Ebook Harrison''s manual of medicine (16th edition): Part 1

(BQ) Part 1 book Harrison''s manual of medicine presents the following contents: Care of the hospitalized patient, medical emergencies, common patient presentations; disorders of the eye, ear, nose, and throat, dermatology, hematology and oncology, infectious diseases.

HARRISON’S Manual of Medicine EDITORS Dennis L Kasper, MD, MA(HON) William Ellery Channing Professor of Medicine, Professor of Microbiology and Molecular Genetics, Harvard Medical School; Director, Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital, Boston Eugene Braunwald, MD, MA(HON), MD(HON), ScD(HON) Distinguished Hersey Professor of Medicine, Harvard Medical School; Chairman, TIMI Study Group, Brigham and Women’s Hospital, Boston Anthony S Fauci, MD, ScD(HON) Chief, Laboratory of Immunoregulation; Director, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda Stephen L Hauser, MD Robert A Fishman Distinguished Professor and Chairman, Department of Neurology, University of California– San Francisco, San Francisco Dan L Longo, MD Scientific Director, National Institute on Aging, National Institutes of Health, Bethesda and Baltimore J Larry Jameson, MD, PhD Irving S Cutter Professor and Chairman, Department of Medicine, Northwestern University Feinberg School of Medicine; Physician-in-Chief, Northwestern Memorial Hospital, Chicago HARRISON’S Manual of Medicine EDITORS Dennis L Kasper, MD Eugene Braunwald, MD Anthony S Fauci, MD Stephen L Hauser, MD Dan L Longo, MD J Larry Jameson, MD, PhD McGraw-Hill Medical Publishing Division New York Chicago San Francisco Lisbon London Madrid Mexico City Milan New Delhi San Juan Seoul Singapore Sydney Toronto Copyright © 2005, 2002, 1998, 1995, 1991, 1988 by The McGraw-Hill Companies, Inc All rights reserved Manufactured in the United States of America Except as permitted under the United States Copyright Act of 1976, no part of this publication may be reproduced or distributed in any form or by any means, or stored in a database or retrieval system, without the prior written permission of the publisher 0-07-146698-3 The material in this eBook also appears in the print version of this title: 0-07-144441-6 All trademarks are trademarks of their respective owners Rather than put a trademark symbol after every occurrence of a trademarked name, we use names in an editorial fashion only, and to the benefit of the trademark owner, with no intention of infringement of the trademark Where such designations appear in this book, they have been printed with initial caps McGraw-Hill eBooks are available at special quantity discounts to use as premiums and sales promotions, or for use in corporate training programs For more information, please contact George Hoare, Special Sales, at george_hoare@mcgraw-hill.com or (212) 904-4069 TERMS OF USE This is a copyrighted work and The McGraw-Hill Companies, Inc (“McGraw-Hill”) and its licensors reserve all rights in and to the work Use of this work is subject to these terms Except as permitted under the Copyright Act of 1976 and the right to store and retrieve one copy of the work, you may not decompile, disassemble, reverse engineer, reproduce, modify, create derivative works based upon, transmit, distribute, disseminate, sell, publish or sublicense the work or any part of it without McGraw-Hill’s prior consent You may use the work for your own noncommercial and personal use; any other use of the work is strictly prohibited Your right to use the work may be terminated if you fail to comply with these terms THE WORK IS PROVIDED “AS IS.” McGRAW-HILL AND ITS LICENSORS MAKE NO GUARANTEES OR WARRANTIES AS TO THE ACCURACY, ADEQUACY OR COMPLETENESS OF OR RESULTS TO BE OBTAINED FROM USING THE WORK, INCLUDING ANY INFORMATION THAT CAN BE ACCESSED THROUGH THE WORK VIA HYPERLINK OR OTHERWISE, AND EXPRESSLY DISCLAIM ANY WARRANTY, EXPRESS OR IMPLIED, INCLUDING BUT NOT LIMITED TO IMPLIED WARRANTIES OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE McGrawHill and its licensors not warrant or guarantee that the functions contained in the work will meet your requirements or that its operation will be uninterrupted or error free Neither McGraw-Hill nor its licensors shall be liable to you or anyone else for any inaccuracy, error or omission, regardless of cause, in the work or for any damages resulting therefrom McGraw-Hill has no responsibility for the content of any information accessed through the work Under no circumstances shall McGraw-Hill and/or its licensors be liable for any indirect, incidental, special, punitive, consequential or similar damages that result from the use of or inability to use the work, even if any of them has been advised of the possibility of such damages This limitation of liability shall apply to any claim or cause whatsoever whether such claim or cause arises in contract, tort or otherwise DOI: 10.1036/0071466983 For more information about this title, click here CONTENTS Contributors Preface xiii xv SECTION CARE OF THE HOSPITALIZED PATIENT Initial Evaluation and Admission Orders for the General Medicine Patient Assessment of Nutritional Status Electrolytes/Acid-Base Balance Enteral and Parenteral Nutrition Transfusion and Pheresis Therapy Principles of Critical Care Medicine Respiratory Failure Pain and Its Management Procedures Commonly Performed by Internists 10 Diagnostic Imaging in Internal Medicine 11 Gastrointestinal Diseases 14 19 22 23 28 32 34 17 SECTION MEDICAL EMERGENCIES 12 Acute Respiratory Distress Syndrome (ARDS) 13 Cardiovascular Collapse and Sudden Death 14 Shock 15 Sepsis and Septic Shock 16 Acute Pulmonary Edema 17 Confusion, Stupor, and Coma 18 Stroke 19 Subarachnoid Hemorrhage 20 Increased Intracranial Pressure and Head Trauma 21 Hypoxic-Ischemic Encephalopathy 22 Status Epilepticus 23 Poisoning and Drug Overdose 24 Diabetic Ketoacidosis and Hyperosmolar Coma 25 Hypoglycemia 26 Infectious Disease Emergencies 27 Oncologic Emergencies 28 Anaphylaxis 29 Bites, Venoms, Stings, and Marine Poisonings 30 Hypothermia and Frostbite 31 Bioterrorism 39 41 44 49 53 54 58 66 67 72 74 89 91 94 101 105 106 115 118 69 SECTION COMMON PATIENT PRESENTATIONS 32 33 34 35 36 Chest Pain Abdominal Pain Headache Back and Neck Pain Fever, Hyperthermia, Chills, and Rash 133 136 139 147 37 38 39 40 156 v Pain or Swelling of Joints Syncope and Faintness Dizziness and Vertigo Acute Visual Loss and Double Vision 161 164 168 171 vi CONTENTS 41 Paralysis and Movement Disorders 42 Aphasias and Related Disorders 43 Sleep Disorders 44 Dyspnea 45 Cough and Hemoptysis 46 Cyanosis 47 Edema 48 Nausea, Vomiting, and Indigestion 49 Weight Loss 50 Dysphagia 175 179 181 185 187 192 194 197 201 203 51 Acute Abdomen 52 Diarrhea, Constipation, and Malabsorption 53 Gastrointestinal Bleeding 54 