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DOM Scripting Web Design with JavaScript and the
Document Object Model 2nd Edition Jeremy Keith
Digital Instant Download
Author(s): Jeremy Keith, Jeffrey Sambells (auth.)
ISBN(s): 9781430233909, 1430233907
Edition: 2
File Details: PDF, 4.21 MB
Year: 2010
Language: english
 DOM Scripting
Web Design with JavaScript and the
Document Object Model
Second Edition

■■■

Jeremy Keith
with Jeffrey Sambells

i
 DOM Scripting: Web Design with JavaScript and the Document Object Model: Second Edition
Copyright © 2010 by Jeremy Keith with Jeffrey Sambells
All rights reserved. No part of this work may be reproduced or transmitted in any form or by any
means, electronic or mechanical, including photocopying, recording, or by any information
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Publisher and President: Paul Manning

Lead Editor: Ben Renow-Clarke
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Editorial Board: Steve Anglin, Mark Beckner, Ewan Buckingham, Gary Cornell, Jonathan
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ii
 For Jessica, my wordridden wife
—Jeremy

For Stephanie, Addison, and Hayden, always by my side

—Jeffrey

iii
 Contents at a Glance

■Contents ................................................................................................................ v

■About the Authors .............................................................................................. xiii

■About the Technical Reviewer............................................................................ xiv

■Acknowledgments............................................................................................... xv

■Introduction ....................................................................................................... xvi
■Chapter 1: A Brief History of JavaScript ............................................................... 1

■Chapter 2: JavaScript Syntax ................................................................................ 7

■Chapter 3: The Document Object Model .............................................................. 31

■Chapter 4: A JavaScript Image Gallery ............................................................... 45

■Chapter 5: Best Practices .................................................................................... 59

■Chapter 6: The Image Gallery Revisited .............................................................. 73

■Chapter 7: Creating Markup on the Fly ............................................................... 95

■Chapter 8: Enhancing Content ........................................................................... 123

■Chapter 9: CSS-DOM .......................................................................................... 149

■Chapter 10: An Animated Slideshow ................................................................. 175

■Chapter 11: HTML5 ............................................................................................ 205

■Chapter 12: Putting It All Together.................................................................... 227

■Appendix: DOM Scripting Libraries ................................................................... 279

■Index ................................................................................................................. 303

iv
Contents

■Contents at a Glance ............................................................................................ iv

■About the Authors .............................................................................................. xiii

■About the Technical Reviewer............................................................................ xiv

■Acknowledgments............................................................................................... xv

■Introduction........................................................................................................ xvi

■Chapter 1: A Brief History of JavaScript ............................................................... 1

The origins of JavaScript ................................................................................................ 1

The Document Object Model ........................................................................................... 2

The browser wars ........................................................................................................... 3

The D word: DHTML ............................................................................................................................... 3

Clash of the browsers ............................................................................................................................ 3

Raising the standard ....................................................................................................... 4

Thinking outside the browser ................................................................................................................ 4

The end of the browser wars ................................................................................................................. 4

A new beginning .................................................................................................................................... 5

What’s next? ................................................................................................................... 5

■Chapter 2: JavaScript Syntax ................................................................................ 7

What you’ll need ............................................................................................................. 7

Syntax ............................................................................................................................. 9

Statements ............................................................................................................................................. 9

Comments ............................................................................................................................................ 10

Variables .............................................................................................................................................. 10

v
■ CONTENTS

Data types ............................................................................................................................................ 12

Arrays ................................................................................................................................................... 14

Objects ................................................................................................................................................. 16

Operations ..................................................................................................................... 17

Arithmetic operators ............................................................................................................................ 17

Conditional statements ................................................................................................. 19

Comparison operators .......................................................................................................................... 20

Logical operators ................................................................................................................................. 21

Looping statements ...................................................................................................... 22

The while loop ...................................................................................................................................... 22

The for loop .......................................................................................................................................... 24

Functions ...................................................................................................................... 24

Objects .......................................................................................................................... 27

Native objects ...................................................................................................................................... 28

Host objects ......................................................................................................................................... 29

What’s next? ................................................................................................................. 29

■Chapter 3: The Document Object Model .............................................................. 31

D is for document.......................................................................................................... 31

Objects of desire ........................................................................................................... 31

Dial M for model............................................................................................................ 32

Nodes ............................................................................................................................ 33

Element nodes ..................................................................................................................................... 34

Text nodes............................................................................................................................................ 34

Attribute nodes..................................................................................................................................... 34

Cascading Style Sheets........................................................................................................................ 35

Getting Elements .................................................................................................................................. 37

Taking stock ......................................................................................................................................... 41

Getting and Setting Attributes ....................................................................................... 41

getAttribute .......................................................................................................................................... 41

vi
 ■ CONTENTS

setAttribute .......................................................................................................................................... 43

What’s next? ................................................................................................................. 44

■Chapter 4: A JavaScript Image Gallery ............................................................... 45

The markup ................................................................................................................... 45

The JavaScript .............................................................................................................. 47

A DOM diversion ................................................................................................................................... 48

Finishing the function .......................................................................................................................... 49

Applying the JavaScript ................................................................................................ 49

Event handlers ..................................................................................................................................... 49

Expanding the function ................................................................................................. 51

Introducing childNodes ........................................................................................................................ 51

Introducing the nodeType property ...................................................................................................... 52

Adding a description in the markup ..................................................................................................... 53

Changing the description with JavaScript ........................................................................................... 54

Introducing the nodeValue property ..................................................................................................... 54

Introducing firstChild and lastChild ...................................................................................................... 55

Using nodeValue to update the description ......................................................................................... 55

What’s next? ................................................................................................................. 58

■Chapter 5: Best Practices .................................................................................... 59

Mistakes of the past ..................................................................................................... 59

Don’t blame the messenger ................................................................................................................. 59

The Flash mob...................................................................................................................................... 60

Question everything ............................................................................................................................. 60

Graceful degradation .................................................................................................... 61

The javascript: pseudo-protocol .......................................................................................................... 62

Inline event handlers ............................................................................................................................ 62

Who cares? .......................................................................................................................................... 63

The lessons of CSS ....................................................................................................... 63

Separation of structure and style ......................................................................................................... 63

vii
 ■ CONTENTS

Progressive enhancement ................................................................................................................... 64

Unobtrusive JavaScript ................................................................................................. 65

Backward compatibility ................................................................................................ 67

Object detection ................................................................................................................................... 67

Browser sniffing ................................................................................................................................... 68

Performance considerations ......................................................................................... 69

Minimizing DOM access and markup................................................................................................... 69

Assembling and placing scripts ........................................................................................................... 70

Minification .......................................................................................................................................... 70

What’s next? ................................................................................................................. 71

■Chapter 6: The Image Gallery Revisited .............................................................. 73

A quick recap ................................................................................................................ 73

Does it degrade gracefully? .......................................................................................... 74

Is the JavaScript unobtrusive? ..................................................................................... 75

Adding the event handler ..................................................................................................................... 75

Share the load ...................................................................................................................................... 80

Assuming too much ...................................................................................................... 82

Fine-tuning.................................................................................................................... 84

Keyboard access ........................................................................................................... 86

Beware of onkeypress ......................................................................................................................... 87

Sharing hooks with CSS................................................................................................ 88

DOM Core and HTML-DOM ............................................................................................ 91

What’s next? ................................................................................................................. 92

■Chapter 7: Creating Markup on the Fly ............................................................... 95

Some old-school methods ............................................................................................ 95

document.write .................................................................................................................................... 95

innerHTML ............................................................................................................................................ 97

DOM methods ............................................................................................................. 100

createElement .................................................................................................................................... 101

viii
 ■ CONTENTS

appendChild ....................................................................................................................................... 102

createTextNode .................................................................................................................................. 103

A more complex combination ............................................................................................................ 105

Revisiting the image gallery ....................................................................................... 107

Inserting a new element before an existing one ................................................................................ 109

Inserting a new element after an existing one................................................................................... 110

The finished image gallery ................................................................................................................. 112

Ajax ............................................................................................................................. 116

The XMLHttpRequest object ............................................................................................................... 116

Progressive enhancement with Ajax .................................................................................................. 121

Hijax ................................................................................................................................................... 121

What’s next? ............................................................................................................... 122

■Chapter 8: Enhancing Content ........................................................................... 123

What not to do............................................................................................................. 123

Making the invisible visible......................................................................................... 124

The content ................................................................................................................. 124

The markup: HTML, XHTML, or HTML5 .............................................................................................. 125

The CSS .............................................................................................................................................. 127

The JavaScript ................................................................................................................................... 128

Displaying abbreviations ............................................................................................. 128

Writing the displayAbbreviations function ......................................................................................... 129

Creating the markup .......................................................................................................................... 131

A browser bomb ................................................................................................................................. 136

Displaying citations ..................................................................................................... 139

Writing the displayCitations function ................................................................................................. 140

Displaying access keys ............................................................................................... 145

Retrieving and attaching information ......................................................................... 148

What’s next? ............................................................................................................... 148

ix
■ CONTENTS

■Chapter 9: CSS-DOM.......................................................................................... 149

Three sheets to the Web ............................................................................................. 149

Structure ............................................................................................................................................ 149

Presentation ....................................................................................................................................... 150

Behavior ............................................................................................................................................. 150

Separation .......................................................................................................................................... 151

The style property ....................................................................................................... 152

Getting styles ..................................................................................................................................... 153

Setting styles ..................................................................................................................................... 158

Knowing when to use DOM styling ............................................................................. 160

Styling elements in the node tree ...................................................................................................... 160

Repetitive styling ............................................................................................................................... 164

Responding to events......................................................................................................................... 168

className .................................................................................................................. 170

Abstracting a function ........................................................................................................................ 173

What’s next? ............................................................................................................... 174

■Chapter 10: An Animated Slideshow ................................................................. 175

Animation basics......................................................................................................... 175

Position .............................................................................................................................................. 175

Time ................................................................................................................................................... 178

Incremental movement ...................................................................................................................... 178

Abstraction ......................................................................................................................................... 181

Practical animation ..................................................................................................... 187

The situation ...................................................................................................................................... 188

The solution ....................................................................................................................................... 189

CSS..................................................................................................................................................... 190

JavaScript .......................................................................................................................................... 192

A question of scope............................................................................................................................ 195

Refining the animation ....................................................................................................................... 197

Adding a safety check ........................................................................................................................ 200

x
 ■ CONTENTS

Generating markup ............................................................................................................................ 201

What’s next? ............................................................................................................... 204

■Chapter 11: HTML5 ............................................................................................ 205

What is HTML5? .......................................................................................................... 205

A little help from a friend ............................................................................................ 206

A few examples .......................................................................................................... 208

Canvas ............................................................................................................................................... 208

Audio/Video ........................................................................................................................................ 213

Forms ................................................................................................................................................. 221

Is there anything else?................................................................................................ 225

What's Next ................................................................................................................. 226

■Chapter 12: Putting It All Together.................................................................... 227

The brief ...................................................................................................................... 227

Raw materials .................................................................................................................................... 227

Site structure ..................................................................................................................................... 227

Page structure.................................................................................................................................... 229

Design ......................................................................................................................... 229

CSS ............................................................................................................................. 230

Color ................................................................................................................................................... 232

Layout ................................................................................................................................................ 234

Typography ........................................................................................................................................ 236

Markup ........................................................................................................................ 238

JavaScript ................................................................................................................... 238

Page highlighting ............................................................................................................................... 240

JavaScript slideshow ......................................................................................................................... 243

Internal navigation ............................................................................................................................. 248

JavaScript image gallery ................................................................................................................... 252

Table enhancements .......................................................................................................................... 256

Form enhancements .......................................................................................................................... 261

xi
 ■ CONTENTS

Minification ........................................................................................................................................ 276

What’s next? ............................................................................................................... 277

■Appendix: DOM Scripting Libraries ................................................................... 279

Choosing a library ....................................................................................................... 280

A few libraries .................................................................................................................................... 281

Content delivery networks ................................................................................................................. 282

Syntax ......................................................................................................................... 283

Selecting elements ..................................................................................................... 284

CSS selectors ..................................................................................................................................... 284

Library-specific selectors .................................................................................................................. 286

Filtering with a callback ..................................................................................................................... 288

Manipulating the DOM document ............................................................................... 289

Creating content................................................................................................................................. 289

Manipulating content ......................................................................................................................... 291

Handling events .......................................................................................................... 291

Load events ........................................................................................................................................ 291

Other events ....................................................................................................................................... 292

Ajax ............................................................................................................................. 293

Ajax with Prototype ............................................................................................................................ 293

Ajax with jQuery ................................................................................................................................. 296

Animation and effects ................................................................................................. 298

CSS property-based animations ........................................................................................................ 299

Packaged animations ......................................................................................................................... 300

Remember accessibility ..................................................................................................................... 301

Summary..................................................................................................................... 301
■Index ................................................................................................................. 303

xii
About the Authors

■ Jeremy Keith is a web developer living and working in Brighton, England. Working with the web
consultancy firm Clearleft (www.clearleft.com), Jeremy enjoys building accessible, elegant websites
using the troika of web standards: XHTML, CSS, and the DOM. His online home is http://adactio.com.
Jeremy is also a member of the Web Standards Project (www.webstandards.org), where he serves as joint
leader of the DOM Scripting Task Force. When he is not building websites, Jeremy plays bouzouki in the
alt.country band Salter Cane (www.saltercane.com). He is also the creator and curator of one of the Web’s
largest online communities dedicated to Irish traditional music, The Session (www.thesession.org).

