(BQ) Part 1 book “Read book Atlas of pediatric infectious diseases” has contents: Adenovirus infections, arcanobacterium haemolyticum infections, astrovirus infections, bacillus cereus infections, bacterial vaginosis, clostridium difficile, clostridial myonecrosis, chlamydia trachomatis,… and other contents.
ATLAS of pediatric infectious diseases 3rd Edition Editor: Carol J Baker, MD, FAAP Incorporating key content from the AAP Red Book®, this newly updated edition provides must-know information for diagnosing, evaluating, and treating more than 100 pediatric conditions A peerless pictorial resource More than 1,200 finely detailed clinical photos and radiographs illustrate disease features Succinct captions illuminate crucial aspects of patient presentation and disease processes and offer valuable insights for differential diagnosis Includes 1,200+ images — with 400+ new! A super-efficient quick reference and learning tool Concise text descriptions step you through diagnosis, evaluation, and management essentials for each condition • Clinical manifestations • Incubation period • Etiology • Diagnostic tests • Epidemiology • Treatment BAKER For other pediatric infectious disease resources, visit the American Academy of Pediatrics at shop.aap.org Red Book ® ATLAS of pediatric infectious diseases Red Book ® AAP Red Book ® ATLAS of pediatric infectious diseases 3rd Edition Editor: Carol J Baker, MD, FAAP Now with 1c,o2lo 00+ r photos Red Book ® ATLAS of pediatric infectious diseases 3rd Edition Editor: Carol J Baker, MD, FAAP American Academy of Pediatrics Publishing Staff Mark Grimes, Director, Department of Publishing Peter Lynch, Manager, Digital Strategy and Product Development Barrett Winston, Digital Solutions Editor Theresa Wiener, Manager, Publishing and Production Services Jason Crase, Manager, Editorial Services Peg Mulcahy, Manager, Art Direction and Production Mary Lou White, Director, Department of Marketing and Sales Linda Smessaert, Marketing Manager, Professional Publications Published by the American Academy of Pediatrics 141 Northwest Point Blvd Elk Grove Village, IL 60007-1019 Telephone: 847/434-4000 Facsimile: 847/434-8000 www.aap.org The recommendations in this publication not indicate an exclusive course of treatment or serve as a standard of medical care Variations, taking into account individual circumstances, may be appropriate The American Academy of Pediatrics is not responsible for the content of the resources mentioned in this publication Web site addresses are as current as possible but may change at any time Products are mentioned for informational purposes only Inclusion in this publication does not imply endorsement by the American Academy of Pediatrics Brand names are furnished for identification purposes only No endorsement of the manufacturers or products mentioned is implied This publication has been developed by the American Academy of Pediatrics The authors, editors, and contributors are expert authorities in the field of pediatrics No commercial involvement of any kind has been solicited or accepted in the development of the content of this publication Every effort is made to keep Red Book® Atlas of Pediatric Infectious Diseases consistent with the most recent advice and information available from the American Academy of Pediatrics Special discounts are available for bulk purchases of this publication E-mail our Special Sales Department at aapsales@aap.org for more information © 2017 American Academy of Pediatrics All rights reserved No part of this publication may be reproduced, stored in a retrieval system, or trans mitted in any form or by any means—electronic, mechanical, photocopying, recording, or otherwise— without prior permission from the publisher (locate title at http://ebooks.aappublications.org and click on © Get Permissions; you may also fax the permissions editor at 847/434-8780 or e-mail permissions@aap.org) First edition published 2010; second, 2013 Printed in the United States of America 9-375/1016 10 MA0805 ISBN: 978-1-61002-060-2 eBook: 978-1-61002-061-9 Library of Congress Control Number: 2016942360 III Contents Preface VII 1/Actinomycosis .1 2/Adenovirus Infections .4 3/Amebiasis .7 4/Amebic Meningoencephalitis and Keratitis (Naegleria fowleri, Acanthamoeba species, and Balamuthia mandrillaris) 13 5/Anthrax 18 6/Arboviruses (Including California serogroup, chikungunya, Colorado tick fever, eastern equine encephalitis, Japanese encephalitis, Powassan, St Louis encephalitis, tick-borne encephalitis, Venezuelan equine encephalitis, western equine encephalitis, and yellow fever viruses) 24 7/Arcanobacterium haemolyticum Infections 33 8/Ascaris lumbricoides Infections 35 9/Aspergillosis 38 10/Astrovirus Infections .43 11/Babesiosis 45 12/Bacillus cereus Infections 49 13/Bacterial Vaginosis 51 14/Bacteroides and Prevotella Infections 53 15/Balantidium coli Infections (Balantidiasis) 56 16/Baylisascaris Infections 58 17/Infections With Blastocystis hominis and Other Subtypes .62 18/Blastomycosis 64 19/Bocavirus 66 20/Borrelia Infections (Relapsing Fever) 67 21/Brucellosis .70 22/Burkholderia Infections 73 23/Campylobacter Infections .76 24/Candidiasis 79 25/Cat-scratch Disease (Bartonella henselae) 88 26/Chancroid 93 27/Chlamydophila (formerly Chlamydia) pneumoniae 95 28/Chlamydophila (formerly Chlamydia) psittaci (Psittacosis, Ornithosis, Parrot Fever) 97 29/Chlamydia trachomatis 99 30/Botulism and Infant Botulism (Clostridium botulinum) .104 31/Clostridial Myonecrosis (Gas Gangrene) 109 32/Clostridium difficile 111 33/Clostridium perfringens Food Poisoning 114 34/Coccidioidomycosis .116 35/Coronaviruses, Including SARS and MERS 122 36/Cryptococcus neoformans and Cryptococcus gattii Infections (Cryptococcosis) .126 