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 Contents

Contributors ix 14 Herpesviruses 257

Preface xi 15
Viruses of Diarrhea 283

16 Arthropod-Borne and
Other Zoonotic Viruses 295
PART I
17 Rabies 319
Infection 1
L. Barth Reller, Megan E. Reller, and Kenneth J. Ryan 18
Retroviruses: Human T-Lymphotropic Virus,
Human Immunodeficiency Virus,
1 Infection—Basic Concepts 3 and Acquired Immunodeficiency
2 Immune Response to Infection 19 Syndrome 327

3 Sterilization, Disinfection, and 19 Papilloma and Polyoma Viruses 355

Infection Control 43
20
Persistent Viral Infections of the
4 Principles of Laboratory Diagnosis Central Nervous System 369
of Infectious Diseases 55
5 Emerging and Reemerging Infectious
Diseases: Emergence and PART III
Global Spread of Infection 85 Pathogenic Bacteria 379
Paul Pottinger, L. Barth Reller, Kenneth J. Ryan, and
Scott Weissman
PART II
21 Bacteria—Basic Concepts 381
Pathogenic Viruses 95
Nafees Ahmad, W. Lawrence Drew, and Michael Lagunoff 22 Pathogenesis of Bacterial Infections 415
6 Viruses—Basic Concepts 97 23 Antibacterial Agents and Resistance 431
7 Pathogenesis of Viral Infection 129 24 Staphylococci 459
8 Antiviral Agents and Resistance 149 25 Streptococci and Enterococci 473
9 Respiratory Viruses 159 26
Corynebacterium, Listeria,
10
Viruses of Mumps, Measles, Rubella, and Bacillus 501
and Other Childhood Exanthems 187 27 Mycobacteria 519
11 Poxviruses 207 28 537
Actinomyces and Nocardia
12 Enteroviruses 217
29
Clostridium, Bacteroides,
13
Hepatitis Viruses 231 and Other Anaerobes 545

vii

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 viii CONTENTS

30
Neisseria 567 46 The Opportunistic Fungi: Candida,
Aspergillus, the Zygomycetes, and
31
Haemophilus and Bordetella 583 Pneumocystis 771
32 Vibrio, Campylobacter, and Helicobacter 599 47 The Systemic Fungal Pathogens:
33 613
Enterobacteriaceae Cryptococcus, Histoplasma, Blastomyces,
787
Coccidioides, Paracoccidioides
34 645
Legionella and Coxiella

35 Pseudomonas and Other Opportunistic

Gram-negative Bacilli 653 PART V

36
Plague and Other Bacterial
Pathogenic Parasites 803
Zoonotic Diseases 665 Paul Pottinger and Charles R. Sterling

37 Spirochetes 679 48 Parasites—Basic Concepts 805

38 701 49 Pathogenesis and Diagnosis

Mycoplasma
of Parasitic Infection 815
39
Chlamydia 707
50 Antiparasitic Agents and Resistance 821
40
Rickettsia, Ehrlichia, Anaplasma,
and Bartonella 717 51 Apicomplexa and Microsporidia 829
41
Dental and Periodontal 52 Sarcomastigophora—The Amebas 861
Infections 729 53
Sarcomastigophora—The Flagellates 875
54 Intestinal Nematodes 899
PART IV 55 Tissue Nematodes 919
Pathogenic Fungi 737
56 Cestodes 939
J. Andrew Alspaugh
57 Trematodes 955
42 Fungi—Basic Concepts 739
43 Pathogenesis and Diagnosis of Infectious Diseases: Syndromes and Etiologies 971
Fungal Infections 747 Practice Questions In USMLE Format 991
44 Antifungal Agents and Resistance 755 Index 1003
45 The Superficial and
Subcutaneous Fungi: Dermatophytes,
Malassezia, Sporothrix, and
Pigmented Molds 761

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 EDITOR
KENNETH J. RYAN, MD
Professor of Immunobiology
Emeritus Professor of Pathology and
Microbiology
University of Arizona College of Medicine
Tucson, Arizona

AUTHORS
NAFEES AHMAD, PhD L. BARTH RELLER, MD
Professor of Immunobiology Professor of Pathology and Medicine
Director, Immunity and Infection Duke University School of Medicine
University of Arizona College of Medicine Durham, North Carolina
Tucson, Arizona
MEGAN E. RELLER, MD, PhD, MPH
J. ANDREW ALSPAUGH, MD Associate Professor of Medicine
Professor of Medicine, Molecular Genetics Duke University School of Medicine
and Microbiology Durham, North Carolina
Duke University School of Medicine
Durham, North Carolina CHARLES R. STERLING, PhD
Professor Emeritus
W. LAWRENCE DREW, MD, PhD School of Animal and Comparative
Emeritus Professor of Laboratory Biomedical Sciences
Medicine and Medicine University of Arizona
University of California, San Francisco Tucson, Arizona
School of Medicine
Mount Zion Medical Center SCOTT WEISSMAN, MD
San Francisco, California Associate Professor of Pediatrics
University of Washington School of
MICHAEL LAGUNOFF, PhD Medicine
Professor of Microbiology Seattle Children’s
University of Washington School of Seattle, Washington
Medicine
Seattle, Washington

PAUL POTTINGER, MD
Associate Professor of Medicine
Division of Allergy and Infectious Diseases
University of Washington School of
Medicine
Seattle, Washington

STUDENT ADVISORY GROUP

Laura Bricklin, Chair
Matthew Cravens
Kieran Hynes
Eric Lander
Danielle Nahal
Ned Premyodhin
Edwin Telemi

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 Preface

W
ith this seventh edition, Sherris Medical Microbiology will complete its fourth
decade. We are pleased to welcome new authors, Andy Alspaugh (mycology)
and Megan Reller (epidemiology) from Duke and Scott Weissman (bacteriology)
from the University of Washington. Sadly, George Ray a founding author and coeditor of the
last three editions is no longer with us (see Dedication). John Sherris, the founding editor,
continues to act as an inspiration to all of us.

BOOK STRUCTURE
The goal of Sherris Medical Microbiology remains unchanged from that of the first edition
(1984). This book is intended to be the primary text for students of medicine and medical
science who are encountering microbiology and infectious diseases for the first time. Part I
opens with a chapter that explains the nature of infection and the infectious agents at the
level of a general reader. The following four chapters give more detail on the immunologic,
diagnostic, and epidemiologic nature of infection with minimal detail about the agents
themselves. Parts II through V form the core of the text with chapters on the major viral,
bacterial, fungal, and parasitic diseases, and each begins with its own chapters on basic biol-
ogy, pathogenesis, and antimicrobial agents.

CHAPTER STRUCTURE
In the specific organism/disease chapters, the same presentation sequence is maintained
throughout the book. First, features of the Organism (structure, metabolism, genetics, etc.)
are described; then mechanisms of the Disease (epidemiology, pathogenesis, immunity)
the organism causes are explained; the sequence concludes with the Clinical Aspects
(manifestations, diagnosis, treatment, prevention) of these diseases. A clinical Case Study
followed by questions in USMLE format concludes each of these chapters. In Sherris Medi-
cal Microbiology, the emphasis is on the text narrative, which is designed to be read com-
prehensively, not as a reference work. Considerable effort has been made to supplement this
text with other learning aids such as the above-mentioned cases and questions as well as
tables, photographs, and illustrations.

STUDENT-DRIVEN STUDY AIDS

This edition includes a number of new study aids which are the product of a Student
Advisory Group (see Authors page) conceived and lead by Laura Bricklin, then a second-
year medical student. They include a boxed narrative OVERVIEW opening each disease-
oriented chapter or major section, highlighted MARGINAL NOTES judged to be “high
yield” for Step 1 preparation, and bulleted lists of KEY CONCLUSIONS at the end of major
sections. A THINK ➔ APPLY feature randomly inserts thought-provoking questions into
the body of the text, which are answered at the bottom of the page. These new features are
explained in detail and illustrated on pages iv and v.
xi

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 xii PREFACE

The back of the book includes two more review tools. Infectious Diseases: Syndromes
and Etiologies is a set of tables that brings together the infectious agents (viruses, bacteria,
fungi, parasites) discussed separately in Parts II through V as probable causes of the major
infection syndromes (pneumonia, arthritis, diarrhea, etc.). It is hoped these will be of value
when the student prepares for case discussion exercises or sees patients. The 100 Practice
Questions are in USMLE format and in addition to the ones at the end of earlier chapters.
For any textbook, dealing with the onslaught of new information is a major challenge.
In this edition, much new material has been included, but to keep the student from being
overwhelmed, older or less important information has been deleted to keep the size of this
book no larger than of the sixth edition. As a rule of thumb, material on classic microbial
structures, toxins, and the like in the Organism section has been trimmed unless its role is
clearly explained in the Disease section. At the same time, we have tried not to eliminate
detail to the point of becoming synoptic and uninteresting. Genetics is one of the greatest
challenges in this regard. Without doubt this is where major progress is being made in
understanding infectious diseases, but a coherent discussion may require using the names
and abbreviations of genes, their products, and multiple regulators to tell a complete story.
Whenever possible we have tried to tell the story without all the code language. We have
also tried to fully describe the major genetic mechanisms in general chapters and then refer
to them again when that mechanism is deployed by a pathogen. For example, Neisseria
gonorrhoeae is used to explain the genetic mechanisms for antigenic variation in a general
chapter on bacterial pathogenesis (Chapter 22), but how it influences its disease, gonorrhea,
is taken up with its genus Neisseria (Chapter 30).
A saving grace is that our topic is important, dynamic, and fascinating—not just to
us but to the public at large. Newspaper headlines now carry not only the new names of
emerging threats like Zika virus but also the antigenic formulas of more familiar pathogens
like E coli and influenza virus. Resistance to antimicrobial agents and the havoc created by
antivaccine movements are regular topics on the evening news. I1t is not all bad news. We
sense a new optimism that deeper scientific understanding of worldwide scourges like HIV/
AIDS, tuberculosis, and malaria will lead to their control. We are hopeful that the basis for
understanding these changes is clearly laid out in the pages of this book.
Kenneth J. Ryan
Editor

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 PART I
Infection
L. Bar t h R eller • M egan E. R eller • Ke n n e t h J. R ya n

Infection—Basic Concepts C H A P T ER 1
Immune Response to Infection C H A P T ER 2
Sterilization, Disinfection, and Infection Control C H A P T ER 3
Principles of Laboratory Diagnosis of Infectious Diseases C H A P T ER 4
Emerging and Reemerging Infectious Diseases: Emergence and Global Spread of Infection C H A P T ER 5

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 1
Infection—Basic
Concepts
Humanity has but three great enemies: fever, famine and war; of these by far the greatest, by far the most terrible, is fever.

— Sir William Osler, 1896*

W
hen Sir William Osler, the great physician/humanist, wrote these words, fever
(infection) was indeed the scourge of the world. Tuberculosis and other forms
of pulmonary infection were the leading causes of premature death among the
well to do and the less fortunate. The terror was due to the fact that, although some of the
causes of infection were being discovered, little could be done to prevent or alter the course
of disease. In the 20th century, advances in public sanitation and the development of vac-
cines and antimicrobial agents changed this (Figure 1–1), but only for the nations that could
afford these interventions. As we move through the second decade of the 21st century,
the world is divided into countries in which heart attacks, cancer, and stroke have sur-
passed infection as causes of premature death and those in which infection is still the leader.
A new uneasiness that is part evolutionary, part discovery, and part diabolic has taken
hold. Infectious agents once conquered have shown resistance to established therapy, such
as multiresistant Mycobacterium tuberculosis, and diseases, such as acquired immunode-
ficiency syndrome (AIDS), have emerged. The spectrum of infection has widened, with
discoveries that organisms earlier thought to be harmless can cause disease under certain
circumstances. Who could have guessed that Helicobacter pylori, not even mentioned in
the first edition of this book (1984), would be the major cause of gastric and duodenal
ulcers and an officially declared carcinogen? Finally, bioterrorist forces have unearthed two
previously controlled infectious diseases—anthrax and smallpox—and threatened their
distribution as agents of biological warfare. For students of medicine, understanding the
fundamental basis of infectious diseases has more relevance than ever.

BACKGROUND
The science of medical microbiology dates back to the pioneering studies of Pasteur and
Koch, who isolated specific agents and proved that they could cause disease by introduc-
ing the experimental method. The methods they developed lead to the first golden age of
microbiology (1875-1910), when many bacterial diseases and the organisms responsible for
them were defined. These efforts, combined with work begun by Semmelweis and Lister,
which showed how these diseases spread, led to the great advances in public health that
initiated the decline in disease and death. In the first half of the 20th century, scientists
studied the structure, physiology, and genetics of microbes in detail and began to answer

*
Osler W. JAMA. 1896;26:999.

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 4 PART I INFECTION

Public health
departments
1000
established Influenza pandemic

Death rate per 100,000 population per year

800

600
Diphtheria immunization (1940)
Chlorination
Penicillin usage (1945)
400 of water
Polio vaccine
Haemophllus influenzae
200 conjugate vaccine (1990)

FIGURE 1–1. Death rates for infectious

disease in the United States in the 20th
century. Note the steady decline in 0
death rates related to the introduction 1900 1920 1940 1960 1980 2000
of public health, immunization, and
antimicrobial interventions. Year

questions relating to the links between specific microbial properties and disease. By the end
of the 20th century, the sciences of molecular biology, genetics, genomics, and proteomics
extended these insights to the molecular level. Genetic advances have reached the point at
which it is possible to know not only the genes involved but also to understand how they are
regulated. The discoveries of penicillin by Fleming in 1929 and of sulfonamides by Domagk
in 1935 opened the way to great developments in chemotherapy. These gradually extended
from bacterial diseases to fungal, parasitic, and finally viral infections. Almost as quickly,
virtually all categories of infectious agents developed resistance to all categories of antimi-
crobial agents to counter these chemotherapeutic agents.