■ Jeffrey Sambells is a Canadian designer of pristine pixel layouts and a developer of squeaky clean
code. Back in the good-old days of the Internet, he started a little company called We-Create. Today, he
is still there as Director of Research and Development / Mobile. The title “Director of R&D” may sound
flashy, but really, that just means he is in charge of learning and cramming as much goodness into
products as possible—ensuring they’re all just awesome. He is currently having fun exploring mobile
design and development techniques. Jeffrey loves to learn. He has as much enthusiasm for digging in the
dirt or climbing a cliff as he does for precisely aligning pixels or forcing that page to load just a little
faster. What really pushes him forward is taking the bits of knowledge he has collected and piecing them
together into something new and unique—something other people can be excited about, too. Along the
way, Jeffrey has managed to graduate university, start a few businesses, write some books, and raise a
wonderful family.

xiii
■ CONTENTS

About the Technical Reviewer

■ Rob Drimmie is lucky. He has an amazing wife, two awesome kids, and a brand-new keyboard. Rob's
creative urges tend to manifest in the form of web applications, and he prefers they be fueled by pho and
hamburgers (the creative urges, that is).

xiv
Acknowledgments

This book owes its existence to my friends and colleagues, Andy Budd (http://andybudd.com) and
Richard Rutter (http://clagnut.com). Andy runs a (free) training event in our hometown of Brighton
called Skillswap (http://www.skillswap.org). Way back in July 2004, Richard and I gave a joint
presentation on JavaScript and the Document Object Model. Afterward, we adjourned to the cozy
confines of a nearby pub, where Andy put the idea in my head of expanding the talk into the first edition
of this book.
I would never have learned to write a single line of JavaScript if it weren’t for two things. The first is the
view source option built in to almost every web browser. Thank you, view source. The second is the
existence of JavaScript giants who have been creating amazing code and explaining important ideas over
the years. Scott Andrew, Aaron Boodman, Steve Champeon, Peter-Paul Koch, Stuart Langridge, and
Simon Willison are just some of the names that spring to mind. Thank you all for sharing.
Thanks to Molly Holzschlag for sharing her experience and advice with me, and for giving me feedback
on early drafts. Thanks to Derek Featherstone for many a pleasurable JavaScriptladen chat; I like the way
your mind works.
Extra-special thanks to Aaron Gustafson who provided invaluable feedback and inspiration during the
writing of this book.
While I was writing the first edition of this book, I had the pleasure of speaking at two wonderful events:
South by Southwest in Austin, Texas, and @media in London. Thanks to Hugh Forrest and Patrick
Griffiths, respectively, for orchestrating these festivals of geekery that allowed me to meet and befriend
the nicest, friendliest bunch of people I could ever hope to call my peers.
Finally, I’d like to thank my wife, Jessica Spengler, not only for her constant support, but also for her
professional help in proofreading my first drafts. Go raibh míle maith agat, a stór mo chroí.

Jeremy Keith

xv
■ CONTENTS

Introduction

This book deals with a programming language, but it isn’t intended for programmers. This is a book for
web designers. Specifically, this book is intended for standards-aware designers who are comfortable
using CSS and HTML. If that sounds like you, read on.
This book is made up of equal parts code and concepts. Don’t be frightened by the code. I know it
might look intimidating at first, but once you’ve grasped the concepts behind the code, you’ll find
yourself reading and writing in a new language.
Learning a programming language might seem like a scary prospect, but it needn’t be. Document
Object Model (DOM) scripting might appear to be more verbose than, say, CSS. But once you have the
hang of the syntax, you’ll find yourself armed with a powerful web development tool. In any case, the
code is there simply to illustrate the concepts.
I’ll let you in on a secret: no one memorizes all the syntax and keywords that are part and parcel of
any programming language. That’s what reference books are for. This isn’t a reference book. I’m going to
cover the bare minimum of syntax required to get up and running with JavaScript.
In this book, I focus on the ideas behind DOM scripting. A lot of these ideas might already be
familiar to you. Graceful degradation, progressive enhancement, and user-centered design are
important concepts in any aspect of front-end web development. These ideas inform all the code
examples given in this book.
You’ll find scripts for creating image galleries, animating slideshows, and enhancing the look and
feel of page elements. If you want, you can simply cut and paste these examples, but it’s more important
to understand the hows and whys that lie behind the code.
If you’re already using CSS and HTML to turn your designs into working web pages, then you
already know how powerful web standards can be. Remember when you discovered that you could
change the design throughout an entire site just by changing one CSS file? The DOM offers an equal level
of power. But with great power comes great responsibility. That’s why I’m not just going to show you
cool DOM scripting effects. I’m also going to show you how to use DOM scripting to enhance your web
pages in a usable, accessible way.
To get all the code examples discussed in the book, pay a visit to www.friendsofed.com and find this
book’s page. At the friends of ED site, you can also find out about all the other great books the publisher
has to offer on web standards, Flash, Dreamweaver, and much more besides.
Your exploration of DOM scripting needn’t end when you close this book. I’ve set up a website at
http://domscripting.com/, where I continue the discussion of modern, standards-based JavaScript. I
hope you’ll pay the site a visit. In the meantime, enjoy the book.

xvi
CHAPTER 1
■■■

A Brief History of JavaScript

What this chapter covers:

• The origins of JavaScript
• The browser wars
• The evolution of the DOM
When the first edition of this book was published in 2005, it was an exciting time to be a web
designer. Thankfully, five years later, it still is. This is especially true for JavaScript, which has been
pulled from the shadows and into the spotlight. Web development has evolved from its chaotic,
haphazard roots into a mature discipline. Designers and developers are adopting a standards-based
approach to building websites, and the term web standards has been coined to describe the technologies
that enable this approach.
Whenever designers discuss the subject of web standards, Hypertext Markup Language (HTML) and
Cascading Style Sheets (CSS) usually take center stage. However, a third technology has been approved
by the World Wide Web Consortium (W3C) and is supported by all standards-compliant web browsers.
This is the Document Object Model (DOM), which allows us to add interactivity to our documents in
much the same way that CSS allow us to add styles.
Before looking at the DOM, let’s examine the language that you’ll be using to make your web pages
interactive. The language is JavaScript, and it has been around for quite some time.

The origins of JavaScript

JavaScript was developed by Netscape, in collaboration with Sun Microsystems. Before JavaScript, web
browsers were fairly basic pieces of software capable of displaying hypertext documents. JavaScript was
later introduced to add some extra spice to web pages and to make them more interactive. The first
version, JavaScript 1.0, debuted in Netscape Navigator 2 in 1995.
At the time of JavaScript 1.0’s release, Netscape Navigator dominated the browser market. Microsoft
was struggling to catch up with its own browser, Internet Explorer, and was quick to follow Netscape’s
lead by releasing its own VBScript language, along with a version of JavaScript called JScript, with the
delivery of Internet Explorer 3. As a response to this, Netscape and Sun, together with the European
Computer Manufacturers Association (ECMA), set about standardizing the language. The result was
ECMAScript, yet another name for the same language. Though the name never really stuck, we should
really be referring to JavaScript as ECMAScript.
JavaScript, ECMAScript, JScript—whatever you want to call it—was gaining ground by 1996. Version
3 browsers from Netscape and Microsoft both supported the JavaScript 1.1 language to varying degrees.

1
CHAPTER 1 ■ A BRIEF HISTORY OF JAVASCRIPT

■ Note JavaScript has nothing to do with Java, a programming language developed by Sun Microsystems.
JavaScript was originally going to be called LiveScript. JavaScript was probably chosen to make the new language
sound like it was in good company. Unfortunately, the choice of this name had the effect of confusing the two
languages in people’s minds—a confusion that was amplified by the fact that web browsers also supported a form
of client-side Java. However, while Java’s strength lies in the fact that it can theoretically be deployed in almost
any environment, JavaScript was always intended for the confines of the web browser.

JavaScript is a scripting language. Unlike a program that does everything itself, the JavaScript
language simply tells the web browser what to do. The web browser interprets the script and does all the
work, which is why JavaScript is often compared unfavorably with compiled programming languages
like Java and C++. But JavaScript’s relative simplicity is also its strength. Because it has a low barrier to
entry, nonprogrammers who wanted to cut and paste scripts into their existing web pages quickly
adopted the language.
JavaScript also offers developers the chance to manipulate aspects of the web browser. For example,
the language could be used to adjust the properties of a browser window, such as its height, width, and
position. Addressing the browser’s own properties in this way can be thought of as a Browser Object
Model. Early versions of JavaScript also provided a primitive sort of DOM.

The Document Object Model

What is the DOM? In short, the DOM is a way of conceptualizing the contents of a document.
In the real world, we all share something that could be called a World Object Model. We can refer to
objects in our environment using terms like car, house, and tree, and be fairly certain that our terms will
be understood. That’s because we have mutually agreed on which objects the words refer to specifically.
If you say “The car is in the garage,” it’s safe to assume that the person you’re talking to won’t take that
to mean “The bird is in the cupboard.”
Our World Object Model isn’t restricted to tangible objects though; it also applies to concepts. For
instance, you might refer to “the third house on the left” when giving directions. For that description to
make sense, the concepts of “third” and “left” must be understood. If you give that description to
someone who can’t count, or who can’t tell left from right, then the description is essentially
meaningless, whether or not the words have been understood. In reality, because people agree on a
conceptual World Object Model, very brief descriptions can be full of meaning. You can be fairly sure
that others share your concepts of left and third.
It’s the same situation with web pages. Early versions of JavaScript offered developers the ability to
query and manipulate some of the actual contents of web documents—mostly images and forms.
Because the terms images and forms had been predefined, JavaScript could be used to address the third
image in the document or the form named details, as follows:
document.images[2]
document.forms['details']
This first, tentative sort of DOM is often referred to as DOM Level 0. In those early, carefree days, the
most common usage of DOM Level 0 was for image rollovers and some client-side form validation. But
when the fourth generation of browsers from Netscape and Microsoft appeared, the DOM really hit the
fan.

2
 CHAPTER 1 ■ A BRIEF HISTORY OF JAVASCRIPT

The browser wars

Netscape Navigator 4 was released in June 1997, and by October of that year, Internet Explorer 4 had also
been released. Both browsers promised improvements on previous versions, along with many additions
to what could be accomplished with JavaScript, using a greatly expanded DOM. Web designers were
encouraged to test-drive the latest buzzword: DHTML.

The D word: DHTML

DHTML is short for Dynamic HTML. Not a technology in and of itself, DHTML is a shorthand term for
describing the combination of HTML, CSS, and JavaScript. The thinking behind DHTML went like this:

• You could use HTML to mark up your web page into elements.
• You could use CSS to style and position those elements.
• You could use JavaScript to manipulate and change those styles on the fly.
Using DHTML, complex animation effects suddenly became possible. Let’s say you used HTML to
mark up a page element like this:
<div id="myelement">This is my element</div>
You could then use CSS to apply positioning styles like this:
#myelement {
position: absolute;
left: 50px;
top: 100px;
}
Then, using JavaScript, you could change the left and top styles of myelement to move it around on
the page. Well, that was the theory anyway.
Unfortunately for developers, the Netscape and Microsoft browsers used different, incompatible
DOMs. Although the browser manufacturers were promoting the same ends, they each approached the
DOM issue in completely different ways.

Clash of the browsers

The Netscape DOM made use of proprietary elements called layers. These layers were given unique IDs
and then addressed through JavaScript like this:
document.layers['myelement']
Meanwhile, the Microsoft DOM would address the same element like this:
document.all['myelement']
The differences didn’t end there. Let’s say you wanted to find out the left position of myelement and
assign it to the variable xpos. In Netscape Navigator 4, you would do it like this:
var xpos = document.layers['myelement'].left;
Here’s how you would do the same thing in Internet Explorer 4:
var xpos = document.all['myelement'].leftpos;

3
CHAPTER 1 ■ A BRIEF HISTORY OF JAVASCRIPT

This was clearly a ridiculous situation. Developers needed to double their code to accomplish any
sort of DOM scripting. In effect, many scripts were written twice: once for Netscape Navigator and once
for Internet Explorer. Convoluted browser sniffing was often required to serve up the correct script.
DHTML promised a world of possibilities, but anyone who actually attempted to use it discovered a
world of pain instead. It wasn’t long before DHTML became a dirty (buzz)word. The technology quickly
garnered a reputation for being both overhyped and overly difficult to implement.

Raising the standard

While the browser manufacturers were busy engaging in their battle for supremacy, and using
competing DOMs as weapons in their war, the W3C was quietly putting together a standardized DOM.
Fortunately, the browser vendors were able to set aside their mutual animosity. Netscape, Microsoft,
and other browser manufacturers worked together with the W3C on the new standard, and DOM Level 1
was completed in October 1998.
Consider the example in the previous section. We have a <div> with the ID myelement, and we’re
trying to ascertain the value that has been applied to its left position so that we can store that value as
the variable xpos. Here’s the syntax we would use with the new standardized DOM:
var xpos = document.getElementById('myelement').style.left
At first glance, that might not appear to be an improvement over the nonstandard, proprietary
DOMs. However, the standardized DOM is far more ambitious in its scope.
While the browser manufacturers simply wanted some way to manipulate web pages with
JavaScript, the W3C proposed a model that could be used by any programming language to manipulate
any document written in any markup language.

Thinking outside the browser

The DOM is what’s known as an application programming interface (API). APIs are essentially
conventions that have been agreed upon by mutual consent. Real-world equivalents would be things
like Morse code, international time zones, and the periodic table of the elements. All of these are
standards, and they make it easier for people to communicate and cooperate. In situations where a
single convention hasn’t been agreed upon, the result is often disastrous. For example, competition
between metric and imperial measurements has resulted in at least one failed Mars mission.
In the world of programming, there are many different languages, but there are many similar tasks.
That’s why APIs are so handy. Once you know the standard, you can apply it in many different
environments. The syntax may change depending on the language you’re using, but the convention
remains the same.
So, while we focus specifically on using the DOM with JavaScript in this book, your new knowledge
of the DOM will also be useful if you ever need to parse an XML document using a programming
language like PHP or Python.
The W3C defines the DOM as “A platform- and language-neutral interface that will allow programs
and scripts to dynamically access and update the content, structure, and style of documents.” The
independence of the standardized DOM, together with its powerful scope, places it head and shoulders
above the proprietary DOMs created by the bickering browser manufacturers.

The end of the browser wars

Microsoft won the battle against Netscape for browser market-share supremacy. Ironically, the clash of
competing DOMs and proprietary markup had little effect on the final outcome. Internet Explorer was
destined to win simply by virtue of the fact that it came preinstalled on all PCs running the Windows
operating system.

