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i

Infectious Disease
Emergencies
ii
iii

Infectious Disease
Emergencies
Edited by

Arjun S. Chanmugam, MD, MBA

Professor of Emergency Medicine
Johns Hopkins University School of Medicine
Baltimore, Maryland

Andrew H. Bissonette, MD
Fellow, Emergency Medicine and Internal Medicine
Henry Ford Hospital
Detroit, Michigan

Sanjay V. Desai, MD
Associate Professor of Medicine
Johns Hopkins University School of Medicine
Baltimore, Maryland

Shannon B. Putman, MD
Assistant Professor of Emergency Medicine
Johns Hopkins University School of Medicine
Baltimore, Maryland

1
iv

1
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above should be sent to the Rights Department, Oxford University Press, at the
address above.
You must not circulate this work in any other form
and you must impose this same condition on any acquirer.
Library of Congress Cataloging-​in-​Publication Data
Names: Chanmugam, Arjun S., editor. | Rothman, Richard, MD, editor. | Desai, Sanjay V., editor. |
Putman, Shannon B., editor.
Title: Infectious disease emergencies / edited by Arjun S. Chanmugam, Richard Rothman,
Sanjay V. Desai, Shannon B. Putman.
Other titles: Infectious disease emergencies (Chanmugam)
Description: Oxford ; New York : Oxford University Press, [2016] |
Includes bibliographical references and index.
Identifiers: LCCN 2016002340 | ISBN 9780199976805 (alk. paper) | ISBN 9780199976829 (e-ISBN)
Subjects: | MESH: Communicable Diseases | Emergencies
Classification: LCC RC112 | NLM WC 100 | DDC 616.9/0425—dc23
LC record available at http://lccn.loc.gov/2016002340
This material is not intended to be, and should not be considered, a substitute for medical or other professional
advice. Treatment for the conditions described in this material is highly dependent on the individual
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this material.
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Printed by WebCom, Inc., Canada
╇ v

Contents

Series Preface â•… xi

Preface â•… xiii
Acknowledgments â•… xv
Contributors â•… xvii

Section I╇ Principals of Infectious Disease Management

1 Laboratory Testing for Microbial Detection
Michael Arce 3
2 Infection Control
Michael Vulfovich 9
3 Infectious Disease Mimics
Tyler Martinez 17
v
Section II╇ General Management of Severe Infection in Acute
and Emergency Environments
4 Sepsis
Kamna S. Balhara, Basem F. Khishfe, and Jamil D. Bayram 25

Section III Central Nervous System Infections

5 Bacterial Meningitis
Mary P. Chang 33
6 Aseptic Meningitis
Michelle Sharp 37
7 Encephalitis
Tyler Martinez 41
8 Brain Abscess
Sneha A. Chinai 45
9 Epidural Abscess
David Mabey 51

Section IV Ear, Nose, and Throat Infections

10 Pharyngitis, Tonsillitis, and Peritonsillar Abscess
Gabrielle Jacquet 57
11 Otitis Externa, Otitis Media, and Mastoiditis
Susan Peterson and Staci Reintjes 61
12 Rhinosinusitis
Staci Reintjes and Susie Peterson 65
vi

13 Odontogenic Infections
Gabrielle Jacquet and Lawrence Page 69
14 Deep Space Infections of the Head and Neck
Gabrielle Jacquet 73

Section V Ocular Infections

15 Periocular Infections
M. DeAugustinas, A Kiely 79
16 Infectious Keratitis
M. DeAugustinas, A Kiely 85
17 Endophthalmitis
M. DeAugustinas, A Kiely 91

Section VI Cardiovascular Infections

18 Infective Endocarditis
Ajar Kocher 97
19 Myocarditis and Pericarditis
Kevin Alexander 103
20 Catheter-╉Associated Infections
Swathi Eluri 107
21 Septic Thrombophlebitis
Sudip Saha 113

Section VII Pulmonary Infections

22 Community-╉Acquired Pneumonia
Ryan Circh 119
23 Hospital Acquired Pneumonia
Joshua Lupton 125
24 Pleural Effusions (Parapneumonic Process and Empyema)
Timothy Niessen 131
25 Lung Abscess
Kevin Gibbs 137
26 Influenza
Gabrielle Jacquet and Andrea Dugas 141
27 Atypical Pulmonary Infections
Rod Rahimi 147
28 Pulmonary Tuberculosis
Bhakti Hansoti 151
29 Acute Uncomplicated Bronchitis
Sarina Sahetya 155
╇ vii

Section VIII Gastrointestinal Infections

30 Viral Gastroenteritis
Ximena Tobar and Shannon B. Putman 161
31 Infectious Colitis
David Scordino 165
32 Peritonitis
Elizabeth Rosenblatt 171
33 Diverticulitis
Bharati Kocher 177
34 Cholecystitis and Cholangitis
Sarah Carle 181
35 Hepatitis
Deanna Wilson 187
36 Appendicitis
David Scordino 193

Section IX Genitourinary Infections

37 Urinary Tract Infections in Women
Arjun S. Chanmugam and Gino Scalabrini 201
38 Cervicitis and Vulvovaginitis
Shannon B. Putman 205
39 Urethritis, Prostatitis, and Epididymitis
Shannon B. Putman and Arjun S. Chanmugam 209
40 Pelvic Inflammatory Disease and Tubo-╉ovarian Abscess
John Holst 213

Section X Skin and Soft Tissue Infections

41 Soft Tissue Infections
Michael Ehmann 223
42 Necrotizing Soft Tissue Infections
Michael Ehmann 227
43 Diabetic Foot Infections
Clare Kelleher 233
44 Dermatologic Manifestations of Infectious Disease
Lisa Cuttle 239
45 Mammalian and Reptile Bites
David Scordino, and Susan Peterson 245

Section XI Bone and Joint Infections

46 Septic Arthritis
Hasan E. Baydoun, Bachar Hamade, Jamil D. Bayram 253
viii

47 Infections of the Hand

Lisa A. Steiner 259
48 Prosthetic Joint Infections
David Mabey, Hasan E. Baydoun, Jamil D. Bayram 269
49 Osteomyelitis
Lisa A. Steiner 275

Section XII Vector-Borne Infections

50 Lyme Disease
Zach Smith 281
51 Ehrlichia, Anaplasma, and Rickettsia
Susan Tuddenham 285
52 Malaria and Dengue Fever
Dana Mueller 291
53 West Nile Virus
Matthew Finn 297

Section XIII Infection in Special Populations

54 Infection in the Cancer Patient
Sri Raghavan 305
55 Infections in the HIV Patient
Michelle Henggeller 311
56 Infections in the Transplant Patient
Alexander Billioux 323
57 Infection in Travelers and Emigrants
Mark Tenforde 333
58 Infection in the Intravenous Drug User
Caren Euster 341
59 Infection in the Pregnant Patient
Vanessa Vasquez 347
60 Infection in the Patient with Sickle Cell Anemia
Raymond Young 353
61 Fever of Unknown Origin
Annie Antar 359

Section XIV Bioterrorism

62 Anthrax
Rebecca Smith 365
63 Smallpox
Rebecca Smith 371
64 Botulism
Monica Mix 375
╇ ix

65 Plague
Trisha Anest, and David Scordino 381
66 Viral Hemorrhagic Fevers (Ebola, Lassa, Hantavirus)
Marcos Schechter 387
67 Tularemia
Alida Gertz 393

Section XV Antibiotic Resistance

68 Antibiotic Resistance
Eili Y. Klein 403

Index â•… 409

x
xi

Series Preface

Emergency physicians care for patients with any condition that may be encountered in an emergency
department. This requires that they know about a vast number of emergencies, some common and
many rare. Physicians who have trained in any of the subspecialties—​cardiology, neurology, obstetrics
and gynecology, and many others—​have narrowed their fields of study, allowing their patients to benefit
accordingly. The Oxford University Press Emergencies series has combined the very best of these two
knowledge bases, and the result is the unique product you are now holding. Each handbook is authored
by an emergency physician and a subspecialist, allowing the reader instant access to years of expertise in
a rapid access, patient-​centered format. Together with evidence-​based recommendations, you will have
access to their tricks of the trade as well as the combined expertise and approaches of a subspecialist
and an emergency physician.
Patients in the emergency department often have quite different needs and require different testing
from those with a similar emergency who are in-​patients. These stem from different priorities; in the
emergency department, the focus is on quickly diagnosing an undifferentiated condition. An emergency
occurring to an in-​patient may also need to be newly diagnosed, but usually the information available
is more complete and the emphasis can be on a more focused and in-​depth evaluation. The authors of
each Handbook have produced a guide for you wherever the patient is encountered, whether in an out-​
patient clinic, urgent care, emergency department, or on the wards.
A special thanks should be extended to Andrea Knobloch, Senior Editor for Medicine at Oxford
xi
University Press, for her vision in bringing this series to press. Andrea is aware of how new electronic
media have impacted the learning process for physician-​assistants, medical students, residents, and fel-
lows, yet, at the same time, she is a firm believer in the value of the printed word. This series contains the
proof that such a combination is still possible in the rapidly changing world of information technology.
Over the last 20 years, the Oxford Handbooks have become an indispensable tool for those in all
stages of training throughout the world. This new series will, I am sure, quickly grow to become the
standard reference for those who need to help their patients when faced with an emergency.