INFECTIOUS AGENTS: THE MICROBIAL WORLD

Microbiology is a science defined by smallness. Its creation was made possible by the inven-
tion of the microscope (Gr. micro, small + skop, to look, see), which allowed visualization of
structures too small to see with the naked eye. This definition of microbiology as the study
Microbes are small of microscopic living forms still holds if one can accept that some organisms can live only in
other cells (eg, all viruses and some bacteria) and that others include macroscopic forms in
their life cycle (eg, fungal molds, parasitic worms). The relative sizes of some microorgan-
isms are shown in Figure 1–2.
Microorganisms are responsible for much of the breakdown and natural recycling of
organic material in the environment. Some synthesize nitrogen-containing compounds
that contribute to the nutrition of living things that lack this ability; others (oceanic algae)
Most play benign roles in the contribute to the atmosphere by producing oxygen through photosynthesis. Because micro-
environment organisms have an astounding range of metabolic and energy-yielding abilities, some can
exist under conditions that are lethal to other life forms. For example, some bacteria can
oxidize inorganic compounds such as sulfur and ammonium ions to generate energy. Oth-
ers can survive and multiply in hot springs at temperatures higher than 75°C.
Some microbial species have adapted to a symbiotic relationship with higher forms of life.
For example, bacteria that can fix atmospheric nitrogen colonize root systems of legumes
and of a few trees, such as alders, and provide the plants with their nitrogen requirements.
When these plants die or are plowed under, the fertility of the soil is enhanced by nitrog-
Products of microbes contribute enous compounds originally derived from the metabolism of the bacteria. Ruminants can
to the atmosphere use grasses as their prime source of nutrition, because the abundant flora of anaerobic bac-
teria in the rumen break down cellulose and other plant compounds to usable carbohy-
drates and amino acids and synthesize essential nutrients including some amino acids and
vitamins. These few examples illustrate the protean nature of microbial life and their essen-
tial place in our ecosystem.

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 CHAPTER 1 I N F E C T I O N — B A S I C CO N C E P T S 5

Limits of 50,000-V Light Unaided

resolution electron microscope microscope human eye
0.003 µm 0.2 µm 40 µm

Microscopic
protozoa and
fungi, 4–10 µm
Classes of
organisms Bacteria
0.1–10 µm

Viruses
0.03–0.3 µm

0.001 0.01 0.1 1 10 100

FIGURE 1–2. Relative size of
Size (µm) microorganisms.

The major classes of microorganisms in terms of ascending size and complexity are
viruses, bacteria, fungi, and parasites. Parasites exist as single or multicellular structures
with the same compartmentalized eukaryotic cell plan of our own cells including a nucleus
and cytoplasmic organelles like mitochondria. Fungi are also eukaryotic, but have a rigid
Increasing complexity: viruses →
external wall that makes them seem more like plants than animals. Bacteria also have a cell
bacteria → fungi → parasites
wall, but with a cell plan called “prokaryotic” that lacks the organelles of eukaryotic cells.
Viruses are not cells at all. They have a genome and some structural elements, but must take
over the machinery of another living cell (eukaryotic or prokaryotic) to replicate. The four
classes of infectious agents are summarized in Table 1–1, and generic examples of each are
shown in Figure 1–3.

VIRUSES
Viruses are strict intracellular parasites of other living cells, not only of mammalian and
plant cells, but also of simple unicellular organisms, including bacteria (the bacteriophages).
Viruses are simple forms of replicating, biologically active particles that carry genetic infor-
mation in either DNA or RNA molecules. Most mature viruses have a protein coat over Viruses contain little more than
their nucleic acid and, sometimes, a lipid surface membrane derived from the cell they DNA or RNA
infect. Because viruses lack the protein-synthesizing enzymes and structural apparatus nec-
essary for their own replication, they bear essentially no resemblance to a true eukaryotic
or prokaryotic cell.
Viruses replicate by using their own genes to direct the metabolic activities of the cell
they infect to bring about the synthesis and reassembly of their component parts. A cell
infected with a single viral particle may, thus, yield thousands of viral particles, which can

TABLE 1–1    Features of Infectious Agents

VIRUSES BACTERIA FUNGI PARASITES
Size (µm) <1 2-8 4+ 2+
Cell wall No Yes Yes No/yesa
Cell plan None Prokaryotic Eukaryotic Eukaryotic
Free living No Yes b
Yes Yes
Intracellular Yes No/yes No No/yesc

a
Parasitic cysts have cell walls.
b
A few bacteria grow only within cells.
c
The life cycle of some parasites includes intracellular multiplication.

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 6 PART I INFECTION

Envelope

Spike
Capsid
Capsid
Nucleic acid
Nucleic acid

Naked virus Enveloped virus

A
Plasma
Capsule Ribosomes Cell wall membrane

Nucleoid

Fimbriae Chromosome Inclusion Flagellum

(DNA) body
B

Flagellum
Bud scar

Ribosomes

Mitochondrion
Endoplasmic
reticulum
Nucleus
Pellicle
Nucleolus
Cell wall
Cell membrane
Golgi apparatus
Water vacuole
Storage vacuole
Centrioles Centrioles

Fungal (Yeast) Cell

C

FIGURE 1–3. Infectious agents.

A. Virus. B. Bacterium. C. Fungus. Cell membrane
D. Parasite. (Reproduced with Glycocalyx
permission from Willey JM: Prescott,
Protozoan Cell
Harley, & Klein’s Microbiology, 7th edition.
McGraw-Hill, 2008.) D

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 CHAPTER 1 I N F E C T I O N — B A S I C CO N C E P T S 7

be assembled almost simultaneously under the direction of the viral nucleic acid. Infec-
tion of other cells by the newly formed viruses occurs either by seeding from or lysis of the Replication is by control of the
infected cells. Sometimes, viral and cell reproduction proceed simultaneously without cell host cell metabolic machinery
death, although cell physiology may be affected. The close association of the virus with the
cell sometimes results in the integration of viral nucleic acid into the functional nucleic Some integrate into the genome
acid of the cell, producing a latent infection that can be transmitted intact to the progeny
of the cell.

BACTERIA
Bacteria are the smallest (0.1-10 μm) independently living cells. They have a cytoplasmic
membrane surrounded by a cell wall; a unique interwoven polymer called peptidoglycan
makes the wall rigid. The simple prokaryotic cell plan includes no mitochondria, lysosomes,
endoplasmic reticulum, or other organelles (Table 1–2). In fact, most bacteria are approxi-
mately the size of mitochondria. Their cytoplasm contains only ribosomes and a single,
Smallest living cells
double-stranded DNA chromosome. Bacteria have no nucleus, but all the chemical ele-
ments of nucleic acid and protein synthesis are present. Although their nutritional require-
Prokaryotic cell plan lacks
ments vary greatly, most bacteria are free living if given an appropriate energy source. Tiny
nucleus and organelles
metabolic factories, they divide by binary fission and can be grown in artificial culture,
often in less than 1 day. The Archaea are similar to bacteria but evolutionarily distinct. They
are prokaryotic, but differ in the chemical structure of their cell walls and other features.
The Archaea (archebacteria) can live in environments humans consider hostile (eg, hot
springs, high salt areas) but are not associated with disease.

FUNGI
Fungi exist in either yeast or mold forms. The smallest of yeasts are similar in size to
bacteria, but most are larger (2-12 μm) and multiply by budding. Molds form tubular
extensions called hyphae, which, when linked together in a branched network, form
the fuzzy structure seen on neglected bread slices. Fungi are eukaryotic, and both yeasts Yeasts and molds are surrounded
and molds have a rigid external cell wall composed of their own unique polymers, by cell wall
called glucan, mannan, and chitin. Their genome may exist in a diploid or haploid state
and replicate by meiosis or simple mitosis. Most fungi are free living and widely distrib-
uted in nature. Generally, fungi grow more slowly than bacteria, although their growth
rates sometimes overlap.

TABLE 1–2    Distinctive Features of Prokaryotic and Eukaryotic Cells

CELL COMPONENT PROKARYOTES
Nucleus No membrane, single circular
chromosome
Extrachromosomal DNA Often present in form of
plasmid(s)
Organelles in cytoplasm None
Cytoplasmic membrane Contains enzymes of respiration; Semipermeable layer not
active secretion of enzymes;
site of phospholipid and DNA
synthesis
Cell wall Rigid layer of peptidoglycan
(absent in Mycoplasma)
Sterols Absent (except in Mycoplasma)
Ribosomes 70 S in cytoplasm
EUKARYOTES
Membrane bounded,
a number of individual
chromosomes
In organelles
Mitochondria (and
­chloroplasts in photosyn-
thetic organisms)
possessing functions of
p
­ rokaryotic membrane
No peptidoglycan (in some
cases cellulose present)
Usually present
80 S in cytoplasmic reticulum

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 8 PART I INFECTION
Range from tiny amoebas to
meter-long worms
Flora may stay for short or
extended periods
If pathogens are involved, the
relationship is called the carrier
state
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PARASITES
Parasites are the most diverse of all microorganisms. They range from unicellular
­amoebas of 10 to 12 μm to multicellular tapeworms 1 m long. The individual cell plan
is eukaryotic, but organisms such as worms are highly differentiated and have their own
organ systems. Most worms have a microscopic egg or larval stage, and part of their life
cycle may involve multiple vertebrate and invertebrate hosts. Most parasites are free liv-
ing, but some depend on combinations of animal, arthropod, or crustacean hosts for their
survival.
THE HUMAN MICROBIOTA
Before moving on to discuss how, when, and where the previously mentioned agents cause
human disease, we should note that the presence of microbes on or in humans is not, by
itself, abnormal. In fact, from shortly after birth on, it is universal; we harbor 10 times the
number of microbial cells than human cells. This population formerly called the normal
flora is now referred to as our microbiota or microbiome. These microorganisms, which
are overwhelmingly bacteria, are frequently found colonizing various body sites in healthy
individuals. The constituents and numbers of the microbiota vary in different areas of the
body and, sometimes, at different ages and physiologic states. Their names are mostly unfa-
miliar because they have not (yet) been associated with disease. They comprise microorgan-
isms whose morphologic, physiologic, and genetic properties allow them to colonize and
multiply under the conditions that exist in particular sites, to coexist with other colonizing
organisms, and to inhibit competing intruders. Thus, each accessible area of the body pres-
ents a particular ecologic niche, colonization of which requires a particular set of properties
of the colonizing microbe.
Organisms of the microbiota may have a symbiotic relationship that benefits the host
or may simply live as commensals with a neutral relationship to the host. A parasitic rela-
tionship that injures the host would not be considered “normal,” but, in most instances,
not enough is known about the organism–host interactions to make such distinctions.
Like houseguests, the members of the normal flora may stay for highly variable periods.
­Residents are strains that have an established niche at one of the many body sites, which
they occupy indefinitely. Transients are acquired from the environment and establish
themselves briefly, but they tend to be excluded by competition from residents or by the
host’s innate or immune defense mechanisms. The term carrier state is used when organ-
isms known to be potentially pathogenic are involved, although its implication of risk is
not always justified. For example, Streptococcus pneumoniae, a cause of pneumonia, and
Neisseria meningitidis, a cause of meningitis, may be isolated from the throat of 5% to 40%
of healthy people. Whether these bacteria represent transient flora, resident flora, or carrier
state is largely semantic. The possibility that their presence could be the prelude to disease
is presently impossible to determine in advance.
It is important for students of medical microbiology and infectious disease to under-
stand the role of the microbiota because of its significance both as a defense mechanism
against infection and as a source of potentially pathogenic organisms. In addition, it is
important for physicians to know the typical composition of the microbiota at various sites
to avoid confusion when interpreting laboratory culture results. The following excerpt
indicates that the English poet W.H. Auden understood the need for balance between the
microbiota and its host. He was influenced by an article in Scientific American about the
flora of the skin.
On this day tradition allots to all for whom my ectoderm
to taking stock of our lives, is as Middle Earth to me.
my greetings to all of you, Yeasts,
For creatures your size I offer
Bacteria, Viruses,
a free choice of habitat,
Aerobics and Anaerobics:
so settle yourselves in the zone
A Very Happy New Year
that suits you best, in the pools
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 CHAPTER 1 I N F E C T I O N — B A S I C CO N C E P T S 9

of my pores or the tropical the sebum and lipids you need,

forests of arm-pit and crotch,
in the deserts of my fore-arms,
or the cool woods of my scalp.
Build colonies: I will supply
adequate warmth and moisture,
on condition you never
do me annoy with your presence,
but behave as good guests should,
not rioting into acne
or athlete’s-foot or a boil.