4
Other documents randomly have
different content
tissue below. In the deeper part of the mucosa, about the muscularis and especially about and
between the acini of the mucous glands, the tissue is infiltrated with lymphoid and plasma cells.
Changes in the mucous glands are invariably present. These changes are distention of ducts and
acini with mucous, degenerative changes occasionally ending in necrosis of cells, disappearance of
acini, dense infiltration of interstitial tissue with lymphoid and plasma cells and finally proliferation of
this interstitial tissue. The duct of a mucous gland, dilated and filled with mucus, may be
surrounded by lymphoid and plasma cells in great number. Acini, similarly dilated, contain mucus
and are composed of cubical cells which have discharged their mucous content. In some instances
(e. g., Autopsy 257) the cells of the acini have undergone necrosis; the cytoplasm stains
homogeneously and the nuclei have disappeared. Where necrosis has occurred, polynuclear
leucocytes may penetrate into the dead cells. In association with degenerative changes in the acini
there is abundant infiltration of the interstitial tissue within and about the glands with lymphoid and
plasma cells. When the acini have disappeared there is proliferation of fibroblasts and new formation
of fibrous tissue, and mucous glands are found in which a few atrophied acini are separated by
newly formed fibrous tissue.
With the bronchitis of influenza the small bronchi (with no cartilage or mucous glands) show
every stage of transition from early acute inflammation characterized by accumulation of polynuclear
leucocytes within the lumen, engorgement of blood vessels, and infiltration of the wall with
polynuclear leucocytes, through various stages of destructive changes to complete disappearance of
the bronchial wall and formation of an abscess cavity at the site of the bronchus. In the early stages
of acute bronchitis, hemorrhage is frequently associated with the lesion. Blood may be abundant
within the lumen of the bronchus, and in the mucosa red blood corpuscles often infiltrate the tissue
around greatly distended blood vessels, or accumulating below the epithelium, separate it from its
basement membrane. Hemorrhage is not limited to the wall of the bronchus, but frequently occurs
into the alveoli in a zone encircling the bronchus.
With acute bronchitis there may be desquamation of epithelial cells with partial or complete loss
of epithelial lining. In the smallest bronchi the single layer of columnar cells may be separated in
places from the underlying tissue, so that intact rows of cells are found within the lumen. In
somewhat larger bronchi, lined by epithelium in multiple layers, superficial columnar ciliated cells
may be lost. In some instances superficial epithelial cells appear to have lost their cohesion and are
separated by narrow spaces; in these instances, polynuclear leucocytes are often numerous
between epithelial cells. Epithelium is occasionally separated from its basement membrane by small
accumulations of serum or blood. Occasionally necrosis of epithelial cells with disappearance of
nuclei is seen and is doubtless caused by the action of bacteria; the affected cells may be raised
from the underlying tissue by accumulated serum (Autopsy 253). The changes which have been
described bring about partial or complete loss of the ciliated lining of the bronchial tube.
The severity of changes in the bronchial wall is in direct relation to the extent of destruction of
the lining epithelium: when the epithelium remains intact polynuclear leucocytes may be found in
considerable number immediately below it, but as the lesion progresses, cells in great part
mononuclear, namely, lymphoid and plasma cells, accumulate in large number throughout the wall
of the bronchus. There is often abundant cellular infiltration within and about the bundles of the
muscular coat. The changes assume the character of chronic inflammation.
When the lining epithelium of the bronchus is lost, fibrin tends to accumulate over the surface of
the defect, to which it is firmly attached. It remains separated by a conspicuous space from
adjacent intact epithelium over which it may project. This superficial network of fibrin merges with a
similar network, extending to a variable depth within the tissue. What may well be described as
coagulative necrosis has often occurred, and structures, such as white fibrous bundles or wall of
blood vessels, are marked out by hyaline material which merges with fibrin. When the walls of the
blood vessels which are invariably engorged are involved, the lumen is plugged by a fibrinous
thrombus.
 Little patches of fibrin adherent to the inner surface of the bronchus may occur in spots where
epithelium has been lost; with uniform loss of epithelium the entire circumference may be lined with
fibrin forming a circular zone occasionally quite uniform in thickness.
Accumulations of polynuclear leucocytes doubtless bring about conditions which cause solution of
fibrin or prevent its formation (when disintegration of leucocytes sets free leucoprotease in
abundance). The activity of the infecting microorganisms, usually hemolytic streptococci or
staphylococci, may cause complete necrosis of a part or all of the bronchial wall. The cavity which is
formed may penetrate into lung tissue that has previously undergone pneumonic consolidation.
Further changes caused by the bronchitis of influenza will be considered under peribronchial
hemorrhage and edema, peribronchial pneumonia and bronchiogenic abscess. Purulent bronchitis is
almost invariably associated with dilatation of the bronchi, the affected bronchi being distended with
pus. With increasing dilatation bronchiectasis becomes evident upon gross examination of the
tissue, and is much more advanced in the small bronchi than in the larger cartilaginous passages.
This subject will be further considered under bronchiectasis.
In association with the acute bronchitis of influenza the epithelium of bronchi not infrequently
looses its superficial columnar ciliated cells and assumes some of the characters of a squamous
epithelium being covered by polygonal or flat cells (Figs. 17 and 18). The condition is often
described a “squamous metaplasia,” although it doubtless represents a stage of regeneration
following injury rather than a true metaplasia. The basal cells of the epithelium have a cubical or
columnar form; above them the cells become polygonal and as the surface is approached, cells are
flat and even scale-like. The nuclei of these superficial cells are often lost. There is no close
resemblance to the squamous epithelium of the skin, for intercellular bridges are not seen.
This change may occur within six days after onset of influenza, though in most instances the
duration of illness has been two weeks or more. It may affect either large or small bronchi, but it is
more frequently found in the latter. Whenever ciliated columnar cells are lost, superficial cells tend
to become flat. Epithelium on one side of a bronchus may have a squamous character, whereas that
elsewhere is columnar and ciliated. The flat epithelium may undergo thickening so that it is 0.1 mm.
or more in thickness. It is noteworthy that regenerating epithelium growing over a denuded surface
has the squamous character which has been described (Plate XIV, Fig. 22).
Bacteriology of the Bronchitis of Influenza.—With the pneumonia of influenza, bronchitis is
invariably present. Cultures have been made from the right or left main bronchus or from the very
small bronchi which contained purulent exudate. A routine method of making the culture has been
adopted. The right main bronchus, exposed by drawing the right lung out of the chest and toward
the midline, was widely seared with a hot knife; the bronchus was partially cut across through the
seared surface with a heated knife and a platinum needle inserted into the lumen. The bacteria
obtained named in the approximate order of their relative frequency have been: B. influenzæ,
pneumococci, hemolytic streptococci, staphylococci (aureus and albus), B. coli, S. viridans, M.
catarrhalis, and diphthoid bacilli which have not been identified. Mixed infections occurred in most
instances. The following list arranged by grouping bacteria in the order cited above, shows how
varied have been the combinations which occur:
 B. influenzæ 3
Pneumococci 5
S. hemolyticus 3
Staphylococci 3
B. coli 3
S. viridans 1
B. influenzæ, pneumococci 17
B. influenzæ, S. hemolyticus 18
B. influenzæ, staphylococci 4
Pneumococci, S. hemolyticus 1
Pneumococci, staphylococci 3
S. hemolyticus, staphylococci 4
S. hemolyticus, B. coli 2
Staphylococci, S. viridans 1
B. influenzæ, pneumococci, S. hemolyticus 6
B. influenzæ, pneumococci, staphylococci 15
B. influenzæ, pneumococci, S. viridans 2
B. influenzæ, S. hemolyticus, staphylococci 16
B. influenzæ, S. hemolyticus, M. catarrhalis 1
B. influenzæ, staphylococci, S. viridans 1
Pneumococci, S. hemolyticus, staphylococci 3
Staphylococci, B. coli, S. viridans 1
B. influenzæ, pneumococci, S. hemolyticus, staphylococci 7
B. influenzæ, pneumococci, staphylococci, M. catarrhalis 1
B. influenzæ, S. hemolyticus, staphylococci, B. coli 1
B. influenzæ, S. hemolyticus, staphylococci, S. viridans 1
B. influenzæ, S. hemolyticus, staphylococci, M. catarrhalis 1
B. influenzæ, staphylococci, S. viridans, M. catarrhalis 1
B. influenzæ has been present in the bronchi in 79.3 per cent of instances of pneumonia referable
to influenza. Combinations which have been found most frequently are B. influenzæ and
pneumococci (17 instances), B. influenzæ and hemolytic streptococci (18 instances), or the same
combinations with staphylococci, namely, B. influenzæ, pneumococci and staphylococci (15
instances), and B. influenzæ, hemolytic streptococci and staphylococci (16 instances). There is little
doubt that B. influenzæ was not identified in some instances in which it was present; when other
microorganisms are very numerous its inconspicuous colonies may be overgrown even though the
presence of pneumococci, streptococci or staphylococci tends to increase the size of its colonies.
Moreover, it is not improbable that the microorganism may disappear from the bronchi. Comparison
with observations made upon influenza suggests that multiple methods of examination might have
demonstrated a much higher incidence of B. influenzæ. Throat cultures alone made during life
demonstrated the presence of B. influenzæ in only 65.7 per cent of patients with acute influenza,
whereas when cultures were made from the nose, throat and sputum, and a mouse was inoculated
with sputum from each patient, B. influenzæ was found in every instance. After the acute stage of
the disease had passed, the number of microorganisms diminished, and in many instances B.
influenzæ disappeared from the upper air passages. In some of our autopsies B. influenzæ
doubtless present during life has similarly disappeared before death due to pneumonia caused by
pneumococci or streptococci. In view of these considerations it is not improbable that B. influenzæ
demonstrated by a single culture in 80 per cent of instances has been constantly present.
Table XXVIII represents the incidence of pneumococci, hemolytic streptococci, staphylococci, and
B. influenzæ in the bronchi, lungs and blood of those individuals with pneumonia in whom
bacteriologic examination has been made at autopsy. The number of cultures made from the
bronchi, lungs or blood of the heart is given in the second column of the table and in other columns
are given the incidence in number and percentage of the microorganisms which have been
mentioned.
Table XXVIII

HEMOLYTIC
PNEUMOCOCCI STREPTOCOCCI STAPHYLOCOCCI B. INFLUENZÆ
NO. OF NO. PER CENT NO. PER CENT NO. PER CENT NO. PER CENT
CULTURES POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE
Bronchus 121 56 46.3 58 47.9 61 50.4 96 79.3
Lung 153 68 44.4 77 50.3 37 24.2 70 45.7
Blood 218 87 39.9 85 39.0 1 0.5 1 0.5

Cultures from the bronchus represent the bacteriology of the bronchitis of influenza. Infection of
the lung following influenza doubtless occurs by way of the bronchi, so that the bacteria which
cause pneumonia are present in the bronchi before they enter the lung tissue. The figures in Table
XXVIII, similar to those previously cited, show the high incidence of B. influenzæ, and the
occurrence of pneumococci, hemolytic streptococci and staphylococci each present in approximately
half of all autopsies.
The figures in Table XXVIII are an index of the capacity of the microorganisms which enter the
bronchi to invade the lungs and finally the blood. Pneumococci were present in the bronchi in 46.3
per cent of instances, in the lungs in only slightly less, and in approximately 40 per cent of autopsies
they had penetrated into the blood. Hemolytic streptococci enter the bronchi with the same
frequency and exhibit an equal ability to penetrate into the lungs and blood. Staphylococci enter the
bronchi in half of these individuals, but penetrate into the lungs in only a fourth of the instances.
They have entered the blood only once (Autopsy 263) in this instance in association with hemolytic
streptococci. B. influenzæ has been present in the bronchi in approximately 80 per cent of
autopsies. It is noteworthy that it has been found in the lung in little more than half this percentage
of instances and has entered the blood only once (Autopsy 474), in this instance in association with
hemolytic streptococci.
In a limited number of autopsies there was purulent bronchitis recognized by the presence of
mucopurulent exudate in small bronchi. It has been stated that this group of cases is not sharply
separable from other instances of bronchitis, because in some cases death has occurred before a
purulent exudate has accumulated or in other instances a purulent exudate has been displaced by
edema. Table XXIX shows the bacteriology of instances of purulent bronchitis:
Table XXIX

HEMOLYTIC
PNEUMOCOCCI STREPTOCOCCI STAPHYLOCOCCI B. INFLUENZÆ
NO. OF NO. PER CENT NO. PER CENT NO. PER CENT NO. PER CENT
CULTURES POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE
Bronchus 66 33 50.0 32 48.5 36 54.5 53 80.3

The percentages of various bacteria with purulent bronchitis do not differ essentially from those
obtained from all autopsies with pneumonia. B. influenzæ is found in approximately 80 per cent of
autopsies. In 16 instances cultures were made from the purulent fluid contained in a small bronchus
and the incidence of B. influenzæ (namely, 81.4 per cent) has not differed from that in the main
bronchus. In 7 of 8 instances in which cultures were made, both from the right main bronchus and
from the purulent fluid in a small bronchus, B. influenzæ was found in one or other in all but one
autopsy (87.5 per cent); in this instance (Autopsy 472) respiratory disease began thirty-seven days
before death and cultures from large and small bronchi at autopsy were overgrown by B. coli. Since
observations upon influenza made during life have shown that B. influenzæ is constantly
demonstrable when multiple methods are employed for its detection, the figures just cited give
support to the suggestion that B. influenzæ is constantly present in the bronchi with the bronchitis
of influenza.
 Lobar Pneumonia
The frequency with which the confluent lobular consolidation of bronchopneumonia involving
whole lobes or parts of lobes follows influenza has emphasized the desirability of distinguishing
carefully between lobar and confluent lobular pneumonia. The pulmonary lesion has been
designated lobar pneumonia when it exhibited the well-known characters of this lesion, namely, firm
consolidation of large parts of lobes, coarse granulation of the cut surface, fibrinous plugs in the
bronchi and, on microscopic examination, homogeneous consolidation and fibrinous plugs within the
alveoli. With confluent lobular consolidation of bronchopneumonia the consolidated area is in most
cases obviously limited by lobule boundaries, and well-defined lobules of consolidation occur
elsewhere in the lungs.
Lobar pneumonia occurred in 98 among 241 instances of pneumonia following influenza, namely,
in 40.7 per cent of autopsies.
The difficulty of separating lobar and bronchopneumonia following influenza has been increased
by the frequent combination of the two lesions in the same individual. There were 34 instances in
which lobar and bronchopneumonia occurred together. The anatomic diagnosis of lobar pneumonia
was made only when lobes or parts of lobes were firmly consolidated and exhibited the characters
of the lesion enumerated above; in several instances, in which there was some doubt concerning
the nature of the lesion, microscopic examination was decisive. The associated bronchopneumonic
lesions represented all the types which have been associated with influenza. In the group of 34
cases of coexisting lobar and bronchopneumonia, lobular consolidation occurred 10 times,
peribronchiolar consolidation 14 times (recognized in all but 4 instances by microscopic
examination), hemorrhagic peribronchiolar consolidation 9 times, peribronchial pneumonia 4 times.
The intimate relation of these lesions to changes in the bronchi is well shown by the frequent
presence of purulent bronchitis. The associated lesions of the bronchi in these cases were as
follows: purulent bronchitis in 23 instances; peribronchial hemorrhage in 6; bronchiectasis in 11.
The frequency of purulent bronchitis and other bronchial lesions in association with coexisting lobar
and bronchopneumonia is in sharp contrast with the occurrence of these lesions in association with
lobar pneumonia alone; with 69 instances of lobar pneumonia alone purulent bronchitis occurred 17
times and bronchiectasis once.
Lobar pneumonia following influenza passes through the usual stages of red and gray
hepatization. Red hepatization was found 16 times, combined red and gray hepatization 28 times,
and gray hepatization 20 times. The average duration of pneumonia with red hepatization was 3.7
days, with combined red and gray hepatization 5.1 days and with gray hepatization 7.5 days. These
figures, it will be shown later, have some importance in relation to the stage at which hemolytic
streptococcus infects lungs the site of lobar pneumonia.
Bacteriology of Lobar Pneumonia.—Table XXX is compiled with the purpose of determining
the bacteriology of the bronchi, lungs and heart’s blood in autopsies performed on individuals with
lobar pneumonia. In some instances bacteriologic examination of one or other of these organs was
omitted; the percentage incidence is an index of the presence of pneumococci, hemolytic
streptococci, staphylococci or B. influenzæ in the bronchi, lungs or heart’s blood and measures the
invasive power of these microorganisms during the course of lobar pneumonia following influenza.
 Table XXX