Jeremy Brown, MD
Series Editor
Associate Professor of Emergency Medicine
The George Washington University Medical Center
xii
xiii

Preface

The history of medicine can be linked to the battle against infectious disease. A striking historical example
is found within the Edwin Smith papyrus, which describes the management of 48 medical cases dating to
about 1600 bce. Impressively, this ancient document may date back much further, as the writings are often
attributed to Imhotep, the great architect and chief physician from the Old Kingdom, 3000–​2500 bce.
Within the papyrus are instructions on a number of medical and surgical interventions, but the inclusion
of treating and preventing infection figures prominently. The struggle against infection is indeed almost
as old as the history of human kind.
The challenges of preventing, diagnosing, and treating infection continue to be a significant part of
medical practice today. In the acute care setting, especially emergency departments, urgent care cen-
ters, and hospitals, diagnosing and treating infectious diseases is a prime concern. Providing the correct
antibiotic or medical intervention after recognizing that an infection is present can be a complicated and
often time-​consuming process. One of the key steps to correctly managing an infection is to have an
understanding of the causes, the associated recommended therapies, and the typical disease course.
This can be even more challenging in the acute setting where time limitations and comorbidities com-
plicate matters.
Although there are a number of excellent references available to medical practitioners, a concise text
that rapidly summarizes the key points of various infectious diseases, especially as it relates to acute
care management, is still in demand. The battle against infectious disease will likely be ongoing, as new
xiii
antibiotics and chemotherapeutics are introduced, as organisms develop resistance, and other defense
mechanisms evolve along with new microbial threats. A succinct reference that provides a rapid under-
standing of the basic interventions and basic process to manage infections can only help to formulate
appropriate initial strategies. In the emergency department, in urgent care centers, in hospitals, and in
clinicians’ offices, having such a reference could make a difference in making the correct diagnosis and
starting the proper treatment in a timely fashion.
The practice of medicine will likely always include a need to consider infectious processes as they con-
tribute to the morbidity and mortality of our patients. To that end, we designed this reference to be
used by clinicians everywhere and to be one more effective reference tool in the battle against infectious
disease.
xiv
xv

Acknowledgments

With thanks to Dr. Richard Rothman for his guidance and contributions to this book.

xv
xvi
xvii

Contributors

Kevin Alexander, MD Sneha A. Chinai, MD, FACEP

Fellow, Cardiovascular Diseases Assistant Professor of Emergency Medicine
Brigham and Women’s Hospital Associate Director, Emergency Medicine
Boston, Massachusetts Residency Program
Department of Emergency Medicine
Trisha Anest, MD, MPH
University of Massachusetts Medical School
Emergency Physician Worcester, Massachusetts
Baltimore, Maryland
Ryan Circh, MD
Annie Antar, MD, PhD
Emergency Physician University of Maryland
Clinical Fellow, Division of Infectious Diseases Baltimore Washington Medical Center
Johns Hopkins University School of Medicine Baltimore, Maryland
Baltimore, Maryland
Lisa Cuttle, MD
Michael Arce
Emergency Physician
Department of Emergency Medicine Knoxville, Tennessee
UMass Memorial Medical Center
Worcester, Massachusetts M. DeAugustinas, MD
Emergency Physician xvii
Kamna Balhara, MD
California
Assistant Professor of Emergency Medicine
UT Health Science Center Sanjay V. Desai, MD
San Antonio, Texas Associate Professor of Medicine
Johns Hopkins University, School of Medicine
Hasan E. Baydoun
Baltimore, Maryland
Department of Orthopaedics
Massachusetts General Hospital Andrea Dugas, MD, PhD
Boston, Massachusetts Assistant Professor of Emergency Medicine
Johns Hopkins University, School of Maryland
Jamil D. Bayram
Baltimore, Maryland
Associate Professor of Emergency Medicine
The Johns Hopkins University School of Medicine Michael Ehmann, MD, MPH, MS
Baltimore, Maryland Instructor
Department of Emergency Medicine
Alexander Billioux
The Johns Hopkins University
Department of Medicine School of Medicine
Johns Hopkins University Baltimore, Maryland
Baltimore, Maryland
Swathi Eluri
Andrew H. Bissonette, MD
Fellow, Gastroenterology
Fellow, Emergency Medicine and Internal Medicine University of North Carolina
Henry Ford Hospital Chapel Hill, North Carolina
Detroit, Michigan
Caren Euster, MD
Sarah Carle, MD
Assistant Professor of Emergency Medicine
Emergency Physician The Johns Hopkins University
Baltimore, Maryland School of Medicine
Mary P. Chang, MD, MPH Baltimore, Maryland
Assistant Professor of Emergency Medicine Matthew Finn
University of Texas Southwestern Medical Fellow, Cardiovascular Diseases
Center Columbia University
Dallas, Texas New York, New York
Arjun S. Chanmugam, MD, MBA Alida Gertz, MD, MPH
Professor of Emergency Medicine The Everett Clinic
Johns Hopkins University, School of Medicine Seattle, Washington
Baltimore, Maryland
xviii

Kevin Gibbs, MD Bharati Kocher, MD

CONTRIBUTORS

Assistant Professor of Pulmonary, Critical Care, Fellow, Gastroenterology

Allergy, and Immunologic Medicine University of North Carolina at Chapel Hill
Wake Forest University Chapel Hill, North Carolina
Winston-Salem, North Carolina
Joshua Lupton, MD
Bachar Hamade, MD, MSc Resident
Chief Resident, Department of Emergency Medicine Department of Emergency Medicine
Johns Hopkins University, School of Medicine The Johns Hopkins University School of Medicine
Baltimore, Maryland Baltimore, Maryland
Bhakti Hansoti, MBChB, MPH David Mabey, MD
Assistant Professor of Emergency Medicine Department of Emergency Medicine
Johns Hopkins University, School of Medicine Ultrasound Education Intermountain Medical
Baltimore, Maryland Center
Murray, Utah
Michelle Henggeller, MD
Department of Emergency Medicine Tyler Martinez, DO
The Johns Hopkins Howard County General Emergency Physician
Hospital Phoenix, Arizona
Columbia, Maryland
Monica Mix
John Holst, DO, RDMS, RDCS Johns Hopkins University
Emergency Medicine Ultrasound Director Baltimore, Maryland
Essentia Health Systems, St. Mary’s Hospital
Dana Mueller
xviii
Duluth, Minnesota
Mary’s Center
Gabrielle Jacquet, MD, MPH, FACP Washington D.C.
Assistant Professor,
Timothy Niessen, MD, MPH
Boston University School of Medicine
Director, Global Health, Dept. of Emergency Assistant Professor of Medicine
Medicine Johns Hopkins University
Assistant Director, Global Health, Boston Baltimore, Maryland
University School of Medicine Lawrence Page, DDS, PhD
Affiliate Faculty, Boston University Center for Periodontist
Global Health and Development Ellicott City, Maryland
Boston, Massachusetts
Susan Peterson, MD
Clare Kelleher
Assistant Professor of Emergency Medicine
Department of Medicine Johns Hopkins University School of Medicine
University of North Carolina Baltimore, Maryland
Chapel Hill, North Carolina
Shannon B. Putman, MD
Basem F. Khishfe, MD
Assistant Professor of Emergency Medicine
Department of Emergency Medicine Johns Hopkins University, School of Medicine
Cook County Stroger Hospital Baltimore, Maryland
Chicago, Ilinois
Sri Raghavan, MD, PhD
Amanda Elizabeth Kiely, M.D.
Clinical Fellow, Hematology/​Oncology
Assistant Professor Dana-​Farber Cancer Institute
Department of Ophthalmology Boston, Massachusetts
The Johns Hopkins University School of Medicine
Baltimore, Maryland Rod Rahimi, MD, PhD
Fellow, Division of Pulmonary and Critical Care
Eili Y. Klein, PhD
Medicine
Associate Professor Massachusetts General Hospital
Department of Emergency Medicine Harvard Medical School
The Johns Hopkins University School of Medicine Boston, Massachusetts
Baltimore, Maryland
Staci Reintjes, DO
Ajar Kocher
Emergency Physician
Fellow, Cardiovascular Diseases Saint Luke’s Health Care System in
Duke University Kansas City, Missouri
Durham, North Carolina
xix

