![Discussion
That wide variations in the conception of influenza have arisen during the recent
pandemic, even a hasty review of the literature makes clear. In its essence this
divergence of opinion seems to depend upon whether pneumonia is considered an
essential part of influenza or a complication due either to the primary cause of
influenza or to secondary infection. One extreme is expressed by Dunn[30]
who says
“the so-called complication is the disease,” the other by Fantus[31]
who finds
influenza a relatively mild disease with pneumonia a relatively infrequent and
largely preventable complication.
A similar divergence of opinion prevails with respect to the bacteriology of
influenza. There is fairly general agreement that the members of the
pneumococcus and streptococcus groups and to a less extent other organisms are
responsible for a large proportion of the secondary pneumonias, and but few
observers hold that they possess any etiologic relationship to influenza. No such
uniformity of opinion exists, however, with respect to the relation of B. influenzæ to
influenza and to the complicating pneumonia. By some it is considered the primary
cause of influenza, by others it is regarded as a secondary invader responsible for a
certain proportion of the secondary pneumonias, and by still others it is not
considered to bear any relation either to influenza or its complications.
A limited number of references to the extensive literature of the recent pandemic
will amply serve to illustrate the various points of view that have developed.
Keegan[32]
regards pneumonia as a complication and considers that B. influenzæ,
the probable cause of influenza, is the primary cause of the pneumonia which may
or may not be still further complicated by pneumococcus or streptococcus infection
as a terminal event. Christian[33]
states that epidemic influenza causes a clinically
demonstrable bronchitis and bronchopneumonia in the larger proportion of cases,
and lays particular emphasis upon the fact that it is quite incorrect to consider
fatalities in the epidemic as due to influenza uncomplicated by bronchopneumonia.
Blanton and Irons[34]
speak of influenza as an “antecedent respiratory infection” of
undetermined etiology, and believe that pneumonia when it occurs is due to
autogenous infection by a variety of secondary invaders, principally of the
pneumococcus and streptococcus groups. Hall, Stone, and Simpson[35]
regard
pneumonia strictly as a complication and quite distinct from influenza itself. Synnott
and Clark[36]
believe that the infection is characterized by a progressive intense
exudative inflammation of the respiratory tract often terminating in an aspiration
pneumonia with a variety of conditions found at autopsy and a multiplicity of
secondary organisms responsible for the fatal termination. B. influenzæ was usually
found but always with other organisms. Friedlander and his collaborators[37]
speak
of a fulminating fatal type of influenza with acute inflammatory pulmonary edema,](https://image.slidesharecdn.com/6787-250526074627-bda7bf83/85/Solution-Manual-for-Systems-Analysis-and-Design-8th-Edition-by-Kendall-32-320.jpg)
![but regard true bronchopneumonia as secondary, due to infection with
pneumococcus or S. hemolyticus. B. influenzæ was not found more frequently than
under normal conditions. Brem[38]
and his collaborators present a clear cut clinical
picture both of influenza and the secondary pneumonia to which it predisposes,
regarding the latter as definitely due to secondary infection with pneumococcus,
streptococcus or B. influenzæ, the virus of influenza being unknown. Ely[39]
and his
collaborators make no distinction between influenza and pneumonia, and
apparently consider the epidemic due to a hemolytic streptococcus of indefinite and
inconstant characters. The Camp Lewis Pneumonia Unit[40]
states “the process
[influenza], whether mild or severe, is etiologically and pathologically the
same; * * *.” B. influenzæ was not found. In a report of The American Public
Health Association[41]
it is stated that deaths resulting from influenza are commonly
due to pneumonias resulting from an invasion of the lungs by one or more forms of
streptococci, by one or more forms of pneumococci, or by the so-called influenza
bacillus. This invasion is apparently secondary to the initial attack. Wolbach[42]
found B. influenzæ in a high proportion of cases, not infrequently in pure culture in
the lung, and believes that there is a true influenzal pneumonia whether B.
influenzæ is the cause of the primary disease or not. Spooner, Scott and Heath[43]
isolated B. influenzæ in a high percentage of cases and consider it reasonable to
suppose that it was the prime factor in the epidemic. Kinsella[44]
found B. influenzæ
infrequently and regards it as a secondary invader. MacCallum[45]
regards B.
influenzæ as a secondary invader and believes that it is responsible for a form of
purulent bronchitis and bronchopneumonia following certain cases of influenza.
