Pathology for the Physical Therapist

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0786_FM_i-xviii.qxd 2/11/11 11:57 AM Page vii
Pathology for the Physical Therapist Assistant is a com-
prehensive pathology text uniquely designed for physical
therapist assistant (PTA) education and practice. As PTAs
graduate and enter clinical practice it will continue to be a
reference volume. The impetus to write this book was the
lack of a specific text for pathology related to PTA prac-
tice. As a PTA program director and educator for the past
15 years with a specialization in teaching the pathology
content of the program, I became acutely aware that none
of the pathology texts available were really appropriate
for the PTA students. The required knowledge level of
pathology for the PTA is less than that of the physical
therapist, but different from other associate degree–level
health care workers. The aim of this book is to highlight
the most important information and diagnoses relevant for
the PTA student and practitioner and fill the gap as far as
pathology content for PTA associate degree programs.
The content of the text includes, but is not restricted to,
that required by “a normative model of physical therapist
assistant education” published by the APTA.
This 14-chapter book was designed to facilitate use
in a 15-week semester of a pathology course or to use
each chapter as stand-alone content within PTA pro-
grams where the pathology content is spread throughout
the curriculum. The features of this book are designed
to assist student learning, encourage critical thinking,
and ensure the appropriate knowledge of pathology re-
quired for both passing the national licensing examina-
tion and functioning within the clinic. Each chapter
and many sections have a heading called “Why does
the physical therapist assistant need to know about. . .,”
which helps to focus the reader on the importance of the
content for practice. An understanding of the relevance
of information for PT practice and PTA work makes the
study of a subject more interesting. Each chapter begins
with the anatomy and physiology of the body system as
a review of the normal system prior to learning about
the pathology. Throughout the text the relationship be-
tween the PTA and the physical therapist is emphasized
and the “scope of work” of the PTA is delineated. Care-
ful consideration has been given to the scope of work of
the PTA, although this does not mean that tests and
measures and specific diagnostic procedures are not de-
scribed in the text where relevant. PTAs need to be able
to read the patient chart and understand the meaning of
P R E FAC E
physical therapy and medical tests. Reference to the
Guide for Physical Therapist Practice is emphasized in
each chapter and Guide language is used throughout the
text. The use of medical terminology is consistent with
explanations within the text of the meaning of medical
terms as well as inclusion of each term within the exten-
sive glossary at the back of the book. Some of the spe-
cific terms and words relevant to the PTA are listed at
the beginning of each chapter as “key terms,” bolded
within the text, and included in the glossary. The exten-
sive use of tables, lists, information boxes, and illustra-
tions gives the chapters a more easily understandable
format. Many tables are provided to make the content
more understandable for the reader and are particularly
useful for more complicated content.
Some of the other unique features of this book
include:
• Each chapter has a distinct focus on a specific body
system.
• Chapter outlines provide an easy method for students
and faculty to find content.
• The anatomy and physiology of the specific body
system is described as a review for the PTA prior to dis-
cussion regarding the pathology of that system.
• Physical therapy interventions are included for all
appropriate pathological conditions.
• Tables, lists, and information boxes facilitate student
learning and break up the text, making for easier
reading.
• Specific content related to precautions and contraindica-
tions for certain patient diagnoses related to physical
therapy practice help to focus students on clinical
practice issues.
• Medical tests are described as they relate to the
pathology of the body system.
• Specific boxes for “geriatric considerations” in each
chapter help to make the chapter content relevant to
clinical practice.
• “It happened in the clinic” boxes in each chapter relate
real-life situations within the clinic that provide interest-
ing insights into physical therapy practice for students
regarding chapter content.
• The use of an icon within the text enables students and
faculty to immediately identify pediatric content.
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viii Preface

• Inclusion of a list of useful Web sites pertaining to the • Review questions for each chapter allow for student self-
chapter content encourages students to further research testing, homework assignments, or team projects.
topics and make use of professional-level sources of
This text was never intended to provide detailed
information.
physical therapy interventions for people with specific
• References for each chapter include those from scien-
diagnoses or manifestations of the disease process, but
tific literature and professional sources to ensure accu-
the inclusion of content more specific to practice for the
racy of information.
PTA hopefully makes this a useful addition to texts for
• Case studies at the end of each chapter assist students to
PTA education.
apply the knowledge gained from the chapter to increase
the clinical relevance of the information and to provide
talking points within class. Penny Lescher
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ACKNOWLEDGMENTS
The task of thanking all those who have helped me dur-
ing the writing of this text is a difficult one since so
many people have helped along the way. Writing this
book has truly been an enormous project made easier by
all the help and encouragement I have received. Many
people encouraged me to write a pathology text, espe-
cially all my fellow PTA educators throughout the coun-
try. Particular thanks go to Pam Ritzline PT, EdD, for all
her help with the content editing; David C. Thomas, PT,
MGA, my fellow PTA educator and friend in Maryland,
for his help in reviewing initial writing of the cardiopul-
monary chapter and writing test questions; Alan Brownlie,
PhD, Associate Professor of English at Anne Arundel
Community College, for his help in re-directing my
grammatical construction; and my friend and colleague
Amy Murphy, PT, for her assistance with writing test
questions for the instructor’s manual.
Particular thanks go to all the people at F. A. Davis for
their encouragement and patience. To Jean Francois Vilain,
retired publisher, for making my dream of writing this
text a reality and Margaret M. Biblis, publisher, for contin-
uing to believe the text would be completed. To Melissa
Duffield, my patient publishing editor; Jill Rembetski, my
developmental editor; Peg Waltner, developmental editor
and all those who were instrumental in helping me achieve
my goal of writing and publishing this book.
And finally many thanks to all the PTA students who
have inspired me to write this text. Without their enthusi-
asm and zest for learning I would never have started this
endeavor.
ix
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REVIEWERS

Wendy D. Bircher, PT, EdD Julie A. Toney, PT, MPH

Director, Physical Therapist Assistant Program Physical Therapy Program
San Juan College University of Findlay and Promedica Health
Farmington, NM System
Toledo, OH
Leila Darress, PT, MHSA
Director, Physical Therapist Assistant Program Christopher H. Wise, PT, MS, OCS, FAAOMPT,
Indian River Community College MTC, ATC
Fort Pierce, FL Physical Therapy Department
Widener University
James W. Farris, PT, PhD Chester, PA
Associate Professor, Physical Therapy Program
Arkansas State University Jane E. Worley, PT, MS
Jonesboro, AR Director, Physical Therapist Assistant Program
Lake Superior College
Diana N. Ploeger, PT, MEd Duluth, MN
Coordinator and Associate Professor, Physical
Therapist Assistant Program
Salt Lake Community College
Salt Lake City, UT

Pamela D. Ritzline, PT, EdD

Director and Assistant Professor, Physical
Therapist Assistant Program
University of Indianapolis
Greenwood, IN

xi
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CONTENTS

Chapter 1: Inflammation and Case Study 1.1, 28

Healing, 1 Case Study 1.2, 29
Introduction, 2 Study Questions, 29
Normal Cell Anatomy and Physiology, 2
Nucleus, 3 Chapter 2: Immunopathology,
Cytoplasm, 3 Neoplasia, and Chromosome
Plasma Membrane, 4 Abnormalities, 33
Cell Injury, 4 Introduction, 34
Cell Injury—Reversible, 5 Immunopathology, 34
Cell Injury—Irreversible, 6 Cells of the Immune Response, 35
Cellular Responses to Damage or Stimuli, 8 Hypersensitivity Reactions, 35
Inflammation, 9 Type I Hypersensitivity, 35
Causes of the Inflammatory Response, 10 Type II Hypersensitivity, 39
Polymorphonucleocytes, 10 Type III Hypersensitivity, 39
Eosinophils, 10 Type IV Hypersensitivity, 39
Monocytes and Macrophages, 10 Vaccination, 40
Platelets, 11 Effects of Exercise on the Immune Response, 40
Basophils, 12 Infections, 41
Lymphocytes and Plasma Cells, 12 Types of Microorganisms, 41
Classification of Inflammation, 12 Development of Infection, 42
Physical Therapy Treatment for Inflammation, 13 Treatment of Infection, 43
Healing, 14 Neoplasia, 45
Cells Involved in the Healing Process, 15 Carcinogens, 46
Types of Healing, 16 Risk Factors for Malignant Tumors, 46
Complications of Wound Healing Other Than Treatment Interventions for Cancer, 49
Delayed Healing, 19 Genetic and Hereditary Chromosome
Special Aspects Regarding Pressure Ulcers, 20 Diseases, 51
Physical Therapy Intervention for Wounds, 21 The Normal Chromosome, 51
Bone Healing, 23 Overview of Genetic and Hereditary Chromosome
Diseases, 52
Ligament Healing, 25
Chromosome Abnormalities, 54
Muscle and Tendon Healing, 25
Chromosome Abnormality Conditions, 54
Pain, 26
Developmental Diseases/Birth Injuries, 58
Pain Control Theories, 27
Genetically Linked Diseases, 67
Physical Therapy Interventions, 27
Case Study 2.1, 70
Pain Assessment, 28
Study Questions, 70