Elizabeth Rosenblatt, MD Lisa Steiner MMS, PA-C

CONTRIBUTORS
Fellow, Gastroenterology Sr. Physician Assistant
University of Washington The Johns Hopkins University School of Medicine
Seattle, Washington Baltimore, Maryland
Richard Rothman, MD, PhD Mark Tenforde, MD, MPH
Professor of Emergency Medicine Division of Allergy and Infectious Diseases
The Johns Hopkins University School of Medicine University of Washington School of Medicine
Baltimore, Maryland Seattle, Washington
Sudip Saha, MD Ximena Tobar MMS, PA-C
Cardiology Fellow Sr. Physician Assistant
Beth Israel Deaconess Medical Center The Johns Hopkins University School of Medicine
Boston, Massachusetts Baltimore, Maryland
Sarina Sahetya, MD Susan Tuddenham, MD, MPH
Postdoctoral Fellow Fellow, Infectious Diseases
Pulmonary and Critical Care Medicine Johns Hopkins University, School of Medicine
Johns Hopkins Hospital Baltimore, Maryland
Baltimore, Maryland
Vanessa Vasquez, MD
Gino Scalabrini Emergency Physician
Johns Hopkins University School of Medicine West Palm, Florida
Baltimore, Maryland
Michael Vulfovich
Marcos Schechter, MD Director of Medical Education
Fellow, Infectious Diseases Department of Emergency Medicine xix
Emory University Metrowest Physicians
Atlanta, Georgia Framingham, Massachusetts
David Scordino, MD Deanna Wilson
Instructor of Emergency Medicine Adolescent Health Program
Johns Hopkins University, School of Medicine Johns Hopkins University
Baltimore, Maryland Baltimore, Maryland
Michelle Sharp Raymond Young, MD
Fellow, Pulmonary and Critical Care Fellow, Cardiovascular Medicine
Johns Hopkins University Georgetown University
Baltimore, Maryland Washington, DC
Zach Smith, MMS, PA-​C
University of Maryland Medical Center
R. Adams Cowley Shock Trauma Center
Critical Care Resuscitation Unit
Baltimore, Maryland
xx
1

Section I

Principals of Infectious
Disease Management
2
3

Chapter 1

Laboratory Testing for Microbial Detection

Michael Arce

Laboratory Modalities 4
Viral Testing 4
Bacterial Testing 5
Sexually Transmitted Infections 6
Parasitic Infection 7
Fungal 7

3
4

Principals of Infectious Disease Management

Laboratory Modalities
The approach to microbial detection in patients who present to the emergency department (ED) should
be focused and should aim for clinically significant findings while minimizing the chances of a clinically
deleterious false negative result. Judicious selection of laboratory tests, efficient sample collection, and
laboratory reporting are all important considerations. In this chapter, general guidelines are provided for
the initial evaluation of potential microbial infections in patients presenting to the ED. In some cases, the
diagnosis will remain uncertain during the patient’s stay, but diagnostic testing initiated in the ED may be
beneficial for the inpatient or outpatient team and for the future care of the patient.
The methodology of point of care testing (POCT) differs from that of core laboratory testing. POCT
is diagnostic testing performed at or near the site of clinical care delivery. It provides the advantage of
rapid test results with the potential for faster patient treatment. When used appropriately, it typically has
high sensitivity and, thus, is an effective screening tool in the ED. The disadvantage of POCT is its lower
specificity. Some POCT is useful in the identification of certain specific organisms that cause infectious
disease, including group A Streptococcus (rapid Strep test or RST), HIV (human immunodeficiency virus),
Influenzavirus A and B, and human respiratory syncytial virus (RSV). Other POCT can also help assess for
the likelihood of a non-​specific microbe being present, such as the urine dipstick.
Reverse transcriptase (RT) polymerase chain reaction (PCR; RT-​PCR) is one of the more well-​
developed molecular techniques to date and has a wide range of clinical applications: specific or broad-​
spectrum pathogen detection, evaluation of emerging novel infections, surveillance, early detection of
bioterrorism agents, and antimicrobial resistance profiling. In regard to emergency care, PCR-​based
methods are often cost-​effective with excellent sensitivity and specificity profiles, and they have a rapid
turnaround time relative to traditional testing procedures.
4 Direct fluorescent antibody (DFA) testing is designed to specifically target antigens unique to the
infecting organism but not present in the human host. This technique can be used to quickly determine
if a subject has a specific viral, bacterial, or parasitic infection. These immunoassays are cost-​effective,
highly specific (99% in some cases), and, generally, moderately sensitive (84% in some cases). Because
of this, DFA tests can be used for both screening and confirmation at a fraction of the turnaround time
and cost of other forms of definitive microbial testing.

Viral Testing
The vast majority of viral infections affecting immunocompetent populations rarely pose significant
morbidity or mortality risks. Therefore, with certain exceptions, there is little gained from viral test-
ing initiated during an ED visit. Some exceptions include suspected cases of meningitis or encephalitis,
respiratory infections of epidemiologic significance (ie, SARS), viral sexually transmitted diseases, and
infectious mononucleosis (IM) in patients at risk for complications.
Certain viral respiratory infections like Influenzavirus and SARS coronavirus are on the forefront of public
consciousness because these viruses have the potential to cause large-​scale epidemics. Given the rise in
concern about recent influenza pandemics, the CDC (Centers for Disease Control and Prevention) and
other infectious disease governing bodies have established testing recommendations for patients with
febrile respiratory illness.
Testing for Influenzavirus infections should be initiated with a screening test such as rapid antigen test-
ing (RAT). A positive RAT is most likely to represent a truly positive patient during peak influenza sea-
son. Likewise, when influenza season has passed, negative RAT most likely represents a true negative
patient, and confirmatory testing is not needed. However, due to the limited sensitivity of RAT, a nega-
tive Influenzavirus screen during peak flu season should be interpreted with caution, and a confirmatory
test should be sent. The test of choice for diagnosing Influenzavirus infection is DFA. DFA is highly sensi-
tive and specific when compared to a viral culture, and it is timely and cost-​effective. Turnaround time
typically is 24 to 48 hours.
The additional advantage of RT-​PCR is its ability to type and subtype strains of Influenzavirus (eg, H1N1
or H5N1). A viral culture may be useful for public health surveillance but has no utility for ED care.
RSV infections can be diagnosed with reasonable accuracy based on clinical features during winter
months. Laboratory confirmation should only be sent during treatment to confirm diagnosis but not nec-
essarily used to guide a decision to treat. Nasopharyngeal washings followed by rapid antigen assays are
generally diagnostic (sensitivity and specificity of 90%). PCR-​based assays are a reasonable alternative
to culture for confirming the rapid antigen detection assay results. Turnaround time is 24 to 48 hours.
The respiratory viral panel is a molecular assay that detects multiple viral pathogens. It is used to con-
firm negative screening tests (eg, rapid antigen assay). These panels typically detect Influenzavirus A and
5

B and RSV as well as adenovirus, rhinovirus, and parainfluenza virus species/​subtypes. Turnaround time

Laboratory Testing for Microbial Detection

is less than 24 hours. IM testing is recommended in adolescents and adults with exam findings consistent
with IM because monitoring for complications may be necessary. Complications are rare but include
splenic rupture, hemolytic anemia, thrombocytopenia, aplastic anemia, thrombotic thrombocytopenic
purpura, and disseminated intravascular coagulation. Heterophile antibody testing (ie, monospot) or
ELISA (enzyme-​linked immunosorbent assay) techniques are approximately 85% sensitive and approach
100% specificity. As a result, further confirmatory testing is generally not indicated.

Bacterial Testing
Bacterial sources of infection are far-​reaching, affect all ages, and are the cause of significant morbidity
and mortality around the globe. An important part of initiating care for these patients includes localizing
the source of infection in order to gain source control and identifying the pathogen in order to provide
appropriate treatment. Common sources for the spread of bacterial infection include cerebrospinal fluid
(CSF), blood, urine, oropharyngeal, pulmonary, intra-​abdominal, bone, and soft-​tissue infections. In this
chapter, testing for specific bacterial infections is organized by localization.

Chapter 1
Suspected central nervous system (CNS) bacterial infections require special attention. Depending on
a patient’s clinical presentation, a screening head computed tomography (CT) may be warranted prior
to obtaining CSF for analysis. Head CT is recommended for patients with alterations in mental status,
papilledema (or other signs of pupillary reactions), or focal neurologic changes in order to assess for the
likelihood of potential cerebral herniation if a lumbar puncture (LP) were performed. Analysis of CSF
by way of lumbar puncture is the test of choice when evaluating a patient for a CNS infection. Some
CSF findings are highly suggestive of bacterial meningitis, but there are a variety of deviations from the
standard findings. It is important to note that CSF pleocytosis can result from noninfectious situations, 5
including traumatic LP, seizure, or subarachnoid hemorrhage. A correction factor can be used to further
clarify whether the measured white blood cell (WBC) elevations in sample CSF are the result of a trau-
matic LP or are truly representative of the WBC in the patient’s CSF (Equation 1.1).