Pritchett and Stillman[46]
found B. influenzæ in 93 per cent of cases of influenza and
bronchopneumonia. Hirsch and McKinney[47]
state that B. influenzæ played no rôle
in the epidemic at Camp Grant and apparently consider it due to a specially virulent
pneumococcus.
No further references to the extensive literature of the recent pandemic seem
necessary, since those cited above serve to illustrate the various points of view that
exist. A similar diversity of opinion may be found in the reports from foreign
sources.
It would appear that much of the divergence of opinion that has been formed
has depended to a considerable extent upon the conditions under which cases have
been observed. This is clearly brought out by contrasting the experience of
Fantus[39]
dealing with private cases in civilian practice, where pneumonia was
relatively uncommon, with that of others dealing only with cases in large hospitals,
where those admitted have been in large part selected seriously ill patients with a
high incidence of pneumonia, the milder cases comprising from 60 to 90 per cent
of those attacked by influenza never reaching the hospital. Variations in opinion
with respect to the bacteriology of the epidemic, especially in regard to B.
influenzæ, would appear to be due for the most part to differences in bacteriologic
technic, in some degree to differences in interpretation. Accumulating evidence can
leave little doubt that B. influenzæ was at least extraordinarily and universally](https://image.slidesharecdn.com/6787-250526074627-bda7bf83/85/Solution-Manual-for-Systems-Analysis-and-Design-8th-Edition-by-Kendall-33-320.jpg)
![is analogous to the exanthemata, the majority of which present a comparatively
long, fairly constant, incubation period.
B. influenzæ has characteristics in accord with the clinical features of influenza. It
is an organism of very labile virulence; it is always present in our experience on the
mucous membranes of the respiratory tract in early uncomplicated cases of
influenza, often in overwhelming numbers; in only very exceptional instances, in
adults at least, does it invade the body producing a general infection, as the
numerous reports of negative blood cultures testify; recent investigations by
Parker[48]
and others indicate that it is capable of producing a toxin quickly fatal for
rabbits; it is predominantly present in the respiratory tract during the active stage
of the disease and disappears in a considerable proportion of cases at time of
recovery, while in others, more particularly those that develop an extensive
secondary bronchitis and bronchiectasis it may persist for an indefinite period of
time.
It is, of course, fully appreciated that the foregoing is in the main merely
argumentative reasoning and it is put forth only to suggest that B. influenzæ merits
a much closer scrutiny with respect to its etiologic relationship to influenza than the
trend of present opinion has awarded it.
Although there remains some difference of opinion as to the relation of influenza
to pneumonia, the majority of observers concur in regarding pneumonia as a
complication and this would seem to be the only logical interpretation of the facts
available. The same may be said with respect to purulent bronchitis and
bronchiectasis. It is of considerable significance in this connection that pneumonia
following influenza presents no uniform clinical picture, no uniform bacteriology and
no uniform pathology. Whether the predisposition of patients with influenza to
contract pneumonia is preponderantly due to lowering of general resistance to
infection by the extremely prostrating effect of the disease and the inhibition of
leucocytic defense, or to a destruction of local resistance against bacterial invasion
by reason of profound injury to the bronchial mucosa, or to a combination of both
factors, is difficult to say. It seems most probable that both are concerned. At any
rate it seems clear that in the presence of influenza a considerable variety of
organisms which under ordinary conditions do not find lodgement in the lungs are
able to gain access to the lower respiratory tract and produce pneumonia.](https://image.slidesharecdn.com/6787-250526074627-bda7bf83/85/Solution-Manual-for-Systems-Analysis-and-Design-8th-Edition-by-Kendall-35-320.jpg)