Jaundice and Evaluation of Liver Function 55 Ascites 56 Azotemia and Urinary Abnormalities 57 Anemia and Polycythemia 58 Lymphadenopathy and Splenomegaly 206 208 214 218 224 227 232 235 SECTION DISORDERS OF THE EYE, EAR, NOSE, AND THROAT 59 Common Disorders of Vision and Hearing 241 60 Infections of the Upper Respiratory Tract 248 SECTION DERMATOLOGY 61 General Examination of the Skin 62 Common Skin Conditions 259 255 SECTION HEMATOLOGY AND ONCOLOGY 63 Examination of Blood Smears and Bone Marrow 64 Red Blood Cell Disorders 65 Leukocytosis and Leukopenia 66 Bleeding and Thrombotic Disorders 67 Prevention and Early Detection of Cancer 68 Cancer Chemotherapy 69 Myeloid Leukemias, Myelodysplasia, and Myeloproliferative Syndrome 70 Lymphoid Malignancies 71 Skin Cancer 265 267 72 73 74 75 272 275 280 284 76 77 78 79 80 290 296 307 81 Head and Neck Cancer Lung Cancer Breast Cancer Tumors of the Gastrointestinal Tract Genitourinary Tract Cancer Gynecologic Cancer Prostate Hyperplasia and Carcinoma Cancer of Unknown Primary Site Paraneoplastic Endocrine Syndromes Neurologic Paraneoplastic Syndromes 309 310 316 320 331 334 338 341 344 346 CONTENTS vii SECTION INFECTIOUS DISEASES 82 Diagnosis of Infectious Diseases 83 Antibacterial Therapy 84 Immunization and Advice to Travelers 85 Infective Endocarditis 86 Intraabdominal Infections 87 Infectious Diarrheas 88 Sexually Transmitted Diseases and Reproductive Tract Infections 89 Infections of the Skin, Soft Tissues, Joints, and Bones 90 Infections in the Immunocompromised Host 91 HIV Infection and AIDS 92 Hospital-Acquired Infections 93 Pneumococcal Infections 94 Staphylococcal Infections 95 Streptococcal/Enterococcal Infections, Diphtheria, and Other Corynebacterial Infections 96 Meningococcal and Listerial Infections 97 Infections Caused by Haemophilus, Bordetella, Moraxella, and HACEK Group Organisms 98 Diseases Caused by GramNegative Enteric Bacteria, Pseudomonas, and Legionella 351 360 365 372 380 383 393 408 417 424 442 445 448 455 462 99 Infections Caused by Other Gram-Negative Bacilli 100 Anaerobic Infections 101 Nocardiosis and Actinomycosis 102 Tuberculosis and Other Mycobacterial Infections 103 Lyme Disease and Other Nonsyphilitic Spirochetal Infections 104 Rickettsial Diseases 105 Mycoplasma Infections 106 Chlamydial Infections 107 Herpesvirus Infections 108 Cytomegalovirus and Epstein-Barr Virus Infections 109 Influenza and Other Viral Respiratory Diseases 110 Rubeola, Rubella, Mumps, and Parvovirus Infections 111 Enteroviral Infections 112 Insect- and Animal-Borne Viral Infections 113 Fungal Infections 114 Pneumocystis Infection 115 Protozoal Infections 116 Helminthic Infections 479 485 492 495 506 510 516 517 520 529 533 539 544 547 555 565 569 580 466 471 SECTION CARDIOVASCULAR DISEASES 117 Physical Examination of the Heart 118 Electrocardiography and Echocardiography 119 Valvular Heart Disease 120 Cardiomyopathies and Myocarditis 121 Pericardial Disease 593 596 603 609 612 122 Hypertension 123 ST-Segment Elevation Myocardial Infarction (STEMI) 124 Chronic Stable Angina, Unstable Angina, and NonST-Elevation Myocardial Infarction 616 621 631 viii CONTENTS 125 Arrhythmias 126 Congestive Heart Failure and Cor Pulmonale 638 648 127 Diseases of the Aorta 128 Peripheral Vascular Disease 129 Pulmonary Hypertension 653 655 658 SECTION RESPIRATORY DISEASES 130 Respiratory Function and Pulmonary Diagnostic Procedures 131 Asthma and Hypersensitivity Pneumonitis 132 Environmental Lung Diseases 133 Chronic Bronchitis, Emphysema, and Acute or Chronic Respiratory Failure 663 668 673 675 134 Pneumonia and Lung Abscess 135 Pulmonary Thromboembolism 136 Interstitial Lung Disease (ILD) 137 Diseases of the Pleura, Mediastinum, and Diaphragm 138 Disorders of Ventilation, Including Sleep Apnea 679 685 687 691 695 SECTION 10 RENAL DISEASES 139 Approach to the Patient with Renal Disease 140 Acute Renal Failure 141 Chronic Kidney Disease (CKD) and Uremia 142 Dialysis 143 Renal Transplantation 699 702 707 709 711 144 145 146 147 148 149 Glomerular Diseases Renal Tubular Disease Urinary Tract Infections Renovascular Disease Nephrolithiasis Urinary Tract Obstruction 713 720 724 728 731 734 SECTION 11 GASTROINTESTINAL DISEASES 150 Peptic Ulcer and Related Disorders 151 Inflammatory Bowel Diseases 152 Colonic and Anorectal Diseases 153 Cholelithiasis, Cholecystitis, and Cholangitis 737 742 746 749 154 155 156 157 Pancreatitis Acute Hepatitis Chronic Hepatitis Cirrhosis and Alcoholic Liver Disease 158 Portal Hypertension 753 757 762 766 769 CONTENTS ix SECTION 12 ALLERGY, CLINICAL IMMUNOLOGY, AND RHEUMATOLOGY 159 Diseases of Immediate Type Hypersensitivity 160 Primary Immunodeficiency Diseases 161 SLE, RA, and Other Connective Tissue Diseases 162 Vasculitis 163 Ankylosing Spondylitis 773 776 779 785 788 164 Psoriatic Arthritis 165 Reactive Arthritis and Reiter’s Syndrome 166 Osteoarthritis 167 Gout, Pseudogout, and Related Diseases 168 Other Arthritides 169 Sarcoidosis 170 Amyloidosis 791 792 794 796 799 802 804 SECTION 13 ENDOCRINOLOGY AND METABOLISM 171 Disorders of the Anterior Pituitary and Hypothalamus 172 Disorders of the Posterior Pituitary 173 Disorders of the Thyroid 174 Disorders of the Adrenal Gland 175 Obesity 176 Diabetes Mellitus 177 Disorders of the Male Reproductive System 807 813 815 823 828 830 835 178 Disorders of the Female Reproductive System 179 Hypercalcemic and Hypocalcemic Disorders 180 Osteoporosis and Osteomalacia 181 Disorders of Lipid Metabolism 182 Hemochromatosis, Porphyrias, and Wilson’s Disease 839 847 852 855 861 SECTION 14 NEUROLOGY 183 The Neurologic Examination 184 Neuroimaging 185 Seizures and Epilepsy 186 Tumors of the Nervous System 187 Acute Meningitis and Encephalitis 188 Chronic Meningitis 189 Multiple Sclerosis (MS) 190 Alzheimer’s Disease and Other Dementias 191 Parkinson’s Disease 192 Ataxic Disorders 867 873 875 883 886 896 899 904 910 914 193 ALS and Other Motor Neuron Diseases 194 Trigeminal Neuralgia, Bell’s Palsy, and Other Cranial Nerve Disorders 195 Autonomic Nervous System Disorders 196 Spinal Cord Diseases 197 Peripheral Neuropathies, Including Guillain-Barre´ Syndrome 198 Myasthenia Gravis (MG) 199 Muscle Diseases 200 Chronic Fatigue Syndrome 917 920 925 932 936 942 944 952 578 SECTION Infectious Diseases lence, a state that sometimes alternates with restlessness and insomnia Extrapyramidal signs may include choreiform movements, tremors, and fasciculations; ataxia is common Progressive neurologic impairment may end in coma and death East African disease is a more acute illness that, without treatment, generally leads to death in weeks or months DIAGNOSIS Examination of fluid from the chancre, thin or thick blood smears, lymph node aspirates, bone marrow biopsy specimens, or CSF samples can reveal the parasite CSF