IV CONTENTS 37/Cryptosporidiosis 129 38/Cutaneous Larva Migrans 134 39/Cyclosporiasis 136 40/Cytomegalovirus Infection 138 41/Dengue 145 42/Diphtheria .149 43/Ehrlichia, Anaplasma, and Related Infections (Human Ehrlichiosis, Anaplasmosis, and Related Infections) 154 44/Enterovirus (Nonpoliovirus) (Group A and B Coxsackieviruses, Echoviruses, Numbered Enteroviruses) 160 45/Epstein-Barr Virus Infections (Infectious Mononucleosis) 165 46/Escherichia coli and Other Gram-Negative Bacilli (Septicemia and Meningitis in Neonates) .169 47/Escherichia coli Diarrhea (Including Hemolytic Uremic Syndrome) 174 48/Fungal Diseases .179 49/Fusobacterium Infections (Including Lemierre Disease) 183 50/Giardia intestinalis (formerly Giardia lamblia and Giardia duodenalis) Infections (Giardiasis) 186 51/Gonococcal Infections 190 52/Granuloma Inguinale (Donovanosis) .198 53/Haemophilus influenzae Infections 200 54/Hantavirus Pulmonary Syndrome 207 55/Helicobacter pylori Infections 213 56/Hemorrhagic Fevers Caused by Arenaviruses 215 57/Hemorrhagic Fevers Caused by Bunyaviruses 218 58/Hemorrhagic Fevers Caused by Filoviruses: Ebola and Marburg .221 59/Hepatitis A 226 60/Hepatitis B .230 61/Hepatitis C .238 62/Hepatitis D 242 63/Hepatitis E 244 64/Herpes Simplex 246 65/Histoplasmosis .258 66/Hookworm Infections (Ancylostoma duodenale and Necator americanus) 264 67/Human Herpesvirus (Including Roseola) and 268 68/Human Herpesvirus 271 69/Human Immunodeficiency Virus Infection 273 70/Influenza 294 71/Isosporiasis (now designated as Cystoisosporiasis) 306 72/Kawasaki Disease 309 73/Kingella kingae Infections 317 74/Legionella pneumophila Infections 319 75/Leishmaniasis .323 CONTENTS V 76/Leprosy 330 77/Leptospirosis 335 78/Listeria monocytogenes Infections (Listeriosis) .339 79/Lyme Disease (Lyme Borreliosis, Borrelia burgdorferi I nfection) .343 80/Lymphatic Filariasis (Bancroftian, Malayan, and Timorian) 355 81/Lymphocytic Choriomeningitis 359 82/Malaria 361 83/Measles 372 84/Meningococcal Infections 378 85/Human Metapneumovirus 385 86/Microsporidia Infections (Microsporidiosis) 386 87/Molluscum Contagiosum 389 88/Mumps 392 89/Mycoplasma pneumoniae and Other Mycoplasma Species Infections 396 90/Nocardiosis 401 91/Norovirus and Other Human Calicivirus Infections .404 92/Onchocerciasis (River Blindness, Filariasis) 405 93/Human Papillomaviruses 407 94/Paracoccidioidomycosis (South American Blastomycosis) 411 95/Paragonimiasis 413 96/Parainfluenza Viral Infections 416 97/Parasitic Diseases 420 98/Parvovirus B19 (Erythema Infectiosum, Fifth Disease) 430 99/Pasteurella Infections 435 100/Pediculosis Capitis (Head Lice) .437 101/Pediculosis Corporis (Body Lice) 441 102/Pediculosis Pubis (Pubic Lice, Crab Lice) 443 103/Pertussis (W hooping Cough) 445 104/Pinworm Infection (Enterobius vermicularis) 452 105/Pityriasis Versicolor (Tinea Versicolor) 455 106/Plague 457 107/Pneumococcal Infections 464 108/Pneumocystis jiroveci Infections 472 109/Poliovirus Infections 476 110/Prion Diseases: T ransmissible Spongiform Encephalopathies 481 111/Q Fever (Coxiella burnetii Infection) 485 112/Rabies 488 113/Rat-bite Fever 492 114/Respiratory Syncytial Virus 494 115/Rickettsial Diseases 498 116/Rickettsialpox .500 117/Rocky Mountain Spotted Fever .502 VI CONTENTS 118/Rotavirus Infections 508 119/Rubella 510 120/Salmonella Infections 516 121/Scabies 524 122/Schistosomiasis 529 123/Shigella Infections 535 124/Smallpox (Variola) .539 125/Sporotrichosis 545 126/Staphylococcal Infections 548 127/Group A Streptococcal Infections 568 128/Group B Streptococcal Infections 582 129/Non–Group A or B Streptococcal and Enterococcal Infections 586 130/Strongyloidiasis (Strongyloides stercoralis) 591 131/Syphilis 594 132/Tapeworm Diseases (Taeniasis and Cysticercosis) .611 133/Other Tapeworm Infections (Including Hydatid Disease) 616 134/Tetanus (Lockjaw) 619 135/Tinea Capitis (Ringworm of the Scalp) 622 136/Tinea Corporis (Ringworm of the Body) .626 137/Tinea Cruris (Jock Itch) .629 138/Tinea Pedis and Tinea Unguium (Athlete’s Foot, Ringworm of the Feet) .631 139/Toxocariasis (Visceral Toxocariasis [previously Visceral Larva Migrans]; Ocular Toxocariasis [previously Ocular Larva Migrans]) 634 140/Toxoplasma gondii Infections (Toxoplasmosis) 637 141/Trichinellosis (Trichinella spiralis and Other Species) 647 142/Trichomonas vaginalis Infections (Trichomoniasis) 651 143/Trichuriasis (Whipworm Infection) .655 144/African Trypanosomiasis (African Sleeping Sickness) .657 145/American Trypanosomiasis (Chagas Disease) 660 146/Tuberculosis 664 147/Diseases Caused by Nontuberculous Mycobacteria (Environmental Mycobacteria, Mycobacteria Other Than Mycobacterium tuberculosis) 686 148/Tularemia 693 149/Endemic Typhus (Murine Typhus) 698 150/Epidemic Typhus (Louseborne or Sylvatic Typhus) .700 151/Varicella-Zoster Virus Infections 703 152/Cholera (Vibrio cholerae) 712 153/Other Vibrio Infections .716 154/West Nile Virus 718 155/Yersinia enterocolitica and Yersinia pseudotuberculosis Infections (Enteritis and Other Illnesses) 723 Index 727 VII Preface The American Academy of Pediatrics (AAP) Red Book® Atlas of Pediatric Infectious Diseases, 3rd Edition, is a summary of key disease information from the AAP Red Book®: 2015 Report of the Committee on Infectious Diseases It is intended to be a study guide for students, residents, and practitioners The visual representations of common and atypical clinical manifestations of infectious diseases provide diagnostic information not found in the print version of the Red Book The juxtaposition of these visuals with a summary of the clinical features, epidemiology, diagnostic methods, and treatment information hopefully will serve as a training tool and a quick reference The Red Book Atlas is not