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xiv Contents

Chapter 3: Cardiovascular Case Study 3.2, 118

Pathologies, 77 Study Questions, 119
Introduction, 79
Anatomy and Physiology of the Chapter 4 Respiratory Diseases, 121
Cardiovascular System, 79 Introduction, 122
The Heart, 79 Anatomy and Physiology of the Respiratory
Neural Control of the Heart, 80 System, 122
Nerve Conduction System of the Heart, 80 The Thoracic Cage and Its Contents, 123
Coronary Circulation, 81 Physiology of Ventilation and Respiration, 127
Cardiac Cycle, 81 Muscles of Ventilation, 131
Heart Sounds, 81 Tests for Respiratory Function, 132
Pulse, 82 Subjective Findings, 132
Cardiac Output, 82 Objective Findings, 132
Blood Pressure, 83 Lung Function Tests, 133
Blood Vessels, 84 Diseases of the Respiratory System, 141
Lymphatic System, 86 General Signs and Symptoms of Pulmonary
Diseases, 141
Pathology of the Cardiovascular System, 87
Pathological Conditions of the Respiratory
General Signs and Symptoms of Cardiac Disease, 89
Tract, 144
Diagnostic Tests Performed for Cardiac Patients, 92
Pulmonary Surgery, 156
Disorders and Pathological Conditions of the
Post-pulmonary Surgery Complications, 158
Heart, 95
Classes of Medications Used to Treat
Cardiac Surgeries and Cardiac
Respiratory Diseases, 159
Rehabilitation, 106
The Role of the PTA in Interventions for
Coronary Artery Bypass Graft, 106
Patients With Respiratory Diseases, 159
Heart Transplant, 106
Specific Physical Therapy Treatment Interventions
Open Heart Surgery, 106 for Patients With Respiratory Pathologies, 160
Pacemaker Insertion, 107 Case Study 4.1, 164
Percutaneous Transluminal Coronary Artery Case Study 4.2, 164
Angioplasty, 107
Study Questions, 165
Arterial Diseases, 107
Venous Diseases, 112 Chapter 5: Degenerative Joint
Blood Disorders, 113 Diseases and Bone Pathologies, 169
Lymphatic Disorders, 115 Introduction, 170
Cardiovascular System Failure, 116 Normal Joint Structure, 171
Physical Therapy Treatment and the Role Normal Anatomy and Physiology of Bone, 172
of the PTA in Cardiac and Circulatory
Degenerative Diseases of Joints, 173
Conditions, 117
Surgical intervention for arthritis, 183
Other Considerations, 117
Diseases of Bone, 188
Home Health Physical Therapy, 118
Bone Diseases Associated With
Outpatient Cardiac Rehabilitation, 118
Hyperparathyroidism and
Case Study 3.1, 118 Hypoparathyroidism, 193
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Contents xv

Bone Tumors, 195 Feldenkrais Method, 301

Cartilage Tumors, 199 Myofascial Release, 301
Joint Abnormalities, 200 Neurodevelopmental Therapy/Bobath
Genetic Bone Abnormalities, 201 Techniques, 301
Case Study 5.1, 205 Proprioceptive Neuromuscular
Facilitation, 302
Study Questions, 206
Sensory Integration, 302
Chapter 6: Rheumatoid Arthritis Tai Chi Chuan in Rehabilitation, 303
and Related Conditions, 213 Neurological Disorders, 303
Introduction, 214 Neurological Conditions Resulting From Deficits in
the Development of the Nervous System or Birth
Rheumatoid Arthritis, 214
Injury, 304
Articular (Joint) Pathological Changes, 215
Common Neurological Disorders, 308
Nonarticular (Nonjoint) Pathological Changes, 220
Case Study 7.1, 331
Juvenile Rheumatoid Arthritis and Still’s
Case Study 7.2, 331
Disease, 228
Study Questions, 332
Rheumatoid-Related Inflammatory Joint
Pathologies, 231
Connective Tissue Diseases, 238 Chapter 8: Burns and Skin
Other Rheumatoid- and Connective Tissue–
Conditions, 341
Associated Diseases, 248 Introduction, 342
Muscle Diseases, 250 Anatomy and Physiology of the Skin, 342
Case Study 6.1, 254 Skin Conditions and Diseases, 345
Case Study 6.2, 254 Thermal Injuries, 347
Case Study 6.3, 255 Cold Injuries, 353
Study Questions, 255 Infectious Diseases of the Skin, 355
Case Study 8.1, 376
Chapter 7: Neurological Disorders, 263 Case Study 8.2, 377
Introduction, 264 Study Questions, 377
The Anatomy and Physiology of the
Neurological System, 264 Chapter 9: Endocrine, Metabolic,
Development of the Nervous System in the Fetus, 265 and Nutritional Disorders, 383
The Neuron, 268 Introduction, 384
Central Nervous System, 272 Anatomy and Physiology of the
Peripheral Nervous System, 282 Endocrine System, 384
Testing for the Neurological System, 292 Endocrine System Diseases and Disorders, 386
Physical Therapy Treatment for People With Pituitary Diseases, 387
Neurological Conditions, 299 Thyroid Diseases, 389
Adverse Mechanical/Neural Tension, 299 Adrenal Cortex Diseases, 393
Alexander Technique, 300 Adrenal Medulla Diseases, 397
Brunnstrom Approach, 300 Diabetes Mellitus, 398
Constraint-Induced Movement Therapy, 300 Diabetic Neuropathy, 404
Craniosacral Therapy, 300 Diabetic Coma, 405
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xvi Contents

Metabolic Disorders, 406 Intervention During Pregnancy, 489

Balance of Acids and Bases, 406 Pregnancy-Related Conditions, 490
Nutritional Disorders, 408 Labor, 496
Overweight and Obesity, 408 Complications of Labor, 498
Eating Disorders, 410 Postpartum Issues and Problems, 500
Mineral Deficiencies, 414 Menopause, 502
Inflammatory Bowel Disease, 414 Male Reproductive Anatomy, 503
Case Study 9.1, 415 Diseases of the Male Reproductive System, 504
Study Questions, 415 Congenital Abnormalities, 505
Prostate Diseases, 507
Chapter 10: Infectious Diseases, 421 Testicular Diseases, 509
Introduction, 422 Case Study 11.1, 512
Hepatitis, 423 Study Questions, 513
Human Immunodeficiency Virus and Acquired
Immune Deficiency Syndrome, 428 Chapter 12: Diseases of the
Sexually Transmitted Diseases, 431 Digestive and Urinary Systems, 521
Nosocomial Infections, 437 Introduction, 522
Insect (Vector)- and Animal-Borne Anatomy and Physiology of the Digestive
Infectious Diseases, 438 System, 522
Preventable Infectious Diseases for Which Diagnostic Medical Tests for Digestive System
Health Care Workers Are Required to Have Diseases, 525
Immunity, 445 Diseases of the Digestive System, 529
Other Infectious Diseases, 453 Diseases of the Esophagus, 530
Case Study 10.1, 458 Diseases of the Mouth and Pharynx, 531
Study Questions, 459 Diseases of the Stomach, 533
Diseases of the Small Intestine, 535
Chapter 11: Female and Male Diseases of the Large Bowel and Large Intestine, 538
Reproductive System Conditions, 467 Diseases of the Liver and Gallbladder, 545
Introduction, 468 Liver Diseases and Conditions Caused by Drugs,
Anatomy and Physiology of the Female Medications, and Toxins, 548
Reproductive System, 468 Diseases of the Pancreas, 550
Diseases and Conditions of the Female The Anatomy and Physiology of the Urinary
Reproductive System, 472 System, 552
Menstrual Cycle Problems, 473 Diagnostic Tests and Procedures for the Urinary
Carcinomas of the female Reproductive System, 475 Tract, 554
Intrauterine Devices and Their Significance in Terms Associated With Urinary Disease, 557
Physical Therapy Intervention, 483 Diseases of the Urinary Tract, 558
Diseases of the Breast, 483 Diseases of the Bladder, 559
Pregnancy, 487 Diseases of the Kidney, 561
Lactation, 488 Case Study 12.1, 568
Monitoring of the Fetus During Pregnancy, 488 Study Questions, 568
Precautions and Contraindications for PT
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Contents xvii