![CHAPTER III
SECONDARY INFECTION IN THE WARD TREATMENT
OF INFLUENZA AND PNEUMONIA
Eugene L. Opie, M.D.; Francis G. Blake, M.D.; James C. Small, M.D.; and Thomas
M. Rivers, M.D.
One of the most pressing problems that presented itself in the care of
influenza and pneumonia patients in the army cantonments during the recent
epidemic was the danger of secondary contact infection because of the
overcrowding of the base hospitals, nearly all of which were taxed far beyond
the limits of their capacity. That this danger was very real was fully
demonstrated by certain studies in ward infection that this commission was
able to make at Camp Pike[49]
. It is the purpose of the present section of the
report to present these studies and to discuss the means whereby this
danger may be most successfully met.
It is perhaps well, first to define exactly what is meant by secondary
contact infection in influenza and pneumonia. In our experience at Camp Pike
it was found that a very large percentage of the pneumonias following
influenza were accompanied by secondary infection with pneumococcus,
some few being caused by hemolytic streptococcus. The types of
pneumococcus encountered were almost entirely those that are found
normally in the mouths of healthy men, approximately 85 per cent being
Types II atypical, III, and IV. It has been generally accepted that infection
with these types of pneumococci is usually autogenous—that is, that under
the proper conditions of lowered resistance an individual becomes infected
with the pneumococcus that he carries in his own mouth. Many observations
made during the course of the present work have suggested that this is
probably not so in many instances and that the influenza patient may not be
so much in danger from the pneumococcus that he normally carries in his
own mouth as he is from that carried by his neighbor, in other words, he is in
danger from contact infection. The same considerations hold true with](https://image.slidesharecdn.com/6787-250526074627-bda7bf83/85/Solution-Manual-for-Systems-Analysis-and-Design-8th-Edition-by-Kendall-36-320.jpg)
![Secondary Infection with S. Hemolyticus in
Pneumonia
Pneumonia caused by streptococci was repeatedly observed[50]
during the
pandemic of influenza which occurred in 1889–90. With clearer recognition of
the characters which distinguish varieties of streptococci several observers
have shown that secondary infection with hemolytic streptococci may occur
during the course of pneumonia and though definite evidence has been
lacking have suggested that it may be acquired within hospital wards. That a
similar secondary infection with S. hemolyticus in pneumococcus pneumonias
following influenza occurred not infrequently at Camp Pike during the
epidemic was shown by bacteriologic studies made during life and at autopsy
in a considerable series of cases. During the early days of the epidemic of
influenza, secondary streptococcus infection was almost entirely limited to
certain wards which were opened for the care of the rapidly increasing
number of patients with pneumonia. During this period these wards were
overcrowded, organization was incomplete, and the opportunities for transfer
of infection from patient to patient were almost unlimited. The spread of
streptococcus contagion and its fatal effect may be clearly brought out by
comparison of these wards with wards that had long been organized for the
care of patients with pneumonia.
Ward 3 had been in use for the care of patients with pneumonia for some
time prior to the outbreak of influenza. It was provided with sheet cubicles
and conducted by medical officers, nurses and enlisted men accustomed to
the care of patients with pneumonia, ordinary precautions being taken
against transfer of infection from one patient to another. The data in Table
XVII show the average number of patients in the ward, the number of new
cases of pneumonia admitted, and the number of deaths among patients
admitted during the corresponding period, for three periods of ten days each
from September 6 to October 5. The types of infection in fatal cases as
determined by cultures taken at autopsy are also shown.](https://image.slidesharecdn.com/6787-250526074627-bda7bf83/85/Solution-Manual-for-Systems-Analysis-and-Design-8th-Edition-by-Kendall-38-320.jpg)
![Table XXI
Secondary Infection with Pneumococcus Type II
NAME BED
OCCUPIED
ADMITTED PNEUMOCOCCUSIN
SPUTUM ON
ADMISSION
SECONDARY
INFECTION
DATE PNEUMOCOCCUS
AT AUTOPSY
Pvt.