Serum WBC − CSFRBC

True CSF WBC = Measured CSF WBC − (1.1)
Serum RBC 
RBC = red blood cell

Gram stain can suggest a bacterial etiology (when positive) 24 hours earlier than culture results.
However, CSF culture remains a gold standard for diagnosing and guiding treatment of CNS infections.
Direct bacterial antigen detection is available for rapid detection of the more concerning causes of bac-
terial CSF infection (e.g. Streptococcus pneumoniae, Haemophilus influenzae type B, group B Streptococcus,
and Neisseria meningitidis). However, these tests have been shown to be of limited sensitivity, and they
are not cost-​effective. Moreover, they rarely change management because neonates, non-​immunized
individuals, and many patients suspected of having bacterial meningitis should receive antibiotic treat-
ment regimens empirically for these pathogens when they are suspected.
Bacterial causes of pharyngitis can lead to significant morbidity in the acute phase of the illness, and
long-​term complications can result from pharyngeal streptococcal infections. A peritonsillar or retro-
pharyngeal abscess can lead to upper airway obstruction or extension of the infection through fascial
planes, potentially leading to CNS infection, mediastinitis, and even cervical osteomyelitis in the right
circumstances.
The most widely recommended testing strategy for the detection of group A beta-​hemolytic
Streptococcus (GABHS) in pediatrics is an RST specific for Streptococcus antigen in order to screen for
infection in patients presenting with symptoms consistent with strep infection, including scarlatiniform
rash. Negative RSTs in pediatric patients should be followed by a throat culture given the risk of false
negatives, but positive RSTs are reliable and are grounds for initiating treatment. Cultures are not use-
ful 2–​3 weeks post infection. Given a lower prevalence of Streptococcus in adults, a negative RST yields
a sufficient negative predictive value to forgo throat culture. Cultures are not recommended for a test
of cure after treatment because they may remain positive due to a low-​level carriage state (ie, some
patients are chronically colonized by GABHS without clinical consequence). RST has a turnaround time
of 3 to 5 minutes.
In contrast, throat culture has a turnaround time of 24 to 48 hours, and an additional 24 hours is
required for isolation and identification from contaminated specimens. For the evaluation of patients
suspected of having poststreptococcal disease (ie, rheumatic fever or glomerulonephritis), streptozyme,
6

antistreptolysin O (ASO), and anti-​DNase B (antideoxyribonuclease B or ADB) titers are used to estab-
Principals of Infectious Disease Management

lish the presence of a preceding streptococcal infection.

Respiratory illness caused by bacteria is generally a clinical diagnosis that is supported by radiologic
imaging (eg, chest x-​ray, CT). However, certain pathogens, if not identified or if inadequately treated,
pose greater risks to patients. Some examples include pulmonary abscesses, pulmonary tuberculosis,
and Legionella infections. Obtaining diagnostic pulmonary secretions and subsequent culturing can be
useful in cases of pulmonary infections that fail appropriate antibiotic management and in cases that are
suspicious for Mycobacterium infections, especially pulmonary tuberculosis. Bacterial respiratory cultures
have a turnaround time of 48 or more hours.
The evaluation of a symptomatic urinary tract infection (UTI) begins with urine collection. In stable
patients who are able to cooperate with specimen collection, a midstream, clean catch urine sample
is as accurate as a catheterized urine sample. A urine dipstick is a POCT that is fast and inexpensive.
A negative urine dipstick in a patient with a low pretest probability can be used to rule out urine as a
source of infection. However, a urine dipstick is not sensitive enough to rule out infection in symptomatic
patients with higher pretest probabilities. Moreover, a urine dipstick can be subject to inaccuracies due
to improper testing and handling practices. A urine dipstick positive for nitrate is 95% specific but only
45% sensitive for a UTI. A urine dipstick positive for leukocyte esterase is anywhere between 50% and
96% sensitive and 91% and 99% specific.
Microscopic urinalysis (UA) can be useful for differentiating between infection and colonization of the
genitourinary (GU) tract. The presence of bacteria alone on microscopic UA is suggestive of coloniza-
tion, which may or may not represent infection. If WBCs are also present, then infection is more likely.
UA also helps to delineate a simple UTI from pyelonephritis. The presence of WBC casts is suggestive
of an ascending infection (ie, pyelonephritis), and treatment for a complicated UTI should be adminis-
tered. However, the accuracy of microscopy in diagnosing UTI is similar to that of a urine dipstick, so a
6 negative test in a symptomatic patient with intermediate to high pretest probability is not enough to rule
out infection. Urine culture can be used when microscopic UA or urine dipstick findings are negative in
patients with intermediate to high pretest probability for a GU infection. Urine culture is also useful for
close monitoring in patients who are not started on antibiotics or in patients with previous treatment
failures. Urine culture is indicated in patients at risk for a complicated UTI.
The detection of bloodstream infections and serious local infections in the setting of systemic inflam-
matory response syndrome (SIRS) or sepsis requires blood culture analysis of two to three indepen-
dently drawn blood samples. Multiple samples yield the greatest sensitivity for detection of a blood
stream infection (BSI) and minimizes the misinterpretation of contaminated samples. Most true positive
blood cultures become positive within 24 to 48 hours, and the pathogen responsible is typically isolated
from a majority of samples. Routine microbial testing for gastrointestinal infection is generally not useful
in the emergency setting.
Stool testing is time consuming, yields little value, and rarely influences management. Patients pre-
senting with abdominal pain or symptoms consistent with colitis in the setting of a diarrheal illness
should prompt consideration of microbial causes that have the potential for serious complications in the
appropriate clinical setting. Detection of Clostridium difficile infection is often done by immunodiagnostic
assays (C. difficile PCR). In adults, C. difficile PCR is reported as 88% sensitive and 96% specific. Cytotoxic
culture remains the gold standard but is slow and labor intensive. ELISA toxin assays are also available.
Sensitivities vary widely, ranging from 50% to 90%. C. difficile PCR has a turnaround time of 24 hours,
and cytotoxic assays have turnaround times of 24 to 72 hours. Stool culture takes 96 hours to produce
results.
Enterohemorrhagic E. coli (E. coli 0157:H7) requires a specialized stool culture that may be of use in
patients who present with signs and symptoms of hemolytic uremic syndrome. Turnaround time is 48 to
72 hours, but additional time is needed for confirmation of a positive test.

Sexually Transmitted Infections

Sexually transmitted infections (STIs) are commonly seen and treated in the emergency setting. A variety
of testing techniques have made ED testing more efficient. For example, N. gonorrhea and Chlamydia
testing can be done by nucleic acid amplification testing (NAAT) from either urogenital or urine samples.
Adding to the convenience of these methods is the availability of combination tests for the simultane-
ous detection of both pathogens. Culture continues to be the gold standard for diagnosis; in cases of
suspected sexual abuse or rape, culture is highly recommended. Turnaround time for amplified nucleic
acid testing is 24 to 72 hours. Turnaround times for cervical or urethral cultures are between 48 and
72 hours.
7

Herpes is generally a clinical diagnosis, but microbial testing can be warranted when isolation of

Laboratory Testing for Microbial Detection

herpes simplex virus (HSV) is required for patient management, such as in cases of disseminated
disease or CNS infection. DFA detection is helpful in detecting HSV in typical skin lesions, and it
provides rapid and specific identification of HSV infection. However, sample collection is somewhat
labor-​intensive.
HSV PCR is the most sensitive method for HSV detection and is particularly useful in the diagnosis of
CNS infections due to the rapid turnaround time when compared to HSV culture, which can take up to
two days.
In the past, HIV antibody screening was difficult to routinely perform during an ED visit because of
the lengthy turnaround time. Recently, six POCTs for the presumptive diagnosis of HIV infection were
approved for use in the United States. When compared to standard antibody screening, these POCTs
have proven to be accurate screening tests with high sensitivity and specificity. HIV POCT is becoming
more widely available in US EDs. A negative screening test is regarded as a true negative. Confirmation
is only indicated for a positive screening test. Western blot assay remains the confirmatory test of choice
for HIV infection in the setting of a positive POCT.
Treponema pallidum is commonly diagnosed by serologic testing as well as by IgG (immunoglobulin G)
and IgM (immunoglobulin M) antibody detection. There are two types of serologic testing. Traditionally,

Chapter 1
nontreponemal tests (ie, rapid plasma reagin [RPR] or the venereal disease research laboratory [VDRL])
are used as screening tests and can be used to follow the response to treatment. Treponemal tests (TP-​
PA [treponema pallidum particle agglutination], FTA-​ABS [fluorescent treponemal antibody-​absorbed],
and MHA-​TP [microhemagglutination assay for antibodies to treponema pallidum]) are used for con-
firmation of a reactive nontreponemal test. In other words, when a VDRL or RPR screen for syphilis is
positive (reactive), then confirmation testing with one of the direct treponemal tests is indicated.