should be examined whenever the diagnosis is being considered Increased opening pressure, increased protein level, and increased mononuclear cell counts are common Parasites can be visualized in the sediment of centrifuged CSF TREATMENT Treatment is toxic and must be closely supervised I Stage I disease A East and West African: suramin (1 g on days 1, 3, 7, 14, and 21) There is a high incidence of serious adverse effects Fever, photophobia, pruritus, arthralgias, skin eruptions, and renal damage can occur Severe reactions can be fatal B Alternatives East African: Pentamidine (4 mg/kg for 10 days) West African: Eflornithine (400 mg/kg per day in divided doses for weeks) II Stage II disease A East African: Melarsoprol (2– 3.6 mg/kg daily in divided doses for days; week later, 3.6 mg/kg per day in divided doses for days; repeat latter course 10– 21 days later) Reactive encephalopathy occurs in up to 18% of pts B West African: Eflornithine (400 mg/kg per day in divided doses for weeks) TOXOPLASMOSIS ETIOLOGY AND EPIDEMIOLOGY Toxoplasmosis is caused by the intracellular parasite Toxoplasma gondii In the United States and most European countries, seroconversion rates increase with age and exposure Cats and their prey are the definitive hosts Transmission occurs when humans ingest oocysts from contaminated soil or tissue cysts from undercooked meat About one-third of women who become acutely infected with T gondii during pregnancy transmit the parasite to the fetus Congenital infection can occur if the mother is infected Ͻ6 months before conception and becomes increasingly likely throughout pregnancy, with a 65% likelihood if the mother is infected in the third trimester PATHOGENESIS Both humoral and cellular immunity are important, but infection commonly persists Such lifelong infection usually remains subclinical Compromised hosts not control infection; progressive focal destruction and organ failure occur CLINICAL FEATURES • Disease in immunocompetent hosts is usually asymptomatic and self-limited and does not require therapy; 80– 90% of cases go unrecognized Cervical lymphadenopathy is the most common finding; nodes are nontender and discrete Generalized lymphadenopathy can occur Fever, headache, malaise, and fatigue are documented in 20– 40% of pts with lymphadenopathy CHAPTER 115 Protozoal Infections 579 • Immunocompromised pts, including those with AIDS and those receiving immunosuppressive treatment for lymphoproliferative disorders, are at greatest risk Most clinical disease is due to reactivated latent infection CNS: principal site of involvement Findings include encephalopathy, meningoencephalitis, and mass lesions Pts may exhibit changes in mental status, fever, seizures, headaches, and aphasia The brainstem, basal ganglia, pituitary gland, and corticomedullary junction are most often involved Pneumonia: Dyspnea, fever, and nonproductive cough can progress to respiratory failure Toxoplasma pneumonia is often confused with Pneumocystis pneumonia Miscellaneous sites: GI tract, pancreas, eyes, heart, liver • Congenital infection affects 400– 4000 infants each year in the United States Severe disease, manifesting as hydrocephalus, microcephaly, mental retardation, and chorioretinitis, is more common the earlier the infection is contracted • Ocular infection: T gondii is estimated to cause ϳ35% of all cases of chorioretinitis in the United States and Europe Most cases are associated with congenital infection Blurred vision, scotoma, photophobia, and eye pain are manifestations of infection; macular involvement can occur with loss of central vision On examination, yellow-white cotton-like patches with indistinct margins of hyperemia are seen Older lesions appear as white plaques with distinct borders and black spots DIAGNOSIS • Acute toxoplasmosis can be diagnosed by the demonstration of tachyzoites in tissue or by documentation of the simultaneous presence of serum IgM and IgG antibodies to T gondii • In AIDS pts, the infection is diagnosed presumptively on the basis of clinical presentation and a positive test for IgG antibody to T gondii In these pts, CT or MRI of the brain shows lesions that are often multiple and contrast enhancing A single lesion may prove to be a CNS lymphoma rather than toxoplasmosis • Congenital toxoplasmosis is diagnosed by PCR of the amniotic fluid (to detect the B1 gene of the parasite) and by the detection of IgG antibody or a positive IgM titer after the first week of life; IgG antibody determinations should be repeated every months • Ocular toxoplasmosis is diagnosed by the detection of typical lesions on ophthalmologic examination and the demonstration of a positive IgG titer TREATMENT • Congenital infection: daily pyrimethamine (0.5– mg/kg) and sulfadiazine (100 mg/kg) for year If infection is diagnosed and treated early, up to 70% of children can have normal findings at follow-up evaluations • Ocular disease: pyrimethamine and sulfadiazine or clindamycin for month • Immunocompromised pts: pyrimethamine (200-mg PO loading dose followed by 50– 75 mg/d) plus sulfadiazine (4– g/d PO, divided into doses) plus leucovorin (10– 15 mg/d) Pyrimethamine (75 mg/d) plus clindamycin (450 mg tid) is an alternative Glucocorticoids are often used to treat intracerebral edema After 4– weeks (or after radiographic improvement), the pt may be switched to chronic suppressive therapy (secondary prophylaxis) with pyrimethamine (25– 50 mg/d) plus sulfadiazine (2– g/d), pyrimethamine (75 mg/d) plus clindamycin (450 mg tid), or pyrimethamine alone (50– 75 mg/ d) 580 SECTION Infectious Diseases PREVENTION Personal Protection Measures Toxoplasma infection can be prevented by avoiding undercooked meats and oocyst-contaminated materials (e.g., cats’ litter boxes) Chemoprophylaxis The risk of disease is very high among AIDS pts who are seropositive for T gondii and have a CD4ϩ T lymphocyte count of Ͻ100/ ␮L Trimethoprim-sulfamethoxazole (one double-strength tablet daily) should be given to these pts as prophylaxis against both Pneumocystis pneumonia and toxoplasmosis Primary or secondary prophylaxis can be stopped if, after institution of antiretroviral treatment, the CD4ϩ T lymphocyte count increases to Ͼ200/␮L and remains above that cutoff for months For a more detailed discussion, see Davis CE: Laboratory Diagnosis of Parasitic Infections, Chap 192, p 1197; Moore TA: Agents Used to Treat Infections Due to Parasites and Pneumocystis, Chap 193, p 1202; White NJ, Breman JG: Malaria and Babesiosis: Diseases Caused by Red Blood Cell Parasites, Chap 195, p 1218; Herwaldt BL: Leishmaniasis, Chap 196, p 1233; Kirchhoff LV: Trypanosomiasis, Chap 197, p 1238; and Kasper LH: Toxoplasma Infection, Chap 198, p 1243, in HPIM-16 116 HELMINTHIC INFECTIONS NEMATODES The nematodes, or roundworms, that