Chapter 13: Intensive Care, 579 Anatomy and Physiology of the Eye, 605
Introduction, 580 Pathological Conditions of the Eye, 606
The Intensive Care Unit, 580 Anatomy and Physiology of the Ear, 610
General Precautions and Recommendations for Pathological Conditions of the Ear, 611
Treating Patients in the ICU, 584 Other Conditions or Disorders Related to
Equipment Used in the ICU, 585 Aging, 615
What Causes a Patient to Be Placed in the ICU? 590 Amputation, 615
Physical Therapy Interventions Used for Patients Arthritis, 615
With Specific Diagnoses on the ICU, 591 Balance Problems, Falls, and Immobility, 616
Prevention of Pressure Ulcers, 596 Bowel and Bladder Dysfunction, 617
Legal and Ethical Issues, 597 Dementia, 617
Pediatric Intensive Care Unit, 597 Diabetes Mellitus, 618
Case Study 13.1, 597 Malnutrition, 618
Study Questions, 598 Parkinson’s Disease, 619
Pressure Ulcers, 620
Chapter 14: The Geriatric Patient, 601 Terminal Illness, 620
Introduction, 602 Special Issues Related to Geriatric Patients, 621
Overview of Geriatrics, 602 Elder Abuse, 621
Physiological Effects of Aging, 603 Case Study 14.1, 623
Effects of Age on the Skin, 604 Study Questions, 623
False Assumptions About the Elderly, 604
Psychological Effects of Aging, 604 Glossary, 627
Specific Diseases Prevalent in the Elderly
Population, 605 Index, 641
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CHAPTER

1
Inflammation and Healing

L E A R N I N G O B J E C T I V E S K E Y T E R M S
After completion of this chapter, students should be able to: Acute on chronic inflammation
• Describe the anatomy and physiology of the cell. Adhesions
• Describe the physiological mechanisms of injury at the cellular level, Autolytic débridement
including necrosis and the inflammatory response. Cardinal signs of inflammation
• Describe the physiology of cellular and tissue repair. Débridement
• Identify the phases of wound healing.
Disuse atrophy
• Explain the complications of wound healing.
• Analyze how physical therapy can be used to reduce inflammation and Edema
facilitate wound healing. Endogenous opiates
• Describe the healing process for bone, ligaments, tendons, and muscle. Eschar
• Discuss various pain-control theories. First intention healing
Gate Control Theory of pain
Granulation tissue
C H A P T E R O U T L I N E Heterotopic calcification/
Introduction ossification
Normal Cell Anatomy and Physiology Hypertrophic scarring
Nucleus Ischemia
Cytoplasm
Plasma Membrane Keloid scarring
Cell Injury Palpation
Cell Injury—Reversible Pus
Cell Injury—Irreversible
Second intention healing
Cellular Responses to Damage or Stimuli
Inflammation
Causes of the Inflammatory Response
Polymorphonucleocytes
Eosinophils
Monocytes and Macrophages
Platelets
Basophils

1
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2 Pathophysiology for the Physical Therapist Assistant

C H A P T E R O U T L I N E (continued)

Classification of Inflammation
Types of Inflammation
Physical Therapy Treatment for Inflammation
Healing
Cells Involved in the Healing Process
Types of Healing
Complications of Wound Healing Other Than Delayed Healing
Special Aspects Regarding Pressure Ulcers
Physical Therapy Intervention for Wounds
Bone Healing
Ligament Healing
Muscle and Tendon Healing
Pain
Pain Control Theories
Physical Therapy Interventions
Pain Assessment

Introduction
regarding the appearance of tissues and present-
ing signs and symptoms. Although selection of
In this first chapter, several basic concepts are introduced
interventions is determined by the PT at the initial
that are crucial to the knowledge base of the physical ther-
examination evaluation and reexamination, the
apist assistant. Although these topics may seem unrelated
PTA must be able to make decisions regarding
to the study of pathology, they are nevertheless important
ongoing therapy. If cellular and tissue changes
as an introduction. Understanding the anatomy and phys-
occur which require intervention by the PT, then
iology of the human body is required before studying
the PTA must know when to alert the supervising
pathology to make accurate comparisons between the nor-
PT to these changes in patient status. If treatment
mal and abnormal states. This chapter focuses on normal
is not effective, the PTA must know when to discuss
cell anatomy and physiology, cell injury, tissue injury, the
this with the supervising PT and how to provide
process of inflammation, the healing of tissues, and the
rationale for possible change of treatment. The
subject of pain. Inflammation is a key concept in physical
PTA must also be familiar with the indications,
therapy because all injuries—whether to cells, tissues, or
contraindications, and precautions for the treat-
body organs—result in the inflammatory process. Inflam-
ment of many pathological conditions. Effective
mation is a necessary initiator of the healing process, and
patient care depends on the knowledge and
pain is the product of both injury and inflammation. Thus,
expertise of all those providing treatment.
what at first may seem different topics are combined into
a chapter that develops the basic concepts necessary to un-
derstanding the subject of pathology in the human body.
Normal Cell Anatomy
and Physiology
Why Does the Physical Therapist
Assistant Need to Know About Normal Understanding the normal functions and cell structure of
Cell Anatomy and Physiology? the healthy human body is an essential part of trying to
understand pathology, or the abnormal state. Although the
The physical therapist assistant (PTA) should be PT examines the patient and establishes the plan of care,
knowledgeable about normal cellular physiology the PTA must understand how the body reacts to certain
and the effects of changes in that physiology. stimuli at the cellular level to ensure use of the correct
The PTA needs to be able to communicate knowl- physical therapy intervention and facilitate the healing
edgeably and effectively with the physical thera- process. The following discussion of normal cell biology
pist (PT), other health-care providers, and patients is merely a review for the PTA. For further information,
the PTA should consult a physiology text.
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1 Inflammation and Healing 3

Most cells within the human body have a nucleus Nucleus

and cytoplasm (Fig. 1-1) and are surrounded and The nucleus contains nucleic acids and nuclear proteins.
contained within the plasma membrane (Fig. 1-2). The Nucleic acids include deoxyribonucleic acid (DNA) and
exceptions to this rule are mature red blood cells and ribonucleic acid (RNA). Some types of RNA are found in
platelets, which do not have a nucleus. Many cells in the the cytoplasm of the cell and some in the nucleolus or
body are specialized for specific functions but retain the nucleus, but DNA is located in the nucleus. DNA is
these common traits. aggregated with other proteins called histones, forming
strands of chromatin. These histones are positively
charged proteins that help bind the negatively charged
Endoplasmic DNA into smaller units that fit within the nucleus of the
reticulum cell. The chromatin plays a role in strengthening DNA so
Ribosomes
Cell
that cell mitosis and meiosis can take place.1 Several dif-
membrane ferences between DNA and RNA exist. RNA consists of a
single-stranded helix, whereas DNA has a double-helix
structure. The sugar in DNA is deoxyribose (no oxygen
molecule), and that of RNA is ribose. Both DNA and
Nucleus RNA are composed of any of five nitrogen bases. Two are
Nuclear the purines adenine and guanine, and three are the pyrim-
membrane
idines thymine, cytosine, and uracil. Of the five, only
Nucleolus
uracil is specific to RNA. The molecules of RNA are
smaller than those of DNA and are found in the cytoplasm
of the cell. Functionally, DNA acts as the store house for
genetic information. The function of RNA depends on
its type. Of the many types of RNA, three of the most im-
portant are ribosomal RNA (rRNA), messenger RNA
Lysosome
(mRNA), and transfer RNA (tRNA).2 Ribosomal RNA
Mitochondrion (rRNA) is found in the cytoplasm of the cell within the
ribosomes where synthesis of proteins occurs. The ribo-
Golgi somes actually consist of approximately 60% rRNA, and
apparatus
the other 40% is protein. Messenger RNA (mRNA) is a
FIGURE 1.1 The cell.
nucleic acid that acts as a messenger service taking infor-
mation from the DNA to the ribosomes. Transfer
RNA (tRNA) is a transport system that takes amino
acids to the ribosomes for the development of proteins.3 A
Exterior surface of cell plasma membrane
special organelle exists within the nucleus called a nucle-
Glycolipids olus, which is the location of the synthesis of three of the
Receptor
site types of RNA.4
During mitosis, when cells divide, the chromatin
changes into chromosomes. DNA is the library of genetic
material that is unique for each individual person. This
genetic material is altered within each organ to enable
differing body functions. Although the genetic material
in cells within the kidney will be the same as that within
a strand of hair, the functions of the cells in each case are
quite different.