7
Parasitic Infection
Parasite and vector-​related infections cause a great deal of morbidity and mortality worldwide but rarely
impact the United States on a large scale. However, there are a few notable infections. Malaria, babe-
siosis, Chagas disease, and leishmaniasis are parasitic infections that can be detected in peripheral blood
samples. Testing for these parasites requires thick and thin smears, which are inspected for the level of
parasitemia. The turnaround time for a positive smear is around 24 hours. If malaria is suspected, a STAT
(signal transducer and activator of transcription) preliminary result should be ordered. STAT testing can
result in less than 4 hours. Repeat samples should be sent during malaria treatment after 24, 48, and 72
hours to assess the effectiveness of therapy by trending the decline of parasitemia.
Borrelia burgdorferi is a tick-​borne disease that is classically diagnosed clinically without laboratory test-
ing. In some cases, testing can help if Lyme disease is suspected in at-​risk patients. If laboratory testing is
performed, an ELISA antibody screen is used for the detection of IgG or IgM antibodies. False negatives
are common in the first one to two weeks of infection because it can take time to create a measurable
concentration of antibodies against B. burgdorferi. If the ELISA is positive or inconclusive, a Western
blot should be done to confirm infection. This two-​tiered approach is recommended by the CDC to
minimize false positive findings.

Fungal
Cultures are the most sensitive routine laboratory method for the detection of fungal infections. Fungal
culture is indicated in patients who are immunocompromised, septic and receiving extensive treatment
with broad-​spectrum antibiotics, and, sometimes, victims of severe trauma. Fungal cultures are rarely
sent from the ED but should be considered in patients who have a lack of response to appropriate anti-
bacterial treatment. Cultures for yeast are incubated for seven days, whereas routine fungal cultures are
incubated for up to four weeks.

Suggested Readings and References

1. Wolfson AB. Harwood-​Nuss’ Clinical Practice of Emergency Medicine. 5th ed. Philadelphia, PA: Lippincott Williams
and Wilkins; 2010:869–​935.
2. Marx JA, Hockberger R, Walls R. Rosen’s Emergency Medicine Concepts and Clinical Practice. 7th ed. Philadelphia,
PA: Mosby; 2010:1676–​1848.
3. Roberts JR, Hedges JR. Clinical Procedures in Emergency Medicine. 5th ed. Philadelphia, PA: Saunders; 2010:1283–​1298.
8

4. Slaven EM, Stone SC, Lopez FA. Infectious Diseases: Emergency Department Diagnosis and Management.
Principals of Infectious Disease Management

New York: McGraw-​Hill; 2007.

5. US Centers for Disease Control and Prevention. Clinical Description and Lab Diagnosis of Influenza. http://​
www.cdc.gov/​flu/​professionals. Accessed October 15, 2012.
6. National Institute of Allergy and Infectious Disease, Lyme Disease http://​www.niaid.nih.gov/​topics/​lymedis-
ease/​research/​pages/​diagnostics.aspx Accessed April 18, 2015.

8
Another random document with
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the world. He has carried on that controversy since his Balliol days.
The exigencies that oblige him to pretend, against his better
knowledge and common civility, that I am petty and provincial and
patriotic and wilfully ignorant and pitifully out-of-date, oblige him to
pretend as much about most of those who stand for modern science
and a modern interpretation of history. He would pretend as hard
about Sir Ray Lankester, for example, or about Professor Gilbert
Murray or Sir Harry Johnston or Professor Barker, as he does about
me. It is a general system of pretence. It is a necessary part of—I will
not say of the Catholic attitude, but of his Catholic attitude towards
modern knowledge.
The necessity for a pose involving this pretence is not very
difficult to understand. Long before Mr. Belloc embarked upon the
present dispute he had become the slave of a tactical fiction, which
reiteration had made a reality for him. He evoked the fiction as early,
I believe, as his Oxford days. It may have been very effective at
Oxford—among the undergraduates. Then perhaps it was
consciously a defensive bluff, but certainly it is no longer that. He
has come at last to believe absolutely in this creature of his
imagination. He has come to believe this: that there is a vast
“modern European” culture of which the English-speaking world
knows nothing, of which the non-Catholic world knows nothing, and
with which he is familiar. It is on his side. It is always on his side. It is
simply and purely Belloccian. He certainly believes it is there. It
sustains his faith. It assuages the gnawing attacks of self-criticism
that must come to him in the night. Throughout these papers he is
constantly referring to this imaginary stuff—without ever coming to
precisions. Again and again and again and again—and again and
again and again, he alludes to this marvellous “European” science
and literature, beyond our ken.
He does not quote it; it does not exist for him to quote; but he
believes that it exists. He waves his hand impressively in the
direction in which it is supposed to be. It is his stand-by, his refuge,
his abiding fortress. But, in order to believe in it, it is necessary for
him to believe that no other English-speaking men can even read
French, and that their scepticism about it is based on some
“provincial” prejudice or some hatred of Catholics, or southern
people, or “Dagoes,” or “foreigners,” or what you will. That is why
Nature wilfully ignores the wonderful science of this “Europe”; and
why our Royal Society has no correspondence with it. But he has to
imagine it is there and make his readers imagine it is there, and that
there is this conspiracy of prejudice to ignore it, before he can even
begin to put up any appearance of a case against such a résumé of
current knowledge as the Outline of History.

Graceful Concessions to Mr. Belloc

All this rough and apparently irrelevant stuff about his own great
breadth and learning and my profound ignorance and provincialism,
to which he has devoted his two introductory papers, is therefore the
necessary prelude to putting over this delusion. That stream of
depreciation is not the wanton personal onslaught one might
suppose it to be at the first blush. If he has appeared to glorify
himself and belittle me, it is for greater controversial ends than a
mere personal score. We are dealing with a controversialist here and
a great apologist, and for all I know these may be quite legitimate
methods in this, to me, unfamiliar field.
Few people will be found to deny Mr. Belloc a considerable
amplitude of mind in his undertaking, so soon as they get thus far in
understanding him. Before he could even set about syndicating this
Companion to the Outline of History he had to incite a partisan
receptivity in the Catholic readers to whom he appeals, by declaring
that a violent hatred for their Church is the guiding motive of my life.
He had to ignore a considerable array of facts to do that, and he has
ignored them with great courage and steadfastness. He had to
arouse an indifferent Catholic public to a sense of urgent danger by
imposing this figure of a base, inveterate, and yet finally
contemptible enemy upon it. His is a greater task than mere dragon-
slaying. He had to create the dragon before he could become the
champion. And then, with his syndication arrangements complete,
while abusing me industriously for ignorance, backwardness, and
general intellectual backwoodism, he had to write the whole of these
articles without once really opening that Humbert safe of knowledge
which is his sole capital in this controversy. Time after time he refers
to it. Never once does he quote it. At most he may give us illusive
peeps....
Now and then as we proceed I shall note these illusive peeps.
I can admire great effort even when it is ill-directed, and to show
how little I bear him a grudge for the unpleasant things he has
induced himself to write about me, and for the still more unpleasant
things he tempts me—though I resist with a success that gratifies me
—to write about him, I contemplate a graceful compliment to Mr.
Belloc. In spite of the incurable ignorance of French and that “dirty
Dago” attitude towards foreigners Mr. Belloc has so agreeably put
upon me, it is my habit to spend a large part of the winter in a house
I lease among the olive terraces of Provence. There is a placard in
one corner of my study which could be rather amusingly covered
with the backs of dummy books. I propose to devote that to a
collection of Mr. Belloc’s authorities. There shall be one whole row at
least of the Bulletins of the Madame Humbert Society, and all the
later researches of the Belloc Academy of Anonymous Europeans,
bound in bluff leather. There will be Finis Darwinis by Hilario
Belloccio, and Hist. Eccles. by Hilarius Belloccius. I may have
occasion to refer to other leading authorities in the course of this
controversy. I shall add to it as we proceed.
And so, having examined, explained, disposed of, and in part
apologised for, Mr. Belloc’s personalities and the pervading
inelegance of his manners, I shall turn with some relief from this
unavoidably personal retort to questions of a more general interest. I
propose as my first study of these modern Catholic apologetics, so
valiantly produced by Mr. Belloc and so magnificently published and
displayed by the Catholic press, to follow our hero’s courageous but
unsteady progress through the mysteries of Natural Selection. And
after that we shall come to Original Sin and Human Origins in the
light of Mr. Belloc’s science and the phantom science of those
phantom naturalists and anthropologists he calls to his assistance.
 II
THE THEORY OF NATURAL SELECTION
STATED