—W.H. Auden, “A New Year Greeting”

ORIGIN AND NATURE

The healthy fetus is sterile until the birth membranes rupture. During and after birth, the
infant is exposed to the flora of the mother’s vagina and to other organisms in the environ-
ment. During the infant’s first few days of life, the microbiota reflects chance exposure to
Initial flora is acquired during
organisms that can colonize particular sites in the absence of competitors. Subsequently,
and immediately after birth
as the infant is exposed to a broader range of organisms, those best adapted to colonize
particular sites become predominant. Thereafter, the flora generally resembles that of other
individuals in the same age group and cultural milieu.
Local physiologic and ecologic conditions determine the microbial makeup of the flora. Physiologic conditions such as
These conditions are sometimes highly complex, differing from site to site, and sometimes local pH influence colonization
with age. Conditions include the amounts and types of nutrients available, pH, oxidation–
reduction potentials, and resistance to local antibacterial substances such as bile and Adherence factors counteract
lysozyme. Many bacteria have adhesin-mediated affinity for receptors on specific types of mechanical flushing
epithelial cells; this facilitates colonization and multiplication and prevents removal by the
flushing effects of surface fluids and peristalsis. Various microbial interactions also deter- Ability to compete for nutrients
mine their relative prevalence in the flora. These interactions include competition for nutri- is an advantage
ents and inhibition by the metabolic products of other organisms.

MICROBIOTA AT DIFFERENT SITES

At any one time, the microbiota of a single person contains hundreds if not thousands
of species of microorganisms, mostly bacteria. The major members known to be impor-
tant in preventing or causing disease, as well as those that may be confused with etiologic
agents of local infections, are summarized in Table 1–3 and are described in greater detail
in subsequent chapters. The Human Microbiome Project is an ongoing effort to bring this
information together.

●● Blood, Body Fluids, and Tissues

In health, the blood, body fluids, and tissues are sterile. Occasional organisms may be dis- Tissues and body fluids such as
placed across epithelial barriers as a result of trauma or during childbirth; they may be blood are sterile in health
briefly recoverable from the bloodstream before they are filtered out in the pulmonary cap-
illaries or removed by cells of the reticuloendothelial system. Such transient bacteremia Transient bacteremia can result
may be the source of infection when structures such as damaged heart valves and foreign from trauma
bodies (prostheses) are in the bloodstream.

●● Skin
The skin surface provides a dry, slightly acidic, aerobic environment. It plays host to an
abundant flora that varies according to the presence of its appendages (hair, nails) and the
Propionibacteria and
activity of sebaceous and sweat glands. The flora is more abundant on moist skin areas (axil-
staphylococci are dominant
lae, perineum, and between toes). Staphylococci and members of the Propionibacterium
bacteria
genus occur all over the skin, and facultative diphtheroids (corynebacteria) are found in
moist areas. Propionibacteria are slim, anaerobic, or microaerophilic gram-positive rods
Skin flora is not easily removed
that grow in subsurface sebum and break down skin lipids to fatty acids. Thus, they are
most numerous in the ducts of hair follicles and of the sebaceous glands that drain into
Conjunctiva resembles skin
them. Even with antiseptic scrubbing, it is difficult to eliminate bacteria from skin sites,
particularly those bearing pilosebaceous units. Organisms of the skin flora are resistant to

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 10 PART I INFECTION
Oropharynx has streptococci and
Neisseria
H pylori turned out to be a
stomach pathogen
Small intestinal flora is scanty
but increases toward lower ileum
Adult colonic flora is abundant
and predominantly anaerobic
Diet affects species composition
Ryan_ch01_p0001-0018.indd 10
TABLE 1–3    Predominant and Potentially Pathogenic Microbiota of Various
Body Sites
POTENTIAL PATHOGENS
BODY SITE (CARRIER) LOW VIRULENCE (RESIDENT)
Blood None Nonea
Tissues None None
Skin Staphylococcus aureus Propionibacterium,
Corynebacterium (diphtheroids),
coagulase-negative
staphylococci
Mouth Candida albicans Neisseria spp., viridans
streptococci, Moraxella,
Peptostreptococcus
Nasopharynx Streptococcus pneumoniae, Neisseria Neisseria spp., viridans
meningitidis, Haemophilus influenzae, streptococci, Moraxella,
group A streptococci, Staphylococcus Peptostreptococcus
aureus (anterior nares)
Stomach None Streptococci, Peptostreptococcus,
others from mouth
Small intestine None Scanty, variable
Colon Bacteroides fragilis, E coli, Eubacterium, Lactobacillus,
Pseudomonas, Candida, Clostridium B
­ acteroides, Fusobacterium,
(C perfringens, C difficile) Enterobacteriaceae,
­Enterococcus, Clostridium
Vagina
Prepubertal and Candida albicans Diphtheroids, staphylococci,
postmenopausal Enterobacteriaceae
Childbearing Group B streptococci, C albicans Lactobacillus, streptococci
Organisms such as viridans streptococci may be transiently present after disruption of a mucosal site.
a
the bactericidal effects of skin lipids and fatty acids, which inhibit or kill many extraneous
bacteria. The conjunctivae have a very scanty flora derived from the skin flora. The low
bacterial count is maintained by the high lysozyme content of lachrymal secretions and by
the flushing effect of tears.
●● Intestinal Tract
The mouth and pharynx contain large numbers of facultative and anaerobic bacteria. Dif-
ferent species of streptococci predominate on the buccal and tongue mucosa because of dif-
ferent specific adherence characteristics. Gram-negative diplococci of the genus Neisseria
and coccobacillary Moraxella make up the balance of the most commonly isolated organ-
isms. Strict anaerobes and microaerophilic organisms of the oral cavity have their niches in
the depths of the gingival crevices surrounding the teeth and in sites such as tonsillar crypts,
where anaerobic conditions can develop readily.
The total number of organisms in the oral cavity is very high, and it varies from site to site.
Saliva usually contains a mixed flora of about 108 organisms per milliliter, derived mostly
from the various epithelial colonization sites. The genera include Actinomyces, ­Bacteroides,
Prevotella, Streptococcus, and others. The stomach contains few, if any, resident organisms
in health because of the lethal action of gastric hydrochloric acid and peptic enzymes on
bacteria. One species, H pylori, long thought to be a common resident is now known to be
the primary cause of ulcers. The small intestine has a scanty resident flora, except in the
lower ileum, where it begins to resemble that of the colon.
The colon carries the most abundant and diverse microbiota in the body. In the adult,
feces are 25% or more bacteria by weight (about 1010 organisms per gram). More than 90%
are anaerobes, predominantly members of the genera Bacteroides, Fusobacterium, Eubacte-
rium, and Clostridium. The remainder of the flora is composed of facultative organisms such
as Escherichia coli, enterococci, yeasts, and numerous other species. There are considerable
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 CHAPTER 1 I N F E C T I O N — B A S I C CO N C E P T S 11

differences in adult flora depending on the diet of the host. Those whose diets include sub-
stantial amounts of meat have more Bacteroides and other anaerobic gram-negative rods in
their stools than those on a predominantly vegetable or fish diet. Recent studies have sug-
gested the composition of the colonic microbiota could play a role in obesity.

●● Respiratory Tract
The external 1 cm of the anterior nares has a flora similar to that of the skin. This is the
primary site of carriage of a major pathogen, Staphylococcus aureus. Approximately 25% to
30% of healthy people carry this organism as either resident or transient flora at any given S aureus is carried in anterior
time. The nasopharynx has a flora similar to that of the mouth; however, it is often the site nares
of carriage of potentially pathogenic organisms such as pneumococci, meningococci, and
Haemophilus species.
The respiratory tract below the level of the larynx is protected in health by the action of
the epithelial cilia and by the movement of the mucociliary blanket; thus, only transient Lower tract is protected by
inhaled organisms are encountered in the trachea and larger bronchi. The accessory sinuses mucociliary action
are normally sterile and are protected in a similar fashion, as is the middle ear by the epi-
thelium of the eustachian tubes.

●● Genitourinary Tract
The urinary tract is sterile in health above the distal 1 cm of the urethra, which has a scanty
flora derived from the perineum. Thus, in health, the urine in the bladder, ureters, and
renal pelvis is sterile. The vagina has a flora that varies according to hormonal influences at Bladder and upper urinary tract
different ages. Before puberty and after menopause, it is mixed, nonspecific, and relatively are sterile
scanty, and it contains organisms derived from the flora of the skin and colon. During the
childbearing years, it is composed predominantly of anaerobic and microaerophilic mem- Hormonal changes affect the
bers of the genus Lactobacillus, with smaller numbers of anaerobic gram-negative rods, vaginal flora
gram-positive cocci, and yeasts (Figure 1–4) that can survive under the acidic conditions
produced by the lactobacilli. These conditions develop because glycogen is deposited in Use of epithelial glycogen by
vaginal epithelial cells under the influence of estrogenic hormones and metabolized to lac- lactobacilli produces low pH
tic acid by lactobacilli. This process results in a vaginal pH of 4 to 5, which is optimal for
growth and survival of the lactobacilli, but inhibits many other organisms.

Bacterial Vaginosis
Bacterial vaginosis (BV) is a long known and unfortunately common syndrome which is
still poorly understood. Its dominant feature is an uncomfortable vaginal discharge with
a “fishy” odor which contains epithelial cells coated with bacteria (clue cells). This change BV is associated with a shift in
is associated with a shift in the vaginal microbiota away from the acidic Lactobacillus flora vaginal microbiota
to one with a higher pH and a greater mixture of species including more anaerobes. Over
the years several of these newcomers have been tagged as the cause of BV, particularly

FIGURE 1–4. Vaginal flora. Vaginal

Gram smear showing budding yeast
(long arrow), epithelial cells (short
arrow) and a mixture of other bacterial
morphologies. The long gram-positive
rods are most likely lactobacilli.
[Redrawn from Centers for Disease
Control and Prevention (CDC).]

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 12 PART I INFECTION
Flora that reach sterile sites may
cause disease
Virulence factors increase the
opportunity for invasion
Mouth flora plays a major role in
dental caries
Competing with pathogens has a
protective effect
Antibiotic therapy may provide
a competitive advantage for
pathogens
Sterile animals have little
immunity to microbial infection
Low exposure correlates with
asthma risk
Intestinal lactobacilli may protect
against diarrheal agents
Ryan_ch01_p0001-0018.indd 12
­ ardnerella vaginalis and Mobiluncus. The BV situation appears to be more complex than
G
this, involving complex interactions of the vaginal microbiota.
ROLES IN HEALTH AND DISEASE
●● Opportunistic Infection
Many species among the microbiota are opportunists in that they can cause infection when
they reach protected areas of the body in sufficient numbers. For example, certain strains of
E coli can reach the urinary bladder by ascending the urethra and cause acute urinary tract
infection. Perforation of the colon from a ruptured diverticulum or a penetrating abdomi-
nal wound releases feces into the peritoneal cavity; this contamination may be followed by
peritonitis or intraabdominal abscesses caused by members of the flora which have virulence
factors allowing them to exploit this situation. There are now examples of the microbiota
supplying a step in the pathogenesis of a classic pathogen. Attachment of Neisseria gonor-
rhoeae to the cervix has been shown to be enhanced when an enzyme produced by the cer-
vicovaginal microbiota unmasks a crucial receptor (see Chapter 30). Caries and periodontal
disease are caused by organisms that are members of the oral microbiota (see Chapter 41).
●● Exclusionary Effect
Balancing the prospect of opportunistic infection is the tendency of the resident microbiota
to produce conditions that compete with extraneous newcomers who happen to be patho-
gens and thus reduce their ability to establish a niche in the host. The microbiota in the
colon of the breastfed infant produces an environment inimical to colonization by enteric
pathogens, as does a vaginal flora dominated by lactobacilli. The benefit of this exclusion-
ary effect has been demonstrated by what happens when it is removed. Antibiotic therapy,
particularly with broad-spectrum agents, may so alter the microbiota of the gastrointesti-
nal tract that antibiotic-resistant organisms multiply in the ecologic vacuum. Under these
conditions, the spore-forming Clostridium difficile has a selective advantage that allows it to
survive, proliferate, and produce a toxic colitis.
●● Priming of Immune System
Organisms of the microbiota play an important role in the development of immunologic
competence. Animals delivered and raised under completely aseptic conditions (“sterile”
or gnotobiotic animals) have a poorly developed reticuloendothelial system, low serum
levels of immunoglobulins, and lack antibodies to antigens that often confer a degree of
protection against pathogens. There is evidence of immunologic differences between chil-
dren who are raised under usual conditions and those whose exposure to diverse flora is
minimized. Some studies have found a higher incidence of immunopathologic states, such
as asthma in the more isolated children.
PROMOTING A GOOD MICROBIOTA
The field of probiotics is based on the notion that we can manipulate the microbiota by pro-
moting colonization with “good” bacteria. Elie Metchnikoff originally suggested this in his
observation that the longevity of Bulgarian peasants was attributable to their consumption
of large amounts of yogurt; the live lactobacilli in the yogurt presumably replaced the colonic
flora to the general benefit of their health. This notion persists today in capsules contain-
ing freeze-dried lactobacilli sold by the sizable probiotics industry and by promotion of the
health benefit of natural (unpasteurized) yogurt, which contains live lactobacilli. Because
these lactobacilli are adapted to food and not the intestine, they are unlikely to persist, much
less replace, the typical microbiota of the adult colon. In some clinical studies, administration
of preparations containing a particular strain of Lactobacillus (Lactobacillus rhamnosus strain
GG, LGG) has been shown to reduce the duration of rotavirus diarrhea in children. The use of
similar preparations to prevent relapses of antibiotic-associated d­ iarrhea caused by C difficile
has shown little success but fecal transplant (a whole new microbiota) has blocked recur-
rences of pseudomembranous colitis, the most serious form of this disease.
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 CHAPTER 1 I N F E C T I O N — B A S I C CO N C E P T S 13

Research into the role of the microbiota in health and disease is one of the most exciting
topics in science. This is by no means limited to topics related to infectious disease. Cur-
rently the most active areas involve mechanisms of obesity, autoimmune disorders (arthri-
tis, asthma) and more subjective subjects like human cravings. Much of the work involves
the interactions between multiple species many of which can only be detected by genomic
methods. Obviously, it is going to take considerable time to sort these relationships out.

