous (sporadic) disease & the most common form of Creutzeldt Jakob disease (CID), with an incidence of per Inillion worldwide. No environmental risk factors are known, Clinical manifestations include rapidly prupressive dementia, Usually ower 4106 months, Ataxia, myoclonus, and pyramidal and extrapyramidal signs may be observed. Loss of vision is, not uncommon, and patients become comatose before dying, | Rapid cogeitive decline Two ofthe following signs or symptoms: Myoclorus Pyromidalextrapyramical dysanction Visualessfunction Cerebellar dysfunction Akinesie vin Focal coal grt example neglect aphasaaclula, | Sal | Typical EEG sndfor MR Otherinvestications should not suegestanalternative diagnosis European MRI-CJD Consortium Criteria (20097 Progressive dermentla | One of the folowing signs or symptoms: | Myoclonas | FyramiclVextrapyramidal symptoms Akinetic matiem AND Either ‘Wool EEG Hlevated CSF protein 14.3: (with total diseave duration: yeas) oR | Typical rl Foutine investigations should nat sugges an atomainve hagnesis [0 Geuatac ine dna Foch Ri Visualicerebeliar csfunction | Skin and Soft Tissue Infections eee Disease Classification Acquired Idiopathiconly {not ‘enaronnnenta) Sporadi fatal frill ncomoia | Sporadic oD | seopabidtamminstle Yaiet Drom | Kru innerted Fail CD | oss | owen “The diagnosis can be made by clinical history and MRI; cer ebrospinal fluid analysis positive for either total Taa or 14.33 protein may also be useful Transmissible Prion Diseases Variant CD (CID) is the human form of bovine spongiform encephalopathy. It generally affects younger persons (age 15-50 years), frequently presenting with rapidly progressive neuropsychiatric manifestations (depression, withdrawal) and peripheral neuropathy, followed by cerebellar ataxia, invotun tary movements, and cognitive deciine over a 22 month, period, Beecause ¥CID can be transmitted throug blood prod. ucts and tissue, iis a serious public health concern world ‘wide, Probable yCID is diagnosed by typical MRI findings (hockey stick sign” in the posterior thalamus) and tonsil biopyy to detect scrapie assoctated prion protein tn a patent witha compatible clinical presentation (ce Table 5). latrogente CID is exccedingly mre, but transmission has been documented with contaminated cadaverte prtultary- derived hnman growth hormone and gonadotropin, dura mater, stereotactic electroencephalogeaphy needles, neurosur- sical instraments, corneal transplants, medical instruments, implanted electroencephalography electrodes, and blood, transfusions Familial Prion Disease ‘Many mtations have been associated with the prion pro gene. Allare autosomally dominant. These inclade the gradu ally proxsessive Gerstmann Striussler Scheinker syndrome andl the rapidly progressive fatal familial insemna a a + Prion disease should he inchaded in the differential diag ‘nosis ofa patient of any age presenting with otherwise unexplained rapidly progressive dementia and ataxia. + Spontancous CreatzfekdL-Jakob disease is the most com. ‘mon form of prion disease and has no known risk RIOT. Skin and Soft Tissue Infections Introduction ‘Skin infections usually result from epidermal compromise that allows skin colonizerssuch as Staphylococcus aureus and Stieprococeus pyogenes to become pathogenic. Predisposing, conditions include vascalar disease, Immunodeficiency, net ropathy, previous cellulitis, obesity, skin trauma, tinea pedis, and lymphedema, Infectionscan be characterized by anatomic, involvement and presence or absence of pus. Nonparulent spreading skin infections include erysipelas, ceulitis, and necrotizing sol isee infection; purulent skin infections refer to absceses (Figure 2), furuncles, and carbuncles. Paralent skin infections are generally caused by staphytococd. inctud- ing. methicillin resistant Staphylococcus aureus (MRSX): rnonpuruient skin infections ate usually caused by 8 hemolytic