intended to provide detailed treatment and management information but rather a big-picture approach that can be refined by consulting reference texts or infectious disease specialists Complete disease and treatment information from the AAP can be found at http:// redbook.solutions.aap.org, the electronic version of the Red Book This Red Book Atlas could not have been completed without the superb assistance of Peter Lynch, Barrett Winston, Jason Crase, Theresa Wiener, and Peg Mulcahy at the AAP and of those physicians who photographed disease manifestations in their patients and shared these with the AAP Some diseases are rarely seen today because of improved preventive strategies, especially immunization programs While photographs can’t replace hands-on experience, they have helped me to consider the likelihood of a correct diagnosis, and I hope this will be so for the reader I also want to thank those individuals at the Centers for Disease Control and Prevention who have generously provided many photographs of the etiologic agents, vectors, and life cycles of parasites and protozoa relevant to these largely domestic infections The study of pediatric infectious diseases has been a challenging and ever-changing professional life that has brought me great joy To gather information with my ears, eyes, and hands (the history and physical examination), to place this into the context of relevant epidemiology and incubation period, and then to select a few appropriate diagnostic studies is still exciting for me Putting these many pieces together and arriving at the correct diagnosis is akin to solving a crime On many occasions, just seeing the clue (a characteristic rash, an asymmetry, a swelling) will solve the medical puzzle, lead to recovery with the proper management, and bring the satisfaction almost nothing can replace It is my hope that the readers of the third edition of the Red Book Atlas might find a similar enthusiasm for the field Carol J Baker, MD, FAAP Editor Actinomycosis Etiology Actinomycosis The most common species causing human disease is Actinomyces israelii Clinical Manifestations Actinomycosis results from pathogen introduction following a breakdown in mucocutaneous protective barriers Spread within the host is by direct invasion of adjacent tissues, typically forming sinus tracts that cross tissue planes There are common anatomic sites of infection Cervicofacial is most common, often occurring after tooth extraction, oral surgery, or other oral/facial trauma, or even from carious teeth Localized pain and induration may progress to cervical abscess and “woody hard” nodular lesions (“lumpy jaw”), which can develop draining sinus tracts, usually at the angle of the jaw or in the submandibular region Infection may contribute to chronic tonsillar airway obstruction Thoracic disease most commonly is secondary to aspiration of oropharyngeal secretions but may be an extension of cervicofacial infection It occurs rarely after esophageal disruption secondary to surgery or nonpenetrating trauma Thoracic presentation includes pneumonia, which can be complicated by abscesses, empyema, and, rarely, pleurodermal sinuses Focal or multi focal mediastinal and pulmonary masses may be mistaken for tumors Abdominal actino mycosis is usually attributable to penetrating trauma or intestinal perforation The appendix and cecum are the most common sites; symptoms are similar to appendicitis Slowly developing masses may simulate abdominal or retroperitoneal neoplasms Intra-abdominal abscesses and peritoneal-dermal draining sinuses occur eventually Chronic localized disease often forms draining sinus tracts with purulent discharge Other sites of infection include the liver, pelvis (which, in some cases, has been linked to use of intrauterine devices), heart, testicles, and brain (which is usually associated with a primary pulmonary focus) Noninvasive primary cutaneous actinomycosis has occurred A israelii and at least other Actinomyces species cause human disease All are slowgrowing, microaerophilic or facultative anaerobic, gram-positive, filamentous branching bacilli They can be part of normal oral, gastrointestinal tract, or vaginal flora Actino myces species frequently are copathogens in tissues harboring multiple other anaerobic or aerobic species Isolation of Aggregatibacter (Actinobacillus) actinomycetemcomitans, frequently detected with Actinomyces species, may predict the presence of actinomycosis Epidemiology Actinomyces species occur worldwide, being components of endogenous oral and gastrointestinal tract flora Actinomyces species are opportunistic pathogens (reported in patients with HIV and chronic granulomatous disease), with disease usually following penetrating (including human bite wounds) and nonpenetrating trauma Infection is uncommon in infants and children, with 80% of cases occurring in adults The male to female ratio in children is 1.5 to Overt, microbiologically confirmed, monomicrobial disease caused by Actinomyces species has become rare in the era of antimicrobial agents Incubation Period Several days to several years Diagnostic Tests Only specimens from normally sterile sites should be submitted for culture Microscopic demonstration of beaded, branched, gram- positive bacilli in purulent material or tissue specimens suggests the diagnosis Acid-fast staining can distinguish Actinomyces species, which are acid-fast negative, from Nocardia species, which are variably acid-fast positive Yellow “sulfur granules” visualized microscopically or macroscopically in drainage or loculations of purulent material also suggest the diagnosis A Gram stain of “sulfur granules” discloses a dense aggregate of bacterial filaments mixed with inflammatory debris