HEMOLYTIC
PNEUMOCOCCI STREPTOCOCCI STAPHYLOCOCCI B. INFLUENZÆ
NO. OF NO. PER CENT NO. PER CENT NO. PER CENT NO. PER CENT
CULTURES POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE
Bronchus 44 56.9 14 31.8 22 37 84.1 96 79.3
Lung 53 77.3 13 24.5 8 26 49.1 70 45.7
Blood 87 65.5 11 12.6 1 0.5

Pneumococci, the recognized cause of lobar pneumonia, were found in the lungs in 73.3 per cent
of autopsies; failure to find the microorganism in all instances is doubtless the result of its
disappearance from the lung, which, it is well known, occurs not infrequently particularly during the
later stages of the disease. In 65.5 per cent of instances of fatal lobar pneumonia pneumococci
have entered the heart’s blood.
Hemolytic streptococci unlike pneumococci were found more frequently in the bronchi than in the
lungs; this microorganism which exhibits little tendency to disappear, once it has established itself
within the body, found entrance into the bronchi in 31.8 per cent of instances of lobar pneumonia
and in 24.5 per cent entered the lungs. Its invasive power is further illustrated by its penetration
into the heart’s blood approximately in half this proportion of autopsies.
Staphylococci enter the bronchi in many instances (50 per cent), but relatively seldom (15.1 per
cent) invade the lung and rarely if ever penetrate into the blood.
The high incidence, namely, 84.1 per cent, of B. influenzæ in the bronchi is particularly
noteworthy; it exceeds that of pneumococci, the well-recognized cause of lobar pneumonia, within
the lung. It is found much less frequently within consolidated lung tissue and shows no tendency to
invade the heart’s blood. B. influenzæ finds the most favorable conditions for its multiplication within
the bronchi.
In view of the frequent occurrence of coexisting lobar and bronchopneumonia it has appeared
desirable to determine how far the existence of obvious bronchopneumonia modifies the
bacteriology of lobar pneumonia. In Table XXXI the incidence of pneumococci, hemolytic
streptococci, staphylococci and B. influenzæ after death with lobar pneumonia on the one hand is
compared with their incidence after combined lobar and bronchopneumonia on the other.
Pneumococci are found in the lung more frequently with lobar than with combined lobar and
bronchopneumonia. The incidence of hemolytic streptococci and of staphylococci in the lung is on
the contrary higher when bronchopneumonia is associated with lobar pneumonia. It is not
improbable that these microorganisms have a part in the production of associated
bronchopneumonia. The frequency with which microorganisms invade the blood is almost identical
in the two groups.
 Table XXXI

With Lobar Pneumonia Alone

HEMOLYTIC
PNEUMOCOCCI STREPTOCOCCI STAPHYLOCOCCI B. INFLUENZÆ
NO. OF NO. PER CENT NO. PER CENT NO. PER CENT NO. PER CENT
CULTURES POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE
Bronchus 30 20 66.6 9 30 15 50 26 86.7
Lung 34 29 85.2 7 20.6 3 8.8 18 52.9
Blood 54 36 66.7 7 13

With Combined Lobar and Bronchopneumonia

HEMOLYTIC
PNEUMOCOCCI STREPTOCOCCI STAPHYLOCOCCI B. INFLUENZÆ
NO. OF NO. PER CENT NO. PER CENT NO. PER CENT NO. PER CENT
CULTURES POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE
Bronchus 14 9 64.3 5 34.3 7 50 11 78.6
Lung 19 12 63.2 6 31.6 5 26.3 8 42.1
Blood 33 21 63.1 4 12.1

The relative frequency with which different types of pneumococci produce lobar pneumonia under
the conditions existing when Camp Pike was attacked by an epidemic of influenza is indicated by
Table XXXII in which instances of lobar pneumonia alone and of combined lobar and
bronchopneumonia are listed separately.
Pneumococcus I and II, which are found approximately in two-thirds of instances of lobar
pneumonia occurring in cities, have an insignificant part in the production of these lesions.
Pneumococcus IV and atypical Pneumococcus II, which are commonly found in the mouth, are the
predominant cause of these lesions, and with Pneumococcus III, also an inhabitant of the mouths of
normal individuals, have been the cause of two-thirds of all instances of lobar pneumonia observed
in this camp.
Table XXXII

With Lobar Pneumonia

PNEUMOCOCCUS II
PNEUMOCOCCUS I PNEUMOCOCCUS II (Atyp.) PNEUMOCOCCUS III PNEUMOCOCCUS IV
PER PER PER PER PER
NO. OF NO. CENT NO. CENT NO. CENT NO. CENT NO. CENT
CULTURES POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE
Bronchus 30 1 3.3 1 3.3 4 13.3 4 13.3 10 33.3
Lung 34 1 2.9 2 5.9 9 26.5 6 17.6 11 32.4
Blood 54 2 3.7 2 3.7 12 22.2 3 5.6 17 31.5

With Combined Lobar and Bronchopneumonia

PNEUMOCOCCUS II
PNEUMOCOCCUS I PNEUMOCOCCUS II (Atyp.) PNEUMOCOCCUS III PNEUMOCOCCUS IV
PER PER PER PER PER
NO. OF NO. CENT NO. CENT NO. CENT NO. CENT NO. CENT
CULTURES POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE
Bronchus 14 2 14.3 1 7.1 3 21.4 3 21.4
Lung 19 1 5.3 5 26.3 6 31.6
Blood 33 2 6.1 3 9.1 4 12.1 12 36.4

There is no noteworthy difference in the occurrence of these types of pneumococci among

instances of lobar pneumonia, on the one hand, and of combined lobar and bronchopneumonia, on
the other. Different types exhibit no noteworthy differences in their ability to penetrate into lungs
and blood.
Hemolytic Streptococcus with Lobar Pneumonia.—There can be no doubt that the
concurrent infection with microorganisms other than pneumococcus modifies the progress of lobar
pneumonia. With lobar pneumonia alone hemolytic streptococci have entered the bronchi in 30 per
cent of instances and have penetrated into the lungs in 20.6 per cent; with associated lobar and
bronchopneumonia the same microorganism has entered the bronchi in 34.3 per cent of instances
and invaded the lung in 31.6 per cent. Hemolytic streptococci are the only microorganisms other
than pneumococci which, in association with lobar pneumonia, have found their way from the lungs
to the blood stream; more than one-third of all instances of lobar pneumonia in which hemolytic
streptococci find entrance into the bronchi die with streptococcus septicemia.
Separation of instances of lobar pneumonia into groups on the basis of the occurrence of red or
gray hepatization shows that infection with hemolytic streptococcus is more likely to occur during
the early stages of the disease. The average duration of lobar pneumonia with red hepatization has
been 3.7 days, with red and gray hepatization, 5.1 days, and with gray hepatization, 7.5 days.
Infection with hemolytic streptococcus has occurred in association with red or gray hepatization as
shown in Table XXXIII.
Table XXXIII

NO. WITH PER CENT WITH

NO. OF HEMOLYTIC HEMOLYTIC
AUTOPSIES STREPTOCOCCUS STREPTOCOCCUS
Lobar pneumonia with red hepatization 16 6 37.5
Lobar pneumonia with red and gray hepatization 28 6 21.4
Lobar pneumonia with gray hepatization 20 1 5.0
Notwithstanding the longer duration of the disease and consequent prolongation of exposure to
infection, lobar pneumonia, which has reached the stage of gray hepatization, has shown the
smallest incidence of infection with hemolytic streptococci. In the stage of gray hepatization there is
diminished susceptibility to secondary infection with this microorganism.
Characteristic histologic changes have been found in the lungs of those who have died with lobar
pneumonia followed by invasion of lungs and blood by hemolytic streptococci (e. g., Autopsies 273,
430), but with no evidence of suppuration found at autopsy. Within the pneumonic lung occur
patches of necrosis implicating both exuded cells and alveolar walls; in some places nuclei have
disappeared; elsewhere nuclear fragments are abundant. In these patches of necrosis Gram-positive
streptococci in short chains occur in immense number. In some instances (e. g., Autopsies 273, 346,
479) interlobular septa are very edematous and often contain a network of fibrin; lymphatics are
dilated and contain polynuclear leucocytes in abundance. Streptococci are found within these
lymphatics. The histologic changes which have been described represent the earliest stages of
abscess formation and interstitial suppuration, lesions almost invariably caused by hemolytic
streptococci.
 Chart 2.—Showing the relation of (a) date of onset of cases
in which autopsy demonstrated lobar pneumonia, indicated
by upper continuous line with single hatch, and of (b) date
of death of these cases, indicated by lower continuous line
with double hatch to (c) the occurrence of influenza,
indicated by the broken line, and to (d) the total number of
fatal cases of pneumonia, indicated by the broken dotted
line. Each case of fatal pneumonia is indicated by one
division of the scale as numbered on the left of the chart;
cases of influenza are indicated by the numbers on the right
of the chart.

Relation of Lobar Pneumonia to Influenza.—Some writers have suggested that lobar

pneumonia, heretofore observed during the course of epidemics of influenza, is an independent
disease with no relation to influenza, both diseases being referable perhaps to similar meteorologic
or other conditions. Chart 2, which shows by weeks from September 1 to October 31 the relation of
deaths from lobar pneumonia (indicated by double hatch) to deaths from all forms of pneumonia,
disproves this suggestion. The two curves follow parallel courses; that representing lobar
pneumonia reaches a maximum approximately one week after the outbreak of influenza had
reached its height. Lobar pneumonia, like other forms of pneumonia, was secondary to influenza.
When a chart is plotted to represent the dates of onset of fatal cases of lobar pneumonia (indicated
by single hatch in Chart 2), it becomes evident that the greatest number of these cases of
pneumonia had their onset at the beginning of the influenza epidemic, approximately one week
before it reached its height. Fatal lobar pneumonia developed less frequently in the latter part of the
epidemic; to obtain an explanation of this relation it is necessary to chart separately cases of lobar
pneumonia with secondary streptococcus infection, for we have already learned that streptococcus
infection was the predominant cause of death in the early period of the influenza epidemic.
Exclusion of these instances of secondary streptococcus infection makes no noteworthy change in
the character of the chart. Fatal lobar pneumonia, like all forms of fatal pneumonia (p. 140), was
more frequent in the first half than in the second half of the epidemic. This difference is referable
either to greater virulence of the virus of influenza or to the greater susceptibility of those first
selected by the disease or, as more probable, to conditions such as crowding together of patients
with influenza, favoring the transmission of microorganisms which cause pneumonia.
 Bronchopneumonia
For the purpose of the present study it is convenient to group together instances of
bronchopneumonia which have been unaccompanied, on the one hand, by lobar pneumonia (p.
155) or, on the other hand, by suppuration, which with few exceptions is caused by hemolytic
streptococci or by staphylococci. A group of cases in which lobar and bronchopneumonia have
occurred in the same individual have already been considered. In many instances,
bronchopneumonia is accompanied by abscess formation or by some other form of suppuration;
these lesions will be discussed elsewhere.
Bronchopneumonia unaccompanied by lobar pneumonia or by suppuration occurred in 80
autopsies.
Pneumonic consolidation distributed with relation to the bronchi exhibits considerable variety, and
an attempt to define a type of bronchopneumonia characteristic of influenza would be futile.
Nevertheless, the bronchopneumonia of influenza has in many instances distinctive characters.
Lesions of bronchopneumonia which are frequently found in the autopsies under consideration
may be conveniently designated by descriptive terms, indicative of their location in the lung tissue.
These lesions, of which two or more often occur in the same lung, are:
1. Peribronchiolar consolidation with which the inflammatory exudate is limited to the alveoli in
the immediate neighborhood of the bronchioles.
2. Hemorrhagic peribronchiolar consolidation in which gray patches of peribronchiolar pneumonia
occur upon a deep red background produced by hemorrhage into alveoli. Pfeiffer believed that this
lesion was characteristic of influenza.
3. Lobular consolidation with which consolidation is limited to lobules or groups of lobules.
4. Peribronchial pneumonia with which small bronchi are encircled by pneumonic consolidation.
Each one of these lesions will be discussed separately.
Following is a list of the bacteria which have been isolated from the consolidated lung of
individuals with bronchopneumonia unaccompanied by lobar pneumonia or by suppuration:
B. influenzæ 1
Pneumococci 5
S. hemolyticus 5
S. viridans 1
B. influenzæ, pneumococci 9
B. influenzæ, S. hemolyticus 4
B. influenzæ, staphylococci 4
Pneumococci, S. hemolyticus 1
Pneumococci, staphylococci 2
S. hemolyticus, staphylococci 1
S. hemolyticus, B. coli 1
Staphylococci, S. viridans 1
Staphylococci, B. coli 1
B. influenzæ, pneumococci, staphylococci 1
B. influenzæ, pneumococci, S. viridans 1
B. influenzæ, S. hemolyticus, staphylococci 2
B. influenzæ, pneumococci, staphylococci, S. viridans 1
No microorganisms found 6