streptococci. Table 7 inclucles other skin Fathogens and their ‘associated risk factors for less common causes of skin infec tion, Complications of infections include systemic infamma, tory response (as in severe cellulitis) or systemic toxin release {as in tose shoek syndome) Erysipelas and Cellulitis Hiysipelay refers to infeetion of the epidermis, upper dermis, and superficial lymphatics. Usually involving the face or lower ‘extremities, this infection is brighily erythematous with dis tinct elevated borders and associated fever, ymphangitis, and regional Iymphaclenopathy see MKSAP 18 Dermatology). Callatitis refers to infection involving the deeper dermis and subcutaneous fat tissue, Inflammatory’ signs of infection are similar to erysipelas, ut the area of involvement ts less weil, demarcated Although thediagnosis of erysipelas ur cellulitis is usally established clinically, appreximately one Unird of patients are FIGURE 2. Acutancous atscss draining purser ae ssw; its ‘used by malin isan Spiyecocus owes bate. a Mine eremonas hydrophila Vinnie wlnifcus, Vibrio. porshaemoltics Ensipelothricdhusiopathiae Contact mith rechanter ake, roam rivore (including brackish water ‘Contact with leeches ‘Contact with alt waterorbractish water ‘Contac: with drippings from raw zesfood Consumption of undercooked shellish (panicdany oysters) Liver cithosis or chronic Iver disease ‘Contac: with saltwater inarine We(can also Infect frestmoter Fah) Posteurelle mubocida Contac: pilmatly wit eats and ogs Ceprocvtophaga canimosses Contact primarily with doge Bacitusardtvac ‘Contact with infected animals or animal ‘products. May be the esut of bicterorism Francisllatulawnsis Contact withorbite om nfected animal (partculary cateachropod bites (pariculaly tees) ‘Burkhoera mall: Contact with tissues or boul fuids of infected mules orhorses Cloetichom perkingens Surgary or other significant rourna Mycobacterium marinum Contactwith fresh water orsalkwiter, inelacing fish tanks and swimming pools Mycobacteriam fortum Expenure to freshwater footbatha/pedicuresat nal zalena partcdatly alter ar shoving: sugery ‘Skin and Soft Tissue Infections ‘Comment Callas nonspecific clnicalapppeerance: ‘miner tourna to skin usuelly lead to Inoculation ‘oforganiem Callus through dee: noculatoninw skin | ligation leads to bacteremia with secandary sk infection Hallmarkshemorhage buloeimaeaot | cellulitis lesion) CCelluits usualy involves the hand or arm, especially nthose Handling fish, shellish of ‘ctasienaly,poutryor meat contaminated with becterum Causes eryineloid dicease ellis occurs as aresut of eat scratch or bite Callie ancicepse ae present, patculerlyin patente with hypospllentan Evemnaious pruritic lesion with central eschor: spore-forming organism Ulzoroglandler syndrome choracteiced by Ulcerative lesion with centraleschar and localzed sander hymohadenyaathy, constitutional symptoms often present Pustules with suppurative localzed lymph nodes or eeratve rule tite o NNecrotiing infection, oten teferredtoas clestial myonecrosisor ges gangrene Lesion is often tauma zssociated and often involes the upper exterrity papular lesions become uicerative at ste af nocuation: ascendna lymphaticspread can be seen (spototicheid! appearance): systemic toxicity usualy absent | Fuuncls: posopentve woundineaien | ‘misdiagnosed. Clinical mimics include contac! or stasis der rratitis, Iymphecema, erythema nodosum, deep ven fyombosis, thmombophlebiuis, lipadermatoscierosis, eryth romelalgia, rauma-related inflammation, and hypersensitiv MKSAP 18 Dermatology). Blood culture results are positive in approximately 5% of patients with ery sipelas and cellulitis and are not routinely indicated: however: ccultures should be performed for those who ereimmunocom ‘or have unususl previpiating, Ciecunistances, including Immersion injury or animal bites Culture of skin tissue aspirate or biopsy should