Glycoprotein Cytoplasm
Cholesterol
Glycoprotein
Phospholipids
Cytoplasm consists of a ground substance called hyalo-
forms a pore plasm, which is composed mainly of water. All cells
Interior surface of cell plasma membrane within the body contain cytoplasm in varying amounts.
FIGURE 1.2 The cell plasma membrane. More cytoplasm is present in mature cells than in
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4 Pathophysiology for the Physical Therapist Assistant

embryonic or tumor cells. The higher the degree of
specialization of the cell, such as those in the liver,
the higher the cytoplasmic content of the cell, and the
greater the number of organelles within the cytoplasm.
Organelles contained within the cytoplasm include mi-
tochondria, endoplasmic reticulum (ER), ribosomes, the
Golgi apparatus, and lysosomes (Table 1-1). In muscle,
there are other specialized organelles, such as the my-
ofilaments of myosin and actin. A plasma membrane
(outer wall of the cell) surrounds the cytoplasm of
each cell.
Plasma Membrane
The plasma membrane is composed of a mixture of pro-
teins, lipids, and carbohydrates. The inner surface of the
cell is continuous with the ER. The outer surface of the
cell may have cilia, projections through the cell mem-
brane that enable certain specialized cells, such as those
lining the respiratory system to move secretions or cells
such as sperm. The plasma membrane protects the cell
and acts as the medium through which the cell reacts to
its environment (refer to Fig. 1-1).
Under normal circumstances, the cell is in a state of
homeostasis (equilibrium) with its environment. This
means that the cell’s oxygen needs are met, and waste prod-
ucts are excreted from the cell. This state of homeostasis
depends on the correct balance of minerals, such as sodium,
potassium, calcium, and iron, within the cell, which are es-
sential for normal cell health. When this state of homeosta-
sis is challenged, the cell responds in several ways. If the
change is minimal, the cell will recover, but if the trauma to
the cell is too great, the cell will necrose (die).
Cell Injury
Cells have the ability to adapt to changes in their environ-
ment. When a cell is exposed to a stimulus, changes, or

Ta b l e 1 . 1 Cytoplasmic Organelles and Their Functions

CYTOPLASMIC
ORGANELLE L O C AT I O N COMPONENTS FUNCTION

Mitochondria Cytoplasm; more prolific in
highly specialized organs,
such as kidney, liver, nerves;
numbers in a cell vary from
a few hundred to several
thousand
Double membrane—inner
membrane has folds of cristae
Main cell energy producers
Energy produced is stored as
Adenosine triphosphate (ATP)
Aerobic cell respiration (requiring
oxygen)
Turn glucose into CO2 and
water through processes of
glycolysis (breakdown of
glucose into pyruvic acid) and
oxidation of pyruvic acid into
CO2 and water

Endoplasmic Between nuclear and cell Rough ER—ribosomes on its Transport system within the
reticulum (ER) membranes surface cell; eg, for proteins synthe-
Smooth ER—no ribosomes sized on rough ER and lipids
by smooth ER

Ribosomes Surface of rough ER Proteins and ribosomal RNA Protein synthesis; turn informa-
Free floating in cytoplasm tion within the mRNA into
polypeptides to produce
energy

Golgi apparatus Cytoplasm Stacks of flat membranous Carbohydrate synthesis;

sacs processes proteins synthe-
sized in the ER into carbohy-
drates; produces lysosomes

Lysosomes Cytoplasm; round bodies pro- Single membrane structure; Digestion of material ingested
duced by the Golgi apparatus contain many enzymes such into the cell or of damaged
as proteases and lipases tissue; “cleanup crew”
(phagocytosis)
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1 Inflammation and Healing 5

injury can be either reversible or irreversible. In the re- Cell Injury—Reversible

versible type, the cell will usually recover from injury, but in
the irreversible type, the cell will either experience apopto-
sis (programmed cell death) or necrosis (death). Depending
on the extent of damage to the plasma membrane, repair
may be possible, or necrosis of the cell may occur.
Reversible cell injury occurs when damage to the cell is
mild or short in duration, in which case the cell can over-
come the damage (see Fig. 1-3). Reversible cell injury may
result from hypoxia (reduction of oxygen to the cell for
brief periods of time) or anoxia (loss of oxygen). Such

Normal

Injury
Normal cell Normal cell

Cell recovery
Reversible Swelling of endoplasmic Recovery with removal of
reticulum and some damaged components
cell injury by lysosomes
mitochondria
Loss of ribosomes

Death

Early stage of death of

Irreversible cell shows loss of nucleolus
cell injury-death No ribosomes
Swelling of ER
Swelling of all mitochondria

Nucleus undergoes pyknosis/ karyolysis

or karyorrhexis
Holes in cell membrane
Ruptured lysosomes

Fragmentation of
all inner membranes
Nuclear disintegration

FIGURE 1.3 Reversible and irreversible cell injury.

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6 Pathophysiology for the Physical Therapist Assistant

brief periods of reduction of oxygen result in edema
(swelling) of the cytoplasm in the cell. Edema is caused by
water passing into the cell through the selectively semiper-
meable cell membrane. When the oxygen supply to the cell
is reduced, the normal pumping mechanism of the cell,
which is performed by the enzyme adenosine triphos-
phatase (ATPase), is restricted. ATPase is a sodium/chlo-
ride pump and normally pumps sodium (Na+) ions out of
the cell together with chloride (Cl–) ions to maintain an
optimal cell environment (see Fig. 1-4). The normal con-
centration of Na+ and Cl– is lower inside than outside the
cell, and the potassium levels are higher within the cell.
When deprived of oxygen, the pump is disturbed, and Na+
and Cl– ions flood into the cell. Water then passes through
the semipermeable plasma membrane into the cell, result-
ing in dilution of the concentration of these ions, which
prevents severe damage to the cell. This engorgement of
the cell causes changes in cell function, including lowered
energy production by the mitochondria. The mitochondria
also become swollen and begin to produce energy through
Selectively permeable
cell plasma membrane
anaerobic (without oxygen) glycolysis, which produces
lactic acid. The ER becomes damaged, and the nucleus
has to muster its defenses to survive. When the nucleus
remains intact, the cell will recover.
Examples of such reversible damage include some
muscle injuries and, to a lesser degree, muscle fatigue.
A muscle cramp results in a buildup of lactic acid in the
muscle due to the process of anaerobic glycolysis in the
muscle cells. The actual mechanism of a muscle cramp is
unknown, but various theories include electrolytic
imbalance, dehydration, mechanical issues, and interfer-
ence with neural control. The muscle cells produce lactic
acid in response to injury, and the buildup of lactic acid
within the cell causes pain. The pain acts as a warning
sign to the individual to protect the muscle and usually
results in the prevention of irreversible cell damage.
Other types of reversible cell adaptation to stimuli oc-
cur that are desirable, such as hypertrophy, hyperplasia,
and metaplasia. Hypertrophy of a muscle occurs in re-
sponse to exercise. Atrophy is also a reversible cell adap-
tation in response to disuse. Some of the irreversible cell
adaptations include anaplasia, dysplasia, dyscrasia, carci-
noma in situ, and various types of necrosis. All of these
are detailed in the following sections.

Interior of Cell Extracellular Space

Cell Injury—Irreversible
All cells have a normal “shelf life,” similar to products in
K+ K+ a grocery store, which varies with the type of cell. This
normal death of cells is due to a programmed death cycle
K+ Osmosis
Na+ (Cl-) called apoptosis. When a healthy cell is damaged beyond
K+
K+ repair, necrosis occurs. Necrosis may occur as a result of
Na+ (Cl-)
K+
major injury to cells caused by toxins, severe anoxia, or
K+ K+ direct trauma, which damage the nucleus of the cell and
K+ cause the plasma membrane to rupture. The nucleus is
K+
essential for cell life, and without it the cell dies. Three
K+
Na+ (Cl-) types of nucleus damage are pyknosis, karyorrhexis, and
ATP
pump karyolysis5 (also see Fig. 1-5).
• Pyknosis—chromatin becomes condensed and shows
Na+ (Cl-)
on electromicroscopy as a dark area
• Karyorrhexis—fragmentation of the nucleus
• Karyolysis—nuclear structure dissolves

Mitochondria Table 1-2 displays several causes of cell injury and

FIGURE 1.4 Sodium pump. Sodium ions (Na+) are higher in
concentration in the extracellular spaces than in the cell. Thus,
NA+ ions continually try to pass into the cell, together with
chlorine ions (CL–), through the process of osmosis. Potassium
ions (K+) are higher in concentration inside the cell. The sodium
pump is driven by ATPase and shunts Na+ out of the cell to
maintain homeostasis.
necrosis, including hypoxia, which occurs when cells are
deprived of sufficient oxygen for short periods of time. If
the cell is healthy prior to oxygen deprivation and is only
deprived of oxygen for a short time, the cell or tissue may
recover. However, recovery may not occur if the cell was
not healthy initially. Anoxia is complete loss of oxygen to
the tissues and results in the death of those cells or tissues
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1 Inflammation and Healing 7