are of medical significance can be broadly classified as either tissue or intestinal parasites Tissue Nematode Infections TRICHINELLOSIS Etiology cies cause human infection T spiralis and six other Trichinella spe- Life Cycle and Epidemiology Infection results when humans ingest meat (usually pork) that contains cysts with Trichinella larvae During the first week of infection, the larvae invade the small-bowel mucosa; during the second and third weeks, they mature into adult worms, which release new larvae that migrate to striated muscle via the circulation and encyst Clinical Features Light infections (Ͻ10 larvae per gram of muscle) are asymptomatic A burden of Ͼ50 larvae per gram can cause fatal disease • Week 1: diarrhea, abdominal pain, constipation, nausea, and/or vomiting • Week 2: hypersensitivity reactions with fever and hypereosinophilia; peri- orbital and facial edema; hemorrhages in conjunctivae, retina, and nail beds; maculopapular rash; headache; cough; dyspnea; dysphagia Deaths are usually due to myocarditis with arrhythmias or CHF and are less often caused by pneumonitis or encephalitis CHAPTER 116 Helminthic Infections 581 • Weeks 2– 3: myositis, myalgias, muscle edema, weakness (especially in extraocular muscles, biceps, neck, lower back, and diaphragm) Symptoms peak at weeks; convalescence is prolonged Diagnosis • Eosinophilia in Ͼ90% of pts, peaking at a level of Ͼ50% at 2– weeks • Elevated IgE and muscle enzyme levels; increase in specific antibody titers by week • A definitive diagnosis is made by the detection of larvae on biopsy of at least g of muscle tissue Yields are highest near tendon insertions TREATMENT Drugs are ineffective against muscle larvae, but mebendazole and albendazole may be active against enteric-stage parasites Glucocorticoids (1 mg/kg daily for days) may reduce severe myositis and myocarditis Prevention Cooking pork until it is no longer pink or freezing it at Ϫ15ЊC for weeks kills larvae and prevents infection VISCERAL AND OCULAR LARVA MIGRANS cases of larva migrans are caused by Toxocara canis Etiology Most Life Cycle and Epidemiology Infection results when humans— most often preschool children— ingest soil contaminated by puppy feces that contain infective T canis eggs Larvae penetrate the intestinal mucosa and disseminate hematogenously to a wide variety of organs (e.g., liver, lungs, CNS), provoking intense eosinophilic granulomatous responses Clinical Features Heavy infections may cause fever, malaise, anorexia, weight loss, cough, wheezing, rashes, and hepatosplenomegaly Ocular disease usually develops in older children or young adults and may cause an eosinophilic mass that mimics retinoblastoma, endophthalmitis, uveitis, or chorioretinitis Diagnosis • No eggs are found in the stool because larvae not develop into adult worms • Blood eosinophilia up to 90%, leukocytosis, and hypergammaglobulinemia may be evident • Toxocaral antibodies detected by ELISA can confirm the diagnosis TREATMENT Glucocorticoids can reduce inflammatory complications Only ocular infections require treatment: albendazole (800 mg bid for adults and 400 mg bid for children) for 5– 20 days in conjunction with glucocorticoids CUTANEOUS LARVA MIGRANS This disease is caused by larvae of animal hookworms, usually the dog and cat hookworm Ancylostoma braziliense Larvae in contaminated soil penetrate human skin; erythematous lesions form along the tracks of their migration and advance several centimeters each day Pruritus is intense Vesicles or bullae may form Ivermectin (a single dose of 200 ␮g/kg) or albendazole (200 mg bid for days) can relieve the symptoms of this self-limited infestation 582 SECTION Infectious Diseases Intestinal Nematode Infections Intestinal nematodes infect Ͼ1 billion persons worldwide in regions with poor sanitation, particularly in developing countries in the tropics or subtropics These parasites contribute to malnutrition and diminished work capacity ASCARIASIS Etiology Ascariasis is caused by Ascaris lumbricoides, the largest intestinal nematode, which reaches lengths up to 40 cm The parasite is transmitted via fecally contaminated soil Life Cycle Swallowed eggs hatch in the intestine, invade the mucosa, migrate to the lungs, break into the alveoli, ascend the bronchial tree, are swallowed, reach the small intestine, mature, and produce up to 240,000 eggs per day that pass in the feces Clinical Features Most infections have a low worm burden and are asymptomatic During lung migration of the parasite, pts may develop a cough and substernal discomfort, occasionally with dyspnea or blood-tinged sputum, fever, and eosinophilia Eosinophilic pneumonitis (Loăfers syndrome) may be evident Heavy infections occasionally cause pain, small-bowel obstruction, perforation, volvulus, biliary obstruction and colic, or pancreatitis Laboratory Findings Ascaris eggs (65 by 45 ␮m) can be found in fecal samples Adult worms can pass in the stool or through the mouth or nose During the transpulmonary migratory phase, larvae can be found in sputum or gastric aspirates TREATMENT A single dose of albendazole (400 mg) or mebendazole (500 mg) is effective Pyrantel pamoate (a single dose of 11 mg/kg, up to g) is safe in pregnancy HOOKWORM Etiology One-fourth of the world’s population is infected with one of two hookworm species: Ancylostoma duodenale or Necator americanus Life Cycle Infectious larvae penetrate the skin, reach the lungs via the bloodstream, invade the alveoli, ascend the airways, are swallowed, reach the small intestine, mature into adult worms, attach to the mucosa, and suck blood and interstitial fluid Clinical Features Most infections are asymptomatic Chronic infection causes iron deficiency and— in marginally nourished persons— progressive anemia and hypoproteinemia, weakness, shortness of breath, and skin depigmentation Laboratory Findings Hookworm eggs (40 by 60 ␮m) can be found in the feces Stool concentration may be needed for the diagnosis of light infections TREATMENT Albendazole (400 mg once), mebendazole (500 mg once), or pyrantel pamoate (11 mg/kg daily for days) is effective Nutritional support, iron replacement, and deworming are undertaken as needed STRONGYLOIDIASIS Etiology and Epidemiology Unlike other helminths, Strongyloides stercoralis can replicate in the human host, permitting CHAPTER 116 Helminthic Infections 583 ongoing cycles of autoinfection from endogenously produced larvae Autoinfection is most common among immunocompromised hosts, including those receiving glucocorticoids Hyperinfection and widespread larval dissemination can occur in these pts However, severe disease due to Strongyloides is unusual in HIV-infected pts Life Cycle Infection results when filariform larvae in fecally contaminated soil penetrate the skin or mucous