Immunofluorescent stains for Actinomyces 2 Actinomycosis species are available, as well as polymerase chain reaction assay and 16s rRNA sequencing for tissue specimens Treatment Initial therapy should include intravenous penicillin G or ampicillin for to weeks followed by high doses of oral penicillin (up to g/d for adults), usually for a total of to 12 months Exclusively oral therapy has been reported as effective as intravenous therapy for cases of cervicofacial disease Amoxicillin, erythromycin, clindamycin, doxycycline, and tetracycline are alternative antimicrobial choices All Acti nomyces appear resistant to ciprofloxacin and metronidazole Surgical drainage or debridement is often a necessary adjunct to medical management and may allow for a shorter duration of antimicrobial treatment Image 1.2 Image 1.1 A sulfur granule from an actinomycotic abscess (hematoxylin-eosin stain) While pathognomonic of actinomycosis, granules are not always present A Gram stain of sulfur granules shows a dense reticulum of filaments Tissue showing filamentous branching rods of Actinomyces israelii (Brown and Brenn stain) Actinomyces species have fastidious growth requirements Staining of a crushed sulfur granule reveals branching bacilli Image 1.4 Image 1.3 A brain heart infusion agar plate culture of Actinomyces species, magnification x573, at 10 days of incubation Courtesy of Centers for Disease Control and Prevention A 10-year-old boy with chronic pulmonary, abdominal, and lower extremity abscesses with chronic draining sinus tracts from which Actinomyces israelii was isolated Prolonged antimicrobial treatment and surgical drainage were required for resolution of this infectious process 320 LEGIONELLA PNEUMOPHILA INFECTIONS predictive value of a single titer of 1:256 or greater is low and does not provide definitive evidence of infection Antibodies to several gram-negative organisms, including Pseudo monas species, Bacteroides fragilis, and Campylobacter jejuni, can cause false-positive immunofluorescent antibody test results Treatment another fluoroquinolone) is the drug of choice for immunocompromised adults Doxycycline and trimethoprim-sulfamethoxazole are alternative drugs Duration of therapy is to 10 days for azithromycin and 14 to 21 days for other drugs Longer courses of therapy are recommended for patients who are immunocompromised or who have severe disease Azithromycin is the drug of choice Once the condition of a patient is improving, oral therapy can be substituted Levofloxacin (or Image 74.1 This Gram-stained micrograph reveals chains and solitary gram-negative Legionella pneumo phila bacteria found within a sample taken from a victim of the 1976 legionnaires’ disease out break in Philadelphia, PA Legionnaires’ disease is the more severe form of legionellosis and is characterized by pneumonia, commencing to 10 days after exposure Pontiac fever is an acuteonset, flu-like, nonpneumonic illness, occurring within to days of exposure Courtesy of Centers for Disease Control and Prevention Image 74.2 Charcoal-yeast extract agar plate culture of Legionella pneumophila Courtesy of Centers for Disease Control and Prevention/Dr Jim Feeley Image 74.4 Transmission electron micrograph of Legionella pneumophila Courtesy of Centers for Disease Control and Prevention/Dr Francis Chandler Image 74.3 Legionella pneumophila multiplying inside a cultured human lung fibroblast Courtesy of Centers for Disease Control and Prevention/ Dr Edwin P Ewing Jr LEGIONELLA PNEUMOPHILA INFECTIONS 321 Image 74.5 Legionellosis Incidence, by year—United States, 1997–2012 Courtesy of Morbidity and Mortality Weekly Report Image 74.6 An adult with pneumonia due to Legionella pneumophila Legionella infections are rare in otherwise healthy children Although nosocomial infections and hospital outbreaks are reported, this infection is not transmitted from person to person 322 LEGIONELLA PNEUMOPHILA INFECTIONS Image 74.7 Imaging studies of a 42-year-old man with severe pneumonia caused by Legionella pneumophila serogroup 11, showing lobar consolidation of the left lower lung lobe, with an air-bronchogram within the homogeneous airspace consolidation Consensual mild pleural effusion was documented by a chest radiograph (A) and high-resolution computed tomography (B) A week after hospital admission, repeat high-resolution computed tomography of the chest showed extensive and homogeneous consolidation of left upper and lower lobes, accompanied by bilateral ground-glass opacities (C and D) Courtesy of Emerging Infectious Diseases Image 74.8 This hematoxylin-eosin–stained micrograph of lung tissue biopsied from a patient with legionnaires’ diseases revealed the presence of an intra-alveolar exudate consisting of macrophages and poly morphonuclear leucocytes The Legionella pneumophila bacteria are not stained in this preparation (magnification x500) Courtesy of Centers for Disease Control and Prevention Leishmaniasis 75 Leishmaniasis Clinical Manifestations The main clinical syndromes are as follows: • Cutaneous leishmaniasis After inoculation by the bite of an infected female Phlebotomus species sand fly (approximately 2–3 mm long), parasites proliferate locally in mononuclear phagocytes, leading to an erythematous papule, which, typically, slowly enlarges to become a nodule and then an ulcerative lesion with raised, indurated borders Ulcerative lesions can become dry and crusted or can develop a moist granulating base with an overlying exudate Lesions can, however, persist as nodules or papules and can be single or multiple Lesions are commonly on exposed areas of the body (eg, face, extremities) and may be accompanied by satellite lesions, sporotrichoid-like nodules, and regional adenopathy Clinical mani festations