MY first article upon Mr. Belloc’s Companion to the Outline of History

dealt, much against my inclination and as charitably and amiably as
possible, with the oddities of Mr. Belloc’s manner and method, and
those remarkable non-existent “European authorities” to whom he
appeals habitually in moments of argumentative stress. I do not
propose to go on thus girding at Mr. Belloc. He is a Catholic
apologist, endorsed by Catholic authorities, and there is matter of
very great importance for our consideration in what he has to say
about the history of life and mankind.
After his second paper is finished his abuse of me becomes
merely incidental or indirect. He goes on to a staggering rush at
Natural Selection. Let us see to where Catholic thought has got—if
Mr. Belloc is to be trusted—in relation to this very fundamental
matter.
It is Mr. Belloc’s brilliant careless way to begin most of his
arguments somewhere about the middle and put the end first. His
opening peroration, so to speak, is a proclamation that this “Natural
Selection”—whatever it is—is “an old and done-for theory of Darwin
and Wallace.” It is “a laughing-stock for half a generation among
competent men.” Mr. George Bernard Shaw does not believe in it!
G. B. S. among the Fathers! That wonderful non-existent “latest
European work” which plays so large a part in Mr. Belloc’s dialectic is
summoned briefly, its adverse testimony is noted, and it is dismissed
to the safe again. And then there is a brief statement of how these
two vile fellows, Darwin and Wallace, set out upon this reprehensible
theorising. What a ruthless exposé it is of the true motives of
scientific people!

“The process of thought was as follows:

“‘There is no Mind at work in the universe; therefore changes
of this sort must come from blind chance or at least
mechanically. At all costs we must get rid of the idea of design:
of a desired end conceived in a Creative Mind. Here is a theory
which will make the whole process entirely mechanical and
dead, and get rid of the necessity for a Creator.’”

And so having invented and then as it were visited and spat

upon the derided and neglected tomb of Natural Selection and
assured us that God, Mr. Shaw, “European opinion,” and all good
Catholics are upon his side, Mr. Belloc plucks up courage and really
begins to write about Natural Selection.

Natural Selection is Pure Common-Sense

What is this Natural Selection which has been dead for half a
century, but which Mr. Belloc still exerts himself industriously through
four long papers to kill all over again? It is the purest common-sense,
the most obvious deduction from obvious facts. I have set out the
idea as plainly as I could in the Outline of History Mr. Belloc is
attacking. It is put so plainly there that, before he can begin to argue
against it, he has to misstate it; he has to tell the story all over again
in his own words and get it suitably askew. It was quite open to him
to quote from my account, but he preferred to compile his own
misstatement. Indeed, in all this argument against Natural Selection
he never once quotes my actual words. He paraphrases throughout.
He has put some words between inverted commas in one place, so
as inadvertently to produce the impression that they are mine, but
they are not mine.
 Now the facts upon which the idea of Natural Selection rests are
matters of universal knowledge. “Every species of living thing is
continually dying and being born again as a multitude of fresh
individuals”; that is the primary fact. No species seems to be
perfectly adapted to its conditions, and even the happiest species
tends to multiply until it is in a state of need and pressure. So far
surely we are dealing with things beyond dispute. And next comes
the fact of individuality. Every living unit is individual with a difference
of its own. Every individual has its own distinctive differences, and
each of these differences may or may not be an advantage or a
disadvantage. Individuals with advantageous differences will
generally get on better in life, prosper and so be able to breed more
freely, than those with disadvantageous differences. Offspring have a
tendency to repeat the distinctive differences of their parents.
Therefore, taking a species as a whole by the million or billion or
million billion—for few species of animals or plants are represented
by fewer individuals than a million—there will be in each successive
generation a greater number of individuals with the differences that
are advantageous relative to the number with disadvantages. In
other words, the average of the species will have moved more or
less in the direction of the advantageous differences, whatever they
may be, and however numerous they may be. If, for example, the
species is chased and has to climb or run for it, there will be rather
more good climbers and sprinters in the new generation. There may
be other dangers and other needs; they will not affect the premium
set on quickness and the fate of the slow. And if the circumstances
of the species continue to press in the same direction, the movement
of the average will be in the same direction in this respect for so long
as they continue to press. Over a few score or even a few hundred
generations, and under conditions not very strenuous, a species may
not change very much. It may seem to be fixed in its general
characteristics, just as the continents seem to be fixed in their
general outline. But, as the range of time extends and the pressure
of necessity continues, the change becomes more striking.
 Natural Selection Has Nothing to Do with
the Origin of Variations
That is the process of Natural Selection, the “laughing-stock” of
Mr. Belloc’s mysterious conclave of “European” savants. Natural
Selection has nothing to do with the reason for the differences
between individuals. It has no more to do with those than gravitation
has to do with the differences in the heaviness of different
substances. But it is necessary to state as much here, because in
some queer muddled way Mr. Belloc seems to be persuaded that it
has. These differences may arise by pure chance; they may come
about through the operation of complex laws, they may come in
shoals and have their seasons. These things have nothing to do with
Natural Selection.
Now, Wallace and Darwin were two excellent Europeans who
happened to be interested in natural history. In spite of the sinister
motives invented for them by Mr. Belloc, I doubt if any Catholic
sufficiently educated to have read their lives will agree that they had
even a latent animus against Catholic truth or even a subconscious
desire to “get rid of a Creator” in their minds. They no more thought
of “getting rid of a Creator” when humbly and industriously they
gathered their facts and put fact to fact than an honest bricklayer
thinks of “getting rid of a Creator” when he lays his bricks with care
and builds a sound piece of wall. They went about the world studying
natural history. They considered life with a patience and
thoroughness and freedom from preconceptions beyond the
imagination of a man of Mr. Belloc’s habits. They found no such
“fixity of species” as he is inspired to proclaim. They found much
evidence of a progressive change in species, and they saw no
reason to explain it by a resort to miracles or magic. A Catholic priest
of the Anglican communion named Malthus had written a very
interesting and suggestive book upon over-population and the
consequent struggle for existence between individuals. It turned the
attention of both these diligent and gifted observers to just that
process of Natural Selection I have stated. Independently both of
them came to the conclusions that species changed age by age and
without any necessary limits, and mainly through the sieve of Natural
Selection, and that, given a sufficient separation to reduce or prevent
interbreeding and a sufficient difference in the selective conditions at
work, two parts of the same species might change in different
directions, so as at last to become distinct and separate species.
Darwin’s book upon the subject was called The Origin of
Species. It was a very modest and sufficient title. He did not even go
to the length of calling it the origin of genera or orders or classes. He
did not at first apply it to man.
This is the theory of the origin of species through Natural
Selection. It was not pretended by either of these pioneers that
Natural Selection was the sole way through which the differences of
species came about. For example, Darwin devoted a considerable
part of his working life to such collateral modes of differentiation as
the hypothesis that Sexual Selection also had its share. Criticism has
whittled down that share to practically negligible proportions, but I
note the hypothesis here because it absolutely disposes of the
assertion which Mr. Belloc hammers on the table, that the Theory of
Natural Selection excludes any other modes of specific
differentiation.

Testing the Theory

Very rapidly this conception of Natural Selection was extended
by naturalists until it came to be regarded as the general process of
life. They came to realise that all species, all genera, all classes of
life, whatever else may be happening to them, are and always have
been varying through the process of Natural Selection, some rapidly,
some slowly; some so slowly as hardly to change at all through vast
ages. I have stated the a priori case by which, given birth and death
and individuality and changing conditions and sufficient time, it
appears logically inevitable that the change and differentiation of
species must occur, and must be now going on. If we had no
material evidence at all it would still be possible to infer the evolution
of species.
That a priori case has never been answered, and it seems to me
unanswerable. But scientific men, with their obstinate preference for
observation and experiment over mere logical gymnastics, rarely rest
their convictions on a priori cases. A sustaining scepticism is a
matter of conscience with them. To them an a priori case is merely a
theory—that is to say, a generalisation under trial. For nearly three-
quarters of a century, therefore, biologists have been examining
whatever instances they could discover that seemed to contradict
this assumption that the process of specific change under Natural
Selection is the general condition of life. To this day this view is still
called the Theory of Natural Selection, though to a great number it
has come to have the substantial quality of an embracing fact.
It would have been amusing if Mr. Belloc had told us more of his
ideas of the scientific world. Apparently he knows scarcely anything
of museums or laboratories or the spirit and methods of research.
And manifestly he has not the faintest suspicion of the way in which
the whole world of vital phenomena has been ransacked and
scrutinised to test, correct, supplement, amplify, or alter this great
generalisation about life. He probably shares the delusion of most
other men in the street, that scientific theories are scientific finalities,
that they are supposed to be as ultimate as the dogmas of some
infallible religion. He imagines them put over chiefly by asseveration,
just as the assertions of a polemical journalist are put over. He has
still to learn that theories are trial material, testing targets, directives
for research. Shooting at established theories is the normal
occupation of the scientific investigator. Mr. Belloc’s figure of the
scientific investigator is probably a queer, frowsty, and often, alas!
atheistical individual, poking about almost aimlessly among facts in
the hope of hitting upon some “discovery” or “getting rid of a God.”
He does not understand the tense relevance of the vast amount of
work in progress. But for three-quarters of a century the thought and
work of myriads of people round and about the world have borne
directly or almost directly upon the probing, sounding, testing, of the
theory of Natural Selection. It stands clarified and, it would seem,
impregnable to-day.