47
 The similarity of this list to that representing the bacteriology of bronchitis is evident; there is the
same multiplicity of microorganisms and the frequent occurrence of mixed infections. B. influenzæ is
much less frequently found in the lung. The relative pathogenicity of the large group of
microorganisms enumerated above is better indicated by the following list which shows what
microorganisms have penetrated into the blood in autopsies performed on individuals with
bronchopneumonia:
Pneumococci 20
S. hemolyticus 23
S. viridans 1
Pneumococci, S. hemolyticus 2
No bacteria found 25

Total 71
Table XXXIV shows the percentage incidence of pneumococcus, hemolytic streptococcus,
staphylococcus and B. influenzæ in the bronchi, lungs and blood and is inserted for comparison with
the similar table (Table XXX) showing the incidence of these bacteria in lobar pneumonia.
Table XXXIV

HEMOLYTIC
PNEUMOCOCCI STREPTOCOCCI STAPHYLOCOCCI B. INFLUENZÆ
NO. OF NO. PER CENT NO. PER CENT NO. PER CENT NO. PER CENT
CULTURES POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE
Bronchus 37 19 48.6 13 35.1 22 59.5 28 75.7
Lung 47 20 42.6 14 29.8 13 27.7 23 48.9
Blood 70 22 31.4 24 34.3

Table XXXIV shows that pneumococci have a less important part in the production of broncho
than of lobar pneumonia; with lobar pneumonia this microorganism was found in the lungs in 77.3
per cent of instances and in the blood, in 65.5 per cent, whereas with bronchopneumonia it was
found in the lungs in 42.6 per cent and in the blood in 31.4 per cent. Hemolytic streptococci (in
lungs and blood) and staphylococci (in lungs), on the contrary, were more common with
bronchopneumonia, and doubtless have a part in the production of the lesion. Streptococcus
viridans, B. coli and M. catarrhalis, which are not infrequently found in the bronchi (p. 151),
occasionally enter the lungs with bronchopneumonia but are rarely found with lobar pneumonia. B.
influenzæ has been found in less than 80 per cent of instances in the bronchi and in about half of
the lungs, maintaining an incidence approximately the same as that with lobar pneumonia.
Table XXXV shows the types of pneumococci found in association with bronchopneumonia and is
inserted for comparison with the similar table (Table XXXII) showing types of pneumococci with
lobar pneumonia.
With broncho as with lobar pneumonia pneumococci commonly found in the mouth, namely,
atypical II, and Types III and IV, have a more important part in production of the lesion than the so-
called fixed types, I and II. Atypical Pneumococcus II has been less frequently encountered with
broncho than with lobar pneumonia.
Table XXXV

PNEUMOCOCCUS II
PNEUMOCOCCUS I PNEUMOCOCCUS II (Atyp.) PNEUMOCOCCUS III PNEUMOCOCCUS IV
PER PER PER PER PER
NO. OF NO. CENT NO. CENT NO. CENT NO. CENT NO. CENT
CULTURES POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE
Bronchus 37 1 2.7 3 8.1 14 37.8
Lung 47 2 4.3 2 4.3 2 4.3 2 4.3 12 25.2
Blood 70 1 1.4 1 1.4 5 7.1 4 5.7 11 15.9

Peribronchiolar Consolidation.—In many instances of bronchopneumonia, usually in

association with lobular or confluent consolidation, small firm nodules of consolidation are clustered
about the bronchioles (Fig. 2). These nodular foci of consolidation are usually 1.5 to 2 mm. in
diameter, being sometimes slightly smaller or slightly larger. They are usually gray and occasionally
surrounded by a red halo; sometimes they are yellowish gray. They are clustered about the smallest
bronchial tubes to form groups which are from 0.5 to 1 cm. across. A group of nodular foci of
consolidation occupies the central part of a lobule of lung tissue. When pneumonia has been of
short duration these foci are fairly soft and not sharply defined, and in many instances this form of
bronchopneumonia is first recognized by microscopic examination. When the disease has lasted
from ten days to two weeks, the consolidated nodules are very firm and sharply circumscribed,
closely resembling tubercles. When they have assumed this character, microscopic examination
shows that chronic changes indicated by new formation of interstitial tissue have occurred.
The lesion may be designated peribronchiolar consolidation. It has occurred usually in association
with other types of pneumonic lesion in 61 instances, being recognized at autopsy in 18 and by
microscopic examination in 43.

Fig. 2.—Acute bronchopneumonia

with nodules of peribronchiolar
consolidation and purulent
bronchitis. Autopsy 429.

In association with this lesion there are almost invariably severe lesions of the bronchi. Purulent
bronchitis was noted in 47 of the 61 instances, in which this nodular bronchopneumonia was found
at autopsy. An index of the severity of the bronchial injury is the frequency with which
bronchiectasis has occurred; dilatation of small bronchi was observed in 24 instances. In 10
instances the bronchi were encircled by conspicuous zones of hemorrhage.
In association with this peribronchiolar lesion the lung is often voluminous and fails to collapse on
removal from the chest. Pressure upon the lung squeezes from the smallest bronchi, both in the
neighborhood of the nodular consolidation and elsewhere, a droplet of viscid, semifluid
mucopurulent material. The presence of this tenacious material throughout the small bronchi
doubtless explains the failure of the lung tissue to collapse. Interstitial emphysema has been
present in some of these lungs.
A red zone of hemorrhage has occasionally been observed about the foci of peribronchiolar
pneumonia. A further stage in the same process is represented by hemorrhage into all of the alveoli
separating these patches of consolidation. This hemorrhagic lesion, which will be described in more
detail later, has been found repeatedly in the same lung with peribronchiolar pneumonia, being
present in 8 among the 61 autopsies cited. Lobular bronchopneumonia accompanied the
peribronchiolar lesion 27 times and lobar pneumonia accompanied it 20 times.
When an abscess caused by hemolytic streptococcus is associated with peribronchiolar
pneumonia, empyema is present, but otherwise pleurisy is absent or limited to a scant fibrinous
exudate.

Fig. 3.—Acute bronchopneumonia with peribronchiolar

consolidation; a respiratory bronchiole partially lined by
columnar epithelium passes into alveolar duct and the
adjacent alveoli are filled by polynuclear leucocytes.
Autopsy 333.

Histologic examination demonstrates very clearly the relation of this lesion to the bronchioles (Fig.
3). These passages are filled and distended with an inflammatory exudate consisting almost entirely
of polynuclear leucocytes. The respiratory bronchioles are beset with alveoli often limited to one
side of the tubule and these alveoli are filled with leucocytes. The alveolar ducts, distinguishable
from the bronchioles by the absence of columnar or cubical epithelium and by possession of smooth
muscle, are similarly filled with leucocytes; the numerous alveoli which form the walls of the alveolar
ducts are distended by an inflammatory exudate. In sections which pass through an alveolar duct
and one or more of its infundibula, the further extension of the lesion may be determined (Fig. 4).
The infundibulum in proximity with the alveolar duct contains polynuclear leucocytes and the same
cells are seen in the alveoli which here form its wall, but the intensity of the inflammatory reaction
diminishes toward the periphery, so that the distal part of the infundibulum, which is much
distended and in consequence more readily definable than usual, is free from inflammatory exudate.
 Fig. 4.—Acute bronchopneumonia with peribronchiolar
consolidation; a respiratory bronchiole is in continuity with
an alveolar duct and two distended infundibula; alveoli
about bronchiole, alveolar duct and proximal part of
infundibula contain polynuclear leucocytes, the distal part of
the infundibula showing no evidence of inflammation.
Autopsy 333.

Occasionally there is irregularly distributed hemorrhage and perhaps some edema in the alveoli
immediately adjacent to those which form the peribronchiolar focus of inflammation. In such
instances small bronchi, that is, air passages, lined by columnar epithelium and devoid of tributary
alveoli, may be surrounded by a zone of hemorrhage; immediately surrounding the bronchus, the
wall of which shows intense inflammation, alveoli, in a zone of which the radius represents several
alveoli, are filled with blood. This hemorrhagic zone is continued from the bronchus over the focus
of inflammation which surrounds the bronchiole.
Another variation in the character of the lesion is doubtless referable to variation in the severity of
primary bronchial injury. Alveoli immediately surrounding small bronchi are filled with dense plugs of
fibrin. The alveoli which besot the walls of the bronchioles contain fibrin, but the alveolar duct and
its tributary alveoli are filled with polynuclear leucocytes.
The bacteria which have been cultivated from the lung in autopsies with peribronchiolar
pneumonia are as follows:
Pneumococcus 5
S. hemolyticus 8
B. influenzæ, pneumococcus 5
B influenzæ, S. hemolyticus 7
B. influenzæ, staphylococcus 1
Pneumococcus, staphylococcus 2
S. hemolyticus, staphylococcus 2
B. influenzæ, pneumococcus, S. hemolyticus 2
B. influenzæ, pneumococcus, staphylococcus 1
B. influenzæ, S. hemolyticus, staphylococcus 2
Pneumococcus, S. hemolyticus, staphylococcus 3
No organism 3

Total 41
 The following list which shows the bacteria found in the blood is an index to the pathogenicity of
pneumococci and hemolytic streptococci:
Pneumococcus 22
S. hemolyticus 20
Pneumococcus, S. hemolyticus 1
No organism 14

Total 57
The percentage incidence of pneumococcus, hemolytic streptococcus, staphylococcus and B.
influenzæ in bronchus, lung and blood, given in Table XXXVI, is inserted to indicate with what
readiness each one of these microorganisms passes from the bronchus through the lung into the
circulating blood.
Table XXXVI

PNEUMOCOCCUS HEMOLYTIC STAPHYLOCOCCUS B. INFLUENZA

STREPTOCOCCUS
Bronchus 39.4% 57.7% 60.6% 84.8%
Lung 43.9% 61.0% 21.9% 43.9%
Blood 40.3% 36.8% 0. % 0. %
B. influenzæ is present in the bronchi in a very large proportion (84.8 per cent) of those in whom
this type of bronchopneumonia has been found at autopsy; it is much less frequently recovered
from the lungs. Staphylococci, in part S. albus and in part S. aureus, are less frequently found in the
bronchi and are recovered from the lungs in a relatively small proportion of autopsies. The
percentage incidence of pneumococci and streptococci in lungs and blood demonstrates the
pathogenicity of these microorganisms, for whereas pneumococci and hemolytic streptococci are
found in the consolidated lungs in 43.9 and 61.0 per cent of instances of the lesion respectively,
they make their way into the blood in 40.3 and 36.8 per cent of instances.
Coexisting infection with pneumococci and hemolytic streptococci has been not uncommon e. g.,
Autopsy 275 in which both were in the blood; in 2 instances (Autopsies 333 and 378) in which
pneumococci were obtained from the blood, hemolytic streptococci were found in the lungs and
bronchi; in 3 instances (Autopsies 258, 273 and 445) in which hemolytic streptococci were present
in the blood, pneumococci were obtained from the lungs.
In the group of autopsies under consideration, examination of the sputum was made during life
and after onset of pneumonia in 11 instances. The microorganisms found in the sputum and at
autopsy were as follows:
SPUTUM IN BLOOD, LUNGS OR BRONCHUS AT AUTOPSY
Autopsy 240 Pneum. IV Pneum. IV
246 Pneum. atyp. II, B. inf.
247 Pneum. IV, B. inf. Pneum. IV
250 Pneum. atyp. II, B. inf. Pneum. atyp. II
253 Pneum. atyp. II Pneum. II
285 Pneum. atyp. II, B. Inf. S. hem., B. inf.
288 S. hem., B. inf. S. hem., B. inf.
291 Pneum. IV, B. inf. Staph., B. inf.
300 Pneum. atyp. II, B. inf. Pneum. atyp. II, B. inf.
312 Pneum. IV, S. hem., B. inf. S. hem., B. inf.
346 Pneum. IV, B. inf. S. hem., B. inf.
In 2 instances (Autopsies 285 and 346) among this small group of cases, pneumococci but no
hemolytic streptococci were found in the sputum several days before death, whereas death occurred
as the result of secondary invasion with hemolytic streptococci and no pneumococci were found at
autopsy. It is probable that this sequence of events is not uncommon. B. influenzæ finds its way
into the bronchi and pneumococci follow it; pneumonia limited to peribronchiolar alveoli may occur
in consequence of this invasion. Later hemolytic streptococci may follow the same path and cause
death with bacteremia.
Hemorrhagic Peribronchiolar Consolidation.—Peribronchiolar pneumonia accompanied by
diffuse accumulation of blood within the alveoli is one of the most frequent complications of
influenza. The lung tissue is laxly consolidated, and on section there is a homogeneous dull deep
red background upon which are seen small gray spots (1.5 to 2 mm. in diameter) grouped in
clusters about the smallest bronchi (Fig. 5). Wide areas of lung tissue are implicated and the lesion
is more common in the dependent parts of the lung than elsewhere. In common with other forms of
bronchopneumonia the lesion is in most instances associated with changes in the bronchi; in 55
instances of hemorrhagic bronchiolar pneumonia purulent bronchitis was found in 43 instances; it is
noteworthy that purulent bronchitis often is not evident in the presence of pulmonary edema and
edema is not infrequent with this pneumonic lesion.
Microscopic examination demonstrates the presence of acute bronchitis; the lumina of the small
bronchi contain polynuclear leucocytes and red blood corpuscles. Accumulation of blood may
separate the epithelium from the basement membrane. The mucosa immediately below the
epithelium contains polynuclear leucocytes in fair abundance and the blood vessels of the bronchial
wall are much engorged. Respiratory bronchioles are distended with polynuclear leucocytes and red
blood corpuscles. In a zone about each bronchiole, in areas corresponding to the small gray spots
seen upon the cut surface of the lung, the alveoli are filled with polynuclear leucocytes. In the lung
tissue intervening between these spots of leucocytic pneumonia the alveoli are distended with red
blood corpuscles.