INFECTIOUS DISEASE
Of the thousands of species of viruses, bacteria, fungi, and parasites, only a tiny portion
is involved in disease of any kind. These are called pathogens. There are plant pathogens,
animal pathogens, and fish pathogens, as well as the subject of this book, human pathogens.
Among pathogens, there are degrees of potency called virulence, which sometimes makes Pathogens are rare
drawing the dividing line between benign and virulent microorganisms difficult. Pathogens
are associated with disease with varying frequency and severity. Yersinia pestis, the cause of Virulence varies greatly
plague, causes fulminant disease and death in 50% to 75% of persons who come in contact
with it. Therefore, it is highly virulent. Understanding the basis of these differences in viru-
lence is a fundamental goal of this book. The better students of medicine understand how a
pathogen causes disease, the better they will be prepared to intervene and help their patients.
For any pathogen, the basic aspects of how it interacts with the host to produce disease
can be expressed in terms of its epidemiology, pathogenesis, and immunity. Usually, our
knowledge of one or more of these topics is incomplete. It is the task of the physician to
relate these topics to the clinical aspects of disease and be prepared for new developments
which clarify, or in some cases, alter them. We do not know everything, and not all of what
we believe we know is correct.

EPIDEMIOLOGY
Epidemiology is the “who, what, when, and where” of infectious diseases. The power of the
science of epidemiology was first demonstrated by Semmelweis, who by careful analysis of
statistical data alone determined how streptococcal puerperal fever is transmitted. He even
devised a means to prevent transmission (handwashing) decades before the organism itself
(Streptococcus pyogenes) was discovered. Since then, each organism has built its own profile
of vital statistics. Some agents are transmitted by air, some by food, and others by insects;
many spread by the person-to-person route. Figure 1–5 presents some of the variables in Each agent has its own mode of
this regard. Some agents occur worldwide, and others only in certain geographic locations spread
or ecologic circumstances. Knowing how an organism gains access to its victim and spreads
is crucial to understanding the disease. It is also essential in discovering the emergence
of “new” diseases, whether they are truly new (HIV/AIDS) or just recently discovered
(Legionnaires disease). Solving mysterious outbreaks or recognizing new epidemiologic
patterns have often pointed the way to the isolation of new agents.
Epidemic spread and disease are facilitated by malnutrition, poor socioeconomic condi-
tions, natural disasters, and hygienic inadequacy. Epidemics, caused by the introduction of
new organisms of unusual virulence, often result in high morbidity and mortality rates. We
are currently witnessing a new and extended Zika virus pandemic, but the prospect of recur-
rence of old pandemic infections (influenza, cholera) remains. Modern times and technol-
Poor socioeconomic conditions
ogy have introduced new wrinkles to epidemiologic spread. Air travel has allowed diseases
foster infection
to leap continents even when they have very short incubation periods. The efficiency of the
food industry has sometimes backfired when the distributed products are contaminated with
Modern society may facilitate
infectious agents. The outbreaks of hamburger-associated E coli O157:H7 bloody diarrhea
spread
and hemolytic uremic syndrome are an example. The nature of massive meat-packing facili-
ties allowed organisms from infected cattle on isolated farms to be mixed with other meat and
distributed rapidly and widely. By the time outbreaks were recognized, cases of disease were
widespread, and tons of meat had to be recalled. In simpler times, local outbreaks from the
same source might have been detected and contained more quickly.
Of course, the most ominous and uncertain epidemiologic threat of these times is not
amplification of natural transmission but the specter of unnatural, deliberate spread.
Anthrax is a disease uncommonly transmitted by direct contact with animals or animal

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 14 PART I INFECTION
FIGURE 1–5. Infection overview.
The sources and potential sites of
infection are shown. Infection may be
endogenous from the internal flora or
exogenous from the sources shown
around the outside.
Anthrax and smallpox are new
bioterrorism threats
Pathogenicity is multifactorial
Pathogens have molecules that
bind to host cells
Invasion requires adaptation to
new environments
Ryan_ch01_p0001-0018.indd 14
Skin
Capillary
Respiratory tract
Alimentary tract
Scratch, injury
products. Under natural conditions, it produces a nasty, but not usually life-threatening,
ulcer. The inhalation of human-produced aerosols of anthrax spores could produce a lethal
pneumonia on a massive scale. Smallpox is the only disease officially eradicated from the
world. It took place sufficiently long ago that most of the population has never been exposed
or immunized and is, thus, vulnerable to its reintroduction. We do not know whether infec-
tious bioterrorism will work on the scale contemplated by its perpetrators; however, in the
case of anthrax, we do know that sophisticated systems have been designed to attempt it.
We hope never to learn whether bioterrorism will work on a large scale.
PATHOGENESIS
When a potential pathogen reaches its host, features of the organism determine whether or
not disease ensues. The primary reason pathogens are so few in relation to the microbial
world is that being successful at producing disease is a very complicated process. Multiple
features, called virulence factors, are required to persist, cause disease, and escape to repeat
the cycle. The variations are many, but the mechanisms used by many pathogens have now
been dissected at the molecular level.
The first step for any pathogen is to attach and persist at whatever site it gains access. This
usually involves specialized surface molecules or structures that correspond to receptors
on human cells. Because human cells were not designed to receive the microorganisms, the
pathogens are often exploiting some molecule important for some other essential function
of the cell. For some toxin-producing pathogens, this attachment alone may be enough to
produce disease. For most pathogens, it just allows them to persist long enough to proceed
to the next stage—invasion into or beyond the surface mucosal cells. For viruses, invasion
of cells is essential, because they cannot replicate on their own. Invading pathogens must
also be able to adapt to a new milieu. For example, the nutrients and ionic environment of
the cell surface differs from that inside the cell or in the submucosa. Some of the steps in
pathogenesis at the cellular level are illustrated in Figure 1–6.
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 CHAPTER 1 I N F E C T I O N — B A S I C CO N C E P T S 15

Pore-forming toxin

Viral receptors Viral entry Injection

Bacterial attachment
secretion system

Viral attachment Cytoskeleton

alterations

Viral Secreted
DNA/RNA Bacterial
invasion proteins

Virus-directed
synthesis

New viral
particles

Bloodstream invasion

FIGURE 1–6. Infection cellular view. Left. A virus is attaching to the cell surface but can replicate
only within the cell. Middle. A bacterial cell attaches to the surface, invades, and spreads through the
cell to the bloodstream. Right. A bacterial cell attaches and injects proteins into the cell. The cell is
disrupted while the organism remains on the surface.

Persistence and even invasion do not necessarily translate immediately to disease. The
invading organisms must disrupt function in some way. For some, the inflammatory
response they stimulate is enough. For example, a lung alveolus filled with neutrophils
responding to the presence of S pneumoniae loses its ability to exchange oxygen. The lon-
Inflammation alone can result in
ger a pathogen can survive in the face of the host response, the greater the compromise in
injury
host function. Most pathogens do more than this. Destruction of host cells through the
production of digestive enzymes, toxins, or intracellular multiplication is among the more
Cells may be destroyed or their
common mechanisms. Other pathogens operate by altering the function of a cell without
function altered
injury. Diphtheria is caused by a bacterial toxin that blocks protein synthesis inside the host
cell. Details of the molecular mechanism for this action are illustrated in Figure 1–7. Some
viruses cause the insertion of molecules in the host cell membrane, which cause other host
cells to attack it. The variations are diverse and fascinating.

IMMUNITY
Although the science of immunology is beyond the scope of this book, understanding the
immune response to infection (see Chapter 2) is an important part of appreciating patho-
genic mechanisms. In fact, one of the most important virulence attributes any pathogen
can have is an ability to neutralize the immune response to it in some way. Some patho-
Evading the immune response is
gens attack the immune effector cells, and others undergo changes that evade the immune
a major feature of virulence
response. The old observation that there seems to be no immunity to gonorrhea turns out
to be an example of the latter mechanism. Neisseria gonorrhoeae, the causative agent of
gonorrhea, undergoes antigenic variation of important surface structures so rapidly that
antibodies directed against the bacteria become irrelevant.
For each pathogen, the primary interest is whether there is natural immunity and, if so,
whether it is based on cell-mediated (TH1, CMI) or humoral (TH2, antibody) mechanisms.

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 16 PART I INFECTION

Diphtheria toxin
A
Receptor for toxin B
Receptor-mediated
endocytosis

A
Cell membrane
B

Active subunit
of toxin
A
B

AA Polypeptide ADP-ribosylated
AA chain (inactive) EF2
AA AA Aminoacyl-tRNA
EF2
ADPR

Ribosome Elongation

EF2

Acceptor site

mRNA

Donor site
FIGURE 1–7. Action of diphtheria toxin, molecular view. The toxin-binding (B) portion
attaches to the cell membrane, and the complete molecule enters the cell. In the cell, the A subunit
dissociates and catalyzes a reaction that ADP-ribosylates (ADPR) and, thus, inactivates elongation
factor 2 (EF-2). This factor is essential for ribosomal reactions at the acceptor and donor sites, which
transfer triplet code from messenger RNA (mRNA) to amino acid sequences via transfer RNA (tRNA).
Inactivation of EF-2 stops building of the polypeptide chain.

Antibody or cell-mediated
mechanisms may be protective
Humoral and CMI responses are broadly stimulated with most infections, but the specific
response to a particular molecular structure is usually dominant in mediating immunity
to reinfection. For example, the repeated nature of strep throat (group A streptococcus) in
childhood is not due to antigenic variation as described for gonorrhea. The antigen against
which protective antibodies are directed (M protein) is stable, but naturally exists in more
than 80 types. Each type requires its own specific antibody. Knowing the molecule against
which the protective immune response is directed is particularly important for devising
preventive vaccines.

CLINICAL ASPECTS OF INFECTIOUS DISEASE

●● Manifestations
Fever, pain, and swelling are the universal signs of infection. Beyond this, the particular
organs involved and the speed of the process dominate the signs and symptoms of disease.

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 CHAPTER 1 I N F E C T I O N — B A S I C CO N C E P T S 17

Cough, diarrhea, and mental confusion represent disruption of three different body
s­ystems. On the basis of clinical experience, physicians have become familiar with the
range of behavior of the major pathogens. However, signs and symptoms overlap consider- Body system(s) involved dictate
ably. Skilled physicians use this knowledge to begin a deductive process leading to a list of clinical findings
suspected pathogens and a strategy to make a specific diagnosis and provide patient care.
Through the probability assessment, an understanding of how the diseases work is a distinct
advantage in making the correct decisions.

●● Diagnosis
A major difference between infectious and other diseases is that the probabilities just
described can be specifically resolved, often overnight. Most microorganisms can be
isolated from the patient, grown in artificial culture, and identified. Others can be seen
microscopically or detected by measuring the specific immune response to the pathogen.
Disease-causing microbes can be
Preferred modalities for diagnosis of each agent have been developed and are available in
grown and identified
clinic, hospital, and public health laboratories all over the world. Empiric diagnosis made
on the basis of clinical findings can be confirmed and the treatment plan modified accord-
ingly. New methods which detect molecular or genomic markers of the agent are now real-
izing their potential for rapid, specific diagnosis.

●● Treatment
Over the past 80 years, therapeutic tools of remarkable potency and specificity have become
available for the treatment of bacterial infections. These include all the antibiotics and an
array of synthetic chemicals that kill or inhibit the infecting organism, but have minimal
or acceptable toxicity for the host. Antibacterial agents exploit the structural and metabolic
differences between microbial and human eukaryotic cells to provide the selectivity neces-
Antibiotics are directed at
sary for good antimicrobial therapy. Penicillin, for example, interferes with the synthesis
structures of bacteria not present
of the bacterial cell wall, a structure that has no analog in human cells. There are fewer
in host
antifungal and antiprotozoal agents because the eukaryotic cells of the host and those of
the parasite have metabolic and structural similarities. Nevertheless, hosts and parasites do
have some significant differences, and effective therapeutic agents have been discovered or
developed to exploit them.
Specific therapeutic attack on viral disease has posed more complex problems, because
of the intimate involvement of viral replication with the metabolic and replicative activities
of the cell. However, recent advances in molecular virology have identified specific viral
targets that can be attacked. Scientists have developed successful antiviral agents, including Antivirals target unique
those that interfere with the liberation of viral nucleic acid from its protective protein coat virus-coded enzymes
or with the processes of viral nucleic acid synthesis and replication. The successful develop-
ment of new agents for human immunodeficiency virus has involved targeting enzymes
coded by the virus genome.
The success of the “antibiotic era” has been clouded by the development of resistance by
the organisms. The mechanisms involved are varied but, most often, involve a mutational
alteration in the enzyme, ribosome site, or other target against which the antimicrobial is
Resistance complicates therapy
directed. In some instances, organisms acquire new enzymes or block entry of the antimi-
crobial to the cell. Many bacteria produce enzymes that directly inactivate antibiotics. To
Mechanisms include mutation
make the situation worse, the genes involved are readily spread by promiscuous genetic
and inactivation
mechanisms. New agents that are initially effective against resistant strains have been devel-
oped, but resistance by new mechanisms usually follows. The battle is by no means lost, but
has become a never-ending policing action.