of Old World and New World (American) cutaneous leishmaniasis are similar Spontaneous resolution of lesions can take weeks to years—depending, in part, on the Leishmania species/strain— and usually results in a flat, atrophic scar • Mucosal leishmaniasis (espundia) traditionally refers to a metastatic sequela of New World cutaneous infection, which results from dissemination of the parasite from the skin to the naso-oropharyngeal mucosa; this form of leishmaniasis is typically caused by species in the Viannia subgenus Mucosal disease usually becomes evident months to years after original cutaneous lesions heal; however, mucosal and cutaneous lesions can be noted simultaneously, as some affected people have subclinical cutaneous infection Granulomatous inflammation may cause hypertrophy of the nose and lips Untreated mucosal leishmaniasis can progress to cause ulcerative destruction (eg, perforation of the nasal septum) and facial disfigurement • Visceral leishmaniasis (kala-azar) After cutaneous inoculation by an infected sand fly, the parasite spreads throughout the reticuloendothelial system (eg, spleen, liver, 323 bone marrow) The stereotypical clinical manifestations include fever, weight loss, pancytopenia, hypoalbuminemia, and hypergammaglobulinemia Peripheral lymphadenopathy is quite common in East Africa (eg, South Sudan) Some patients in South Asia (the Indian subcontinent) develop grayish discoloration of their skin; this manifestation gave rise to the Hindi term kala-azar (“black sickness”) Untreated, advanced cases of visceral leishmaniasis are almost always fatal, directly from the disease or from complications such as secondary bacterial infections or hemorrhage At the other end of the spectrum, visceral infection can be asymptomatic or oligosymptomatic Latent visceral infection can activate years to decades postexposure in people who become immunocompromised (eg, because of coinfection with HIV; posttransplantation immunosuppression) or who receive immunomodulatory therapy (eg, with an antitumor necrosis factor-α agent) because of other medical conditions Etiology In the human host, Leishmania species are obligate intracellular parasites of mononuclear phagocytes To date, approximately 20 Leishmania species (in the Leishmania and Viannia subgenera) are known to infect humans Cutaneous leishmaniasis is typically caused by Old World species Leishmania tropica, Leishmania major, and Leishmania aethiopica and by New World species Leish mania mexicana, Leishmania amazonensis, Leishmania (Viannia) braziliensis, Leishmania (V) panamensis, Leishmania (V) guyanensis, and Leishmania (V) peruviana Mucosal leishmaniasis is typically caused by species in the Viannia subgenus (especially L [V] braziliensis but also L [V] panamensis and, sometimes, L [V] guyanensis) Most cases of visceral leishmaniasis are caused by Leishmania donovani or Leishmania infantum (Leishmania chagasi is synonymous) L donovani and L infantum can also cause cutaneous leishmaniasis; however, people with typical cutaneous leishmaniasis caused by these organisms rarely develop visceral leishmaniasis 324 Leishmaniasis Epidemiology Diagnostic Tests In most settings, leishmaniasis is a zoonosis, with mammalian reservoir hosts, such as rodents or dogs However, some transmission cycles are anthroponotic; infected humans are the primary or only reservoir hosts of L donovani in South Asia (potentially also in East Africa) and of L tropica Congenital and parenteral transmission have also been reported Definitive diagnosis is made by detecting the parasite in infected tissue by light-microscopic examination of stained slides (eg, of aspirates, touch preparations, histologic sections), by in vitro culture, or by molecular methods In cutaneous and mucosal disease, tissue can be obtained by a 3-mm punch biopsy, lesion scrapings, or needle aspiration of the raised nonnecrotic edge of the lesion In visceral leishmaniasis, although the sensitivity is highest for splenic aspiration (approximately 95%), the procedure can be associated with life-threatening hemorrhage; bone marrow aspiration is safer Other potential sources of specimens include liver, lymph node, and, in some patients (eg, those coinfected with HIV), whole blood or buffy coat Identification of the Leishmania species may affect prognosis and influence treatment decisions The Centers for Disease Control and Prevention (CDC) (www.cdc.gov/parasites/leishmaniasis) can assist in all aspects of diagnostic testing Serologic testing is not usually helpful in cases of cutaneous leishmaniasis but can provide supportive evidence for the diagnosis of visceral or mucosal leishmaniasis, particularly if the patient is immunocompetent Overall, leishmaniasis is endemic in more than 90 countries in the tropics, subtropics, and southern Europe Visceral leishmaniasis (an estimated 0.2–0.4 million new cases annually) is found in focal areas of more than 60 countries: in the Old World, in parts of Asia (particularly South, Southwest, and Central Asia), Africa (particularly East Africa), the Middle East, and southern Europe; in the New World, particularly in Brazil, with scattered foci elsewhere Most (>90%) of the world’s cases of visceral leishmaniasis occur in South Asia (India, Bangladesh, and Nepal), East Africa (Sudan, South Sudan, and Ethiopia), and Brazil Cutaneous leishmaniasis is more common (an estimated total of 0.7–1.2 million new cases annually) and more widespread than visceral leishmaniasis Cutaneous leishmaniasis is found in focal areas of more than 90 countries: in the Old World, in parts of the Middle East, Asia (particularly Southwest and Central Asia), Africa (particularly North and East Africa, with some cases elsewhere), and southern Europe; in