pathogens such as bacteria, viruses, or parasites; or toxic

Normal Cell
Pyknosis Karyorrhexis Karyolysis
FIGURE 1.5 Pyknosis, karyorrhexis, and karyolysis.
if it occurs for more than a matter of a few minutes.
Ischemia, or lack of blood supply to an area of tissue or
part of an organ, can cause injury or cell death. In many
cases, ischemic tissue is capable of recovery; in contrast,
infarction is cell death, and no recovery is possible in
these cells. Because blood supply is the means through
which oxygen reaches the tissue, this has the same effect
as anoxia. Toxicity is another factor in cell injury and oc-
curs in many forms. Toxic effects in cells can be caused
by high levels of toxic metals, such as lead or mercury;
levels of chemicals, including medicines. In addition, tox-
icity can be caused by substances that the body needs to
function normally, such as sodium and glucose if these
substances are found in too high a concentration.
NECROSIS
Necrosis (death of cells) occurs naturally in apoptosis
when cells die because they have reached the limit of
their programmed life. Autolysis is the term used for
disintegration of cells within a dead body or organism as
a result of loss of respiration and thus oxygen to the tis-
sues. Necrosis of cells in a living body is a response to
abnormal stimuli. Knowledge of the types of necrosis is of
importance to the PTA when working with wounds.
Necrosis occurs in several forms, such as liquefactive,
coagulative, caseous, and fat necrosis.
Liquefactive necrosis occurs when cells die and be-
come liquid. Infarcts in the brain most often cause lique-
faction of brain tissue, forming a cavity with a liquid cen-
ter. This process is precipitated by leukocytes, which
release lytic enzymes that break down the cells into liquid
form to eliminate them. If the appearance of the liquid is
yellow, it is called pus. Pus consists of leukocytes and
dead cell debris.
Coagulative necrosis is so called because the cyto-
plasm has a coagulated appearance. The cells retain a
clear outline, but their nuclei disintegrate. This often oc-
curs in the heart in response to a myocardial infarct
(MI) when the cells experience anoxia (lack of oxygen).
Coagulative necrosis often becomes liquefactive.

Ta b l e 1 . 2 Causes of Cell Injury

CAUSE MECHANISM R E S U LT

Hypoxia Reduced oxygen, eg, suffocation, pneumonia, Short periods—reversible damage

anemia Tissue dependent: heart cells more resilient
than brain cells

Anoxia Complete lack of oxygen Prolonged—irreversible damage

Toxicity Direct—heavy metals such as mercury
Indirect—excessive amounts of certain
drugs or chemical compounds that are
inhaled and cause toxic substances to be
formed inside the body
Death of cells if in large enough concentra-
tion; may be organ specific and depends
on the dose/concentration of the substance
taken

Pathogens—bacteria, Bacteria produce toxins Toxins may kill cells in certain parts of the
viruses Some are directly cytopathic body

Ischemia Loss of blood supply to an area Death of cells due to lack of oxygen transfer
from blood supply
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8 Pathophysiology for the Physical Therapist Assistant

Gangrene is the result of infected coagulative necrotic Cellular Responses to Damage or Stimuli
tissue (see Figure 1-6). The resulting inflammation Changes in cells of either reduction or increase in size or
causes a liquefactive process called wet gangrene. number occur as a result of external stimuli. Some of these
When this turns to a dry, blackened mass of necrotic tis- changes are reversible, and others, such as metaplasia, are
sue, it is known as dry gangrene. PTAs commonly see irreversible. Review Table 1-3 for a comparison of the var-
dry gangrene in the distal lower extremities of clients ious types of growth changes of cells.
with peripheral vascular disease (PVD) and diabetes.
ATROPHY
The condition may also occur in the residual limb of the
Atrophy is a reduction in the size of cells, resulting in a
person with lower extremity amputation as a result of
reduced size of tissue or organs (Fig. 1-7). The PTA is
poor circulation.
often concerned with muscle atrophy in clients due to
Caseous necrosis is a type of coagulative necrosis
that occurs in tuberculosis (TB). Patients with TB form
granulomas in the lung (lumps or foci of granular mate- Ta b l e 1 . 3 Types of Growth Changes of Cells
rial) in which the center of the granuloma becomes
cheese-like in consistency (Latin: caseum = cheese). TYPE CHARACTERISTICS
Fat necrosis occurs in fat tissue due to special lipoly-
Atrophy Reduction in cell size
tic enzymes that only act on fat. One of the most common
Hypertrophy Increase in cell size
examples occurs after a motor vehicle accident (MVA) in Hyperplasia Increase in number of cells
which the seat belt ruptures the pancreas, and the pancre- Involution/hypoplasia Decrease in number of cells
atic enzymes degrade the adjacent fat into fatty acids and Metaplasia Change of cell from one type to
glycerol. another
Dystrophic calcification is a process of hardening or
calcification of necrotic tissues that occurs in arteries,
heart valves, and certain tumors as a result of too much
calcium production. Such calcification can also occur in
cancer, in which case it is called metastatic calcification. Normal cells
Heterotopic calcification, or heterotopic ossifica-
tion, is the development of bone in areas where it is not
normally found, such as in muscles and fascia. This may
occur in cases of posttrauma, such as specific muscle
Atrophy
trauma, traumatic brain injury, spinal cord injury, or fol-
lowing myocardial infarction (MI). Heterotopic calcifica-
tion is most frequently found in muscles and soft tissue in
the areas of the hip, knee, or shoulder.6 The formation of
bone within muscle results in reduced function of the Hypertrophy
structure involved.