Some Irrelevant Questions

Among questions bearing upon it but not directly attacking it has
been the discussion of the individual difference. For example, are
differences due to individual experiences ever inherited? Or are only
inherent differences transmissible? What rôle is played by what one
might call “normal,” relatively slight differences, and what by the
“sports” and abnormal births in specific change? Do species under
stress, and feeding on strange food or living in unaccustomed
climates, betray any exceptional tendency to produce abnormality?
Have there been, so to speak, storms and riots of variation in some
cases? Can differences establish themselves while outer necessity
remains neutral? Can variations amounting to specific differences in
colour and form arise as a sort of play of the germ plasm and be
tolerated rather than selected by nature? In what manner do normal
differences arise? What happens to differences in cases of
hybridisation? Here are sample questions that have been the seeds
of splendid work and great arguments. Some of them were already
under discussion in Darwin’s time; he was a pioneer in such
explorations; many ideas of his have stood the test of time, and
many suggestions he threw out have been disproved. When some
casual “may be” of Darwin’s is examined and set aside, it is the
custom of polemical journalists to rush about and proclaim to all who
may be sufficiently ill-informed to listen that Darwin is “exploded.”
Such explosions of Darwin are constantly recurring like gun-fire near
a garrison town, and still he remains. None of these subsidiary
questions affect the stability of this main generalisation of biology,
the Theory of Natural Selection.
The actual attack and testing of the Theory of Natural Selection
have yielded negative results. The statement of the theory may have
been made finer and exacter, that is all. And yet the conditions of its
survival have been very exacting. If the theory is to stand, the whole
of plant and animal life in time and space must be arranged in a
certain order. It must be possible to replace classification by a
genealogical tree. Every form must fall without difficulty into its
proper place in that tree. If it is true that birds are descended from
reptiles or men from apes, then there must be no birds before the
reptiles appear, and no men before apes. The geological record is
manifestly a mere fragmentary history, still for the most part unread,
but, however fragmentary it is, it must be consistent. One human
skull in the coal measures blows the whole theory to atoms. The
passage from form to form must be explicable by intermediate types
capable of maintaining themselves; there may be gaps in the record,
but there must be no miraculous leaps in the story. If an animal living
in the air is to be considered as a lineal descendant of some animal
living in the water, then the structure of the former bit by bit and step
by step must be shown to be adapted, modified, changed about from
that of the latter; it must have ears for water-hearing modified for air-
hearing, and its heart and breathing arrangements must be shown to
be similarly changed over, and so on for all its structure. All these
requirements will follow naturally from the necessities of a process of
Natural Selection. They follow logically upon no other hypothesis.
They are not demanded, for example, by the idea of a Creator
continually interfering with and rectifying some stately,
unaccountable process of “Evolution,” which seems to be Mr.
Belloc’s idea—so far as he ventures to display any idea of his own—
in the matter. Such things as vestigial structures and a number of
odd clumsinesses in living things—many still very imperfect
adaptations to an erect position, for example—become grotesque in
relation to such a view. A Creator who put needless or inconvenient
fish structures into the anatomy of a land animal and made the whole
fauna and flora of the land a patch-up of aquatic forms of life must be
not so much a Divinity as a Pedant. But it is the burthen of the whole
beautiful science of comparative anatomy that the structure of
animals and plants, and their succession in time, fall exactly into the
conditions defined by the Theory of Natural Selection. In the most
lovely and intricate detail, in a vast multitude of examples, in plants
and in animals alike, this theme of the adaptation of pre-existing
structure is worked out.
We should in accordance with the Theory of Natural Selection
expect to find traces of the ancestral form, not only in the lay-out of
the adult animal, but in every phase of its life history, and that, in
fact, is just what we do find. There is no more fascinating branch of
comparative anatomy than embryology. Each life cycle we discuss
tends to repeat the ancestral story, and only under the stress of
necessity does it undergo modification at any point. There is little
toleration in the life process for unnecessary divergencies.
Economies are effected by short cuts and reductions, and special
fœtal structures are granted reluctantly. So that even in man we find
peeping through the adaptations imposed upon the human type by
its viviparous necessities, and in spite of the advantage of every
economy of force, memories, for example, of the gill slits, of the fish
heart and kidney, of the reptilian skull, of the mammalian tail. I
mention this fact in the Outline, and upon it Mr. Belloc comments in a
manner that leaves one’s doubts poised between his honesty and
his intelligence. He declares, which is totally untrue, that I “repeat the
old Victorian tag”—I doubt if there ever was such a tag—that the
embryo “climbs up the family tree.” He puts these words in inverted
commas as though I have really adopted and used them, and for the
life of me it is only by straining my charity to the utmost that I can
accept that this was an accident. Of course every text-book of
embryology for the last forty years has made it perfectly plain, as I
have stated here, that the life cycle can be and is modified at any
point, and that an embryo has much more serious work in hand than
reciting its family history. It betrays its ancestral origins to analysis;
but that is an altogether different matter. Mr. Belloc, however, is so
densely ignorant himself upon these questions that he can imagine,
or think it worth while to pretend to imagine and attempt to persuade
his readers by the expedient of these inverted commas, that I
entertain such a view. And then follow this, which I quote that the
reader may the better understand a certain occasional acerbity in my
allusions to Mr. Belloc:—
 “He doesn’t know that Vailleton of Montpellier has knocked
the last nail into the coffin of that facile and superficial Victorian
shortcut (and blind alley). He has probably never heard of
Vailleton, and when he does he will suspect him for a foreigner.
That is what I mean by being provincial and not abreast of one’s
time.”

It is perfectly true that I have never heard of any Vailleton in

biological science. Nor has anyone else. There is “no sich person.”
Perhaps Mr. Belloc has not been able to read the manuscript of
some adviser, or his memory may have played a trick upon him.
Possibly he has in mind that eminent Victorian embryologist,
Vialleton, who, so far from being the very newest thing in “European”
biology, must now be getting on for seventy. He is half-way back to
Haeckel, the originator of the family-tree idea, a German
embryologist and not, as a matter of fact, the Victorian English
Protestant Mr. Belloc supposes him to be. Possibly years and years
ago some French student may have run away with the idea that
embryos conscientiously repeat their phylogeny, and Professor
Vialleton may have thought it well to discuss this idea in one of his
books. It is not an idea I have ever entertained, much less stated,
and its only interest here is that it gives Mr. Belloc a chance of
showing how rudely he can set out his inaccuracies and his
misconceptions.
But this is an incidental comment. I will reserve for my next
section a consideration of the remarkable arguments—“crushing
arguments” the enthusiastic cross-heads of his editor declare them
to be—that Mr. Belloc produces against this view of life as being in a
state of change under the action of Natural Selection, that I have put
here before the reader.
 III
MR. BELLOC AS A SPECIMEN CRITIC OF
NATURAL SELECTION

THE chief arguments against the Theory of Natural Selection with

which Mr. Belloc has favoured us are neatly set out by him in two
triads. His passion for orderly arrangement is greater than his logic,
and we shall find that the second and third arguments of his second
triad are substantially the same. He is rather exceptionally ignorant
of modern scientific literature, and his arguments do not cover all the
countervailing considerations upon which systematic observation
and research work have been based—the speculations of Dr.
Fairfield Osborn would have been a godsend for him—but the things
he has to say are conveniently simple; they embody some prevalent
misconceptions, and they will be useful in accentuating the more
salient points in my account of the theory given in my second paper.
He produces first certain remarkable a priori arguments—his
“three a prior arguments.” The first is beautifully absurd. It is difficult
to believe it is advanced in anything but a spirit of burlesque. He
says that an advantage is not an advantage. He says that an
advantage does not give an advantage unless it is combined with
other advantages. You will think I am misrepresenting him. Then
please read this:—

“(1) The advantageous differences making for survival are

not of one kind in any particular case, but of an indefinitely large
number (e.g., climate getting colder needs not only warmer coat,
but power to digest new food, protective colouring so as not to
show dark against snow, etc., an indefinitely large number of
qualities). Now the chance of all being combined (and co-
 ordinated) in a single individual, without design, accidentally, let
alone of their thus appearing in many individuals accidentally
and without design, approximates to zero.”