●● Prevention
The goal of the scientific study of any disease is its prevention. In the case of infectious
diseases, this has involved public health measures and immunization. The public health
measures depend on knowledge of transmission mechanisms and on interfering with them. Public health and immunization
Water disinfection, food preparation, insect control, handwashing, and a myriad of other are primary preventive measures
measures prevent humans from coming in contact with infections agents. Immunization
relies on knowledge of immune mechanisms and designing vaccines that stimulate protec-
tive immunity.

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 18 PART I INFECTION

Attenuated strains stimulate
immunity
Live vaccines rarely cause disease
Purified components are safe
vaccines
Vaccines can be genetically
engineered
Immunization follows two major strategies—live vaccines and inactivated vaccines. The
former uses live organisms that have been modified (attenuated) so they do not produce
disease, but still stimulate a protective immune response. Such vaccines have been effec-
tive, but carry the risk that the vaccine strain itself may cause disease. This event has been
observed with the live oral polio vaccine. Although this rarely occurs, it has caused a shift
back to the original Salk inactivated vaccine. This issue has reemerged with a debate over
strategies for the use of smallpox immunization to protect against bioterrorism. This vac-
cine uses vaccinia virus, a cousin of smallpox, and its potential to produce disease on its
own has been recognized since its original use by Jenner in 1798. Serious disease would be
expected primarily in immunocompromised individuals (eg, from cancer chemotherapy
or AIDS), who represent a significantly larger part of the population than when smallpox
immunization was stopped in the 1970s. Could immunization cause more disease than it
prevents? Despite the claims of those who oppose the use of all vaccines as “unnatural” the
risk/benefit ratio of all currently licensed vaccines is greatly on the positive side.
The safest immunization strategy is the use of organisms that have been killed or, better
yet, killed and purified to contain only the immunizing component. This approach requires
much better knowledge of pathogenesis and immune mechanisms. Vaccines for meningitis
use the polysaccharide capsule of the bacterium, and vaccines for diphtheria and tetanus
use only a formalin-inactivated protein toxin. Pertussis (whooping cough) immunization
has undergone a transition in this regard. The original killed whole-cell vaccine was effec-
tive, but caused a significant incidence of side effects. A purified vaccine containing pertus-
sis toxin and a few surface components has reduced side effects, but its efficacy compared
with the previous vaccine is now in question.
The newest approaches for vaccines require neither live organisms nor killed, purified
ones. As the entire genomes of more and more pathogens are being reported, an entirely
genetic strategy is emerging. Armed with knowledge of molecular pathogenesis and immu-
nity and the tools of genomics and proteomics, scientists can now synthesize an immuno-
genic protein without ever growing the organism itself. Such an idea would have astonished
even the great microbiologists of the last two centuries.

SUMMARY
Infectious diseases remain as important and fascinating as ever. Where else do we find
the emergence of new diseases, together with improved understanding of the old ones?
At a time when the revolution in molecular biology and genetics has brought us to the
threshold of new and novel means of infection control, the perpetrators of bioterrorism
threaten us with diseases we have already conquered. Meeting this challenge requires a
secure knowledge of the pathogenic organisms and how they produce disease, as well
as an understanding of the clinical aspects of these diseases. In the collective judgment
of the authors, this book presents the principles and facts required for students of medi-
cine to understand the most important infectious diseases.

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 2
Immune Response to
Infection
Within a very short period immunity has been placed in possession not only of a host of medical ideas of the highest
­importance, but also of effective means of combating a whole series of maladies of the most formidable nature in man and
domestic animals.

—Elie Metchnikoff, 1905

T
he “maladies” Metchnikoff and the other pioneers of immunology were fighting
infections and, for decades, their field was defined in terms of the immune response
to infection. We now understand that the immune system is as much a part of every-
day human biologic function as the cardiovascular or renal systems. In its adaptive and
disordered states, infectious diseases are only one of the major player along with cancer and
autoimmune diseases. Students of medicine take up immunology as a separate unit with its
own text covering the field broadly. This chapter is not intended to fulfill that function, or
to be a shortened but comprehensive version of those sources. It is included as an overview
of aspects related to infection for other students and as an internal reference for topics that
reappear in later pages of this book. These include some of the greatest successes of medical
science. The early and continuing development of vaccines that prevent and potentially elimi-
nate diseases is but one example. In addition, knowledge of the immune response to infection
is integral to understanding the pathogenesis of infectious diseases. It turns out that one of
the main attributes of a successful pathogen is evading or confounding the immune system.
The immune response to infection is presented as two major components—innate
immunity and adaptive immunity. The primary effectors of both are cells that are part
of the white blood cell series derived from hematopoietic stem cells in the bone marrow
(­ Figure 2–1). Innate immunity includes the role of physical, cellular, and chemical systems
that are in place and that respond to all aspects of foreignness. These include mucosal bar-
riers, phagocytic cells, and the action of circulating glycoproteins such as complement. The
adaptive side is sometimes called specific immunity because it has the ability to develop
new responses that are highly specific to molecular components of infectious agents, called
antigens. These encounters trigger the development of new cellular responses and produc-
tion of circulating antibody, which have a component of memory if the invader returns.
Artificially creating this memory is, of course, the goal of vaccines.

INNATE (NATURAL) IMMUNITY

Innate immunity acts through a series of specific and nonspecific mechanisms, all working
to create a series of hurdles for the pathogen to navigate (Table 2–1). The first are mechani- Skin, mucosa are barriers
cal barriers such as the tough multilayered skin or the softer but fused mucosal layers of
internal surfaces. As discussed in Chapter 1, the microbiota on these surfaces presents for- Cells engulf, digest, and present
midable competition for space and nutrients. Turbulent movement of the mucosal surfaces antigens from microbes
and enzymes or acid secreted on their surface make it difficult for an organism to persist.

19

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 20 PART I INFECTION

Hematopoietic
stem cell
(in bone marrow)

Myeloid stem cell

Lymphoid
stem cell
Natural killer
(NK) cells

Erythroblast Megakaryoblast Putative Myeloblast Monoblast Lymphoblasts

mast cell
precursor

White blood cells (leukocytes)

Megakaryocyte

Granulocytes Agranulocytes

T B

Monocytes Lymphocytes
Essential blood phagocytes;

and inflammatory reactions

active engulfers and killers

Blood phagocytes that Primary cells involved in

Function in inflammatory

fungal infections, allergy,

Involved in blood clotting

rapidly leave the circulation; specific immune reactions

events and allergies

mature into macrophages to foreign matter

Active in worm and
Carry O2 and CO2

and dendritic cells

and inflammation

T cells
Red blood cells

Eosinophils

Perform a number of specific

Neutrophils

Basophils
of bacteria

cellular immune responses

Platelets

such as assisting B cells and

killing foreign cells (cell-
mediated immunity)

Macrophages B cells
Largest phagocytes that Differentiate into plasma cells
ingest and kill foreign cells; and form antibodies (humoral
strategic participants in immunity)
certain specific immune
Mast cells reactions
Specialized tissue cells
similar to basophils that Dendritic cells
trigger local inflammatory Relatives of macrophages that
reactions and are responsible reside throughout the tissues
for many allergic symptoms and reticuloendothelial system;
responsible for processing
foreign matter and presenting
it to lymphocytes
FIGURE 2–1. Human blood cells. Stem cells in the bone marrow divide to form two blood
cell lineages: (1) the lymphoid stem cell gives rise to B cells that become antibody-secreting
plasma cells, T cells that become activated T cells, and natural killer cells. (2) The common myeloid
progenitor cell gives rise to granulocytes and monocytes that give rise to macrophages and
dendritic cells. (Reproduced with permission from Willey JM: Prescott, Harley, & Klein’s Microbiology,
7th edition. McGraw-Hill, 2008.)

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 CHAPTER 2 I M M U N E R E S P O N S E TO I N F E C T I O N 21

TABLE 2–1    Features of Innate Immunity in Infection

ACTIVITY AGAINST
LOCATION PATHOGENS
Cells
Macrophage Circulation, tissues Phagocytosis, digestion
Dendritic cell Tissues Phagocytosis, digestion
Polymorphonuclear Circulation, tissues (by Phagocytosis, digestion
n
­ eutrophil (PMN) migration)
M cell Mucus membranes Endocytosis and delivery to
phagocytes
Surface Receptors
Lectin Phagocyte Recognize carbohydrates
Arginine-glycine-arginine Phagocyte Recognize arginine-glycine-
(RGD) aspartic acid sequence
Toll-like receptor (TLR) Phagocyte Recognizes PAMP, such
as bacterial LPS (TLR-4),
p
­ eptidoglycana (TLR-2)
Inflammation
Selectins Endothelium Attract and attach PMNs
Integrins PMNs Attach to selectins
Kallikrein Extracellular fluid Release bradykinin,
prostaglandins
Chemical Mediators
Cathelicidin PMNs, macrophages, Ionic membrane pores
e
­ pithelial cells
Defensins PMN granules Ionic membrane pores
Complement (classical, Serum, extracellular fluid Membrane pores, phagocyte
a­ lternative, lectin) receptors

LPS, lipopolysaccharide of gram-negative bacterial outer membrane; PAMP, pathogen-associated molecular

pattern.
a
Cell wall component of gram-positive and gram-negative bacteria.

Organisms that are able to pass the mucosa encounter a population of cells with the ability
to engulf and destroy them. In addition, body fluids contain chemical agents such as com-
plement, which can directly injure the microbe. The entire process has cross-links to the
adaptive immune system. The endpoint of phagocytosis and digestion in a macrophage is
the presentation of the antigen on its surface; the first step in specific immune recognition.

PHYSICAL BARRIERS
The thick layers of the skin containing insoluble keratins present the most formidable
­barrier to infection. The mucosal membranes of the alimentary and urogenital tract are
not as tough but, often, are bathed in secretions inhospitable to invaders. Lysozyme is an
enzyme that digests peptidoglycan—a unique structural component of the bacterial cell Lysozyme digests bacterial walls
wall. Lysozyme is secreted onto many surfaces and is particularly concentrated in conjunc-
tival tears. The acid pH of the vagina and particularly the stomach makes colonization dif- Cilia move particles away from
ficult for most organisms. Only small particles (5-10 μm) can be inhaled deep into the lung pulmonary alveoli
alveoli because the lining of the respiratory tract includes cilia that trap and move them
back toward the pharynx.
The skin and mucosal surfaces of the intestinal and respiratory tract also contain concen-
trations of lymphoid tissue within or just below their surfaces, which provide a next-level
defense for invaders surviving the above described barriers. These lymphoid collections are

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 22 PART I INFECTION
B cell
M cells deliver to macrophages
and lymphocytes
Stem cells differentiate to
myeloid and lymphoid series
Thymus, spleen, and lymph
nodes are immune organs
Surface receptors recognize
uniquely microbial PAMPs
Ryan_ch02-p0019-0042.indd 22
Mucous
Bacteria membrane
M cell
Epithelial
Bacteria
cell
Pocket
Macrophage
HeIper T cell
FIGURE 2–2. M cell. An M cell is shown between two epithelial cells in a mucous membrane. It has
endocytosed a pathogen and released it into a pocket containing macrophages and other immune
cells.
designed to entrap and deliver invaders to some of the phagocytes described in the follow-
ing text. For example, in the intestine, M cells (Figure 2–2) that lack the villous brush bor-
der of their neighbors endocytose bacteria and then release them into a pocket containing
macrophages and lymphocytic components (T and B cells) of the adaptive immune system.
The enteric pathogen Shigella exploits this receptiveness of the M cell to attack the adjacent
enterocytes from the side.
IMMUNORESPONSIVE CELLS AND ORGANS
Not all the cells shown in Figure 2–1 are involved in the immune system; of those that
are, not all respond to infection. What the immunoresponsive cells have in common is
derivation from hematopoietic stem cells in the bone marrow, which create the myeloid
and lymphoid series followed by further differentiation into their mature cell types. Of the
types shown, the erythroblast and megakaryocyte do not participate in immune reactions.
In the myeloid series, basophils and mast cells are primarily involved in allergic reactions
rather than infection. The immunoresponsive cells are found throughout the body in the
circulation or at fixed locations in tissues. They are concentrated in the lymph nodes and
spleen, and form a unified filtration network designed as a sentinel warning system. In the
lymphoid series, cells destined to become T cells mature in the thymus (the source of their
name). Thus, the thymus, spleen, and lymph nodes might be thought of as the organs of the
immune system. These are collectively referred to as the lymphoid tissues.
●● Cellular Receptors for Microbes
Fixed and circulating phagocytes express surface receptors which recognize a limited array
of uniquely microbial structures based on the pattern of their molecular structure. These
pathogen-associated molecular patterns (PAMPs) include bacterial cell wall peptidoglycan,
the lipopolysaccharide endotoxin of gram-negative bacteria, mannose and other glyco-
proteins, lipids and polysaccharides. Nucleic acids are also recognized such as the double-
stranded RNA found in many viruses. These PAMP-recognizing receptors may be found
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 DANCE ON STILTS AT THE GIRLS’ UNYAGO, NIUCHI