the New World, in parts of Mexico, Central America, and South America (not in Chile or Uruguay) Occasional cases of cutaneous leishmaniasis have been acquired in Texas and Oklahoma The geographic distribution of leishmaniasis cases identified in the United States reflects immigration and travel patterns (eg, the locations of popular tourist destinations in Latin America and of various military activities) Incubation Period Ranges from weeks to years In cutaneous leishmaniasis, skin lesions typically appear within several weeks; in visceral, from to 6 months Treatment Systemic antileishmanial treatment is always indicated for patients with visceral or mucosal leishmaniasis, but not all patients with cuta neous leishmaniasis need to be treated Consultation with infectious disease or tropical medicine specialists or with staff of the CDC Division of Parasitic Diseases and Malaria is recommended (telephone: 404/718-4745; e-mail: parasites@cdc.gov; CDC Emergency Operations Center [after business hours and on weekends]: 770/488-7100) The relative merits of various treatment approaches or regimens for an individual patient should be considered, taking into account that the therapeutic response may vary not only for different Leishmania species but also for the same species in different geographic regions In addition, special considerations apply in the United States for the availability of particular Leishmaniasis medications For example, the pentavalent antimonial compound sodium stibogluconate is not commercially available but can be obtained through the CDC Drug Service (404/639-3670), under an investigational new drug protocol Liposomal amphotericin B, which is administered by intravenous infusion, is recommended for treatment 325 of visceral leishmaniasis The oral agent, iltefosine, is approved for treatment of m cutaneous and mucosal as well as visceral leishmaniasis but is limited to infection caused by particular Leishmania species and for patients 12 years and older who are not pregnant or breastfeeding Image 75.1 Leishmania tropica amastigotes from a skin touch preparation A, Still intact macrophage is practically filled with amastigotes, several of which have a clearly visible nucleus and a kinetoplast (arrows) B, Amastigotes are being freed from a rupturing macrophage The patient has a history of travel to Egypt, Africa, and the Middle East Culture in Novy-MacNeal-Nicolle medium followed by isoenzyme analysis identified the species as L tropica minor Courtesy of Centers for Disease Control and Prevention Image 75.2 Leishmania donovani in bone marrow cell Smear Courtesy of Centers for Disease Control and Prevention/L L Moore Jr, MD 326 Leishmaniasis Image 75.3 This image depicts a mounted male Phlebotomus species fly, which, due to its resemblance, may be mistaken for a mosquito Phlebotomus species sand flies are bloodsucking insects that are very small and sometimes act as the vectors for various diseases, such as leishmaniasis and bartonellosis (also known as Carrión disease) Courtesy of Centers for Disease Control and Prevention/Donated by the World Health Organization Image 75.4 Leishmaniasis is transmitted by the bite of female Phlebotomus species sand flies The sand flies inject the infective stage, promastigotes, during blood meals (1) Promastigotes that reach the puncture wound are phagocytized by macrophages (2) and transform into amastigotes (3) Amastigotes multiply in infected cells and affect different tissues, depending, in part, on the Leishmania species (4) This originates the clinical manifestations of leishmaniasis Sand flies become infected during blood meals on an infected host when they ingest macrophages infected with amastigotes (5, 6) In the sand fly’s midgut, the parasites differentiate into promastigotes (7), which multiply and migrate to the proboscis (8) Courtesy of Centers for Disease Control and Prevention/Alexander J da Silva, PhD/Blaine Mathison Leishmaniasis 327 Image 75.5 Homes built in newly cleared forest areas (here, outside Rio de Janeiro) expose settlers to the sand flies that transmit leishmaniasis Courtesy of World Health Organization Image 75.6 A shantytown, another environment where Leishmania infection proliferates due to inadequate housing and lack of sanitation Courtesy of World Health Organization Image 75.7 Natural uncut forests are transmission sites for leishmaniasis People who collect rubber or clear such areas for agriculture are prone to infection Courtesy of World Health Organization/TDR/Lainson/ Wellcome Trust 328 Leishmaniasis Image 75.8 Cutaneous leishmaniasis, as in this boy from India, seldom disseminates in immunocompetent persons Multiple organisms can usually be found on biopsy of the border of a lesion Image 75.9 Cutaneous leishmaniasis Infected sand fly inocu lation site with satellite lesions The organism may be demonstrated by punch biopsy of the margin of a cutaneous lesion This is the same child as in Image 75.9 Image 75.10 Skin ulcer due to leishmaniasis, hand of Central American adult Courtesy of Centers for Disease Control and Prevention/Dr D.S Martin Image 75.11 Crater lesion of leishmaniasis, skin Courtesy of Centers for Disease Control and Prevention Image 75.12 Two young boys suffering visceral leishmaniasis, with distended abdomens due to hepatospleno megaly Courtesy of World Health Organization/TDR/Lainson/Wellcome Trust Leishmaniasis Image 75.13 A young girl with cutaneous leishmaniasis Courtesy of World Health Organization Image 75.14 A young girl with cutaneous leishmaniasis with multiple cutaneous lesions Courtesy of World Health Organization 329 330 Leprosy 76 Leprosy Clinical Manifestations Leprosy (Hansen disease) is a curable infection involving skin, peripheral nerves, mucosa