Fig. 5.—Bronchopneumonia with hemorrhagic

peribronchiolar consolidation.

In favorable sections it is occasionally possible to follow the bronchiole and alveolar duct, both
filled with leucocytes, into an infundibulum. The proximal part of the infundibulum contains
polynuclear leucocytes, whereas the distal part and its tributary alveoli are filled with serum and red
blood corpuscles.
When the lesion has persisted for a short time there is evidence of beginning migration of
polynuclear leucocytes from the blood vessels into the alveoli which are filled with blood. The
alveolar walls contain numerous polynuclear leucocytes and leucocytes which have entered the
intraalveolar blood are numerous in contact with the wall but occur in scant number in the center of
the alveolar lumen.
Alveolar epithelium in contact with the blood in the lumen is usually swollen and often uniformly
nucleated.
 The inflammatory process is evidently transmitted from the bronchioles and to a less degree from
the small bronchi to the adjacent alveoli. Polynuclear leucocytes fill the lumen of the bronchiole and
the alveoli immediately adjacent; at the periphery of the focus of pneumonia, the alveoli may
contain fibrin. In such instances small bronchi (lined by a continuous layer of columnar epithelial
cells) may be surrounded by alveoli containing fibrin.
In sections from one part of the lung, the alveoli between the peribronchiolar foci of pneumonia
may be uniformly filled with red blood corpuscles, whereas in sections from another part pneumonic
foci may be surrounded by a zone of intraalveolar hemorrhage or of hemorrhage and edema outside
of which some air-containing tissue occurs. There are transitions between this halo of intraalveolar
hemorrhage and edema surrounding each bronchiolar focus and complete hemorrhagic infiltration of
all intervening alveoli.
Large mononuclear cells are occasionally fairly numerous within the alveoli containing blood.
These cells act as phagocytes ingesting red corpuscles, so that at times they are filled with
corpuscles. Disintegration of red corpuscles occurs and brown pigment remains within the cell. It is
not uncommon to find numerous mononuclear pigment containing cells which resemble those found
with chronic passive congestion of the lungs.
Lungs, the site of hemorrhagic peribronchiolar pneumonia, may undergo chronic changes which
will be described elsewhere.
The lesion which has been designated hemorrhagic peribronchiolar pneumonia is that which
Pfeiffer regarded as the characteristic type of influenzal pneumonia. In the small bronchi containing
pus and in lung tissue, Pfeiffer states, influenza bacilli are predominant and present in astonishing
number in smear preparations. The demonstration of B. influenzæ by cultures from pneumonic lung
is mentioned by him but its association with other microorganisms in such cultures is not discussed.
Microorganisms which we have isolated from the lungs of individuals with hemorrhagic
peribronchiolar pneumonia are as follows:
B. influenzæ 1
Pneumococcus 2
S. hemolyticus 10
B. influenzæ, pneumococcus 7
B. influenzæ, S. hemolyticus 3
B. influenzæ, staphylococcus 2
S. hemolyticus, B. coli 3
B. influenzæ, pneumococcus, staphylococcus 2
B. influenzæ, S. hemolyticus, staphylococcus 5
Pneumococcus, S. hemolyticus, staphylococcus 1
No organisms 2

Total 38
With this type of pneumonia B. influenzæ has not been isolated in pure culture; B. influenzæ
alone is recorded only once (Autopsy 435), but in this instance the culture has been so obscured by
contamination that the occurrence of pneumococci or streptococci cannot be excluded; S.
hemolyticus has doubtless been present in this lung, for it has been found in the heart’s blood, in
the bronchus, and in the peritoneal exudate of the same individual.
The incidence of pneumococci and hemolytic streptococci in this list does not differ materially
from that with peribronchiolar pneumonia unaccompanied by extensive intraalveolar hemorrhage,
though hemolytic streptococci are somewhat more frequent with the hemorrhagic lesion. The
following table shows the frequency with which pneumococci and hemolytic streptococci have
penetrated into the blood:
 Pneumococcus 11
S. hemolyticus 24
Pneumococcus, S. hemolyticus 1
No organism 12

Total 48
Table XXXVII showing the percentage incidence of pneumococci, hemolytic streptococci,
staphylococci and B. influenzæ further emphasizes the similarity between the bacteriology of
peribronchiolar pneumonia (Table XXXVI) and the closely related hemorrhagic lesion:
Table XXXVII

HEMOLYTIC
PNEUMOCOCCUS STREPTOCOCCUS STAPHYLOCOCCUS B. INFLUENZÆ
Bronchus 44.0% 64.0% 44.0% 72.0%
Lung 31.6% 57.9% 26.8% 52.6%
Blood of heart 25.0% 52.1% 0% 0%
Pneumococci have been found in the lungs (31.6 per cent) and blood (25 per cent), somewhat
less frequently than with peribronchiolar pneumonia (43.9 and 40.3 per cent respectively), and
hemolytic streptococci have been found in the blood more frequently (52.1 per cent) than with the
latter (36.8 per cent) but otherwise the bacteriology of the two lesions corresponds closely. The low
incidence of B. influenzæ in the bronchi (72 per cent) with hemorrhagic peribronchiolar pneumonia
is perhaps incorrect as the result of the relatively small number of bacteriologic examinations
(namely, 25), but the incidence of the same microorganism in the lung has been higher (52.6 per
cent) than with nonhemorrhagic peribronchiolar lesion (43.9 per cent).
In some instances infection with hemolytic streptococci has occurred after the onset of
pneumonia. The following list compares the results of bacteriologic examination of the sputum
made after the onset of pneumonia with that of blood, lungs or bronchus after death:
SPUTUM IN BLOOD, LUNGS OR BRONCHUS AT AUTOPSY
Autopsy 237 S. hem. S. hem.
242 Pneum. atyp. II, B. inf. Pneum. atyp. II
247 Pneum. IV, B. inf. Pneum. IV
266 S. hem. S. hem., B. inf.
346 Pneum. IV, B. inf. S. hem., B. inf.
376 (No. S. hem.) S. hem., staph., B. inf.
Instances of secondary infection with hemolytic streptococcus occur in the list, namely, Autopsies
346 and 376.
From the foregoing studies of the bacteriology of peribronchiolar and hemorrhagic peribronchiolar
pneumonia the following conclusions may be drawn: (a) B. influenzæ is found in most instances of
these lesions in the bronchi and in about half of all instances in the lungs, but does not occur
unaccompanied by other microorganisms. (b) In a considerable number of autopsies pneumococcus
is the only microorganism that accompanies B. influenzæ; from the lungs it penetrates into the
blood from which it is obtained in pure culture. (c) In a considerable number of instances S.
hemolyticus accompanies B. influenzæ, and in some of these instances (representing a large
proportion of the relatively small number of cases examined during life), examination of the sputum
has demonstrated that infection has been secondary to a pneumonia with which no hemolytic
streptococci have been found in the sputum.
Lobular Consolidation.—Consolidation of scattered lobules or groups of lobules has occurred in
nearly all instances, namely, 71 of 80 autopsies with bronchopneumonia unaccompanied by lobar
pneumonia or by suppuration. When death follows shortly after the onset of pneumonia, patches of
consolidation have a dull deep red color; blood-tinged fluid escapes from the cut surface which is
almost homogeneous or finely granular. The consolidated tissue seen through the pleura, which is
raised above the general level, has a bluish red color. Isolated lobules or groups of lobules which
have undergone consolidation may be scattered throughout the lungs, but not infrequently there is
confluent consolidation of the greater part of lobes, of whole lobes or of almost an entire lung. Such
lungs are very heavy and may weigh 1,400 or 1,500 grams; bloody serous fluid exudes from the cut
surface. The lesion resembles the red hepatization of lobar pneumonia, but confluent patches of
pneumonia are usually well defined by lobule boundaries. The tissue is soft and the granulation of
lobar pneumonia is absent. In many instances the lobular or confluent areas of consolidation are
reddish gray; in some instances consolidated tissue is in places red and elsewhere gray, and in a
smaller group of autopsies there is gray consolidation only (Fig. 6). Red lobular consolidation is
often seen in those who have died within the first four days following the onset of pneumonia, but is
almost equally frequent after from five to ten days; the average duration of pneumonia in these
cases was 5.5 days. Combined red and gray consolidation was more frequently found when
pneumonia had lasted more than five days, the average duration of pneumonia being 7.3 days. The
greater number of instances of gray consolidation were found after seven days of pneumonia, the
average duration of the disease being 10.0 days. These figures are cited to show that lobular, like
lobar, consolidation passes gradually from a stage of red to gray hepatization, but the change occurs
more slowly and is often long delayed.
Lobular pneumonia, which occurred 71 times among 80 cases classified as bronchopneumonia,
may be regarded as an almost constant lesion of the disease. It is found not only in association with
other lesions of bronchopneumonia, but with lobar pneumonia of influenza as well.
The bacteriology of this lesion shows no deviation from that of the slightly larger group of
bronchopneumonia (p. 163). All types of pneumococcus have been found in association with the
lesion, Pneumococcus I in 2 instances, Pneumococcus II in 1 instance; atypical Pneumococcus II
and Pneumococcus IV have been found much more frequently. Pneumococci have been found in
more than a third of these autopsies (42.9 per cent in the lungs, 33.3 per cent in the blood);
hemolytic streptococci in less than one-third (28.5 per cent in the lungs, 30.2 per cent in the blood).

Fig. 6.—Acute bronchopneumonia

with confluent gray lobular
consolidation in lower part of upper
lobe and hemorrhagic
peribronchiolar pneumonia in lower
lobe; purulent bronchitis.
 The following list shows the bacteriology of a small group of autopsies in which the sputum was
examined after onset of pneumonia:
SPUTUM BLOOD, LUNGS OR BRONCHUS AT AUTOPSY
Autopsy 233 Pneum. atyp. II Pneum.
237 S. hem. S. hem.
242 Pneum. atyp. II, B. inf. Pneum. atyp. II
250 Pneum. atyp. II, B. inf. Pneum. atyp. II
253 Pneum. atyp. II Pneum. atyp. II, staph., B. inf.
266 S. hem. S. hem., B. inf.
274 Pneum. IV S. hem.
291 Pneum. IV, B. inf. Staph., B. inf.
312 Pneum. IV, S. hem., B. inf. S. hem., staph., B. inf.
In one instance of streptococcus pneumonia (Autopsy 274) infection with streptococci occurred
subsequent to the examination of the sputum made five days before death; pneumococcus was
found in the washed sputum.
With lobar pneumonia there was evidence that superimposed infection occurred more frequently
during the stage of red than of gray hepatization. With the lobular consolidation of
bronchopneumonia this relation has not been found. Among 27 instances of red lobular
consolidation, hemolytic streptococcus has occurred 6 times, namely in 22.2 per cent; among 26
instances of red and gray consolidation, 8 times, namely, in 30.7 per cent; among 13 instances of
gray consolidation, 5 times, namely, in 38.5 per cent. Infection with hemolytic streptococci is more
frequent when the lesion has persisted to the stage of gray hepatization. This difference between
lobar and bronchopneumonia is probably dependent in part at least upon the more severe and
persistent lesions of the bronchi with bronchopneumonia.
The histology of consolidation which is definitely limited to secondary lobules or groups of lobules
varies considerably. When death occurs in the early stage of the lesion, consolidated patches are
deep red and somewhat edematous, so that bloody serous fluid escapes from the cut surface of the
lung and red blood corpuscles are present in the alveoli in great abundance together with
polynuclear leucocytes, fibrin and serum in varying quantity. It is not uncommon to find evidence
that the lesion has had its origin in the bronchioles and extended from them to other parts of the
lobule. Polynuclear leucocytes may be relatively abundant within and immediately about the
bronchioles and alveolar ducts, whereas the intervening alveoli and infundibula are filled with red
blood corpuscles among which are polynuclear leucocytes and perhaps some fibrin. It may be
evident that bronchiolar pneumonia with hemorrhage into intervening alveoli is in process of
transformation into a more diffuse leucocytic pneumonia, for polynuclear leucocytes are making
their way from the alveolar wall into the blood-filled lumen and, as the result of the presence of
blood, remain for a time close to the lining of the alveolus.
When the consolidated lobules have assumed a gray or reddish gray color, polynuclear leucocytes
are more abundant and often almost homogeneously pack every alveolus within the boundaries of
the lobule. In some instances there is fibrin partially obscured by the presence of leucocytes in great
number.
Although fibrin is less abundant with bronchopneumonia than with lobar pneumonia, nevertheless
in a considerable proportion of instances it is a very conspicuous element of the inflammatory
exudate within the bronchioles, alveolar ducts and alveoli. It is unusual to find the alveolar ducts
and alveoli uniformly plugged with fibrin containing leucocytes; there is a variegated distribution of
exudate which has little resemblance to that of lobar pneumonia. Occasionally (Autopsies 242 and
247) polynuclear leucocytes fill the bronchioles, alveolar ducts and infundibula, whereas the
surrounding tributary alveoli contain fibrin and polynuclear leucocytes in moderate number; red
blood corpuscles may be present in sufficient number to give a homogeneously red color to the
lobular consolidation.
 In association with lobular pneumonia, fibrin within the lung tissue undergoes certain changes
which outline very sharply the alveolar ducts and the other structures usually ill defined in
preparations of the lung. A remarkable appearance is produced by the deposit of hyalin fibrin upon
the surface of the alveolar ducts and infundibula. This lesion has been described by LeCount.
Within the alveolar tissue of the lung, spaces are seen lined by a layer of fibrin which stains
homogeneously and very brightly with eosin. They are recognized as alveolar ducts by the presence
of scattered bundles of smooth muscle in their wall. The layer of hyaline fibrin overlying the surface
of the alveolar duct usually forms a continuous lining and covers over the orifices of the alveoli
which surround the alveolar duct. These ducts are rendered still more conspicuous by the character
of their contents which exhibits a sharp contrast with that of the surrounding alveoli. The alveoli
duct occasionally contains a bubble of air, but more frequently it is filled with serum in which red
blood corpuscles are sometimes numerous. There is within the lumen scant fibrin and very few cells,
among which polynuclear leucocytes are predominant. In the surrounding alveoli on the contrary
leucocytes and fibrin are abundant. A similar change is found in the infundibula very clearly defined
by their conical form, which is especially well outlined below the pleura or in contact with
interlobular septa. The infundibulum is outlined by hyaline fibrin which passes over the orifices of
the tributary alveoli and separates the serous contents of the infundibulum from the cellular
fibrinous contents of the alveoli about.
The lesion which has been described is often associated with acute bronchitis and bronchiolitis,
and the alveoli immediately about the respiratory bronchioles may be filled with polynuclear
leucocytes. It is very common to find large bubbles of air sharply defined within the purulent
contents of the bronchiole. In some lobules the alveolar ducts, infundibula and alveoli intervening
between these foci of leucocytic pneumonia are almost uniformly filled with fibrin and polynuclear
leucocytes, but in other places the formation of complete layers of hyaline fibrin is in process.
Bubbles of air are often seen within the alveolar ducts, and about them is an irregular layer of fibrin
formed by the penetration of air into a channel previously filled with a loose network of fibrin
containing serum in its meshes. The fibrin compressed against the walls of alveolar duct and
infundibulum remains as a compact layer separating these structures from the alveoli which project
from their walls. The bubble of air is doubtless later absorbed and replaced by serum, so that many
alveolar ducts are filled with serum almost wholly free from cells, whereas alveoli outside the
fibrinous membrane contain a network of fibrin with leucocytes in greater or less abundance.
In association with this fibrinous pneumonia, which has been described, hyaline thrombosis of the
capillaries is not uncommon. This hyalin material within the capillaries gives reactions of fibrin, and
in sections stained by the Gram-Weigert method for demonstration of fibrin, these thrombosed
vessels have the appearance of capillaries irregularly injected with a blue material.
The interstitial tissue surrounding consolidated lobules is often edematous; the lymphatics are
distended with serum and contain a moderate number of lymphocytes and polynuclear leucocytes.
Among the lungs which have been studied histologically, pneumococcus has been almost
invariably associated with the lobular lesions which have just been described, whether hemorrhagic,
leucocytic or fibrinous; the histologic changes accompanying infection of the lung with streptococcus
will be described later. Pneumococcus has been cultivated from the consolidated lung and is found
in section of the lung. B. influenzæ is found in cultures made from the bronchi. Table XXXVIII
includes those instances in which the histology of the consolidated lung accords with the description
given above.
 Table XXXVIII