Newala, too, suffers from the distance of its water-supply—at least

the Newala of to-day does; there was once another Newala in a lovely
valley at the foot of the plateau. I visited it and found scarcely a trace
of houses, only a Christian cemetery, with the graves of several
missionaries and their converts, remaining as a monument of its
former glories. But the surroundings are wonderfully beautiful. A
thick grove of splendid mango-trees closes in the weather-worn
crosses and headstones; behind them, combining the useful and the
agreeable, is a whole plantation of lemon-trees covered with ripe
fruit; not the small African kind, but a much larger and also juicier
imported variety, which drops into the hands of the passing traveller,
without calling for any exertion on his part. Old Newala is now under
the jurisdiction of the native pastor, Daudi, at Chingulungulu, who,
as I am on very friendly terms with him, allows me, as a matter of
course, the use of this lemon-grove during my stay at Newala.
 FEET MUTILATED BY THE RAVAGES OF THE “JIGGER”
(Sarcopsylla penetrans)

The water-supply of New Newala is in the bottom of the valley,

some 1,600 feet lower down. The way is not only long and fatiguing,
but the water, when we get it, is thoroughly bad. We are suffering not
only from this, but from the fact that the arrangements at Newala are
nothing short of luxurious. We have a separate kitchen—a hut built
against the boma palisade on the right of the baraza, the interior of
which is not visible from our usual position. Our two cooks were not
long in finding this out, and they consequently do—or rather neglect
to do—what they please. In any case they do not seem to be very
particular about the boiling of our drinking-water—at least I can
attribute to no other cause certain attacks of a dysenteric nature,
from which both Knudsen and I have suffered for some time. If a
man like Omari has to be left unwatched for a moment, he is capable
of anything. Besides this complaint, we are inconvenienced by the
state of our nails, which have become as hard as glass, and crack on
the slightest provocation, and I have the additional infliction of
pimples all over me. As if all this were not enough, we have also, for
the last week been waging war against the jigger, who has found his
Eldorado in the hot sand of the Makonde plateau. Our men are seen
all day long—whenever their chronic colds and the dysentery likewise
raging among them permit—occupied in removing this scourge of
Africa from their feet and trying to prevent the disastrous
consequences of its presence. It is quite common to see natives of
this place with one or two toes missing; many have lost all their toes,
or even the whole front part of the foot, so that a well-formed leg
ends in a shapeless stump. These ravages are caused by the female of
Sarcopsylla penetrans, which bores its way under the skin and there
develops an egg-sac the size of a pea. In all books on the subject, it is
stated that one’s attention is called to the presence of this parasite by
an intolerable itching. This agrees very well with my experience, so
far as the softer parts of the sole, the spaces between and under the
toes, and the side of the foot are concerned, but if the creature
penetrates through the harder parts of the heel or ball of the foot, it
may escape even the most careful search till it has reached maturity.
Then there is no time to be lost, if the horrible ulceration, of which
we see cases by the dozen every day, is to be prevented. It is much
easier, by the way, to discover the insect on the white skin of a
European than on that of a native, on which the dark speck scarcely
shows. The four or five jiggers which, in spite of the fact that I
constantly wore high laced boots, chose my feet to settle in, were
taken out for me by the all-accomplished Knudsen, after which I
thought it advisable to wash out the cavities with corrosive
sublimate. The natives have a different sort of disinfectant—they fill
the hole with scraped roots. In a tiny Makua village on the slope of
the plateau south of Newala, we saw an old woman who had filled all
the spaces under her toe-nails with powdered roots by way of
prophylactic treatment. What will be the result, if any, who can say?
The rest of the many trifling ills which trouble our existence are
really more comic than serious. In the absence of anything else to
smoke, Knudsen and I at last opened a box of cigars procured from
the Indian store-keeper at Lindi, and tried them, with the most
distressing results. Whether they contain opium or some other
narcotic, neither of us can say, but after the tenth puff we were both
“off,” three-quarters stupefied and unspeakably wretched. Slowly we
recovered—and what happened next? Half-an-hour later we were
once more smoking these poisonous concoctions—so insatiable is the
craving for tobacco in the tropics.
Even my present attacks of fever scarcely deserve to be taken
seriously. I have had no less than three here at Newala, all of which
have run their course in an incredibly short time. In the early
afternoon, I am busy with my old natives, asking questions and
making notes. The strong midday coffee has stimulated my spirits to
an extraordinary degree, the brain is active and vigorous, and work
progresses rapidly, while a pleasant warmth pervades the whole
body. Suddenly this gives place to a violent chill, forcing me to put on
my overcoat, though it is only half-past three and the afternoon sun
is at its hottest. Now the brain no longer works with such acuteness
and logical precision; more especially does it fail me in trying to
establish the syntax of the difficult Makua language on which I have
ventured, as if I had not enough to do without it. Under the
circumstances it seems advisable to take my temperature, and I do
so, to save trouble, without leaving my seat, and while going on with
my work. On examination, I find it to be 101·48°. My tutors are
abruptly dismissed and my bed set up in the baraza; a few minutes
later I am in it and treating myself internally with hot water and
lemon-juice.
Three hours later, the thermometer marks nearly 104°, and I make
them carry me back into the tent, bed and all, as I am now perspiring
heavily, and exposure to the cold wind just beginning to blow might
mean a fatal chill. I lie still for a little while, and then find, to my
great relief, that the temperature is not rising, but rather falling. This
is about 7.30 p.m. At 8 p.m. I find, to my unbounded astonishment,
that it has fallen below 98·6°, and I feel perfectly well. I read for an
hour or two, and could very well enjoy a smoke, if I had the
wherewithal—Indian cigars being out of the question.
Having no medical training, I am at a loss to account for this state
of things. It is impossible that these transitory attacks of high fever
should be malarial; it seems more probable that they are due to a
kind of sunstroke. On consulting my note-book, I become more and
more inclined to think this is the case, for these attacks regularly
follow extreme fatigue and long exposure to strong sunshine. They at
least have the advantage of being only short interruptions to my
work, as on the following morning I am always quite fresh and fit.
My treasure of a cook is suffering from an enormous hydrocele which
makes it difficult for him to get up, and Moritz is obliged to keep in
the dark on account of his inflamed eyes. Knudsen’s cook, a raw boy
from somewhere in the bush, knows still less of cooking than Omari;
consequently Nils Knudsen himself has been promoted to the vacant
post. Finding that we had come to the end of our supplies, he began
by sending to Chingulungulu for the four sucking-pigs which we had
bought from Matola and temporarily left in his charge; and when
they came up, neatly packed in a large crate, he callously slaughtered
the biggest of them. The first joint we were thoughtless enough to
entrust for roasting to Knudsen’s mshenzi cook, and it was
consequently uneatable; but we made the rest of the animal into a
jelly which we ate with great relish after weeks of underfeeding,
consuming incredible helpings of it at both midday and evening
meals. The only drawback is a certain want of variety in the tinned
vegetables. Dr. Jäger, to whom the Geographical Commission
entrusted the provisioning of the expeditions—mine as well as his
own—because he had more time on his hands than the rest of us,
seems to have laid in a huge stock of Teltow turnips,[46] an article of
food which is all very well for occasional use, but which quickly palls
when set before one every day; and we seem to have no other tins
left. There is no help for it—we must put up with the turnips; but I
am certain that, once I am home again, I shall not touch them for ten
years to come.
Amid all these minor evils, which, after all, go to make up the
genuine flavour of Africa, there is at least one cheering touch:
Knudsen has, with the dexterity of a skilled mechanic, repaired my 9
× 12 cm. camera, at least so far that I can use it with a little care.
How, in the absence of finger-nails, he was able to accomplish such a
ticklish piece of work, having no tool but a clumsy screw-driver for
taking to pieces and putting together again the complicated
mechanism of the instantaneous shutter, is still a mystery to me; but
he did it successfully. The loss of his finger-nails shows him in a light
contrasting curiously enough with the intelligence evinced by the
above operation; though, after all, it is scarcely surprising after his
ten years’ residence in the bush. One day, at Lindi, he had occasion
to wash a dog, which must have been in need of very thorough
cleansing, for the bottle handed to our friend for the purpose had an
extremely strong smell. Having performed his task in the most
conscientious manner, he perceived with some surprise that the dog
did not appear much the better for it, and was further surprised by
finding his own nails ulcerating away in the course of the next few
days. “How was I to know that carbolic acid has to be diluted?” he
mutters indignantly, from time to time, with a troubled gaze at his
mutilated finger-tips.
 Since we came to Newala we have been making excursions in all
directions through the surrounding country, in accordance with old
habit, and also because the akida Sefu did not get together the tribal
elders from whom I wanted information so speedily as he had
promised. There is, however, no harm done, as, even if seen only
from the outside, the country and people are interesting enough.
The Makonde plateau is like a large rectangular table rounded off
at the corners. Measured from the Indian Ocean to Newala, it is
about seventy-five miles long, and between the Rovuma and the
Lukuledi it averages fifty miles in breadth, so that its superficial area
is about two-thirds of that of the kingdom of Saxony. The surface,
however, is not level, but uniformly inclined from its south-western
edge to the ocean. From the upper edge, on which Newala lies, the
eye ranges for many miles east and north-east, without encountering
any obstacle, over the Makonde bush. It is a green sea, from which
here and there thick clouds of smoke rise, to show that it, too, is
inhabited by men who carry on their tillage like so many other
primitive peoples, by cutting down and burning the bush, and
manuring with the ashes. Even in the radiant light of a tropical day
such a fire is a grand sight.
Much less effective is the impression produced just now by the
great western plain as seen from the edge of the plateau. As often as
time permits, I stroll along this edge, sometimes in one direction,
sometimes in another, in the hope of finding the air clear enough to
let me enjoy the view; but I have always been disappointed.
Wherever one looks, clouds of smoke rise from the burning bush,
and the air is full of smoke and vapour. It is a pity, for under more
favourable circumstances the panorama of the whole country up to
the distant Majeje hills must be truly magnificent. It is of little use
taking photographs now, and an outline sketch gives a very poor idea
of the scenery. In one of these excursions I went out of my way to
make a personal attempt on the Makonde bush. The present edge of
the plateau is the result of a far-reaching process of destruction
through erosion and denudation. The Makonde strata are
everywhere cut into by ravines, which, though short, are hundreds of
yards in depth. In consequence of the loose stratification of these
beds, not only are the walls of these ravines nearly vertical, but their
upper end is closed by an equally steep escarpment, so that the
western edge of the Makonde plateau is hemmed in by a series of
deep, basin-like valleys. In order to get from one side of such a ravine
to the other, I cut my way through the bush with a dozen of my men.
It was a very open part, with more grass than scrub, but even so the
short stretch of less than two hundred yards was very hard work; at
the end of it the men’s calicoes were in rags and they themselves
bleeding from hundreds of scratches, while even our strong khaki
suits had not escaped scatheless.