of the upper respiratory tract, and testes The clinical forms of leprosy reflect the cellular immune response to Mycobacterium leprae and, in turn, the number, size, structure, and bacillary content of the lesions The organism has unique tropism for peripheral nerves, and all forms of leprosy exhibit nerve involvement Leprosy lesions usually not itch or hurt They lack sensation to heat, touch, and pain but otherwise may be difficult to distinguish from other common maladies There can be madarosis (loss of eyelashes or eyebrows) and ocular problems However, the stereotypical presentations of leonine facies with nasal deformity or clawed hands with loss of digits are manifestations of late-stage untreated disease that are seldom seen today Although the nerve injury caused by leprosy is irreversible, early diagnosis and drug therapy can prevent sequelae Leprosy manifests over a broad clinical and histopathologic spectrum In the United States, the Ridley-Jopling scale is used to classify patients according to the histopathologic features of their lesions and organization of the underlying granuloma The scale includes tuberculoid, borderline tuberculoid, borderline, borderline lepromatous, and lepromatous A simplified scheme introduced by the World Health Organization for circumstances in which pathologic examination and diagnosis are unavailable is based purely on clinical skin examination Under this scheme, leprosy is classified by the number of skin patches seen on skin examination, classifying disease as paucibacillary (1–5 lesions, usually tuberculoid or borderline tuberculoid) or multibacillary (>5 lesions, usually borderline, borderline lepromatous, or lepromatous) Patients in the tuberculoid spectrum have active cell-mediated immunity with low antibody responses to M leprae and few well-defined lesions contain- ing few bacilli Lepromatous spectrum cases have high antibody responses with little cellmediated immunity to M leprae and several somewhat-diffuse lesions usually containing numerous bacilli Serious consequences of leprosy occur from immune reactions and nerve involvement with resulting anesthesia, which can lead to repeated unrecognized trauma, ulcerations, fractures, and even bone resorption Injuries can have a significant effect on life quality Leprosy is a leading cause of permanent physical disability among communicable diseases worldwide Eye involvement can occur, and patients should be examined by an ophthalmologist A diagnosis of leprosy should be considered in any patient with hypoesthetic or anesthetic skin rash or skin patches, especially those that not respond to ordinary therapies, and among those with a history of residence in areas with endemic leprosy or contact with armadillos • Leprosy reactions Acute clinical exacerbations reflect abrupt changes in the immunologic balance They are especially common during initial years of treatment but can occur in the absence of therapy Two major types of leprosy reactions (LRs) are seen: type (reversal reaction, LR-1) is predominantly observed in borderline tuberculoid and borderline lepromatous leprosy and is the result of a sudden increase in effective cell-mediated immunity Acute tenderness and swelling at the site of cutaneous and neural lesions with development of new lesions are major manifestations Ulcerations can occur, but polymorphonuclear leukocytes are absent from the LR-1 lesion Fever and systemic toxicity are uncommon Type (erythema nodosum leprosum, LR-2) occurs in borderline and lepromatous forms as a systemic inflammatory response Tender, red dermal papules or nodules resembling erythema nodosum, along with high fever, migrating polyarthralgia, painful swelling of lymph nodes and spleen, irido cyclitis, and, rarely, nephritis, can occur Leprosy Etiology 331 Leprosy is caused by M leprae, an obligate intracellular bacterium that can have variable staining by Gram stain It is best visualized using the Fite method M leprae is the only bacterium known to infect peripheral nerves Other areas of high endemicity include Angola, Brazil, Central African Republic, Democratic Republic of Congo, Madagascar, Mozambique, the Republic of the Marshall Islands, South Sudan, the Federated States of Micronesia, and the United Republic of Tanzania Epidemiology Incubation Period Leprosy is considered a neglected tropical disease and is most prevalent in tropical and subtropical zones It is not highly infectious Fewer than 5% of people appear to be genetically susceptible to the infection Accordingly, spouses of leprosy patients are not likely to develop leprosy, but biological parents, children, and siblings who are household contacts of untreated patients with leprosy are at increased risk Usually to years (range, 1–20 years) Transmission is thought to be through longterm close contact with an infected individual, and it likely occurs through respiratory shedding of infectious droplets by untreated cases or individuals incubating subclinical infections The 9-banded armadillo (Dasypus novemcinc tus) and 6-banded armadillo (Euphractus sexcinctus) are the only known nonhuman reservoirs of M leprae; zoonotic transmission is reported in the southern United States Like many other chronic infectious diseases, onset of leprosy is increasingly associated with use of anti-inflammatory autoimmune therapies and immunologic senescence among elderly patients There are approximately 6,500 people with leprosy living in the United States, with 3,300 under active medical management During 1994–2011, there were 2,323 new cases of leprosy Over this period, a decline in the rate of new diagnoses from 0.52 (1994–1996) to 0.43 (2009–2011) per million was observed The rate among foreign-born people decreased from 3.66 to 