Metaplasia

Hyperplasia

FIGURE 1.7 Abnormal cellular growth patterns: atrophy, hypertrophy,

FIGURE 1.6 Gangrene of toes. hyperplasia, metaplasia.
0786_Ch01-001-032.qxd 2/11/11 11:13 AM Page 9
inactivity called disuse atrophy. Atrophy occurs after pro-
tracted periods of enforced immobilization, such as after a
fracture or a prolonged illness. Disuse atrophy is usually re-
versible. The PTA assists clients to regain muscle strength,
bulk, and endurance after these episodes of immobility or
inactivity. Other types of atrophy include physiological ag-
ing of the brain, which results in reduced size, and osteo-
porosis of the bones. Pathological atrophy occurs because
of lack of nutrition as in cancer or malnutrition. Senile de-
mentia is a form of brain cell atrophy. In many cases, the
pathological types of atrophy may not be reversible.
HYPERTROPHY
Hypertrophy is an increase in the size of the individual
cells, resulting in an increased size of tissues and organs.
An example is hypertrophy of the left ventricle of the
heart in response to hypertension (high blood pressure).
Heart striated muscle cells are unable to divide, so they re-
spond to the need to work harder by increasing in size.
This increase in individual cell size increases the overall
size of the heart.
HYPERPLASIA
Hyperplasia is an increase in the number of cells within a tis-
sue or organ. An example includes male benign prostate dis-
ease (benign fibroadenoma), in which the walls of the
prostate gland hypertrophy and cause restriction of the ureter
with associated interference with micturition (passing urine).
Other examples include hyperplasia of the uterus during
pregnancy caused by hormonal changes and hyperplasia of a
kidney in response to surgical removal or disease of the other
kidney. Hyperplasia also occurs as a result of friction on the
skin, which produces calluses and corns. Hyperplastic
polyps within the intestine are common with no known eti-
ology (cause), but these can become neoplastic (cancerous)
and are usually surgically removed as a precaution.
INVOLUTION AND HYPOPLASIA
Involution and hypoplasia are both names for a reduction
in the number of cells within a tissue or organ. However,
involution usually refers to the return to normal size of
an organ, as when the uterus returns to normal size after
delivery of a baby, and also pertains to the process of in-
folding of structures during fetal development to form
such structures as the bladder and other hollow organs. In
contrast, hypoplasia more often refers to the abnormal re-
duction in size of an organ that occurs as an abnormality
of the developmental process of the fetus.
METAPLASIA
In metaplasia, cells change from one type into another.
For example, the columnar cells of the bronchial mucosa
of the respiratory system change into stratified squamous
epithelium cells in response to smoke irritation in the
1 Inflammation and Healing 9
bronchi. Another example of metaplasia is the transition
within tissue that takes place when a tendon graft is used
to replace the anterior cruciate ligament. Over time, the
graft tissue takes on the histological properties of a liga-
ment rather than the original tendon.7–8
When tissue becomes cancerous, as in carcinoma in
situ, the changes in cells lead to loss of function of the tis-
sue, which is referred to as anaplasia, rather than metapla-
sia. Another term applied to tissue changes is dysplasia in
which the tissue develops abnormally in utero. The term
dyscrasia is sometimes used to indicate disease, especially
as in plasma cell dyscrasias such as multiple myeloma,
amyloidosis, and other immune or blood diseases.9
Why Does the Physical Therapist
Assistant Need to Know About
Inflammation?
The treatment of inflammation is basic to physical
therapy. All injuries and illnesses cause inflamma-
tion of body cells, tissues, and organs. Because
the PTA works with people with inflammation re-
sulting from many diseases and injuries, a detailed
knowledge of the inflammatory process is essen-
tial to understanding the treatment interventions
provided at each stage of inflammation. A sound
knowledge of the basics also is essential to be
able to speak knowledgeably to the PT and the
physician. Knowledge of the basic principles of in-
flammation also helps when explaining to pa-
tients the reasons for the advice and treatment
to gain compliance with a home program of
management and exercises.
Inflammation
Inflammation is the body’s response to injury. Short-term in-
flammation is both necessary and desirable after injury be-
cause it promotes healing of tissues and allows the return of
the tissue to the normal state of homeostasis. Any living tis-
sue in the body will react in a typical way to injury with the
four cardinal signs of inflammation: heat (Latin: calor),
redness (rubor), swelling (tumor), and pain (dolor). These
cardinal signs have been recognized since Roman times
when Celsus, a Roman physician, wrote about them.10 In
physical therapy, five cardinal signs of inflammation are re-
ferred to, with the addition of loss of function of the tissue.
The inflammatory response acts both to isolate the injured
area and to resolve the problem. Inflammation can be acute
or chronic. Additionally, in rehabilitation, acute on chronic
0786_Ch01-001-032.qxd 2/11/11 11:13 AM Page 10
10 Pathophysiology for the Physical Therapist Assistant
inflammation is frequently seen, which is an acute injury
superimposed on a preexisting chronic state of inflamma-
tion. Acute inflammation is of sudden onset and short
duration. When this process continues for more than a short
time, it becomes chronic inflammation, which can last for
considerable periods, up to months or even years. Acute on
chronic inflammation is often seen in ankle sprains. When
an ankle is sprained and healing is not complete, a state of
chronic inflammation exists. When a further sprain occurs,
the inflammatory process starts again, and acute inflamma-
tion is added to the already chronic inflammatory state of the
ankle. The mechanisms of inflammation are complicated
but are important for the PTA to understand because of the
implications for physical therapy intervention.
Causes of the Inflammatory Response
Causes of the inflammatory response are varied. Skin
abrasions; burns; cuts; trauma from direct blows or acci-
dents; sunburn; chemical burns; infective organisms such
as bacteria, viruses, fungi, and protozoa; chemicals in-
cluding medicines; and foreign bodies are all possible ini-
tiators of inflammation.
When tissue such as skin is damaged, the mast cells and
platelets release chemicals that affect the surrounding tis-
sues. Histamine, bradykinin, serotonin, and prostaglandins
are some of these chemical mediators of inflammation. His-
tamine is a protein released by damaged platelets, basophils,
and mast cells11 within seconds of tissue damage. First, how-
ever, an immediate vasoconstriction of the tissue is noted,
sometimes as an area of lighter colored skin, due to lack of
blood in the immediate area, and then a weal (red mark)
starts to appear as the result of histamine release. Histamine
causes transudation, increased blood vessel permeability
that allows blood cells and fluid to leak into the extracellu-
lar and interstitial spaces. As a result of transudation, vasodi-
lation occurs, the red effect and edema (swelling) of the
skin. The effect of histamine lasts for about 30 minutes be-
cause the cells quickly produce histaminase, which neutral-
izes the histamine and helps to prevent extensive tissue dam-
age. The release of fluids into the interstitial spaces causes
edema. The effects of this histamine-mediated inflammation
are hyperemia (redness or rubor), edema (swelling or tu-
mor), and mild warmth (calor).12
Following this initial phase of inflammation, conges-
tion of the dilated vessels occurs due to slowing of blood
flow, which results in erythrocytes forming rouleaux or
stacks. White cells attach to the epithelium, causing a
pavementing effect and, in combination with the action of
the platelets, produce clotting. Bradykinin is a plasma
protein with similar effects to those of histamine, includ-
ing vasodilation of blood vessels,13 but it reacts more
slowly, hence the term bradykinin (Greek: brady = slow).
Bradykinin prolongs the inflammatory response and
causes pain, the fourth cardinal sign of inflammation. The
roles of cytokines and fibrin are described in the sections
on healing and immunopathology.
CELLS INVOLVED IN THE INFLAMMATORY RESPONSE
Increased permeability of the blood vessel walls second-
ary to the inflammatory response can last several days.
The transudate, mainly composed of water and a few
blood cells, collects in the extracellular and interstitial
spaces, causing edema.14,15 Another process occurs called
diapedesis in which cells cross the vessel walls into the
affected tissue, forming an exudate that, unlike transu-
date, is rich in protein and inflammatory cells. Most of
the cells initially contained in exudate are polymor-
phonuclear leucocytes (PMNs) closely followed by
eosinophils, and after about 48 hours, monocytes,
macrophages, platelets, basophils, lymphocytes, and
plasma cells appear (see Table 1-4). Exudate can be of
various consistencies, including serous (watery) as in
burns, fibrinous with a thick, gluelike consistency, puru-
lent (containing pus), or hemorrhagic (containing
blood).16
Polymorphonucleocytes
Polymorphonucleocytes, or polymorphonuclear leuco-
cytes (PMNs), also known as neutrophils, are white blood
cells with multiple segmented nuclei, which are mobile
and phagocytic (amoeba-like) and ingest the bacteria and
cell debris in the area of the inflammation (Fig. 1-8).
PMNs release proteins called cytokines, which increase
the inflammatory response. Cytokines stimulate the hypo-
thalamus and cause systemic effects such as fever. The
PMNs only last about 2 to 4 days and are thus part of the
acute phase of inflammation.
Eosinophils
Eosinophils are white blood cells (leukocytes), which are
so called because they stain pink with eosin. These cells
appear approximately 2 to 3 days after the PMNs.
Eosinophils are mobile but slower moving than PMNs
and are phagocytic, bacteriocidal (kill bacteria chemi-
cally), and have a single nucleus with two lobes.17
Eosinophils contain chemicals that are toxic to bacteria
and parasites. These cells are present in respiratory aller-
gic reactions such as asthma and can also be found in
chronic inflammation.
Monocytes and Macrophages
Monocytes are white blood cells produced by the myeloid
stem cells, which are precursors of macrophages. After
these cells are approximately 24 hours old, they mature
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1 Inflammation and Healing 11

Ta b l e 1 . 4 Cells of Inflammation
CELL TYPE DESCRIPTION FUNCTION

Polymorphonucleocytes White blood cells Phagocytic—ingest cell debris/foreign

(PMNs; also known
as neutrophils)
Multiple segmented nuclei
Mobile cells—amoeba-like
Only live approximately 2 days and thus are
part of acute inflammatory response
material from injured site
Migrate to area of injury to engulf debris
Release cytokines, which stimulate a
systemic response of fever by affecting
the hypothalamus

Eosinophils White blood cells Phagocytic

Mobile—slower moving than PMNs and Bacteriocidal—give off chemicals that kill
arrive at inflammation site 2–3 days after bacteria and parasites
PMNs
Single nucleus
Present in chronic inflammation

Monocytes White blood cells Develop into macrophages

Precursors to macrophages

Macrophages (histiocytes) White blood cells Phagocytic

Differentiated from monocytes

Platelets (thrombocytes) Fragments of cytoplasm Release serotonin at site of damaged

tissue which causes vasoconstriction of
the damaged blood vessels
Form rouleaux which help in blood clotting
mechanism
Release histamine and plasma proteins
that facilitate clotting

Basophils White blood cells Precursors of mast cells

Contain histamine which is released during
inflammatory response

Granules
into macrophages18 and enter various tissues of the body.
Trisegmented Macrophages or histiocytes are larger than PMNs and are
neucleus
Golgi also phagocytes. They are the main scavenger cells of the
apparatus immune system.19 The macrophages arrive at the inflam-
mation site around Day 4, and because these cells live a
long time, they are present in chronic inflammation. The
macrophages produce cytokines, which in turn stimulate
an increase in the inflammatory response.