Wolfe
No. 6 Sept. 17 IV Sept.
23
II[51]
Pvt.
Pullam
No. 5 Sept. 9 IV Sept.
24
II
Pvt.
Swain
No. 3 Sept. 16 II](https://image.slidesharecdn.com/6787-250526074627-bda7bf83/85/Solution-Manual-for-Systems-Analysis-and-Design-8th-Edition-by-Kendall-44-320.jpg)
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- 5. Chapter 1 Systems Analysis and Design Instructor’s Manual 1-1 Copyright © 2011 Pearson Education, Inc. Publishing as Prentice Hall Solution Manual for Systems Analysis and Design 8th Edition by Kendall Download full chapter at: https://testbankbell.com/product/solution-manual- for-systems-analysis-and-design-8th-edition-by-kendall/ Chapter 1 Systems, Roles, and Development Methodologies Key Points and Objectives 1. Information is an organizational resource that must be managed as carefully as other resources. 2. Information systems fall into one of the following eight categories: A. Transaction processing systems (TPS) process large volumes of data, routine business transactions. B. Office automation systems (OAS) manipulate information and share it throughout the organization. Software, such as spreadsheets, word processing, email, teleconferencing and so on are routinely used in OAS. C. Knowledge work systems (KWS) help professionals to develop new knowledge, often in teams. D. Management information systems (MIS) are computerized information systems that support a broader range of business functions than do data processing systems. E. Decision support systems (DSS) are information systems that help support decision makers in making semi-structured decisions. F. Expert systems capture the expertise of a human expert or experts for solving particular organizational problems. G. Artificial intelligence research is part of expert systems and has two avenues: understanding natural language and analyzing the ability to reason through a problem to its logical conclusion H. Group decision support systems (GDSS) and computer supported collaborative work systems (CSCWS) allow group members to interact and help facilitate group problem solving. I. Executive support systems (EES) help senior management to make strategic decisions. 3. New technologies, such as ecommerce, Enterprise or Enterprise Resource Planning, wireless and mobile devices, and open source software are being integrated into traditional systems. 4. Ecommerce uses the Web to perform business activities. The benefits of using the Web are: A. Increasing awareness of the availability of the service, product, industry, person, or group B. 24-hour access for users C. Improving the usefulness and usability of interface design
- 6. Chapter 1 Systems Analysis and Design Instructor’s Manual 1-2 Copyright © 2011 Pearson Education, Inc. Publishing as Prentice Hall D. Creating a global system 5. Enterprise Resource Planning (ERP) has the goal of integrating many different information systems within the corporation, using proprietary software. 6. Systems must be designed for wireless and mobile devices, including mobile commerce (mcommerce). 7. Open source software (OSS) provides both software and the program source code used to create the software. Many users and programmers may provide modifications to the programs. Open source software may be categorized into four types of communities: A. Ad hoc B. Standardized C. Organized D. Commercial 8. Open source communities differ from each other on six key dimensions: A. General structure B. Environment C. Goals D. Methods E. User community F. Licensing 9. Systems analysis and design is a systematic approach to identifying problems, opportunities, and objectives; analyzing the information flows in organizations; and designing computerized information systems to solve a problem. 10. User involvement throughout the systems project is a critical success factor. 11. Systems analysts act as outside consultants to businesses, as supporting experts within a business and as change agents. 12. Analysts are problem solvers and require communication skills. 13. It is important for analysts to be aware of their ethical framework as they work to build relationships with users and customers. 14. The systems development life cycle is a systematic approach to solving business problems. 15. The human-computer interaction (HCI) is a human-centered approach that places an emphasis on human needs before the needs of an organization or a system. 16. The human-computer interaction should be included into every phase of the systems development life cycle. 17. The systems development life cycle is divided into seven phases: A. Identifying problems, opportunities, and objectives