also he consid cred for these patients. Radiograph maging snot helpnl foe the diagnosis of erysipelas or cellulitis but may be helpful when a deeper necrotizing infection is suspected, For immunocompetent patients with cellulitis orerysip elas who have no systemicsigns or symptoms (mild infection), ity renetions (se promised, exhibit sever: ses empiric onl therapy directed against streplacocet is recom rmencled as outlined in Table & (see MKSAP 18 Dermatoigy. Treatment duration for uncemplicated infection can be as short as days but should be extended as necessiry until the infection improves. In patien 5 with systemic signs (moderate {infection), ineravencus treatment is recoramencded (see Fable 8). Treating predisposing factors (aich as tinea pedis. edema, and primary skin disorders) may decrease the risk for recur rent infection. Propaylactie anubinties such as penicilin or erythromyein can be considered In patients with more than three episodes of celllitis anmaally Patients who are immupocompromised, who have ss temic inflammatory response syndrome and hypotension, oF who have evidence of deeper necrotizing infection such as bullae and desyuamation (severe infection) should receive urgent uation for debridement. Initial ermpirie al € 9 ‘Skin and Soft Tissue Infections In Sn Treatment Enipolasorcelllitis Mic: Ox peniclin, amoxclie, caphalesn, diclexacilin,cincamycin Moderate: Intravenous penicilin ceftriaxone, cefazolin, lindemcin Severe: Surgical azzeszmentfor possible necrotizing component and empiric inravenous vancomycin pls Piperscilin-tazobactem, injrencin,cr merspenem Necrotizing fasitis Plymic-obial infection: Surgical sscessment/dexidement and combination theeapy such as vancomycin plus piperaollintazeboctam 0: migenem er meropenem Supeococcus pyogenes or Cesium perkingens: Surgical assessmertidebridementand pencilin plas | 389 °C (120°) Syitelicblood praceura <90 mm Hg Difuse maculaecash with subsequerk desquamatr, espacial ise cant Involvomontofthroe or more of the following organ syst Gestrontestinal (nates, vor, ciarhoa) Musculor severe myalgia or ivefoldor greeter increase sehurn Gens rua level. Mucous membrane hyperemia ofthe vagina, conjuncivae, | | orphan) | Kidney (blood wea rivogen orserum creatine evelat | leastiwicethe upper imiof narmal) | Livor(biieubin, aspaate aminotransferase, or alanine aminotraniferace concentration twice the upper init of normal Blood (plarelat count <1 00,0001 [100107 | Central nervous ystern(ciserientation without foal paula tare) Negative results on serolagietestng fer RockyMountain =| spotied fever lepiosoioss, and meas; negative cerebrospinal fg cultures lororganisms other tan Staphylococcus aureus sho deh Pa chloe 508 eros vies | Definite case | tocleion of GABHS frome tere site (bloud,cerebroypnel Mid, operative wound) | | Probable case Isolation of GABHS fom a nonsterile ste(Jhrout, vagina skin lesion) | Hypotension (stoic prossure-<#0 mm Ha) “The presence cf 22 of the following findings: Kidnay{acata kidney irjury ile) Liver (elevated aminotransferase concentrations) Shin erythematous mactacrash, soft issue necrosis) Blood (coagulopathy, incucing thrombecyopeniaard disseminated intravascular cougulation) Pulmonary (ocite respiratory cstess syndeome) 13 Community-Acquired Pneumonia [Ee 2a atte an injcton drag se Streptococcal 1855 associaied with skin an soft ussue infection, particularly NE Bacteremia anil mortality rales are higher with streptococcal than staphylococesl surgical debridement. Antibioties for streptococcal ISS consist of penicilin plusclincamyein, the atter added to eradicate the Aigh inoculum of bacteria present and to suppress toxin pro duction. IF methieilin- susceptible aureus isthe cause, na cillin and clindamycin are recommended: for MRSA. vancomycin plus clindamycin or linezolid monotherapy is preferred. More studies are needed fo establish the exact role