Endoplasmic Platelets
reticulum
Platelets, or thrombocytes, are fragments of cells pro-
duced in bone marrow20 from cells called megakary-
ocytes.21 They circulate in the blood system for about
10 days and are not true cells because they have no nu-
cleus. Platelets release platelet factor, which starts the
Mitochondrion clotting process of blood and the formation of connective
tissue essential for the healing process. The release of
Phagocytic serotonin by the platelets adds to this clotting mechanism
vacuole by causing vasoconstriction of damaged blood vessels
FIGURE 1.8 Polymorphonuclear neutrophils. that helps to seal the damaged blood vessels and thus
0786_Ch01-001-032.qxd 2/11/11 11:13 AM Page 12
12 Pathophysiology for the Physical Therapist Assistant
reduce blood loss (see Chapter 2 for further details).
Platelets are active components of inflammation, appear-
ing especially in the first phases.
Basophils
Basophils are white blood cells that play a part in chronic
inflammation. They are the precursors of mast cells and
produce histamine and platelet activating factor in the
immune response.22
Lymphocytes and Plasma Cells
Lymphocytes and plasma cells play a part mainly in
chronic inflammation; more important, they serve as part
of the immune system. Both of these cell types are de-
scribed in Chapter 2.
Classification of Inflammation
As briefly discussed earlier in this chapter, inflammation
may be subdivided into different categories, including
acute, subacute, chronic, and acute on chronic. In addi-
tion, the difference between transudate and exudate
should be understood. Transudate is a watery fluid that
can build up in the tissues, especially in extracellular
spaces, as a result of fluid passing through the cell mem-
branes of the blood vessels in response to changes in
pressure gradients. This occurs secondary to hyperten-
sion, which causes an increase in hydrostatic pressure
across the blood vessel walls, and there is a leakage of
water and perhaps a few proteins and cells from the ves-
sels into the surrounding tissues. However, hypertension
does not change the selective permeability of the vessel
walls, and therefore most cells are unable to pass
through. Transudate can create edema of the tissues. In
contrast, exudate is the fluid buildup that occurs as a
result of the inflammatory process. Exudate also can
cause edema but consists of water, proteins, and many
of the cells of inflammation previously described. The in-
flammatory process changes the selective permeability of
the vessel walls, resulting in passage of the inflammatory
cells into the interstitial and extracellular spaces. Several
types of inflammation are detailed in Table 1-5.
ACUTE INFLAMMATION
Acute inflammation lasts anywhere from a few hours to
several days.23 In some cases, the area affected remains hot
or warm to palpation (touch) for several days. This heat
may subside somewhat, and the injury is then termed suba-
cute inflammation. Acute inflammation may also reoccur.
The presence of acute inflammation is at least a precaution
and usually a contraindication for most physical therapy
interventions. During this phase, active exercise, most
electrical stimulation techniques, ultrasound, and other heat
modalities are contraindicated. The exception to this rule
may be interferential electrical stimulation.
SUBACUTE INFLAMMATION
The term “subacute inflammation” is sometimes used to
refer to the phase of inflammation that starts after resolu-
tion of the immediate acute inflammation, in most cases
during the first 24 hours postinjury. However, the subacute
phase can last from a few hours to several weeks and may
or may not turn into chronic inflammation. This subacute
phase is actually part of the acute phase. Sometimes the in-
flammation subsides during this phase when factors that
caused the inflammation are removed or resolved. In this
stage, there may still be some heat, erythema, and edema
in the area of injury, but it will have subsided from the
acute phase. This phase is of importance to the PTA be-
cause at this point modalities and PT intervention can be
initiated. After the extreme heat, pain, and edema begin to
subside, the PT and PTA can start to provide modalities to
further reduce the effects of the inflammatory process.
CHRONIC INFLAMMATION
Chronic inflammation can be a sequel to the acute and sub-
acute phases, occur as a result of prolonged healing of the
acute and subacute stages, or be chronic from the onset.
Tuberculosis (TB) is considered a chronic inflammatory
condition from the onset. If the inflammation does not re-
solve within a few days, the tissue is considered to be in a
chronic inflammatory state. In certain cases in which the
inflammation subsides during the subacute phase, there
may not be a chronic inflammatory phase. In other cases,
there may not be an acute phase. The initial injury may not
be severe enough to produce an acute response. If a low-
grade irritant is present, then the area may go straight into
a chronic inflammatory response. Problems that occur due
to chronic inflammation have implications for physical
therapy interventions. Chronic inflammation is more likely
to result in considerable scar tissue within the connective
tissues24 and interferes with the function of the tissue in-
volved. The role of physical therapy intervention in such
cases is to reduce the amount of scar tissue formation and
improve the function of the area. Interventions such as heat
modalities, ultrasound, electrical stimulation, active range
of motion and isometric exercises, massage, and mobiliza-
tion can help improve tissue, joint, and muscle function
during rehabilitation after injury.
ACUTE ON CHRONIC INFLAMMATION
In physical therapy, a pattern of acute on chronic inflam-
mation is often observed. Acute on chronic inflammation
occurs when an injury never fully heals and the area is
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1 Inflammation and Healing 13

Ta b l e 1 . 5 Types of Inflammation
TYPE EXAMPLES CHARACTERISTICS

Serous Burns Clear fluid exudate containing few inflammatory

Skin paper cuts cells as seen in a blister after a burn
Skin abrasions

Fibrinous Bacterial pneumonia Exudate contains a lot of fibrin

Strep throat

Purulent Streptococcal infections Pus producing areas of inflammation

Abscesses Infection usually indicated by yellow or greenish
Sinus exudate
Fistula Abscesses localized within a tissue or organ
Empyema Abscess may have a sinus—a cavity that drains to
the surface of the body, allowing the pus to drain
from the infected abscess
Fistula may form—abnormal cavity or tunnel that
forms joining together two previously existing
cavities or connecting a hollow organ with the
skin surface
Empyema—accumulation of pus in a cavity

Ulcerative Diabetic skin ulcers on lower extremities
secondary to peripheral vascular dis-
ease, causing poor circulation
Intestinal and stomach ulcers
Local areas of skin ulceration (wounds) usually on
the lower extremities; usually in persons with
peripheral vascular disease or diabetes
Ulcers may occur on the epithelial linings of the
stomach or small or large intestines

Pseudomembranous Diphtheria Inflamed areas in bronchi that become covered with

a membrane that can close off the bronchi and
Colitis produce suffocation if not treated
Pseudomembranous inflammation of the colon

Granulomatous Sarcoidosis in lungs Granulomas formed within selective tissue. Walled

Syphilis off, encapsulated areas of inflammatory tissue
TB lungs In tuberculosis, these granulomas may show up on
chest X-ray as an area of white, dense matter
within the lung tissue; these tuberculosis granulo-
mas may remain in the lung indefinitely, but if they
remain encapsulated, they are not dangerous

reinjured. Acute on chronic inflammation also occurs in
chronic inflammatory diseases when an acute exacerba-
tion takes place. Other examples include acute respira-
tory infections in a person with a chronic lung disease,
acute exacerbations of chronic diseases such as multiple
sclerosis, and cases of low back pain in which the origi-
nal injury has not healed correctly or fully and an addi-
tional injury produces an acute inflammatory response in
addition to the chronic problem. Another example is a
sprained ankle in which the ligaments and tendons are
not fully healed, adhesions are present, and the ankle is
resprained, resulting in an acute response superimposed
on the chronically inflamed state of the ankle tissue. One
of the major factors in the resprain of ankles arises from
adhesion formation in the tissues secondary to the origi-
nal injury that are susceptible to reinjury. One aim of PT
intervention is therefore to minimize the formation of
adhesions during intervention for the original injury.
Physical Therapy Treatment for Inflammation
The inflammatory process occurs with all injuries and
open wounds. The following physical therapy interven-
tion is described for closed injuries only. Interventions for
open wounds are described later in this chapter.
Some simple rules apply when dealing with a part of
the body that is inflamed. If it is hot, cool it down. If it is
0786_Ch01-001-032.qxd 2/11/11 11:13 AM Page 14

14 Pathophysiology for the Physical Therapist Assistant

cool, heat it up. Never heat an area that is already hot.