NO. OF CHARACTER OF PREDOMINANT CULTURE CULTURE CULTURE

AUTOPSY LOBULAR TYPE OF FROM HEART’S FROM LUNG FROM
CONSOLIDATION INFLAMMATORY BLOOD BRONCHUS
EXUDATE
242 Red Fibrinous Pneum. atyp. II
244 Red Leucocytic and Pneum. IV B. Pneum. IV, B.
hemorrhagic inf. inf.
247 Red and gray Fibrinous Pneum. IV
249 Red and gray Fibrinous Pneum. III
252 Red and gray Fibrinous Pneum. II B. Pneum. II, B.
inf. inf., S. vir.
257 Red and gray Leucocytic Pneum. I B. inf., staph.
303 Red Fibrinous Pneum. IV B. Pneum. IV, B.
inf. inf., staph.
314 ? Fibrinous Pneum. IV Pneum. IV Pneum. IV, B.
inf., staph.
336 Red Fibrinous
395 Red and gray Leucocytic Pneum. atyp. II Pneum. atyp. II
464 Red Leucocytic and Pneum. I B. inf. Pneum. I, B.
hemorrhagic inf., staph.
476 Red Leucocytic and
hemorrhagic
498 Red and gray Fibrinous S. aur.
506 Red Fibrinous Pneum. IV Pneum. IV S. Pneum. IV, B.
aur. inf., S. aur., M.
catarrh
Pneumococcus was found in all but 2 instances, and in one of these (Autopsy 336) the only
culture was from the heart’s blood and in the other (Autopsy 498) cultures were unsatisfactory
because proper media were not obtainable. Pneumococci of Types I, II, II atypical, III and IV are
represented in the list. B. influenzæ has been found in a considerable number of instances in which
cultures have been made from the lung and in every instance in which cultures have been made
from the bronchi. Staphylococci are often found in the bronchi, but in most instances they do not
penetrate into the lung.
Another group of cases of lobular pneumonia are important because in association with necrosis
of lung tissue recognized by the microscope hemolytic streptococci have been found in the lungs. In
such instances serum is abundant and polynuclear leucocytes are relatively scant though their
distribution varies considerably; in some places leucocytes are fairly abundant though elsewhere
almost absent, but this distribution bears no obvious relation to the bronchioles. In some instances
(Autopsies 274 and 487) red blood corpuscles are numerous but in others (Autopsies 275 and 312)
they are inconspicuous. The characteristic feature of the lesion is the occurrence of patches of
necrosis within which the nuclei both of exudate and of alveolar walls have partially or completely
disappeared. In these areas of necrosis short chains of streptococci are found in immense number
whereas in living tissue they are present in moderate number. There has been a relatively inactive
inflammatory reaction, great proliferation of streptococci and necrosis of invaded tissue. The
bacteriology of instances of lobular pneumonia with necrosis is shown in Table XXXIX.
 Table XXXIX

NO. OF CHARACTER OF PREDOMINANT CULTURE CULTURE CULTURE

AUTOPSY LOBULAR TYPE OF FROM HEART’S FROM LUNG FROM
CONSOLIDATION INFLAMMATORY BLOOD BRONCHUS
EXUDATE
274 Red Leucocytic and S. hem. S. hem. S. hem., staph.
hemorrhagic
275 Red and gray Leucocytic Pneum. IV S. S. hem., B. inf., S. hem., B. inf.,
hem. staph. staph.
312 Red and gray Leucocytic S. hem. S. hem., B. inf. S. hem., B. inf.,
staph.
478 Red Leucocytic and S. hem. S. hem.
hemorrhagic
Lobular pneumonia, in some of these instances at least, has been caused primarily by
pneumococci; necrosis has been the result of secondary invasion by streptococci. In Autopsy 275
Pneumococcus IV has been obtained from the blood, but in the presence of streptococci has
presumably disappeared from the lung and bronchus. In the case represented by Autopsy 274,
Pneumococcus IV has been found in the sputum five days before death at the onset of pneumonia,
but at this time no hemolytic streptococci have been found. In the case represented by Autopsy
312, Pneumococcus IV, B. influenzæ and a few colonies of hemolytic streptococci have been
obtained from the sputum two days after recognition of pneumonia and five days before death.
The hemorrhagic and edematous consolidation of the early pulmonary lesions of influenzal
pneumonia is their most distinctive feature. Red confluent lobular pneumonia is frequently found in
those who have died within the first week following the onset of influenza. The lungs are
voluminous and heavy and may weigh as much as 1,500 grams; the pleura which overlies the
consolidated area is blue or plum colored and usually shows scant if any evidence of pleurisy.
Scattered patches of consolidation are accurately limited to lobules, but in addition there are large
areas often involving the greater part of the lobes and not infrequently situated in the lowermost
part of the lower lobes. This confluent consolidation may be obviously limited by lobule boundaries.
The consolidated tissue is deep red and laxly consolidated; red serous fluid escapes from the cut
surface. The lesion not infrequently occurs in association with hemorrhagic peribronchiolar
pneumonia.
The histology of this confluent lesion has been studied in Autopsies 242, 244, 303, 336, 464, 474
and 506. The histology varies, because, in some instances, leucocytes, in other instances, fibrin, is
abundant, but the presence of red blood corpuscles in large number within the alveoli gives a red
color to the consolidated tissue. In these cases pneumococci, associated in the lungs or in the
bronchi with B. influenzæ, have been the cause of pneumonia. In two autopsies studied
histologically (Autopsies 274 and 478) there was red lobular and confluent pneumonia and the blood
and lungs contain hemolytic streptococci demonstrated by cultures; microscopic examination
showed the presence of a widespread necrosis of the lung tissue.
In the group of autopsies in Table XL there was red confluent lobular pneumonia. These autopsies
are separated from those just cited because there was no histologic examination of the tissue.
 Table XL

NO. OF AUTOPSY BACTERIOLOGY OF BACTERIOLOGY OF BACTERIOLOGY OF

HEART’S BLOOD LUNGS BRONCHUS
289 Pneum. IV Pneum. IV Pneum. IV, B. inf., staph.
297 Pneum. IV, B. inf. Pneum. IV, B. inf., S. hem.
(a few)
306
339 Pneum. IV
364 S. hem.
418 Pneum. atyp. II Pneum. atyp. II, B. inf., S.
vir.
424 Pneum. IV.
This group of autopsies confirms the view that the red confluent lobular pneumonia is caused by
pneumococci in association with B. influenzæ. Hemolytic streptococci may invade secondarily. In
Autopsy 297 a few hemolytic streptococci were found in the bronchus but apparently had not
entered the lungs. In the absence of histologic examination it is not possible to determine if the
invasion of hemolytic streptococcus (in Autopsy 364) has caused necrosis of the pneumonic tissue.

Fig. 7.—Bronchopneumonia with purulent bronchitis and

peribronchial hemorrhage.
 Peribronchial Hemorrhage and Pneumonia
In a considerable number of instances, namely, in 19 autopsies, hemorrhage about the small
bronchi has been recognizable upon gross examination of the lung. A conspicuous zone of
hemorrhage 2 or 3 mm. in thickness surrounds small (with no cartilage) often dilated bronchi and
on longitudinal section may be tracted for a considerable distance along the bronchus (Fig. 7). In
many additional instances peribronchial hemorrhage has been found by microscopic examination. In
some instances the peribronchial zone of hemorrhage is firmer than the tissue elsewhere and it is
occasionally difficult to determine whether the lesion is hemorrhage or pneumonia. In 7 instances
frank red consolidation of peribronchial tissue was recognized at autopsy; this lesion will be
considered later under peribronchial pneumonia. Hemorrhage about bronchi, like other evidences of
severe injury to bronchi following influenza, is more frequently found in the lowermost parts of the
lungs than elsewhere. It is invariably associated with severe bronchitis; the bronchi have contained
purulent fluid in 15 of 19 instances of peribronchial hemorrhage and in 10 instances the lesion has
been associated with dilatation of the bronchi.
Microscopic examination furnishes further evidence of the severity of the bronchial changes which
have brought about hemorrhage into the surrounding alveoli. The lumen of the bronchus contains
blood and leucocytes; the epithelium is sometimes raised in places from the underlying basement
membrane by blood; blood vessels of the bronchial wall are engorged, and there is hemorrhage into
the tissue of the bronchus. More frequently the bronchial epithelium is completely lost and the
denuded surface is often covered by a layer of fibrin intimately adherent to the inflamed mucosa.
Transitions between simple hemorrhage and pneumonia are found, polynuclear leucocytes being
mingled with red blood corpuscles. In several instances the alveoli in immediate contact with the
bronchial wall have contained fibrin, whereas those in the surrounding zone have contained blood.
Bacteria found in the bronchi in 10 instances of peribronchial hemorrhage have been as follows:
Staphylococci 1
B. influenzæ, pneumococci 1
B. influenzæ, S. hemolyticus 2
B. influenzæ, pneumococci, staphylococci 1
B. influenzæ, S. hemolyticus, staphylococci 4
No organism found 1
The high incidence of B. influenzæ and the frequent association of B. influenzæ and hemolytic
streptococci are noteworthy. The instance in which no organisms were found is probably due to a
defect in media and should perhaps be excluded from the list.
The percentage incidence of pneumococci, hemolytic streptococci, staphylococci and B. influenzæ
in the bronchus, lungs and blood of the heart is an index of the facility with which these
microorganisms penetrate internal organs when the bronchi are the site of this hemorrhagic lesion.
Table XLI

HEMOLYTIC
PNEUMOCOCCI STREPTOCOCCI STAPHYLOCOCCI B. INFLUENZÆ
NO. OF NO. PER CENT NO. PER CENT NO. PER CENT NO. PER CENT
CULTURES POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE
Bronchus 10 2 20.0 6 60.0 6 60.0 8 80.0
Lung 13 4 30.8 7 53.8 3 23.1 5 38.5
Blood 17 4 23.5 9 52.9

When these figures are compared with those for all forms of bronchitis no very noteworthy
differences are found; the incidence of pneumococci here is less and that of hemolytic streptococci
greater. In association with the severe changes present in the bronchi, hemolytic streptococci which
enter the lungs almost invariably find their way into the blood.
 In 6 instances there has been frank pneumonic consolidation limited to a zone encircling small
and medium-sized bronchi which have often been obviously dilated. On cross section these patches
of pneumonia are circular, from 1 to 2 cm. in diameter and each contains a bronchus at its center.
When the bronchus is cut longitudinally it is evident that pneumonic consolidation forms a cylindrical
sheath about the tube. The consolidation varies in color from red to grayish red. In one instance
(Autopsy 253) the consolidated tissue has formed a gray zone in contact with the bronchus and is
red in a peripheral zone; microscopic examination shows that the alveoli about the bronchus contain
fibrin, whereas those at a greater distance contain red blood corpuscles. In this instance, the
associated pneumonia in another part of the lung has been somewhat anomalous and has had
characters both of lobar and bronchopneumonia, for scattered in the left lung there have been
patches of firm consolidation not more than 2 cm. across. The smaller of these patches are deep
red, but the larger are coarsely granular and gray in the center. The patchy character of the lesion
has suggested bronchopneumonia, but the coarse granulation on section and the presence of
fibrinous plugs within the small bronchi have presented a close resemblance to lobar pneumonia.
This autopsy is one of the few instances in which Pneumococcus II has been found, Pneumococcus
II being present in blood and lungs, B. influenzæ, in lungs and bronchi. In 2 additional instances
(Autopsies 374 and 392) peribronchial pneumonia, recognizable at autopsy, has been associated
with consolidation having the characters of lobar pneumonia. In one instance, Autopsy 374, the
right lung has contained two patches of firm, mottled red and pinkish red coarsely granular
consolidation each about 6 cm. across, one situated in the upper lobe and the other in the lower
lobe. Elsewhere in the lung, in definite relation to dilated bronchi, occur patches of firm, red,
coarsely granular consolidation from 1 to 1.5 cm. in diameter when cut transversely. The bronchus
in the center has contained purulent fluid. In the opposite lung similar consolidation has been
limited to zones about dilated bronchi which contain purulent fluid. Pneumococcus IV has been
obtained from the blood of the heart.
The peribronchial pneumonia which has been described occurs in association with evidence of
profound injury to the bronchial wall. In 5 of 6 instances purulent bronchitis has been found at
autopsy; in half of these instances bronchiectasis has been noted. The epithelium of the bronchus
has been found separated from the underlying tissue by serous exudate, blood and leucocytes;
epithelial cells undergo necrosis and disappear, the denuded surface being covered by fibrin.
Necrosis extends a varying depth into the wall of the bronchus; blood vessels are engorged, and
there is in some instances hemorrhage throughout the wall of the bronchus.
The character of the exudate in the alveoli surrounding the bronchus differs considerably in
different instances. In some instances (Autopsies 374 and 392) red blood corpuscles are
predominant in the alveoli in contact with the bronchial wall, whereas in a peripheral zone
polynuclear leucocytes are more abundant. In other instances (Autopsies 253 and 402) alveoli next
the bronchial wall contain abundant fibrin and these are surrounded by a zone in which the alveoli
are filled with blood.
Peribronchial pneumonia is the result of the direct extension of the inflammatory process through
the wall of the bronchus; it occurs when the epithelium of the bronchus is destroyed and the
underlying tissues are injured, but may be present in a wide encircling zone even when the lesion
has not penetrated the bronchial wall. The distribution of the pneumonia demonstrates very clearly
that the inflammatory process does not reach the affected peribronchial alveoli by way of the
bronchioles tributary to the bronchus.
The bacteriology of these instances of peribronchial pneumonia is noteworthy. (Table XLII.)
 Table XLII