of intravenous immune giobalin in this setting. and i is not recommended in the most revent guidelines by the Infectious, Diseases Society of Amertca. ‘+ Source control fortoxie shack syndrome typically requires surgical debridement Streptococcal texie shock syndrame is treatel with penicilin and clindamycin, Infection with methicillin-suscepéible Staphylecoceus ‘aureus is treated with nafeillin and clindamyeins line- zolid monotherapy or vancornyein plus clindamycin is, preferred forinfection with methicillin resistant S.qureus. TSS. Source control typically requires Community-Acquired Pneumonia 1 Epidemiology Communiy acquired peuronia (CAP) is aKaling cane of Infection and hoyptalzaton tn the United States, asoclated ‘wih more than $10 alin array n helt ere expend tans. The spectram of lies due to CAP ranges from lasses, ts aporolmacly 0% of patie cman in th amtulaory sutra iretons, katesornosptaiation Increase with advanced az: the incidence of hospitalization farCAParnongadults 80 years or clderis 25 times higher thn inadats younger han 0 yar, The definition of CAP has recently expanded 10 inclade sora ati prv our angiciacs tag eat cae ssacited paceronta (HAP) Ti chang ws tae Deane the mlcrobiclogy and iretment of patients wath CAP long ere alts GF who Were tepid ta te eee Frith eet aiersabaan nay from var oCeomarniy well patients with sniar comorbidities Praca elim enor ilibote aed implica none, eaing W « aces theuse of unnecessarily brad antibites, ierentaing CAP iin tre cept -scquied ppeamond BIA retin os cally canta fae Health Ghe-Aavoclate nfretions fo HAP dseusiom P classification simplifies treatment and hes 14 Microbiology CAP fs usually caused by infection with a viral or bacterial pathogen: fungal or mycobacterial infections occur much less frequenth The probabilty of infection witha speetic oganism ‘aries hase! on age, comorbldtes, seasonality, and geagraphy. Epldemtologicisk actors or conditions associated with speciic pathogens sre Fisted in Table 1. Hecause causative organisms have variable virulence, severity of tines, whicl influences site ofeare, is use to guide empiric antibatie therapy (Table 12). Streptococeus pneumoniae, previously considered the leading cause of CAP, aecounts for only 8% to s%OF Hospital ied cases in recent stcies. Ths decreas in incidence a east partially results from the siecess of vaccination strates Comerses ratesof CAP causcelby Siaphyloccccts aueeusand Enlerobacteriacene are rising, even among patients without identifiable health care exposure. The CDC EPIC trial a recent rmallicenter study that performed prospective microbiotogte snc! molecular testing on patients hospitalized with CAR more frequently ident bacterial pathogen in CAP infections requiting hosplalzation (Pgure 4), 5. pneumoniae was the most common bacteriat use. although rhinovirus (%) and influence vines (6) were higher in incidence. The significance of vizal detection i CAP is unclear; an antecedent mild respiratory viral infection may increase the risk fora secondary bacterial jfeetion. This phe nomenon is well documented for postinflucnza CAP caused by S. aureus, S. pneumoniae, ant Streptococcus pyogenes: Despite extensive laboratory investigation, no aasatieeorgan ism was identified in 62% of patients in the CDC EPIC tr Atypical pneumonia refers to CAP caused by organisms not cuhivatsble on standart bacterial media, ielding vinases and fastidious bacterizsuch as Legfonellaspecies, Mycoplasina 114 Sngle or multiple viruses rather than a Legion pocurophia Stptylacenee Pree re erahucrsone Mycoplasma me foro! — mycobacteda Srepacoccis oe — = Vins ls bacteria Es FIGURE 4. The that oops ocertages ot gathogensdeecedamong spitaae patents ith conmunty cquiedgrearona inthe COCEPE Sud se mt pips Community-Acqui sk Factor Heswyaicchol use corp Structural ling dicoaco fhronchisessie, ‘Common Pathogens Sreptococeus