NATIVE PATH THROUGH THE MAKONDE BUSH, NEAR

MAHUTA

I see increasing reason to believe that the view formed some time
back as to the origin of the Makonde bush is the correct one. I have
no doubt that it is not a natural product, but the result of human
occupation. Those parts of the high country where man—as a very
slight amount of practice enables the eye to perceive at once—has not
yet penetrated with axe and hoe, are still occupied by a splendid
timber forest quite able to sustain a comparison with our mixed
forests in Germany. But wherever man has once built his hut or tilled
his field, this horrible bush springs up. Every phase of this process
may be seen in the course of a couple of hours’ walk along the main
road. From the bush to right or left, one hears the sound of the axe—
not from one spot only, but from several directions at once. A few
steps further on, we can see what is taking place. The brush has been
cut down and piled up in heaps to the height of a yard or more,
between which the trunks of the large trees stand up like the last
pillars of a magnificent ruined building. These, too, present a
melancholy spectacle: the destructive Makonde have ringed them—
cut a broad strip of bark all round to ensure their dying off—and also
piled up pyramids of brush round them. Father and son, mother and
son-in-law, are chopping away perseveringly in the background—too
busy, almost, to look round at the white stranger, who usually excites
so much interest. If you pass by the same place a week later, the piles
of brushwood have disappeared and a thick layer of ashes has taken
the place of the green forest. The large trees stretch their
smouldering trunks and branches in dumb accusation to heaven—if
they have not already fallen and been more or less reduced to ashes,
perhaps only showing as a white stripe on the dark ground.
This work of destruction is carried out by the Makonde alike on the
virgin forest and on the bush which has sprung up on sites already
cultivated and deserted. In the second case they are saved the trouble
of burning the large trees, these being entirely absent in the
secondary bush.
After burning this piece of forest ground and loosening it with the
hoe, the native sows his corn and plants his vegetables. All over the
country, he goes in for bed-culture, which requires, and, in fact,
receives, the most careful attention. Weeds are nowhere tolerated in
the south of German East Africa. The crops may fail on the plains,
where droughts are frequent, but never on the plateau with its
abundant rains and heavy dews. Its fortunate inhabitants even have
the satisfaction of seeing the proud Wayao and Wamakua working
for them as labourers, driven by hunger to serve where they were
accustomed to rule.
But the light, sandy soil is soon exhausted, and would yield no
harvest the second year if cultivated twice running. This fact has
been familiar to the native for ages; consequently he provides in
time, and, while his crop is growing, prepares the next plot with axe
and firebrand. Next year he plants this with his various crops and
lets the first piece lie fallow. For a short time it remains waste and
desolate; then nature steps in to repair the destruction wrought by
man; a thousand new growths spring out of the exhausted soil, and
even the old stumps put forth fresh shoots. Next year the new growth
is up to one’s knees, and in a few years more it is that terrible,
impenetrable bush, which maintains its position till the black
occupier of the land has made the round of all the available sites and
come back to his starting point.
The Makonde are, body and soul, so to speak, one with this bush.
According to my Yao informants, indeed, their name means nothing
else but “bush people.” Their own tradition says that they have been
settled up here for a very long time, but to my surprise they laid great
stress on an original immigration. Their old homes were in the
south-east, near Mikindani and the mouth of the Rovuma, whence
their peaceful forefathers were driven by the continual raids of the
Sakalavas from Madagascar and the warlike Shirazis[47] of the coast,
to take refuge on the almost inaccessible plateau. I have studied
African ethnology for twenty years, but the fact that changes of
population in this apparently quiet and peaceable corner of the earth
could have been occasioned by outside enterprises taking place on
the high seas, was completely new to me. It is, no doubt, however,
correct.
The charming tribal legend of the Makonde—besides informing us
of other interesting matters—explains why they have to live in the
thickest of the bush and a long way from the edge of the plateau,
instead of making their permanent homes beside the purling brooks
and springs of the low country.
“The place where the tribe originated is Mahuta, on the southern
side of the plateau towards the Rovuma, where of old time there was
nothing but thick bush. Out of this bush came a man who never
washed himself or shaved his head, and who ate and drank but little.
He went out and made a human figure from the wood of a tree
growing in the open country, which he took home to his abode in the
bush and there set it upright. In the night this image came to life and
was a woman. The man and woman went down together to the
Rovuma to wash themselves. Here the woman gave birth to a still-
born child. They left that place and passed over the high land into the
valley of the Mbemkuru, where the woman had another child, which
was also born dead. Then they returned to the high bush country of
Mahuta, where the third child was born, which lived and grew up. In
course of time, the couple had many more children, and called
themselves Wamatanda. These were the ancestral stock of the
Makonde, also called Wamakonde,[48] i.e., aborigines. Their
forefather, the man from the bush, gave his children the command to
bury their dead upright, in memory of the mother of their race who
was cut out of wood and awoke to life when standing upright. He also
warned them against settling in the valleys and near large streams,
for sickness and death dwelt there. They were to make it a rule to
have their huts at least an hour’s walk from the nearest watering-
place; then their children would thrive and escape illness.”
The explanation of the name Makonde given by my informants is
somewhat different from that contained in the above legend, which I
extract from a little book (small, but packed with information), by
Pater Adams, entitled Lindi und sein Hinterland. Otherwise, my
results agree exactly with the statements of the legend. Washing?
Hapana—there is no such thing. Why should they do so? As it is, the
supply of water scarcely suffices for cooking and drinking; other
people do not wash, so why should the Makonde distinguish himself
by such needless eccentricity? As for shaving the head, the short,
woolly crop scarcely needs it,[49] so the second ancestral precept is
likewise easy enough to follow. Beyond this, however, there is
nothing ridiculous in the ancestor’s advice. I have obtained from
various local artists a fairly large number of figures carved in wood,
ranging from fifteen to twenty-three inches in height, and
representing women belonging to the great group of the Mavia,
Makonde, and Matambwe tribes. The carving is remarkably well
done and renders the female type with great accuracy, especially the
keloid ornamentation, to be described later on. As to the object and
meaning of their works the sculptors either could or (more probably)
would tell me nothing, and I was forced to content myself with the
scanty information vouchsafed by one man, who said that the figures
were merely intended to represent the nembo—the artificial
deformations of pelele, ear-discs, and keloids. The legend recorded
by Pater Adams places these figures in a new light. They must surely
be more than mere dolls; and we may even venture to assume that
they are—though the majority of present-day Makonde are probably
unaware of the fact—representations of the tribal ancestress.
 The references in the legend to the descent from Mahuta to the
Rovuma, and to a journey across the highlands into the Mbekuru
valley, undoubtedly indicate the previous history of the tribe, the
travels of the ancestral pair typifying the migrations of their
descendants. The descent to the neighbouring Rovuma valley, with
its extraordinary fertility and great abundance of game, is intelligible
at a glance—but the crossing of the Lukuledi depression, the ascent
to the Rondo Plateau and the descent to the Mbemkuru, also lie
within the bounds of probability, for all these districts have exactly
the same character as the extreme south. Now, however, comes a
point of especial interest for our bacteriological age. The primitive
Makonde did not enjoy their lives in the marshy river-valleys.
Disease raged among them, and many died. It was only after they
had returned to their original home near Mahuta, that the health
conditions of these people improved. We are very apt to think of the
African as a stupid person whose ignorance of nature is only equalled
by his fear of it, and who looks on all mishaps as caused by evil
spirits and malignant natural powers. It is much more correct to
assume in this case that the people very early learnt to distinguish
districts infested with malaria from those where it is absent.
This knowledge is crystallized in the
ancestral warning against settling in the
valleys and near the great waters, the
dwelling-places of disease and death. At the
same time, for security against the hostile
Mavia south of the Rovuma, it was enacted
that every settlement must be not less than a
certain distance from the southern edge of the
plateau. Such in fact is their mode of life at the
present day. It is not such a bad one, and
certainly they are both safer and more
comfortable than the Makua, the recent
intruders from the south, who have made USUAL METHOD OF
good their footing on the western edge of the CLOSING HUT-DOOR
plateau, extending over a fairly wide belt of
country. Neither Makua nor Makonde show in their dwellings
anything of the size and comeliness of the Yao houses in the plain,
especially at Masasi, Chingulungulu and Zuza’s. Jumbe Chauro, a
Makonde hamlet not far from Newala, on the road to Mahuta, is the
most important settlement of the tribe I have yet seen, and has fairly
spacious huts. But how slovenly is their construction compared with
the palatial residences of the elephant-hunters living in the plain.
The roofs are still more untidy than in the general run of huts during
the dry season, the walls show here and there the scanty beginnings
or the lamentable remains of the mud plastering, and the interior is a
veritable dog-kennel; dirt, dust and disorder everywhere. A few huts
only show any attempt at division into rooms, and this consists
merely of very roughly-made bamboo partitions. In one point alone
have I noticed any indication of progress—in the method of fastening
the door. Houses all over the south are secured in a simple but
ingenious manner. The door consists of a set of stout pieces of wood
or bamboo, tied with bark-string to two cross-pieces, and moving in
two grooves round one of the door-posts, so as to open inwards. If
the owner wishes to leave home, he takes two logs as thick as a man’s
upper arm and about a yard long. One of these is placed obliquely
against the middle of the door from the inside, so as to form an angle
of from 60° to 75° with the ground. He then places the second piece
horizontally across the first, pressing it downward with all his might.
It is kept in place by two strong posts planted in the ground a few
inches inside the door. This fastening is absolutely safe, but of course
cannot be applied to both doors at once, otherwise how could the
owner leave or enter his house? I have not yet succeeded in finding
out how the back door is fastened.

MAKONDE LOCK AND KEY AT JUMBE CHAURO

 This is the general way of closing a house. The Makonde at Jumbe
Chauro, however, have a much more complicated, solid and original
one. Here, too, the door is as already described, except that there is
only one post on the inside, standing by itself about six inches from
one side of the doorway. Opposite this post is a hole in the wall just
large enough to admit a man’s arm. The door is closed inside by a
large wooden bolt passing through a hole in this post and pressing
with its free end against the door. The other end has three holes into
which fit three pegs running in vertical grooves inside the post. The
door is opened with a wooden key about a foot long, somewhat
curved and sloped off at the butt; the other end has three pegs
corresponding to the holes, in the bolt, so that, when it is thrust
through the hole in the wall and inserted into the rectangular
opening in the post, the pegs can be lifted and the bolt drawn out.[50]

MODE OF INSERTING THE KEY

With no small pride first one householder and then a second

showed me on the spot the action of this greatest invention of the
Makonde Highlands. To both with an admiring exclamation of
“Vizuri sana!” (“Very fine!”). I expressed the wish to take back these
marvels with me to Ulaya, to show the Wazungu what clever fellows
the Makonde are. Scarcely five minutes after my return to camp at
Newala, the two men came up sweating under the weight of two
heavy logs which they laid down at my feet, handing over at the same
time the keys of the fallen fortress. Arguing, logically enough, that if
the key was wanted, the lock would be wanted with it, they had taken
their axes and chopped down the posts—as it never occurred to them
to dig them out of the ground and so bring them intact. Thus I have
two badly damaged specimens, and the owners, instead of praise,
come in for a blowing-up.
The Makua huts in the environs of Newala are especially
miserable; their more than slovenly construction reminds one of the
temporary erections of the Makua at Hatia’s, though the people here
have not been concerned in a war. It must therefore be due to
congenital idleness, or else to the absence of a powerful chief. Even
the baraza at Mlipa’s, a short hour’s walk south-east of Newala,
shares in this general neglect. While public buildings in this country
are usually looked after more or less carefully, this is in evident
danger of being blown over by the first strong easterly gale. The only
attractive object in this whole district is the grave of the late chief
Mlipa. I visited it in the morning, while the sun was still trying with
partial success to break through the rolling mists, and the circular
grove of tall euphorbias, which, with a broken pot, is all that marks
the old king’s resting-place, impressed one with a touch of pathos.
Even my very materially-minded carriers seemed to feel something
of the sort, for instead of their usual ribald songs, they chanted
solemnly, as we marched on through the dense green of the Makonde
bush:—
 “We shall arrive with the great master; we stand in a row and have
no fear about getting our food and our money from the Serkali (the
Government). We are not afraid; we are going along with the great
master, the lion; we are going down to the coast and back.”
With regard to the characteristic features of the various tribes here
on the western edge of the plateau, I can arrive at no other
conclusion than the one already come to in the plain, viz., that it is
impossible for anyone but a trained anthropologist to assign any
given individual at once to his proper tribe. In fact, I think that even
an anthropological specialist, after the most careful examination,
might find it a difficult task to decide. The whole congeries of peoples
collected in the region bounded on the west by the great Central
African rift, Tanganyika and Nyasa, and on the east by the Indian
Ocean, are closely related to each other—some of their languages are
only distinguished from one another as dialects of the same speech,
and no doubt all the tribes present the same shape of skull and
structure of skeleton. Thus, surely, there can be no very striking
differences in outward appearance.
 Even did such exist, I should have no time
to concern myself with them, for day after day,
I have to see or hear, as the case may be—in
any case to grasp and record—an
extraordinary number of ethnographic
phenomena. I am almost disposed to think it
fortunate that some departments of inquiry, at
least, are barred by external circumstances.
Chief among these is the subject of iron-
working. We are apt to think of Africa as a
country where iron ore is everywhere, so to
speak, to be picked up by the roadside, and
where it would be quite surprising if the
inhabitants had not learnt to smelt the
material ready to their hand. In fact, the
knowledge of this art ranges all over the
continent, from the Kabyles in the north to the
Kafirs in the south. Here between the Rovuma
and the Lukuledi the conditions are not so
favourable. According to the statements of the
Makonde, neither ironstone nor any other
form of iron ore is known to them. They have
not therefore advanced to the art of smelting
the metal, but have hitherto bought all their
THE ANCESTRESS OF
THE MAKONDE
iron implements from neighbouring tribes.
Even in the plain the inhabitants are not much
better off. Only one man now living is said to
understand the art of smelting iron. This old fundi lives close to
Huwe, that isolated, steep-sided block of granite which rises out of
the green solitude between Masasi and Chingulungulu, and whose
jagged and splintered top meets the traveller’s eye everywhere. While
still at Masasi I wished to see this man at work, but was told that,
frightened by the rising, he had retired across the Rovuma, though
he would soon return. All subsequent inquiries as to whether the
fundi had come back met with the genuine African answer, “Bado”
(“Not yet”).
 BRAZIER

Some consolation was afforded me by a brassfounder, whom I

came across in the bush near Akundonde’s. This man is the favourite
of women, and therefore no doubt of the gods; he welds the glittering
brass rods purchased at the coast into those massive, heavy rings
which, on the wrists and ankles of the local fair ones, continually give
me fresh food for admiration. Like every decent master-craftsman he
had all his tools with him, consisting of a pair of bellows, three
crucibles and a hammer—nothing more, apparently. He was quite
willing to show his skill, and in a twinkling had fixed his bellows on
the ground. They are simply two goat-skins, taken off whole, the four
legs being closed by knots, while the upper opening, intended to
admit the air, is kept stretched by two pieces of wood. At the lower
end of the skin a smaller opening is left into which a wooden tube is
stuck. The fundi has quickly borrowed a heap of wood-embers from
the nearest hut; he then fixes the free ends of the two tubes into an
earthen pipe, and clamps them to the ground by means of a bent
piece of wood. Now he fills one of his small clay crucibles, the dross
on which shows that they have been long in use, with the yellow
material, places it in the midst of the embers, which, at present are
only faintly glimmering, and begins his work. In quick alternation
the smith’s two hands move up and down with the open ends of the
bellows; as he raises his hand he holds the slit wide open, so as to let
the air enter the skin bag unhindered. In pressing it down he closes
the bag, and the air puffs through the bamboo tube and clay pipe into
the fire, which quickly burns up. The smith, however, does not keep
on with this work, but beckons to another man, who relieves him at
the bellows, while he takes some more tools out of a large skin pouch
carried on his back. I look on in wonder as, with a smooth round
stick about the thickness of a finger, he bores a few vertical holes into
the clean sand of the soil. This should not be difficult, yet the man
seems to be taking great pains over it. Then he fastens down to the
ground, with a couple of wooden clamps, a neat little trough made by
splitting a joint of bamboo in half, so that the ends are closed by the
two knots. At last the yellow metal has attained the right consistency,
and the fundi lifts the crucible from the fire by means of two sticks
split at the end to serve as tongs. A short swift turn to the left—a
tilting of the crucible—and the molten brass, hissing and giving forth
clouds of smoke, flows first into the bamboo mould and then into the
holes in the ground.
The technique of this backwoods craftsman may not be very far
advanced, but it cannot be denied that he knows how to obtain an
adequate result by the simplest means. The ladies of highest rank in
this country—that is to say, those who can afford it, wear two kinds
of these massive brass rings, one cylindrical, the other semicircular
in section. The latter are cast in the most ingenious way in the
bamboo mould, the former in the circular hole in the sand. It is quite
a simple matter for the fundi to fit these bars to the limbs of his fair
customers; with a few light strokes of his hammer he bends the
pliable brass round arm or ankle without further inconvenience to
the wearer.
SHAPING THE POT