membranes Larvae travel through the bloodstream to the lungs, break through alveolar spaces, ascend the bronchial tree, are swallowed, reach the small intestine, mature into adult worms, and penetrate the mucosa of the proximal small bowel; eggs hatch in intestinal mucosa Rhabditiform larvae can pass with the feces into the soil or can develop into filariform larvae that penetrate the colonic wall or perianal skin and enter the circulation to establish ongoing autoinfection Clinical Features Uncomplicated disease is associated with mild cutaneous and/or abdominal manifestations such as urticaria, larva currens (a pathognomonic serpiginous, pruritic, erythematous eruption along the course of larval migration that may advance up to 10 cm/h), abdominal pain, nausea, diarrhea, bleeding, and weight loss Colitis, enteritis, or malabsorption can develop Disseminated disease involves extraintestinal tissues, including the CNS, peritoneum, liver, and kidney Bacteremia can develop when enteric flora components enter the bloodstream through disrupted mucosal barriers Gram-negative sepsis, pneumonia, or meningitis can complicate the disease Diagnosis Eosinophilia is common, with levels that fluctuate over time Eggs are rarely found in feces because they hatch in the colon A single stool examination detects rhabditiform larvae (200– 250 ␮m long) in about one-third of uncomplicated infections If stool examinations are negative, duodenojejunal contents can be sampled Antibodies can be detected by ELISA In disseminated infection, filariform larvae (550 ␮m long) can be found in stool or at sites of larval migration TREATMENT Ivermectin (200 ␮g/kg daily for or days) is more effective than albendazole (400 mg daily for days, repeated at weeks) and is better tolerated than thiabendazole (25 mg/kg bid for days) Disseminated disease should be treated for 5– days ENTEROBIASIS Etiology obius vermicularis Enterobiasis (pinworm) is caused by Enter- Life Cycle Adult worms dwell in the bowel lumen and migrate nocturnally out into the perianal region, releasing immature eggs that become infective within hours Autoinfection results from perianal scratching and transport of infective eggs to the mouth Person-to-person spread occurs Pinworm is common among schoolchildren and their household contacts and among institutionalized populations Clinical Features Perianal pruritus is the cardinal symptom and is often worst at night Diagnosis Eggs in the perianal region are detected by application of cellulose acetate tape in the morning Eggs measure 55 by 25 ␮m and are flattened on one side 584 SECTION Infectious Diseases TREATMENT One dose of mebendazole (100 mg), albendazole (400 mg), or pyrantel pamoate (11 mg/kg; maximum, g) is given, with the same treatment repeated after 10– 14 days Household members should also be treated Filarial and Related Infections Filarial worms are nematodes that dwell in the SC tissue and lymphatics More than 170 million people are infected worldwide Infection is established only with repeated and prolonged exposures to infective larvae Disease tends to be more intense and acute in newly exposed individuals than in natives of endemic areas Life Cycle Insects transmit infective larvae to humans Adult worms reside in lymphatics or SC tissues; their offspring are microfilariae (200– 250 ␮m long, 5– ␮m wide) that either circulate in the blood or migrate through the skin Subperiodic forms are those that are present in peripheral blood at all times and peak in the afternoon Nocturnally periodic forms are scarce in peripheral blood by day and increase by night Adult worms live for years; microfilariae live for 3– 36 months A rickettsia-like endosymbiont of Wolbachia has been found in all stages of the four major filarial species that cause human disease and may prove to be a target for future antifilarial chemotherapy LYMPHATIC FILARIASIS Etiology Wuchereria bancrofti, Brugia malayi, or B timori can reside in lymphatic channels or lymph nodes W bancrofti is most common and usually is nocturnally periodic Pathology Adult worms cause inflammatory damage to the lymphatics Clinical Features Asymptomatic microfilaremia, hydrocele, acute adenolymphangitis (ADL), and chronic lymphatic disease are the main clinical presentations ADL is associated with high fever, lymphatic inflammation, and transient local edema W bancrofti particularly affects genital lymphatics ADL may progress to lymphatic obstruction and elephantiasis with brawny edema, thickening of the SC tissues, and hyperkeratosis Superinfection is a problem Diagnosis Detection of the parasite is difficult, but microfilariae can be found in peripheral blood, hydrocele fluid, and occasionally other body fluids Timing of blood collection is critical Two assays are available to detect W bancrofti circulating antigens, and a PCR has been developed to detect DNA of both W bancrofti and B malayi in the blood High-frequency ultrasound of the scrotum or the female breast can identify motile adult worms Pts have eosinophilia and elevated IgE levels The presence of antifilarial antibody supports the diagnosis, but cross-reactivity with other helminthic infections makes interpretation difficult TREATMENT Diethylcarbamazine (DEC) given at mg/kg daily for 12 days is the standard regimen, but one dose may be equally efficacious An alternative is albendazole (400 mg bid for 21 days) Prevention • Mosquito control or personal protective equipment can minimize bites • Mass annual distribution of albendazole with DEC or ivermectin for com- munity-based control reduces microfilaremia and interrupts transmission CHAPTER 116 Helminthic Infections 585 ONCHOCERCIASIS Etiology Onchocerciasis (“river blindness”) is caused by Onchocerca volvulus, is the second leading cause of infectious blindness worldwide, and is transmitted by the bite of an infected blackfly The blackfly vector breeds along free-flowing rivers and streams and restricts its flight to an area within several kilometers of these breeding sites Life Cycle Larvae develop into adult worms that are found in SC nodules (onchocercomata) After months or years, microfilariae migrate out of the nodules and concentrate in the dermis Onchocerciasis affects primarily the skin, eyes, and lymph nodes Microfilariae cause inflammation and fibrosis Neovascularization and corneal scarring cause corneal opacities and blindness Clinical Features • Skin: Pruritus and rash are the most common manifestations • Onchocercomata: palpable and/or visible, firm and nontender • Ocular tissue: Conjunctivitis with photophobia is an early finding Sclerosing keratitis, anterior uveitis, iridocyclitis, and secondary glaucoma due to anterior uveal tract deformity are complications • Lymphadenopathy: especially in the inguinal and femoral areas Diagnosis