pneumoniae, oralflars(arpiraion) Klebsial preumanize Haemophilus nfuuenzae, S, preamorise, Moraxall catarrhals, Legionella preumophils, Peeudomoras aeruginosa P asraginosa, Burthaiclericepocis, Stonotoshomonas maltophila, Staphylococcus aureus Spticfbreie| Aspiction (scizures, neurclogie ‘mparmer, loss of conseiourness) Age 65 years Postural ness Ramat oxposwe ra anaorches, Ecorobacreinceoe Influoras.inus,S proviroriae, thinovirus S aureus, Sreptoceceus pyogenes, S.proumoniae Bids Chorcophit sta Hcoplra canal, Cooticoeusreomas ose sea ero ones oe Peterlee ire snetrdomesicned hot bine uch specs Soo = SS Rodent droppings Hantavirus | — Facet sine | Heb exoare Lagi poms est yc ast parts —— Fe red tes Fisopleae caputum Boson: demas Sune eee Gosidies a Se ee id ot wes Pe clapmiaivgmetiones — Wiretarna paiRiouawes tiachin Seer) ‘pneumoniae, and Chlamydophila pneumoniae. Respiratory irae account for ncarly al ial pneumonia infections, but Jess common pathogens inclice varicella-zoster virus or Hantavirus Legionelia pneumophila isa roengized cause of AP requiring hosptlalizaon or CU admission, Legjonetosis ‘associated with waler exposure, inluding hot tubs and air ecncitioning units: however. infection may oceur without an @bvious source. A bivory of travel has been reported in spproximately 10% of Lgionela cases eporie tothe CDC CAP cause by araerobic bacteria uncommon, & primar 2 seen with sspaten, and i caused by microserophic oo pharyngeal ora. Rsk factors for aspiration pneumonia inchade Secreased consciousness (aeahol or iid! substance use, se sere, soke), poor dentition gastmcsophageareix, an so sang, Zoonotic cases of CAP include Coxiella bumeté and Fancivella rularensis Mycobacterial or fungal causes of CAP sould be considered tn patients with framuocompromising ‘editions, epidemiologic risk facors for infection (such as ecarcerajion, certain hobises oF occupations, and pertinent seenal or foreign tre, or aabacute presertationsanin thre ‘eno do no respond to conventional antibactena treatment. EI «© The definition of community-acgaited paeamonia (CAP) has recently expanded to inchide some patients previously categorized as having health care associaled pneumonia beans: the microbiology and treatment of patients with CAP in Jong-term care Bellies or who ‘were hospitalized in the preceding 3 months do not dif fer substantially from that of community dwelling patients with similar comorbidities, ‘+ Streptococcus pneumoniae sccunts for onky 5% tb 15% ofcommunity acquired pneumonia (CAP) infections requiring hospitalization, whereas rates of CAP caused. by Staphylocaceus aureusand Enterobacteriaceae are rising, even among patients without identifiable health care exposure. ‘+ The significance of viral detection in community acquired pneumonia is unclear; bowever, an antecedent mild respiratory viral infection may increase the risk for a secondary bacterial infection. 15 Healthy patientwthout antbictic. inpreceding3 months Stoptoceccus prewmoniae Mycoplasma oR Chlornycophile Macrlide Doxyeycine Respiratory viruses Healthy patient from region with | 225% nacolde resciance anong 5. pneumoniae Comorbicities' or antbioticuse in Seme as above Same at inpations,nor.iCU Respiratery quinolene oR Batam plusa macrolide Racpirstory quinolone Blactom plus a macrolide | eal a | ‘Oralanaerodes enema se eateries my Sey eae & Paar lf penicillin allergic, a respiratory ee Magee decrees oe | Any Risk factorfor CA-MRSA (see text) Standard therapy PLUS | CAMRSA conmanin ocainedmebici-estnStnhyomcus aves | tpn wit wcrsin Foe Maral A ed 5, rent Bae J, Carp GD, Dean NC. Deel St vancomycin oR linesotal iM J Miser M Nader MS ores, [1] Diagnostic Evaluation CAP should be suspected and chest imaging performed in any fall presente gail er amouled rah ugh, een OF chest pin, Symptons may be sublle or absent In older ats or murstpnresed patina. ana ica shou feather freed for purrs