AUTOPSY BLOOD LUNG BRONCHUS

253 Pneum. II Pneum. II, B. inf. Staph., B. inf.
374 Pneum. IV
387 Pneum. II, S. hem. Pneum. II, staph., B. inf. Pneum. II, S. hem., staph.,
B. inf.
392 Pneum. II
402 Pneum. IV, S. hem.
424 ? Pneum. IV
Pneumococcus has been found in every instance either in the lungs or blood. Pneumococcus II,
which has been uncommon with the pneumonia following influenza at Camp Pike and has occurred
only ten times in more than 200 autopsies, has been present in one-half of these cases. The
constant association of the lesion with pneumococcus is particularly significant when a comparison
is made between the incidence of pneumococcus with peribronchial hemorrhage, on the one hand,
and peribronchial pneumonia on the other; pneumococcus has been present in less than a third of
the instances of hemorrhage but in all instances of pneumonia.
In addition to the instances in which gross peribronchial consolidation has been noted at autopsy,
microscopic examination has demonstrated the presence of fibrinous pneumonia surrounding
bronchi in a considerable number of autopsies. In a zone encircling small bronchi (with no cartilage)
alveoli are filled by plugs of dense fibrin (Fig. 20) containing in variable number polynuclear
leucocytes and mononuclear cells. The width of the zone is often equal or greater than the diameter
of the bronchus. Alveoli outside the zone of fibrinous inflammation may contain red blood corpuscles
or serum, and desquamated epithelial cells are often abundant.
Of 21 instances of peribronchial fibrinous pneumonia 20 were associated with purulent bronchitis.
Further evidence of the relation of the lesion to profound injury to the bronchi is its association with
bronchiectasis in 17 instances.
Peribronchial fibrinous pneumonia, like other lesions encircling the small bronchi, bears a direct
relation to the severity of microscopic changes in the bronchus. The epithelium of the bronchus is
either partially or completely lost. Occasionally epithelium is raised by hemorrhage or leucocytes
from the underlying tissue but more frequently it is wholly lost and the surface is covered by a layer
of fibrin. In the early stages of the lesion, polynuclear leucocytes may be numerous throughout the
bronchial wall, indicating that the inflammatory irritant within the lumen is affecting the entire wall
and extending its influence to the surrounding pulmonary tissue. Later lymphoid and plasma cells
are more abundant than polynuclear leucocytes. Coagulative necrosis and disintegration of the
bronchial wall, proceeding from the inner surface outward, may extend more or less deeply, and
fibrinous inflammation of adjacent alveoli is often more extensive about that segment of the
bronchus which shows the greatest change. In some instances segments of the bronchial wall or
even the entire wall has disappeared, so that alveoli containing fibrin form part of the wall of the
cavity thus formed. When bronchiectasis has occurred, there are often fissures from the lumen
through the entire wall extending into the surrounding lung tissue: here fibrinous pneumonia is
particularly conspicuous, occurring in a zone about the edges of the defect. This deposition of fibrin
within the alveoli adjacent to the injury doubtless has a part in limiting the distribution of bacterial
infection. Nevertheless breaks in the continuity of the bronchial wall are not essential to the
production of the lesion and the irritant, which is responsible for the lesion, may penetrate through
the bronchial wall to surrounding alveoli and from alveoli to other alveoli immediately adjacent.
With this peribronchial pneumonia the smallest bronchi are distended with pus and their walls are
infiltrated with polynuclear leucocytes, lymphoid and plasma cells. In a broad zone encircling the
bronchus the alveoli are filled with plugs of fibrin. Bronchioles are similarly distended with
polynuclear leucocytes; the alveoli which occur upon the wall of the bronchiole are often limited to
one side of the wall and are filled with fibrin. This fibrin occasionally projects into the lumen of the
bronchiole and forms a continuous layer in contact with the wall on the same side. The alveolar duct
and infundibulum are distended with polynuclear leucocytes. The alveoli upon the wall of the
alveolar duct and upon the proximal part of the infundibulum are filled with fibrin. The bronchus,
bronchiole, alveolar duct and part of the infundibulum are thus surrounded by a continuous zone of
alveoli containing fibrin. The alveoli about the distal part of the infundibulum may be filled with
polynuclear leucocytes. Lung tissue between adjacent zones of fibrinous pneumonia may contain
serum and desquamated epithelial cells.
Organization of peribronchial fibrin was found in 10 of the 22 autopsies in which peribronchial
fibrinous pneumonia had been found. Fibroblasts have invaded the fibrin and newly formed
capillaries have penetrated into it. In some instances the interalveolar septa are thickened and
infiltrated with lymphoid and plasma cells, and in 7 instances there was chronic pneumonia with
thickening and mononuclear infiltration of the interstitial tissue about the bronchi and blood vessels,
and elsewhere. The duration of the fatal illness in 12 instances with no organization was usually
from ten days to two weeks, though in 3 instances there was no organization although the
respiratory disease had lasted from seventeen to nineteen days (average duration with no
organization, 13.5 days). The duration of illness in 10 instances with organization of fibrin was
slightly less than three weeks (average 18.9 days). These figures do not accurately represent the
duration of pneumonia which usually develops after a period of several days following onset of
influenza.
This group of instances of peribronchial fibrinous pneumonia has offered an opportunity to study
the bacteriology of pneumonia with organization and to determine if it presents any unusual
characters. The bacteriology of autopsies with peribronchial fibrinous pneumonia with no
organization is shown in Table XLIII:
Table XLIII

AUTOPSY BLOOD LUNG BRONCHUS

289 Pneum. IV Pneum. IV Pneum. IV, B. inf., staph.
372
376 S. hem. S. hem. S. hem., B. inf., S. aur.
409 0
410 S. hem., B. inf. S. aur.
412 Pneum. II Pneum. II, B. inf.
420 S. hem. S. hem., B. inf. S. aur.
423 S. hem. S. hem., B. inf.
440 0 B. inf., S. aur. B. inf., S. aur.
448 0 0 0
482 0 B. inf., Pneum. IV B. inf., Pneum. IV, S. hem.
489 0 Pneum. IV, B. inf. Pneum. IV, B. inf.
The bacteriology of instances of peribronchial fibrinous pneumonia with organization of the
intraalveolar fibrin is shown in Table XLIV:
 Table XLIV

AUTOPSY BLOOD LUNG BRONCHUS

283 Pneum. IV Staph., B. inf. B. inf., Pneum. IV, staph.
291 0 0 B. inf., staph.
398 0
419 0 Pneum. II, B. inf. Pneum. II, B. inf.
421 S. hem. Pneum. IV, S. hem.
422 0 Pneum. II atyp., B. inf.
425 S. hem. S. hem., B. inf., S. alb.
433 0 S. hem., B. inf., S. aur.
460 S. hem. S. hem., B. inf. S. hem., B. inf., staph.
463 0 B. inf., staph. B. inf., staph., Pneum. IV
B. influenzæ has been present in the bronchi in every instance save one in which cultures have
been made, and it is probable that in this exceptional instance cultures have remained sterile
because the media employed have been defective. The incidence of B. influenzæ in the lung has
been unusually high both with and without organization (66.7 per cent with no organization; 77.8
per cent with organization). Streptococci and staphylococci have been found in a considerable
proportion of all instances of peribronchial fibrinous pneumonia, but there has been no notable
preponderance of these microorganisms when organization has occurred. Organization has been
present in instances in which pneumonia is referable to pneumococcus associated with B. influenzæ
and unaccompanied by either streptococci or staphylococci (Autopsies 419 and 422). Wadsworth[81]
found no organization after inoculation of the lungs of dogs with pneumococcus or with
staphylococcus alone, but produced organization when he inoculated animals with both
microorganisms.
Injury to bronchi produced in part at least by B. influenzæ exposes the bronchi and lung tissue to
repeated infection with a variety of microorganisms; absorption of fibrin and regeneration of alveolar
epithelium are prevented, resolution fails to occur and organization of fibrin follows.
 Suppurative Pneumonia With Necrosis and Abscess Formation
Three varieties of suppurative pneumonia have occurred in association with influenza.
A. Necrosis and suppuration with formation of one or several abscesses usually below the pleura
and almost invariably caused by hemolytic streptococci.
B. Interstitial suppurative pneumonia caused by hemolytic streptococcus.
C. Multiple abscesses in clusters caused by staphylococci.
Suppurative pneumonia with necrosis and abscess formation will be discussed in this section.
Pulmonary abscesses which occurred in 43 autopsies may be included in this group; in 4 of these
autopsies abscess and interstitial suppurative pneumonia occurred in the same individual. These
abscesses were much more frequently situated in the lower than in the upper lobes and more often
in the right than in the left lung. In most instances there was one or several abscesses situated
below the pleura of one lobe; occasionally abscesses occurred in two lobes of the same lung or in
both lungs. The distribution was as follows: Abscess in only one lung occurred in right upper lobe in
6 autopsies; middle lobe, 3; lower lobe, 15; left upper lobe, 2; lower lobe, 16. Abscesses occurred in
both right and left lower lobes, twice. The usual situation was at the lower and posterior part of the
lower lobe at or near the basal edge, less frequently below the posterior border or upon the basal
surface of the lobe. These abscesses in almost every instance were found immediately below the
pleural surface, so that they appeared upon the pleura as opaque yellow spots usually surrounded
by narrow zones of hemorrhage. In one instance (Autopsy 376) the abscess cavity was separated
from the pleural cavity by remains of the pleura which was as thin as tissue paper and in other
instances perforation had occurred (Fig. 9). In Autopsy 480 the abscess cavity which had perforated
the pleura was in free communication with a bronchus of medium size.
In most instances of suppurative pneumonia there have been associated lesions of
bronchopneumonia which have been peribronchiolar, hemorrhagic or lobular and have exhibited no
unusual characters. The abscess or abscesses are situated within an area of pneumonic
consolidation which is not limited by lobule boundaries and has not the characters of
bronchopneumonic consolidation. In some instances this consolidation is limited to a zone
immediately about the abscess, but often it involves the greater part of a lobe. The tissue is laxly
consolidated and flabby; on section it has a dull, conspicuously cloudy appearance and is grayish
red, pinkish gray or gray; it is homogeneous or very finely granular. Turbid gray fluid, which
sometimes resembles thin pus, oozes from the cut surface.
Widespread necrosis of tissue is not infrequently a conspicuous feature of this pyogenic
pneumonia (Fig. 8). Upon a cloudy gray background of consolidation are numerous opaque
yellowish gray or yellow patches, occasionally 2 or 3 cm. across, giving a mottled character to the
cut surface. Upon the pleura these necrotic patches appear as dull opaque yellow spots. They may
be surrounded by a zone of hemorrhage. The opaque material is at first firm but may undergo
softening, becoming semisolid and finally purulent. Necrotic patches may be scattered throughout a
lobe, but fully formed abscesses are with few exceptions immediately below the pleura (Fig. 9).
 Fig. 8.—Streptococcus
pneumonia with massive
necrosis. Autopsy 354.
 Fig. 9.—Abscess below pleura
with perforation caused by
hemolytic streptococci. Healing
suppurative interstitial
pneumonia indicated by
yellowish gray lines marking
interlobular septa at base of
lower lobe. Autopsy 474; right
lung. (See left lung, Fig. 10.)

The duration of illness in cases of pneumonia with abscess varied from a week or less
(11 instances) to more than four weeks. The duration of the greater number of cases
(17 instances) was between one and two weeks. In one instance onset occurred with
symptoms of influenza, pneumonia was recognized two days later, and death occurred
only four days after the onset of illness. When the duration of the illness was less than
a week the symptoms of onset were in some instances those of pneumonia.
Table XLV shows the incidence of pneumococcus, S. hemolyticus, staphylococcus and
B. influenzæ in instances of suppurative pneumonia with abscess formation, 4 instances
of abscess with interstitial suppurative pneumonia being excluded:
Table XLV

HEMOLYTIC
PNEUMOCOCCI STAPHYLOCOCCI B. INFLUENZÆ
NO. OF STREPTOCOCCI
CULTURES NO. PER CENT NO. PER CENT NO. PER CENT NO. PER CENT
POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE POSITIVE
Bronchus 24 5 20.8 22 91.6 12 50.0 18 75.0
Lung 36 9 25.0 30 83.3 14 35.6 8 22.2
Blood 37 6 16.2 31 83.8

In over 80 per cent of instances of pulmonary abscess hemolytic streptococcus has

been found in blood, lungs and bronchus and, when cultures have been made, in the
inflamed pleural cavity as well. Streptococci have been found in immense number in
sections from the necrotic lung tissue and the abscesses which have been formed. It is
evident that hemolytic streptococci have caused suppurative pneumonia and death,
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