Why Does the Physical Therapist
This could cause a drastic increase in temperature and
Assistant Need to Know About the
lead to irreversible tissue damage. The general adage is
Healing Process?
to use ice in the first 24 hours (acute stage) after injury,
but if the area remains hot or warm to the touch, it is ac-
The process of healing is necessary for all types of
ceptable to continue to use ice on the area. A study by
pathological conditions to return the human
Bleakley et al in 2004 showed that there is insufficient
body to functional levels. Encouraging and en-
evidence-based research to conclude the efficacy of the
hancing the normal physiological healing process
use of ice. The use of ice is according to experience and
is one of the main aims of physical therapy inter-
anecdotal evidence of practice.25 Some people do, how-
ventions. Without an understanding of the stages
ever, respond better to ice than heat at all stages of their
of healing of body tissues, the PTA cannot relate
recovery. Because ultrasound produces thermal effects,
to specific physical therapy interventions that
it is contraindicated for acute inflammation. Interferen-
can enhance the healing process and return pa-
tial therapy, but no other form of electrical stimulation,
tients to their fully functional capacity. The ability
may be used to treat an acute area. If asked whether it is
to identify delays in the healing process also as-
safe to use electrical stimulation on an acute joint or in-
sists the PTA in appropriate communication with
jury, it is always safest to say no and then qualify it with
the supervising PT and physician.
the possibility of interferential therapy. The acronym
A large part of physical therapy practice is in-
RICE is used for inflammation management meaning
volved with stimulating the healing process of
Rest, Ice, Compression, and Elevation. Rest allows the
body tissues. Whether damage to tissues results
body’s healing processes to occur and relieves pain. In a
from disease, injury, illness, or surgery, the PTA will
weight-bearing limb, this means no weight bearing, and
work with many people who have tissue injury.
in an upper extremity, this could mean using a sling to
An understanding of the normal and complex
rest the injured arm. In severe cases such as fracture, a
process of tissue healing is essential to deter-
cast may be used; a splinting device can be used for a
mine which physical therapy interventions are
bad sprain. Ice helps to reduce pain and edema, com-
appropriate at a particular stage of tissue heal-
pression controls edema, and elevation assists with
ing. Recognizing when the healing process has
edema control and may reduce pain as well as stimulate
been compromised is also important so that
venous and lymphatic drainage.
specific physical therapy interventions can be
In the subacute phase, after the first 24 hours, if the
used to stimulate the healing process.
area is not warm to the touch with erythema (red in
appearance), then physical therapy may include such
modalities as electrical stimulation for edema reduction,
pain control and reduction of inflammation, nonthermal Healing
ultrasound to stimulate the healing process, and gentle
active range of motion exercises as tolerated by the HINTS ON THE USE OF THE GUIDE TO PHYSICAL
patient. If the area affected remains warm to the THERAPIST PRACTICE (1-1)
touch with an erythema, continue to apply cold packs to
the area. Skin wounds fall within various areas of the Guide to
If the chronic stage of inflammation develops, types Physical Therapist Practice
of PT intervention can include any modality such as elec- Preferred Practice Pattern: “Integumentary” 7.
trical stimulation to stimulate healing and reduce pain; • 7A practice pattern, “primary prevention/risk reduc-
ultrasound to break down scar tissue, mobilize tissue, and tion for integumentary disorders” (p. 589): patients at
reduce pain; and exercise as appropriate. Transverse risk for developing skin wounds due to factors such as
friction massage may also be necessary to mobilize the reduced skin sensation or reduced physical activity
area and release scar tissue to improve function. This is • 7B “impaired integumentary integrity associated
not an all-inclusive list of interventions. Consult a physi- with superficial skin involvement” (p. 601): patients
cal modalities textbook to determine the parameters for with Stage 2 pressure ulcers, superficial burns, and
electrical stimulation and ultrasound suitable for specific vascular disease due to venous or arterial insuffi-
conditions. ciency and diabetes
0786_Ch01-001-032.qxd 2/11/11 11:13 AM Page 15
• 7C “impaired integumentary integrity associated
with partial-thickness skin involvement and scar for-
mation” (p. 619): if skin involvement is more exten-
sive, as in partial thickness burns, Stage 2 pressure
ulcers, surgical wounds, among others
• 7D “impaired integumentary integrity associated
with full-thickness skin involvement and scar forma-
tion” (p. 637): patients with full-thickness skin
lesions such as frostbite, burns, vascular ulcers, and
Stage 3 pressure ulcers
• 7E “impaired integumentary integrity associated
with skin involvement extending into fascia, muscle,
or bone and scar formation” (p. 655): patients with
problems that extend deeper than the skin into the
muscle, fascia, and bone
Remember that patients may have other comorbid
conditions that place them in other practice patterns
such as those involved with cardiac or musculoskeletal
conditions.
(From the American Physical Therapy Association, 2003. Guide to
physical therapist practice, revised 2nd edition. Alexandria, VA:
APTA. Used with permission.)
Wound healing is classified into two categories.26 First
intention (or primary intention) healing27 is healing of a
clinical or surgical wound or of a skin-penetrating injury
with clear, clean margins that have not become separated
or that can be closed using sutures, staples, or Steristrips.
Examples of such wounds might be a knife or paper cut.
Second intention healing is delayed healing of a surgi-
cal wound or healing of a nonsurgical wound. Second in-
tention healing can also include healing of a wound that
has a loss of skin or where the subcutaneous tissue has
been exposed too long to enable closing of the wound
through use of stitches, staples, or Steristrips. Wounds in
which there is loss of a significant amount of tissue also
fall within this category. This method also covers the
healing of venous stasis ulcers and pressure ulcers. Heal-
ing takes place as the result of the inflammatory process.
Some wounds may never heal, whereas others heal
quickly. Many factors are involved in determining the
rate of healing of a wound. Understanding which cells as-
sist in healing and what their individual functions are in
relation to the process is important for the PTA. Some
areas of the body, such as the skin, heal quickly. Tissues
of the heart and brain were once thought to be unable to
regenerate, but recent findings suggest that new tissue
starts to generate in the areas of loss and revasculariza-
tion of tissue occurs in cases of ischemia.28,29 With the
1 Inflammation and Healing 15
recent scientific work with stem cells, the possibilities of
renewal of tissues in the heart, brain, and spinal cord are
even more encouraging.30,31 However, if there is necrosis
of heart or neuronal cells, there is likely to be permanent
damage to these structures, resulting in varying degrees
of loss of function depending on the location and extent
of the injury.
Cells Involved in the Healing Process
Some of the key cells involved in the healing process in-
clude leucocytes (PMNs), myofibroblasts-angioblasts,
and fibroblasts. As described earlier in the chapter, the
PMNs play a role in the initial phases of healing. PMNs
are among the first cells to arrive at the injury site to start
the cleanup of damaged cells. PMNs live for a few days at
the most, and then the macrophages take over. These
macrophages are present both in chronic inflammation
and in the healing wound. The macrophages produce
chemicals such as cytokines that stimulate the healing
process by acting on the myofibroblasts, fibroblasts, and
angioblasts. In bone healing, the PMNs also stimulate the
osteoblasts.32
MYOFIBROBLASTS
Myofibroblasts are cells with a mixture of properties sim-
ilar to those of smooth muscle cells (myo) and fibroblasts.
Because the cells have similar contractile properties to
those of muscle, they play a part in the contraction of the
wound during the initial phases of healing. This holds the
wound together and allows a network of epithelial cells to
gather and cover the affected area.
ANGIOBLASTS
Angioblasts are precursors of blood vessels. These cells en-
able the macrophages and other phagocytic cells to reach
the wound and remove necrotic tissue, such as the scab. In
a larger open wound, they form a red dotted effect in the
wound bed called granulation tissue (see Fig. 1-9). The
appearance of granulation tissue in the base of a wound
indicates that the wound is healthy and healing.
FIBROBLASTS
Fibroblasts produce fibrin and collagen (fibronectin).
The fibrin acts as a sticky mesh across the wound to bind
the cells together, forming a network of fibers across the
wound and holding the entire wound together. Collagen is
the basic structure of the network that forms across the
wound to strengthen the healing area and is known as con-
nective tissue. Collagen is composed of protein molecules
and is found throughout the body in all tissues and organs.
Many types of collagen exist, but four main types are of
significance in physical therapy: Types I through IV.33
0786_Ch01-001-032.qxd 2/11/11 11:13 AM Page 16

16 Pathophysiology for the Physical Therapist Assistant

providing tensile strength to skin, and the Type III giving

it the resistance to friction. The first type to form in the
wound is similar to Type III collagen. Type III collagen
contains thin strands, which give body tissues strength
and flexibility. Type III collagen forms the initial scar tis-
sue of a wound. This collagen is the one that provides a
network of fibers across the wound to support the under-
lying healing blood vessels and cells. As the wound ma-
tures, the Type III collagen is replaced by Type I collagen.
Type I collagen forms the scar tissue, which replaces the
original skin. Type I collagen is fairly strong but lacks the
elasticity of the original skin.35,36

FIGURE 1.9 Granulation tissue in the base of a wound. From
Sussman, C., & Bates-Jensen, B. M. (2001). Wound care: a col-
laborative practice manual for physical therapists and nurses,
2nd edition. Gaithersburg, MD: Aspen, Plate 8, color plate p. 3.
Reproduced with permission.
Each type of collagen serves a different purpose (see
Table 1-6). Normal skin contains a lot of both Type I and
Type III collagen, giving it elasticity and strength. The
proportions of types of collagen in skin change over
the life span.34 In most cases, normal tissue is composed
of several types of collagen fibers, the Type I fibers
Types of Healing
Healing takes place in one of two ways, either through the
process of regeneration of tissue that was minimally dam-
aged or a process of repair in which the original tissue is
replaced with scar tissue. In reversible cell injury, as previ-
ously described, the process of healing is through regener-
ation. The cells recover and are replaced with cells of the
same type that were damaged. This process is achieved
through cell mitosis of the involved organ or tissue.
Irreversible cell injury in most tissues and organs re-
sults in repair with fibrous connective tissue. In this
process, tissues that have undergone necrosis are replaced
by tissue that is not the same as the original tissue. When
replaced in this way, there is a loss of function of the
tissue because the cells no longer have the functional
properties of the ones they replace, and the result is a fi-
brosis. Cirrhosis of the liver is an example of fibrosis. This
replacement of original tissue by fibrotic connective tissue

Ta b l e 1 . 6 Types of Collagen
TYPE STRUCTURE L O C AT I O N FUNCTION

Type I A thick bundle of protein fibers Tendons, bones, mature scar Provides strength
that mixes with other types of tissue
collagen

Type II Thin filaments Cartilage Flexibility and strength

Type III Thin filaments with cross-
bridges of disulfide molecules
Wound healing in initial scarring
Skin and blood vessels
Supports the developing blood
vessels in the base of a
wound in initial stages of
healing
Pliability and strength

Type IV Protein mass not fibers Basement membranes through- Provides an attachment for the
out the body cells of epithelium and en-
dothelium when mixed with
other proteins
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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