mdicgaphie worn these populations Foseroanteror and late chest raiogra phy isrecommended, In adiition to confirming the diagnosis, tepagc patarca’ may jrowtle dhaaea pase 16 pathogens (fable 13) and guide clinteal decisions regarding, appropriate ste of eare. When plain radiographs are normal bbut suspicion for CAP remains high, chest radiography may be repeated after 24 hours: for patents at high risk (febrile neu. ropenia, risk for anthna, or acute respinatory distress sym drome requiring Inervention) wich normal ridiographs, chest CT should be pursued. Routine laboratory studies are indicated to ascertain the severity of infection, determine the optanal sie of eare, and, ensure appropriate antimicrobial dosing, HIV testing, should yt ea aetna Rightlowerlobe Oral anacrobes (spiration) | pneumonia Lingabstess/ Oralanacrabes Staphylococcus aureus, cesiaylesion _Klebsiellapneumoniae, Nocardia ‘Aatinomyces, Phodocccws, ‘ycobactera, encemic fungi ieentital ‘Avypical pathogens(Leaionella, sefitate Mycoplasma, Chlamycophiia) viruses | Flewalefusorw — Otalanserobes anginosus-constelats enpyems (g}uP seeprococd)§ aureus S-preumonive be performed if indicated: 4 positive result expands the spec ‘ram of potentially causative organisms, Procalciionin lee, iF ‘sealable as 2 point of care test, is insufficiently sensitive or specific to independently diagnosis CAP or a microbiologic cause but may support s diagnosis along with other clinical “Snddings Mapid testing for mfluenza virus may assist in ident Sing patients who woukl benefit from oseltamivir and who sequire droplet precautions at hospital admission, but a past five fest result does not exclude 2 concomitant bacterial pathogen. Diagnostiestudiesto identify a causative onpinism are not ‘outinely indicated in outpatients with CAP but should be considered in non ICU hespitalized patients when this informa Son would change therapy crallow treatment de escalation. All patients with CAP who require admission 10 the ICU should fendergo diagnostic evaluation In an attempt to confirm a seicrobial cause. Interpretation of sputum Gram stain and ccoure is hampered by the pesenve of oropharyngeal eolont zation, ani growth may reflect nonpathogenic organisms, & eed quality sputum culture obiained before antibiotie initia, ‘jon fs suggestive or dlagnostie i up 10 80% af eases of pret. -mococeal pneumonia sensitivity decreases afer antibiotic herapy. Sputum Gram stain and culture are appropriate for patients admitied to the ICL, patients who did noc respond 19 patient antibiotic therapy, patients with cavitary Tang Scions, and patients with underlying stractural lung disease. Jn these cases, consideration for mycobacterial or fungal eases may be newessary, flood enlture results are positive in 20% to 25% ofpatients Jeth pneumococeal pneumonia; ever culture resultsare pos ithe in patients with oher bacterial causes. Pneumocoxcal frinary antigen testing is more than 70% sensitive, and results are nol affected by artibioticauminisiration, Legionetea uri rary antigen test results are positive In most patients with L pneumophila serotype | infection. However, the test does 10; tee! other strains: and resulls can remain positive for prolonged periods after infection, Rapid antigen testing fer Community-Acquired Pneumonia influcrza virus on nasal swabs offers the adeantage of point ff care diagnosis but 'S less sensitive tan polymerase Chala reaction based techniques. Respiratory viral panel results using niicleie acid amplification are positive in up to patients hospitalized with GAP: however, a positive result may reflec viral coinfection or antecedent predisposing infection rather than current clinical liness. Although these panelsare Jess helpful in guiding, ‘bie Uhetaps a positive respiratory viral panel might have sig nificant infection control implications among patients admit led othe hospital Additional