This is, so to speak, the short uncompleted form of the first

argument. It is expanded later to a copiousness too great to admit of
quotation. This expansion carries the statement right to its
conclusion, that only an individual possessing all the possible
differences that are advantageous at any particular time can survive.
Otherwise its differences have no “survival value.” They may be
advantages, but not sufficient advantages to score an advantage. I
know this sounds tipsy, but there it is in black and white in Mr.
Belloc’s wonderful Article V for any one to consult. It follows plainly
that, except for a miracle, every species must be exterminated in
every generation. I can see no other way out of it. No individual, he
declares, can survive without the full set of advantageous
differences, and the chance of any individual having the full set of
advantageous differences, he declares after some abstruse verbal
gestures, is zero. There is Mr. Belloc with his unfailing logic, his clear
mathematical demonstration, and all the rest of it. There is the lucid
Latin mind shining above my Nordic fog! Yet the previous generation
got along without any of the set! And species do survive.
Did Mr. Belloc imagine he was saying something else? It is not
for me to speculate. Helping out an antagonist in a controversy is apt
to be resented. He has, I think, simply got into a muddle here, and
he is not sufficiently self-critical to get out of it again. So he tries to
muddle through. It is quite reasonable to say that when a species is
under stress of changing conditions it is usual for the need for
adaptation to be felt upon a number of points and not simply upon
one, and that, since every advantage counts, the individuals with the
greatest combination of advantageous differences have the best
chances. But that does not alter the fact that even a single
advantage is an advantage. What happens in nature is not an
extermination of all who are not completely in the fashion of the new
differences. That seems to be Mr. Belloc’s idea, but it is a wrong
idea. What does happen is a diminution in each generation of the
number of the disadvantaged in relation to the number of the
advantaged. That is quite another affair. Mr. Belloc has not grasped
this. His third a priori argument shows as much even more plainly
than his first, and to that I shall presently come.

Mr. Belloc’s Mental Indigestion

I fancy this stuff he has written here is an outcome of an
indigestion of Samuel Butler by Mr. Belloc. I should not have thought
Mr. Belloc had read Samuel Butler, and I doubt if he has read him
much. But there is a decided echo of Luck or Cunning in the one
indistinct paragraph in which, without committing himself too deeply,
Mr. Belloc seems to convey his own attitude towards the procedure
of Evolution. “Design,” whatever that is, is at work, and Natural
Selection is not. “There is an innate power possessed by the living
thing to attempt its own adaptation.” It is quite a delusion apparently
that rabbits that cannot run or sparrows that are not quick on the
wing are killed off more frequently than the smarter fellows. That
never happens, though to the atheistically minded it may seem to
happen. If it happens, it would “get rid of a God.” But there are
rabbits which, unlike Mrs. Micawber, do make an effort. You must
understand that all creation, inspired by design, is striving. The good
fungus says to itself, “Redder and more spots will benefit me
greatly,” and tries and tries, and presently there are redder hues and
more spots. Or a happily inspired fish says: “There is a lot of food on
land and the life is more genteel there, so let me get lungs.” And
presently it gets lungs. Some day Mr. Belloc must take a holiday in
Sussex and flap about a bit and get himself some wings and
demonstrate all this. But perhaps this is caricature, and Mr. Belloc
when he talks about that “innate disposition” just means nothing very
much—just an attempt or something. I will not pretend to understand
Mr. Belloc fully upon this point.
 Mr. Belloc’s Bird-Lizard
I will return to the essential misconception of the Theory of
Natural Selection betrayed in this first a priori when I consider Mr.
Belloc’s third feat of logic. But first let me glance at his second. In
this he says, very correctly, that every stage in the evolution of a
living creature must be a type capable of maintaining itself and every
change must be an advantageous change. I have noted this very
obvious point already in my second paper. But then Mr. Belloc
instructs us that the chances of its being so are, for no earthly
reason, zero—that fatal zero again!—and goes on to a passage so
supremely characteristic that it must be read to be believed:—

“A bird has wings with which it can escape its enemies. If it

began as a reptile without wings—when, presumably, it had
armour or some other aid to survival—what of the interval?
Natural Selection sets out to change a reptile’s leg into a bird’s
wing and the scales of its armour into feathers. It does so by
making the leg less and less of a leg for countless ages, and by
infinite minute gradations, gradually turning the scales into
feathers.
“By the very nature of the theory each stage in all these
millions is an advantage over the last towards survival! The thing
has only to be stated for its absurdity to appear. Compare the
‘get away’ chances of a lizard at one end of the process or a
sparrow at the other with some poor beast that had to try and
scurry off on half-wings! or to fly with half-legs!
“Postulate a design, say, ‘Here was something in the
making,’ and the process is explicable, especially if fairly rapid
so as to bridge over the dangerously weak stage of imperfection.
Postulate Natural Selection and it is manifestly impossible.”

Let us note a few things of which Mr. Belloc shows himself to be

unaware in this amusing display of perplexity. In the first place he
does not know that the Mesozoic reptiles most closely resembling
birds were creatures walking on their hind-legs, with a bony structure
of the loins and a backbone already suggestive of the avian
anatomy. Nor is he aware that in the lowliest of living birds the fore-
limbs are mere flappers, that the feathers are simpler in structure
than any other bird’s feathers, and that the general development of a
bird’s feather points plainly to the elongation of a scale. He has
never learnt that feathers came before wings, and that at first they
had to do, not with flying, but with protection against cold. Yet all this
was under his nose in the Outline of History in text and picture. The
transition from a quilled to a feathered dinosaur presents indeed no
imaginative difficulties, and the earliest birds ran and did not fly. One
of the earliest known extinct birds is Hesperornis, a wingless diving
bird. It is figured on page 30, and there is another bird on page 34
that Mr. Belloc might ponder with advantage. A whole great section
of living birds, like the ostrich and the emu, have no trace in their
structure of any ancestral flying phase; their breast-bones are
incapable of carrying the necessary muscular attachments.
 H. G. Wells.
Low

But after the feather was fully developed it opened up great

possibilities of a strong and light extension of the flapper, helpful in
running or useful in leaps from tree to tree. Archæopteryx, another
early bird, which is also figured in the Outline, has a sort of bat-wing
fore-limb with feathers instead of membrane. It was a woodland
creature, and flew as a flying fox or a flying lemur or even a bat flies.
All these facts are widely known, and all that trouble about the half-
leg, half-wing, dissolves before them. But consider what a hash they
make of Mr. Belloc’s argument, and how pitifully it scurries off before
them on its nondescript stumps of pretentious half-knowledge, half-
impudence! So much for zero the second.

Troubles of Mr. Belloc as a Matrimonial

Agent
The final of this wonderful trinity of a prioris is a repetition of an
argument advanced ages ago by Queen Victoria’s Lord Salisbury,
when he was President of the British Association. Even then it struck
people that he had been poorly coached for the occasion. Assuming
that one or two individuals have got all these “survival value”
differences in the correct proportions—against which the chances
are zero—how by any theory of Natural Selection are we to suppose
they will meet, breed, and perpetuate them? So this argument runs.
The chances are again declared to be zero, the third zero, and Mr.
Belloc, I gather, calls in Design again here and makes his Creative
Spirit, which has already urged these two individuals, lions, or liver
flukes or fleas or what not, to make an effort and adapt themselves,
lead them now to their romantic and beneficial nuptials, while the
Theory of Natural Selection grinds its teeth in the background and
mutters “Foiled again.”
But this third argument reinforces the first, in showing what is the
matter with Mr. Belloc’s ideas in this group of questions. He has got
the whole business upside down. I rather blame the early Darwinians
in this matter for using so inaccurate a phrase as the “Survival of the
Fittest.” It is to that phrase that most of Mr. Belloc’s blunderings are
due. Yet he ought not to have been misled. He had a summary of
modern views before him. He criticises my Outline of History, he
abuses it, and yet he has an extraordinary trick of getting out of its
way whenever it swings near his brain-case. I warn the readers of
that modest compendium expressly (and as early as page 16) that
the juster phrase to use is not the Survival of the Fittest, but the
Survival of the Fitter. I do what I can throughout to make them see