2.29, whereas the rate among USborn people was 0.16 in both 1994–1996 and 2009–2011 The majority of leprosy cases reported in the United States occurred among residents of Texas, California, and Hawaii or among immigrants or those who lived or worked in leprosy-endemic countries More than 65% of the world’s leprosy patients reside in South and Southeast Asia— primarily India Diagnostic Tests Histopathologic examination of skin biopsy by an experienced pathologist is the best method of establishing the diagnosis and is the basis for classification of leprosy These specimens can be sent to the National Hansen’s Disease (Leprosy) Program (NHDP) [800/642-2477; www.hrsa.gov/hansensdisease] in formalin or embedded in paraffin Acid-fast bacilli may be found in slit smears or biopsy specimens of skin lesions of patients with lepromatous forms but are rarely visualized from patients with tuberculoid and indeterminate forms of disease A polymerase chain reaction assay for M leprae is available to assist diagnosis after consultation with the NHDP and can be performed on the basis of clinical suspicion Treatment Leprosy is curable The primary goal of therapy is prevention of permanent nerve damage, which can be accomplished by early diagnosis and treatment Combination antimicrobial multidrug therapy can be obtained free of charge from the NHDP in the United States and from the World Health Organization in other countries Certain criteria must be met for physicians wishing to obtain the antimicrobial therapy from the NHDP (www.hrsa.gov/hansensdisease/diagnosis/ recommendedtreatment.html) It is important to treat M leprae infections with more than antimicrobial agent to minimize development of antimicrobial- resistant organisms Adults are treated with dapsone, rifampin, and clofazimine Resistance to all 3 drugs has been documented but is rare. The infectivity of leprosy patients ceases within a few days of initiating standard multidrug t herapy 332 Leprosy • Multibacillary leprosy (6 patches or more) Dapsone and rifampin and clofazimine for 24 months are recommended Clarithromycin can be used in place of clofazimine for children Clofazimine is not available commercially; in the United States, it is available only as an investigational drug for treatment of leprosy and is obtained through the NHDP • Paucibacillary leprosy (1–5 patches) Dapsone and rifampin for 12 months are recommended Before beginning anti microbial therapy, patients should be tested for glucose-6-phosphate dehydrogenase deficiency, have baseline complete blood cell counts and liver function test results documented, and be evaluated for any evidence of tuberculosis infection, especially if the patient is infected with HIV Skin darkening typically resolves within several months of completing therapy Leprosy reactions should be treated aggressively to prevent peripheral nerve damage Treatment with prednisone can be initiated All patients with leprosy should be educated about signs and symptoms of neuritis and cautioned to report signs and symptoms of neuritis immediately so corticosteroid therapy can be instituted Patients should receive counseling because of the social and psychological effects of this disease Relapse of disease after completing multidrug therapy is rare (0.01%–0.14%); the presentation of new skin patches is usually attributable to a late type reaction When it does occur, relapse is usually attributable to reactivation of drugsusceptible organisms People with relapses of disease require another course of multidrug therapy Therapy for patients with leprosy should be undertaken in consultation with an expert in leprosy Image 76.2 Image 76.1 A photomicrograph of Mycobacterium leprae taken from a leprous skin lesion M leprae is the cause of leprosy, or Hansen disease A slowmultiplying bacterium, it mainly affects the skin, nerves, and mucous membranes In 1999, the world incidence level was estimated to be 640,000; in 2000, 738,284 cases were identified In 2007, 101 new cases of leprosy were reported in the United States Courtesy of Centers for Disease Control and Prevention Hansen disease A young Vietnamese boy who spent years in a refugee camp in the Philippines presented with the nodular violaceous skin lesion shown The results of a biopsy of the lesion showed acid-fast organisms surrounding blood vessels A diagnosis of lepromatous leprosy was made and the child was treated with a multidrug regimen Copyright Barbara Jantausch, MD, FAAP Leprosy 333 Image 76.3 Erythema nodosum leprosum in a 29-year-old Asian man Copyright Gary Williams Image 76.4 Erythema nodosum leprosum in the same patient as in Image 76.3 Copyright Gary Williams Image 76.5 Erythema nodosum leprosum in the same patient as in images 76.3 and 76.4 Copyright Gary Williams Image 76.6 Lepromatous leprosy in an Asian man Newly diagnosed cases are considered contagious until treatment is established and should be reported to local and state public health departments Courtesy of Hugh Moffet, MD 334 Leprosy Image 76.7 An adult male with lepromatous leprosy Courtesy of Hugh Moffet, MD Image 76.8 Number of reported cases, by year—United States, 1992–2012 Courtesy of Morbidity and Mortality Weekly Report ... United States of America 9-375 /10 16 10 MA0805 ISBN: 978 -1- 610 02-060-2 eBook: 978 -1- 610 02-0 61- 9 Library of Congress Control Number: 2 016 942360 III Contents Preface VII 1/ Actinomycosis... of Pediatrics (AAP) Red Book Atlas of Pediatric Infectious Diseases, 3rd Edition, is a summary of key disease information from the AAP Red Book : 2 015 Report of the Committee on Infectious Diseases. .. .500 11 7/Rocky Mountain Spotted Fever .502 VI CONTENTS 11 8/Rotavirus Infections 508 11 9/Rubella 510 12 0/Salmonella Infections 516 12 1/Scabies