- 7. Chapter 1 Systems Analysis and Design Instructor’s Manual 1-3 Copyright © 2011 Pearson Education, Inc. Publishing as Prentice Hall B. Determining human information requirements C. Analyzing system needs D. Designing the recommended system E. Developing and documenting software F. Testing and maintaining the system G. Implementing and evaluating the system 18. System maintenance is removing undetected errors and enhancing existing software. 19. Systems are enhanced for the following reasons: A. Adding additional features to the system. B. Business and governmental requirements change over time. C. Technology, hardware, and software are rapidly changing. 20. CASE tools are software packages for systems analysis and design. 21. Reasons for using CASE tools are: A. To increase analyst productivity. B. Facilitate communication among analysts and users. C. Providing continuity between life cycle phases. 22. CASE tools may be divided into several categories, namely: A. Upper CASE tools are used to perform analysis and design. B. Lower CASE tools are used to generate computer language source code from CASE design. The advantage in generating source code are: a. The time to develop new systems decreases. b. The time to maintain generated code is less than to maintain traditional systems. c. Computer programs may be generated in more than one language. d. CASE design may be purchased from third-party vendors and tailored to organizational needs. e. Generated code is free from program coding errors. 23. The agile approach is based on: A. Values B. Principles C. Core practices 24. The four values of the agile approach are: A. Communication B. Simplicity C. Feedback D. Courage 25. Four resources may be adjusted for successful completion of an agile project:
- 8. Chapter 1 Systems Analysis and Design Instructor’s Manual 1-4 Copyright © 2011 Pearson Education, Inc. Publishing as Prentice Hall A. Time B. Cost C. Quality D. Scope 26. An agile project is interactive and incremental 27. The agile development process has five distinct stages: A. Exploration B. Planning C. Iterations to the first release D. Productionizing E. Maintenance 28. The planning game spells out rules that help formulate the agile development team from their business customers. 29. Object-oriented (O-O) analysis and design is used to build object-oriented programs. This includes not only data, but the instructions about operations that manipulate the data. 30. The Unified Modeling Language (UML) is a standardized object-oriented modeling language. 31. Object-oriented methodologies focus on small, quick iterations of development. 32. Object-oriented phases include: A. Define the use case model. B. Begin drawing UML diagrams. C. Develop class diagrams. D. Draw statechart diagrams. E. Modify the UML diagrams. F. Develop and document the system. Consulting Opportunity 1.1 (p. 7) Healthy Hiring: Ecommerce Help Wanted The qualifications that the systems analysis team should be looking for when hiring their new ecommerce development team member should focus on interpersonal skills as well as technical skills. The system development project is not analyzing an existing business area and does not have to focus on how the current system works or the problems present in the current system. This implies that the analysis team will have to do extensive work with the users to define the new system before writing any program code. One of the primary qualities of the new analyst is to get along well with the other team members as well as users. A second quality is the ability to learn new languages rather than know specific languages. Because this is a new project and the software used to develop ecommerce Web sites as well as the other systems needed to support ecommerce is rapidly changing.