testing Is indicated only in setect patients ‘asedlon epidemiologic risk factors (see Table 1), clinical find Ings, or radiographic patterns (sce"Teble 13). Fungal an acl fas hucilli stains of sputum or fungal antigen testing can be performed. Serology for Coxiella burnett, Francisella tular of cisions about discontinuing antibi ensis, Legionella, Mycoplasma, anid. Chlamggtophila, wsing acute and convalescent sera, ean document seroconversion or 2 far inerease ia titers Patients with pleural effusions of unknown cause o those thicker than 1 cm should undergo thoracentesis to exclude concomitant empyema requiring drainage (ee MKSAP 18 Pulmonary and Critical Care Medicine) Bronchoscopy with transbronchial biopsy should be consid ered in patients with an unrevealing noninvasive evaluation who do not respond te empiric dherapy. ED SORA + Diagnostic studies to identify a eusative organism are HVC ‘not roatinely indicated in outpatients with community acquired pneumonia (CAP) but should be considered in ‘non ICU hospitalized patients when this information ‘would change management; diagnostic studies should bee performed in ail patients admitted to the CU with car ‘For patients with pneumococcal pneumonta, a good ‘quality sputum culture obtained before antibiotic initia tion is suggestive or diagnostic in up to 80% of cases; blood culture results are positive in 20% to 25% of cases; pneumococcal urinary antigen testing is more than 70% sensitive, and results are not affected by antibiotic administration. ‘= Legionella urinary antigen test results are posit ‘most patients with £. pneumophila serotype 1 infection, butit doesnot detect other strains, and results can remain positive for prolonged periods after infection. Management Site of Care oO Ambulatory management is adequate for many patients with CAP. Multiple clinical prediction models are available to tden- tify patients who would most benefit from hospital or ICL admission (Table 14), bat complexity and lack of consensus limit their use. Although prediction rules may ald in 7 PsP >S0yeers | Comortidties Malignancy Congestive heartfaiure | Carebrovasculardizease Kidrey disease iva caso Heartrate2!25/min Respiration rato 230/erin Temperature <35°C (99 For BAO NC(I04°F} 5090 men Hg Vital signs Physical examination Atered mentation | acme tae Radiographic findings site of care decisions, scores should not supersede clinical judgment “The Pneumonia Severity Index (PSD) isa validated predic tor of all cause mortality at 50 days. The initial assescment determines the presence of 1 variables assoctated with adverse ‘outcomes (ee Table 14) Patients with mo risk factors (severity isk class J can Iypieally be managed as outpatients, Those ‘with at least one risk factor are strattied using. second scor ing system into a risk classification between IT and V based on ‘4 more complex point system that includes residence in ruursiig home, abnormal Iahoratory test resulis, anid radio graphic findings. ‘Tae CURB 65 (Conti Jood Urea nitrogen [EUNI, spiratory rate, ilood pressure, and age 265 years) score Is asimplified, albeit slightly less predictive, tool for identity ing patients at low risk. Thirty day mortality among palients with 2 CURB 65 score of © oF 1 was Tess than 3%, 8 ambulatory treatment is appropriate for most patients ‘with scores les than 2. The modified CRB 65 omits BUN measurement and supports ambulatory elinteal assess ment: patients with aseore of Lor more warrant considera tion for hospitalization 18 Respiration rate 10min ‘SEP <90 mm Hy or DBP dmmbg, Confusion BUN=20 mg/el (7.1 nmol) 1331p Sowey trotoaonam peren;potents signed cent ye mona en cttw at IDSAJATS Criteria: Rospiatin rate>30/min | Temperature <6 C96.8°F) Hypotension requiring aggressive fluid wesveetation Cenfusionor disorientation BUNS20 mg/dL (27.1 mmol) Levkogrecoure

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