SMOOTHING WITH MAIZE-COB

CUTTING THE EDGE

 FINISHING THE BOTTOM

LAST SMOOTHING BEFORE

BURNING

FIRING THE BRUSH-PILE

 LIGHTING THE FARTHER SIDE OF
THE PILE

TURNING THE RED-HOT VESSEL

NYASA WOMAN MAKING POTS AT MASASI

Pottery is an art which must always and everywhere excite the
interest of the student, just because it is so intimately connected with
the development of human culture, and because its relics are one of
the principal factors in the reconstruction of our own condition in
prehistoric times. I shall always remember with pleasure the two or
three afternoons at Masasi when Salim Matola’s mother, a slightly-
built, graceful, pleasant-looking woman, explained to me with
touching patience, by means of concrete illustrations, the ceramic art
of her people. The only implements for this primitive process were a
lump of clay in her left hand, and in the right a calabash containing
the following valuables: the fragment of a maize-cob stripped of all
its grains, a smooth, oval pebble, about the size of a pigeon’s egg, a
few chips of gourd-shell, a bamboo splinter about the length of one’s
hand, a small shell, and a bunch of some herb resembling spinach.
 Nothing more. The woman scraped with the
shell a round, shallow hole in the soft, fine
sand of the soil, and, when an active young
girl had filled the calabash with water for her,
she began to knead the clay. As if by magic it
gradually assumed the shape of a rough but
already well-shaped vessel, which only wanted
a little touching up with the instruments
before mentioned. I looked out with the
MAKUA WOMAN closest attention for any indication of the use
MAKING A POT. of the potter’s wheel, in however rudimentary
SHOWS THE a form, but no—hapana (there is none). The
BEGINNINGS OF THE embryo pot stood firmly in its little
POTTER’S WHEEL
depression, and the woman walked round it in
a stooping posture, whether she was removing
small stones or similar foreign bodies with the maize-cob, smoothing
the inner or outer surface with the splinter of bamboo, or later, after
letting it dry for a day, pricking in the ornamentation with a pointed
bit of gourd-shell, or working out the bottom, or cutting the edge
with a sharp bamboo knife, or giving the last touches to the finished
vessel. This occupation of the women is infinitely toilsome, but it is
without doubt an accurate reproduction of the process in use among
our ancestors of the Neolithic and Bronze ages.
There is no doubt that the invention of pottery, an item in human
progress whose importance cannot be over-estimated, is due to
women. Rough, coarse and unfeeling, the men of the horde range
over the countryside. When the united cunning of the hunters has
succeeded in killing the game; not one of them thinks of carrying
home the spoil. A bright fire, kindled by a vigorous wielding of the
drill, is crackling beside them; the animal has been cleaned and cut
up secundum artem, and, after a slight singeing, will soon disappear
under their sharp teeth; no one all this time giving a single thought
to wife or child.
To what shifts, on the other hand, the primitive wife, and still more
the primitive mother, was put! Not even prehistoric stomachs could
endure an unvarying diet of raw food. Something or other suggested
the beneficial effect of hot water on the majority of approved but
indigestible dishes. Perhaps a neighbour had tried holding the hard
roots or tubers over the fire in a calabash filled with water—or maybe
an ostrich-egg-shell, or a hastily improvised vessel of bark. They
became much softer and more palatable than they had previously
been; but, unfortunately, the vessel could not stand the fire and got
charred on the outside. That can be remedied, thought our
ancestress, and plastered a layer of wet clay round a similar vessel.
This is an improvement; the cooking utensil remains uninjured, but
the heat of the fire has shrunk it, so that it is loose in its shell. The
next step is to detach it, so, with a firm grip and a jerk, shell and
kernel are separated, and pottery is invented. Perhaps, however, the
discovery which led to an intelligent use of the burnt-clay shell, was
made in a slightly different way. Ostrich-eggs and calabashes are not
to be found in every part of the world, but everywhere mankind has
arrived at the art of making baskets out of pliant materials, such as
bark, bast, strips of palm-leaf, supple twigs, etc. Our inventor has no
water-tight vessel provided by nature. “Never mind, let us line the
basket with clay.” This answers the purpose, but alas! the basket gets
burnt over the blazing fire, the woman watches the process of
cooking with increasing uneasiness, fearing a leak, but no leak
appears. The food, done to a turn, is eaten with peculiar relish; and
the cooking-vessel is examined, half in curiosity, half in satisfaction
at the result. The plastic clay is now hard as stone, and at the same
time looks exceedingly well, for the neat plaiting of the burnt basket
is traced all over it in a pretty pattern. Thus, simultaneously with
pottery, its ornamentation was invented.
Primitive woman has another claim to respect. It was the man,
roving abroad, who invented the art of producing fire at will, but the
woman, unable to imitate him in this, has been a Vestal from the
earliest times. Nothing gives so much trouble as the keeping alight of
the smouldering brand, and, above all, when all the men are absent
from the camp. Heavy rain-clouds gather, already the first large
drops are falling, the first gusts of the storm rage over the plain. The
little flame, a greater anxiety to the woman than her own children,
flickers unsteadily in the blast. What is to be done? A sudden thought
occurs to her, and in an instant she has constructed a primitive hut
out of strips of bark, to protect the flame against rain and wind.
This, or something very like it, was the way in which the principle
of the house was discovered; and even the most hardened misogynist
cannot fairly refuse a woman the credit of it. The protection of the
hearth-fire from the weather is the germ from which the human
dwelling was evolved. Men had little, if any share, in this forward
step, and that only at a late stage. Even at the present day, the
plastering of the housewall with clay and the manufacture of pottery
are exclusively the women’s business. These are two very significant
survivals. Our European kitchen-garden, too, is originally a woman’s
invention, and the hoe, the primitive instrument of agriculture, is,
characteristically enough, still used in this department. But the
noblest achievement which we owe to the other sex is unquestionably
the art of cookery. Roasting alone—the oldest process—is one for
which men took the hint (a very obvious one) from nature. It must
have been suggested by the scorched carcase of some animal
overtaken by the destructive forest-fires. But boiling—the process of
improving organic substances by the help of water heated to boiling-
point—is a much later discovery. It is so recent that it has not even
yet penetrated to all parts of the world. The Polynesians understand
how to steam food, that is, to cook it, neatly wrapped in leaves, in a
hole in the earth between hot stones, the air being excluded, and
(sometimes) a few drops of water sprinkled on the stones; but they
do not understand boiling.
To come back from this digression, we find that the slender Nyasa
woman has, after once more carefully examining the finished pot,
put it aside in the shade to dry. On the following day she sends me
word by her son, Salim Matola, who is always on hand, that she is
going to do the burning, and, on coming out of my house, I find her
already hard at work. She has spread on the ground a layer of very
dry sticks, about as thick as one’s thumb, has laid the pot (now of a
yellowish-grey colour) on them, and is piling brushwood round it.
My faithful Pesa mbili, the mnyampara, who has been standing by,
most obligingly, with a lighted stick, now hands it to her. Both of
them, blowing steadily, light the pile on the lee side, and, when the
flame begins to catch, on the weather side also. Soon the whole is in a
blaze, but the dry fuel is quickly consumed and the fire dies down, so
that we see the red-hot vessel rising from the ashes. The woman
turns it continually with a long stick, sometimes one way and
sometimes another, so that it may be evenly heated all over. In
twenty minutes she rolls it out of the ash-heap, takes up the bundle
of spinach, which has been lying for two days in a jar of water, and
sprinkles the red-hot clay with it. The places where the drops fall are
marked by black spots on the uniform reddish-brown surface. With a
sigh of relief, and with visible satisfaction, the woman rises to an
erect position; she is standing just in a line between me and the fire,
from which a cloud of smoke is just rising: I press the ball of my
camera, the shutter clicks—the apotheosis is achieved! Like a
priestess, representative of her inventive sex, the graceful woman
stands: at her feet the hearth-fire she has given us beside her the
invention she has devised for us, in the background the home she has
built for us.
At Newala, also, I have had the manufacture of pottery carried on
in my presence. Technically the process is better than that already
described, for here we find the beginnings of the potter’s wheel,
which does not seem to exist in the plains; at least I have seen
nothing of the sort. The artist, a frightfully stupid Makua woman, did
not make a depression in the ground to receive the pot she was about
to shape, but used instead a large potsherd. Otherwise, she went to
work in much the same way as Salim’s mother, except that she saved
herself the trouble of walking round and round her work by squatting
at her ease and letting the pot and potsherd rotate round her; this is
surely the first step towards a machine. But it does not follow that
the pot was improved by the process. It is true that it was beautifully
rounded and presented a very creditable appearance when finished,
but the numerous large and small vessels which I have seen, and, in
part, collected, in the “less advanced” districts, are no less so. We
moderns imagine that instruments of precision are necessary to
produce excellent results. Go to the prehistoric collections of our
museums and look at the pots, urns and bowls of our ancestors in the
dim ages of the past, and you will at once perceive your error.
MAKING LONGITUDINAL CUT IN
BARK

DRAWING THE BARK OFF THE LOG

REMOVING THE OUTER BARK

 BEATING THE BARK

WORKING THE BARK-CLOTH AFTER BEATING, TO MAKE IT

SOFT

MANUFACTURE OF BARK-CLOTH AT NEWALA

To-day, nearly the whole population of German East Africa is
clothed in imported calico. This was not always the case; even now in
some parts of the north dressed skins are still the prevailing wear,
and in the north-western districts—east and north of Lake
Tanganyika—lies a zone where bark-cloth has not yet been
superseded. Probably not many generations have passed since such
bark fabrics and kilts of skins were the only clothing even in the
south. Even to-day, large quantities of this bright-red or drab
material are still to be found; but if we wish to see it, we must look in
the granaries and on the drying stages inside the native huts, where
it serves less ambitious uses as wrappings for those seeds and fruits
which require to be packed with special care. The salt produced at
Masasi, too, is packed for transport to a distance in large sheets of
bark-cloth. Wherever I found it in any degree possible, I studied the
process of making this cloth. The native requisitioned for the
purpose arrived, carrying a log between two and three yards long and
as thick as his thigh, and nothing else except a curiously-shaped
mallet and the usual long, sharp and pointed knife which all men and
boys wear in a belt at their backs without a sheath—horribile dictu!
[51]
Silently he squats down before me, and with two rapid cuts has
drawn a couple of circles round the log some two yards apart, and
slits the bark lengthwise between them with the point of his knife.
With evident care, he then scrapes off the outer rind all round the
log, so that in a quarter of an hour the inner red layer of the bark
shows up brightly-coloured between the two untouched ends. With
some trouble and much caution, he now loosens the bark at one end,
and opens the cylinder. He then stands up, takes hold of the free
edge with both hands, and turning it inside out, slowly but steadily
pulls it off in one piece. Now comes the troublesome work of
scraping all superfluous particles of outer bark from the outside of
the long, narrow piece of material, while the inner side is carefully
scrutinised for defective spots. At last it is ready for beating. Having
signalled to a friend, who immediately places a bowl of water beside
him, the artificer damps his sheet of bark all over, seizes his mallet,
lays one end of the stuff on the smoothest spot of the log, and
hammers away slowly but continuously. “Very simple!” I think to
myself. “Why, I could do that, too!”—but I am forced to change my
opinions a little later on; for the beating is quite an art, if the fabric is
not to be beaten to pieces. To prevent the breaking of the fibres, the
stuff is several times folded across, so as to interpose several
thicknesses between the mallet and the block. At last the required
state is reached, and the fundi seizes the sheet, still folded, by both
ends, and wrings it out, or calls an assistant to take one end while he
holds the other. The cloth produced in this way is not nearly so fine
and uniform in texture as the famous Uganda bark-cloth, but it is
quite soft, and, above all, cheap.
Now, too, I examine the mallet. My craftsman has been using the
simpler but better form of this implement, a conical block of some
hard wood, its base—the striking surface—being scored across and
across with more or less deeply-cut grooves, and the handle stuck
into a hole in the middle. The other and earlier form of mallet is
shaped in the same way, but the head is fastened by an ingenious
network of bark strips into the split bamboo serving as a handle. The
observation so often made, that ancient customs persist longest in
connection with religious ceremonies and in the life of children, here
finds confirmation. As we shall soon see, bark-cloth is still worn
during the unyago,[52] having been prepared with special solemn
ceremonies; and many a mother, if she has no other garment handy,
will still put her little one into a kilt of bark-cloth, which, after all,
looks better, besides being more in keeping with its African
surroundings, than the ridiculous bit of print from Ulaya.
MAKUA WOMEN