- 9. Chapter 1 Systems Analysis and Design Instructor’s Manual 1-5 Copyright © 2011 Pearson Education, Inc. Publishing as Prentice Hall In this situation, it is important that the team members have some basic business understanding, because ecommerce is much more than just building a Web site. However, it is probably advantageous if the team members do not possess identical skills and competencies. Team member skills that complement one another will help the team as it encounters project complexities and has to draw on a broad base of experience and knowledge. The personality traits that are desirable in a systems analyst who will be working in ecommerce development are good interpersonal and team player skills, good communication skills, curiosity, creativity, ability to deal with stress and pressure, an understanding of how systems are put together, diagramming and design skills, and skills related to coding, testing, and debugging software. HyperCase Experience 1 As stated in the general introduction, it is strongly suggested that students review the instructions. Click on the link on the home page. This will enable them to understand the principles of how to use the HyperCase environment and assist them in having a valuable learning experience with it. You may wish to make assignments starting with the exercises, and have the students download the Visible Analyst files and restore them into their copy of Visible Analyst. The Visible Analyst project name is MRE. A review session or class discussion of what they learned would be a useful learning experience. Students may also download the Visio files and the repository Web page. The students should also go to the reception area and take a stroll around the building, clicking on links and examining the office environment. Have the students print out the telephone directory. Answers to Review Questions 1. Compare treating information as a resource to treating humans as a resource. Information fuels business and can be the critical factor in determining the success or failure of the business. Treating information as a resource includes physical or ergonomic factors, usability factors, aesthetic and enjoyable aspects, and behavioral aspects relating to the usefulness of the system. Treating humans as a resource means learning frustrations and feelings that humans have when working with a system. 2. List the differences between OAS and KWS. An office automation system (OAS) is a set of familiar commercial software tools that allow data workers to manipulate data, rather than create it. General tools, such as word processing and spreadsheets, are used to manipulate the data. A knowledge work system (KWS) is used by professionals to create new knowledge. 3. Define what is meant by MIS. Management information systems (MIS) includes transaction processing, decision analysis, and produce output that is used in decision making. 4. How does MIS differ from DSS? Both depend on a database as a source of data; however, DSS emphasizes the support of decision
- 10. Chapter 1 Systems Analysis and Design Instructor’s Manual 1-6 Copyright © 2011 Pearson Education, Inc. Publishing as Prentice Hall making in all phases and is more closely tailored to the person or group using them. 5. Define the term expert systems. How do expert systems differ from decision support systems? An expert system captures and uses the knowledge of an expert for solving organizational problems. Expert systems select the best solutions to problems, whereas DSSs leave the ultimate judgment to the decision maker. 6. List the problems of group interaction that group decision support systems (GDSS) and computer-supported collaborative work systems (CSCWS) were designed to address. The problems of group interaction that group decision support systems address are: A. Lack of participation B. Domination by group members C. Group think decision making. 7. Which is the more general term, CSCWS or GDSS? Explain. CSCW is a more general term, and may include software support called groupware for team collaboration. 8. Define the term mcommerce. Mcommerce is mobile commerce, performing ecommerce using handheld wireless devices. 9. List the advantages of mounting applications on the Web. The advantages of mounting applications on the World Wide Web are: A. Increasing awareness of the availability of the service, product, industry, person, or group B. The possibility of 24-hour access for users C. Standardizing the design of the interface D. Creating a global system without worry about time zones 10. What is the overarching reason for designing ERP systems? The overarching reason for designing ERP systems is the integration of many information systems existing on different managerial levels and within different functions. 11. Provide an example of an open source software project. There are many open source software projects that are available. Students may be familiar with ones that are not mentioned. Mozilla Firefox, Apache, and Linux are mentioned in this chapter. 12. List the advantages of using systems analysis and design techniques in approaching computerized information systems for business. System analysis and design techniques provide the analyst with a systematic procedure for analyzing data input, UML diagrams or data flow, and information output; furthermore, the techniques can improve the functioning of business.
- 11. Chapter 1 Systems Analysis and Design Instructor’s Manual 1-7 Copyright © 2011 Pearson Education, Inc. Publishing as Prentice Hall 13. List three roles that the systems analyst is called upon to play. Provide a definition for each one. The three roles of a system analyst are: A. Consultant—hired from outside an organization to address information systems issues within that organization. B. Supporting Expert—serves as a resource for those who are managing a systems project. C. Change Agent—an analyst who serves as a catalyst for change, develops a plan for change, and works with others in facilitating that change. 14. What personal qualities are helpful to the systems analyst? List them. Personal qualities helpful to systems analysts include: A. Problem-solving abilities B. Communication skills C. Computer experience D. Self-discipline and self-motivation E. Project management capabilities 15. List and briefly define the seven phases of the systems development life cycle (SDLC). The seven phases of the SDLC are: A. Identifying problems, opportunities, and objectives—recognizing problems and opportunities confronting the business and determining business objectives. B. Determining information requirements—understanding what information users need to perform their jobs. C. Analyzing system needs—structured analysis of information needs and decision making. D. Designing the recommended system—logical design of the information system. E. Developing and documenting software—structured development of software and documentation. F. Testing and maintaining the system—testing and revising the system. G. Implementing and evaluating the system—training users and reviewing system. 16. What are CASE tool used for? The reasons for using CASE tools are: A. Increasing analyst productivity B. Improving analyst-user communication C. Integrating life cycle activities 17. What is the difference between upper and lower CASE tools? Upper CASE tools are used for creating and modifying the system design. Lower CASE tools are used to generate computer source code, eliminating the need for programming the system. 18. Define what is meant by the agile approach?