A definitive diagnosis is based on the finding of an adult worm in an excised nodule or of microfilariae in a skin snip Eosinophilia and elevated serum IgE levels are common Assays to detect specific antibodies and PCR to detect onchocercal DNA in skin snips are available in some laboratories TREATMENT Nodules on the head should be excised to avoid ocular infection Ivermectin in a single dose of 150 ␮g/kg given yearly or semiannually is the mainstay of treatment Doxycycline therapy for weeks may render adult female worms sterile for long periods and also may target the Wolbachia endosymbiont TREMATODES The trematodes, or flatworms, may be classified according to the tissues invaded by the adult flukes The life cycle involves a definitive mammalian host in whom adult worms produce eggs and an intermediate host (e.g., snails) in which larval forms multiply Worms not multiply within the definitive host Human infection results from either direct penetration of intact skin or ingestion Schistosomiasis Etiology Schistosomes are blood flukes that infect 200– 300 million persons worldwide Five species cause human schistosomiasis: the intestinal species Schistosoma mansoni (found in South America, Africa, and the Middle East), S japonicum (found in China, the Philippines, and Indonesia), S mekongi (found in Southeast Asia), and S intercalatum (found in West and Central Africa); and the urinary species S haematobium (found in Africa and the Middle East) Infection is initiated by penetration of intact skin by infective cercariae— the form of the parasite released from snails in freshwater bodies As they mature into schistosomes, the parasites reach the portal vein, mate, then migrate to the venules of the bladder and ureters (S haematobium) or the mesentery (S mansoni, S japonicum, S mekongi, S intercalatum) and deposit eggs Some mature ova are extruded into the intestinal or urinary lumina, from which they may be voided and ultimately may reach water and perpetuate the life cycle The persistence of other ova in tissues leads to a granulomatous host response 586 SECTION Infectious Diseases and fibrosis Factors governing disease manifestations include the intensity and duration of infection, the site of egg deposition, and the genetic characteristics of the host Pathogenesis In the liver, granulomata cause presinusoidal portal blockage, hemodynamic changes (including portal hypertension), and periportal fibrosis Similar processes occur in the bladder Clinical Features Clinical manifestations vary by species, intensity of infection, and host factors • Cercarial invasion (“swimmers’ itch”): An itchy maculopapular rash develops 2– days after parasitic invasion This condition is most frequently caused by S mansoni or S japonicum but is most severe if due to avian schistosomes, which invade human skin but then die in SC tissue • Acute schistosomiasis (Katayama fever): A serum sickness– like illness with fever, generalized lymphadenopathy, hepatosplenomegaly, and peripheral blood eosinophilia may develop during worm maturation and at the start of oviposition Parasite-specific antibodies may be detected before eggs are seen in excreta • Chronic schistosomiasis causes manifestations that depend primarily on the schistosome species Intestinal species cause colicky abdominal pain, bloody diarrhea, malabsorption, hepatosplenomegaly, and portal hypertension Esophageal varices with bleeding, ascites, hypoalbuminemia, and coagulation defects are late complications Urinary species cause dysuria, frequency, hematuria, obstruction with hydroureter and hydronephrosis, fibrosis of bladder granulomas, and late development of squamous cell carcinoma of the bladder Granulomata and fibrosis at other sites (e.g., in the lungs and the CNS) may occur Diagnosis Diagnosis is based on clinical presentation, blood eosinophilia, and a positive serologic assay for schistosomal antibodies Examination of stool or urine can yield positive results Infection may also be diagnosed by examination of tissue samples (e.g., rectal biopsies) TREATMENT Severe acute schistosomiasis requires hospitalization and supportive measures along with a consideration of glucocorticoid treatments After the acute critical phase has resolved, praziquantel results in parasitologic cure in ϳ85% of cases The recommended doses are 20 mg/kg bid for day for S mansoni, S intercalatum, and S haematobium infections and 20 mg/kg tid for day for S japonicum and S mekongi infections Late established manifestations, such as fibrosis, not improve with treatment Prevention Travelers should avoid contact with all freshwater bodies Liver (Biliary) Flukes Stool ova and parasite (O & P) examination diagnoses infection with liver flukes • Clonorchiasis and opisthorchiasis occur in Southeast Asia Infection is acquired by ingestion of contaminated raw freshwater fish Chronic infection causes cholangitis, cholangiohepatitis, and biliary obstruction and is associated CHAPTER 116 Helminthic Infections 587 with cholangiocarcinoma Therapy for acute infection consists of praziquantel administration (25 mg/kg tid for day) • Fascioliasis is endemic in sheep-raising countries Infection is acquired by ingestion of contaminated aquatic plants (e.g., watercress) Acute disease causes fever, RUQ pain, hepatomegaly, and eosinophilia Chronic infection is associated with bile duct obstruction and biliary cirrhosis For treatment, triclabendazole is given as a single dose of 10 mg/kg Lung Flukes Infection with Paragonimus spp is acquired by ingestion of contaminated crayfish and freshwater crabs Acute infection causes lung hemorrhage, necrosis with cyst formation, and parenchymal eosinophilic infiltrates A productive cough, with brownish or bloody sputum, in association with peripheral blood eosinophilia is the usual presentation in pts with heavy infection In chronic cases, bronchitis or bronchiectasis may predominate CNS disease can also occur and can result in seizures The diagnosis is made by O & P examination of sputum or stool Praziquantel (25 mg/kg tid for day) is the therapeutic agent of choice CESTODES The cestodes, or tapeworms, can be classified into two groups, according to whether humans are the definitive or the intermediate hosts The tapeworm attaches to intestinal mucosa via sucking cups or hooks located on the scolex Proglottids (segments) form behind the scolex and constitute the bulk of the tapeworm Eggs of the various Taenia species are identical; thus diagnosis to the species level relies on differences in the morphology of the scolex or proglottids Taeniasis Saginata Etiology and Pathogenesis Humans are the definitive host for Taenia saginata, the beef tapeworm, which inhabits the upper jejunum Eggs are excreted in feces and ingested by cattle or other herbivores; larvae encyst (cysticerci) in the striated muscles of these animals When humans ingest raw or undercooked beef, the cysticerci mature into adult worms Clinical Features Pts may experience perianal discomfort, mild abdominal pain, nausea, change in appetite, weakness, and weight loss Diagnosis The diagnosis is made by detection of eggs or proglottids in the stool Eggs may be found in the perianal area Eosinophilia may develop, and IgE levels may be elevated TREATMENT Praziquantel is given in a single dose of 10 mg/kg Taeniasis Solium and Cysticercosis Etiology and Pathogenesis Humans are the definitive host and pigs the intermediate host for T solium, the pork tapeworm The disease, which is due to ingestion of pork infected with cysticerci, is similar to taeniasis saginata If humans ingest T solium eggs (e.g., as a result of close contact with a tapeworm carrier or via autoinfection), they develop cysticercosis Larvae penetrate the intestinal wall and are carried to many tissues, where cystercerci develop Clinical Features • Intestinal infections: Epigastric discomfort, nausea, a sensation of hunger, weight loss, and diarrhea can occur, but most infections are asymptomatic 588 SECTION Infectious Diseases • Cysticercosis: Cysticerci can be found anywhere in the body but most often are detected in the brain, skeletal muscle, SC tissue, or eye Neurologic manifestations are most common and include seizures due to inflammation surrounding cysticerci in the brain, hydrocephalus (from obstruction of CSF flow by cysticerci and accompanying inflammation or by arachnoiditis), headache, nausea, vomiting, changes in vision, dizziness, ataxia, and confusion Diagnosis Intestinal infection is diagnosed by detection of eggs or proglottids in stool The diagnosis of cysticercosis is confirmed in pts with either one absolute criterion or a combination of two major criteria, one minor criterion, and one epidemiologic criterion (Table 116-1) Findings on neuroimaging include cystic lesions with or without enhancement, one or more nodular calcifications, or focal enhancing lesions TREATMENT Intestinal infections respond to a single dose of praziquantel (10 mg/kg) Neurocysticercosis can be treated with albendazole (15 mg/kg per day for 8– 28 days) or praziquantel (50– 60 mg/kg daily in divided doses for 15 days or 100 mg/kg in doses given over day) Pts should be carefully monitored, given the potential for an inflammatory response to treatment High-dose glucocorticoids can be administered during treatment, particularly if symptoms become worse during therapy; since glucocorticoids induce praziquantel metabolism, cimetidine should be given with praziquantel to inhibit this effect Supportive measures include antiepileptic administration and treatment of hydrocephalus as indicated Table 116-1 Proposed Diagnostic Criteria for Human Cysticercosis, 2001 Absolute criteria a Demonstration of cysticerci by histologic or microscopic examination of biopsy material b Visualization of the parasite in the eye by funduscopy c Neuroradiologic demonstration of cystic lesions containing a characteristic scolex Major criteria a Neuroradiologic lesions suggestive of neurocysticercosis b Demonstration of antibodies to cysticerci in serum by enzyme-linked immunoelectrotransfer blot c Resolution of intracranial cystic lesions spontaneously or after therapy with albendazole or praziquantel alone Minor criteria a Lesions compatible with neurocysticercosis detected by neuroimaging studies b Clinical manifestations suggestive of neurocysticercosis c Demonstration of antibodies to cysticerci or cysticercal antigen in cerebrospinal fluid by ELISA d Evidence of cysticercosis outside the central nervous system (e.g., cigarshaped soft tissue calcifications) Epidemiologic criteria a Residence in a cysticercosis-endemic area b Frequent travel to a cysticercosis-endemic area c Household contact with an individual infected with Taenia solium Source: Modified from OH Del Brutto et al: Neurology 57:177, 2001 CHAPTER 116 Helminthic Infections 589 Echinococcosis Etiology and Pathogenesis Echinococcosis is an infection of humans that is caused by Echinococcus larvae The adult worm of E granulosus lives in the jejunum of dogs and releases eggs that humans may ingest Disease is prevalent in areas where livestock is raised in association with dogs After ingestion, embryos escape from the eggs, penetrate the intestinal mucosa, enter the portal circulation, and are carried to many organs but particularly the liver and lungs Larvae develop into fluid-filled unilocular hydatid cysts within which daughter cysts develop, as germinating cystic structures Cysts expand over years E multilocularis, found in arctic or subarctic regions, is similar, but rodents are the intermediate hosts The parasite is multilocular, and vesicles progressively invade host tissue by peripheral extension of processes from the germinal layer Clinical Features Expanding cysts exert the effects of space-occupying lesions, causing symptoms in the affected organ Pts with hepatic disease most commonly present with abdominal pain or a palpable mass in the RUQ Compression of a bile duct may cause biliary obstruction or may mimic cholelithiasis Rupture or leakage from a hydatid cyst may cause fever, pruritus, urticaria, eosinophilia, or anaphylaxis Pulmonary cysts may rupture into the bronchial tree or the peritoneal cavity and cause cough, chest pain, or hemoptysis Rupture of cysts may result in multifocal dissemination E multilocularis disease may present as a hepatic tumor, with destruction of the liver and extension into vital structures Diagnosis Radiographic imaging is important in evaluating echinococcal cysts Daughter cysts within a larger cyst are pathognomonic Eggshell or mural calcification on CT is indicative of E granulosus infections Serology may be useful but can be negative in up to half of pts with lung cysts Serology is usually positive in pts with hepatic disease Aspiration of cysts usually is not attempted because leakage of cyst fluid can cause dissemination or anaphylactic reactions TREATMENT Ultrasound staging is recommended for E granulosus infection Therapy is based on considerations of the size, location, and manifestations of cysts and the overall health of the pt For some uncomplicated lesions, percutaneous aspiration, infusion of scolicidal agents, and reaspiration are recommended Albendazole (15 mg/kg daily in divided doses for days before the procedure and for at least weeks afterward) is given for prophylaxis of secondary peritoneal echinococcosis due to inadvertent spillage of fluid during this treatment Surgery is the treatment of choice for complicated E granulosus cysts Albendazole should also be given prophylactically, as just described Praziquantel (50 mg/kg daily for weeks) may hasten the death of protoscolices Medical therapy alone with albendazole for 12 weeks to months results in cure in ϳ30% of cases and in clinical improvement in another 50% E multilocularis infection is treated surgically, and albendazole is given for at least years after presumptively curative surgery If surgery is not curative, albendazole should be continued indefinitely Diphyllobothriasis Diphyllobothrium latum, the longest tapeworm (up to 25 cm), attaches to the ileal and occasionally the jejunal mucosa Humans are infected by eating raw fish Symptoms are rare and usually mild, but infection can cause vitamin B12 deficiency because the tapeworm absorbs large amounts of vitamin B12 and 590 SECTION Infectious Diseases interferes with ileal B12 absorption Up to 2% of infected pts, especially the elderly, have megaloblastic anemia resembling pernicious anemia and can suffer neurologic sequelae due to B12 deficiency The diagnosis is made by detection of eggs in the stool Praziquantel (5– 10 mg/kg once) is highly effective ECTOPARASITES Ectoparasites are helminths that infest the skin of other animals, from which they derive sustenance These organisms can incidentally inflict direct injury, elicit hypersensitivity, or inoculate toxins or pathogens Scabies Etiology Scabies is caused by the human itch mite Sarcoptes scabiei Life Cycle and Epidemiology Gravid female mites burrow beneath the stratum corneum, deposit eggs that mature in weeks, and emerge as adults to reinvade the same or another host Scabies transmission is facilitated by intimate contact with an infested person and by crowding, uncleanliness, or contact with multiple sexual partners The itching and rash are due to a sensitization reaction against excreta of the mite Scratching destroys the mite, and most infestations are limited to Ͻ15 mites per person Norwegian or crusted scabies— hyperinfestation with thousands of mites— is associated with glucocorticoid use and immunodeficiency diseases, including HIV disease Clinical Features Itching is worst at night and after a hot shower Burrows appear as dark wavy lines that end in a pearly bleb containing the female mite Most lesions are between the fingers or on the volar wrists, elbows, and penis Bacterial superinfection can occur Diagnosis Scrapings from unroofed burrows reveal the mite, its eggs, or fecal pellets TREATMENT Permethrin cream (5%) should be applied thinly behind the ears and from the neck down after bathing and removed h later with soap and water Alternatives include topical crotamiton cream, benzyl benzoate, and sulfur ointments A dose of ivermectin (200 ␮g/kg) is also effective but is not yet approved by the FDA for scabies treatment For crusted scabies, first a keratolytic agent (e.g., 6% salicylic acid) and then scabicides are applied to the scalp, face, and ears in addition to the rest of the body Several doses of ivermectin may be required in pts with crusted scabies Itching and hypersensitivity may persist for weeks or months in scabies and should be managed with symptom-based treatment Bedding and clothing should be washed in hot water and dried in a heated dryer, and close contacts should be treated to prevent reinfestations Pediculosis Etiology and Epidemiology Nymphs and adults of human lice— Pediculus capitis (the head louse), P humanus (the body louse), and Pthirus pubis (the pubic louse)— feed at least once a day and ingest human blood exclusively The saliva of these lice produces an irritating rash in sensitized persons Eggs are cemented firmly to hair or clothing, and empty eggs (nits) remain affixed for months after hatching Lice are generally transmitted from person to person Head lice are transmitted among schoolchildren, body lice are transmitted between persons who not change their clothes often, and pubic lice are usually CHAPTER 116 Helminthic Infections 591 transmitted sexually The tendency of the body louse to leave febrile persons or corpses may facilitate the transmission of diseases such as louse-borne typhus, relapsing fever, and trench fever Diagnosis The diagnosis can be suspected if nits are detected, but confirmatory measures should include the demonstration of a live louse TREATMENT If live lice are found, treatment with 1% permethrin (two 10-min applications 10 days apart) is usually adequate If this course fails, treatment for 8– 12 h with 0.5% malathion may be indicated Ivermectin may be useful in cases resistant to permethrin and malathion Eyelid infestations should be treated with petrolatum applied for 3– days or with 1% yellow oxide of mercury ointment applied times daily for weeks The hair should be combed with a fine-toothed comb to remove nits Pediculicides must be applied from head to foot to remove body lice Clothes and bedding should be deloused by placement in a hot dryer for 30 minutes or by fumigation Myiasis In this infestation, maggots invade living or necrotic tissue or body cavities and produce clinical syndromes that vary with the species of fly In wound and bodycavity myiasis, flies are attracted to blood and pus, and newly hatched larvae enter wounds or diseased skin Treatment consists of maggot removal and tissue debridement Leech Infestations Medicinal leeches can reduce venous congestion in surgical flaps or replanted body parts Aeromonas hydrophila colonizes the gullets of commercially available leeches Prophylactic antibiotics are indicated for the prevention of human infection For a more detailed discussion, see Davis CE: Laboratory Diagnosis of Parasitic Infections, Chap 192, p 1197; Moore TA: Agents Used to Treat Infections Due to Parasites and Pneumocystis, Chap 193, p 1202; Weller PF: Trichinella and Other Tissue Nematodes, Chap 200, p 1253; Weller PF, Nutman TB: Intestinal Nematodes, Chap 201, p 1256; Nutman TB, Weller PF: Filarial and Related Infections, Chap 202, p 1260; Mahmoud AAF: Schistosomiasis and Other Trematode Infections, Chap 203, p 1266; White AC Jr, Weller PF: Cestodes, Chap 204, p 1272; and Maguire JH et al: Ectoparasite Infestations and Arthropod Bites and Stings, Chap 379, p 2600, in HPIM-16 This page intentionally left blank ... 16 5 51. 9 52.4 52.9 53.5 54.0 54.5 55.0 55.6 56 .1 56.6 57.2 57.9 58.6 59.3 59.9 60.5 61. 1 61. 7 62.3 62.9 63.5 16 6 16 7 16 8 16 9 17 0 17 1 17 2 17 3 17 4 17 5 17 6 17 7 17 8 17 9 18 0 18 1 18 2 18 3 18 4 18 5 18 6... 66.6 67.3 68.0 68.7 69.4 70 .1 70.8 71. 6 72.4 73.3 74.2 75.0 75.8 76.5 77.3 78 .1 78.9 14 0 14 1 14 2 14 3 14 4 14 5 14 6 14 7 14 8 14 9 15 0 15 1 15 2 15 3 15 4 15 5 15 6 15 7 15 8 15 9 16 0 44.9 45.4 45.9 46.4 47.0... Ͻ 18 .5 Table 2 -1 Ideal Weight for Height Men a a Women Height Weight Height Weight Height Weight Height Weight 14 5 14 6 14 7 14 8 14 9 15 0 15 1 15 2 15 3 15 4 15 5 15 6 15 7 15 8 15 9 16 0 16 1 16 2 16 3 16 4 16 5