- 12. Chapter 1 Systems Analysis and Design Instructor’s Manual 1-8 Copyright © 2011 Pearson Education, Inc. Publishing as Prentice Hall The agile approach is based on values, principles, and core practices. It values communication, simplicity, feedback, and courage. 19. What is the meaning of the phrase “the planning game”? The planning game spells out rules that can help formulate the agile development team’s relationship with their business customers. The rules are a basis for building and maintaining a relationship. 20. What are the stages in agile development? The five stages in agile development are exploration, planning, iterations to the first release, productionizing, and maintenance. 21. Define the terms object-oriented analysis and object-oriented design. Object-oriented analysis and object-oriented design are techniques intended to facilitate the development of systems that must change rapidly in response to dynamic business environments. 22. What is UML? UML is the Unified Modeling Language, a standardized object-oriented language used to break down a system into a use case model. Central Pacific University—Problems 1. From the introductory conversation Chip and Anna shared, which elements mentioned might suggest the use of CASE tools? CASE tools would be used to help Chip and Anna communicate with each other and share portions of the design that they have completed. Because there are many users for the Computer System, CASE tools will help to facilitate communication among the users and analyst and document the information that they have received as a result of interviews, document analysis, and questionnaires.
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- 14. Purulent Bronchitis It has been stated that a considerable number of cases of influenza developed a more or less extensive purulent bronchitis. This term is used as descriptive of a group of cases showing clinically evidence of a diffuse bronchitis as manifested by numerous medium and fine moist râles scattered throughout the chest and evidence of a definitely purulent inflammatory reaction as indicated by the expectoration of fairly copious amounts of mucopurulent or frankly purulent sputum. This condition is regarded as quite distinct, on the one hand, from the common type of mucoid bronchitis frequently associated with “common colds” and a fairly common feature of uncomplicated cases of influenza, in which physical examination of the chest reveals only transient sibilant and musical râles without evidence of extension to finer bronchi, and, on the other hand, from bronchopneumonia. Bacteriology.—Thirteen cases of purulent bronchitis following influenza in none of which was there any evidence of pneumonia at the time cultures of the sputum were made nor later were subjected to careful bacteriologic study. Specimens of bronchial sputum were collected in sterile Petri dishes and selected portions thoroughly washed to remove surface contaminations before bacteriologic examinations were made. The results are shown in Table XIII.
- 15. Table XIII Bacteriology of the Sputum in Cases of Purulent Bronchitis Following Influenza CASE STAINED FILM OF SPUTUM DIRECT CULTURE ON BLOOD AGAR PLATE MOUSE INOCULATION GJ B. influenzæ + + + B. influenzæ + + + + B. influenzæ Gram + diplococci + Pneumococcus + Pneumococcus (type undetermined) WAL B. influenzæ + + B. influenzæ + + + Gram + diplococci + + Pneumococcus IV + + TH B. influenzæ + + + B. influenzæ + + + + Gram + diplococci + + + Pneumococcus IV + + LH B. influenzæ + B. influenzæ + + Gram + diplococci + Pneumococcus IV + + FBD Gram + diplococci + + + + Pneumococcus IV + + + Pneumococcus IV B. influenzæ + B. influenzæ Wa B. influenzæ + + B. influenzæ + + Gram + diplococci + + Pneumococcus IV + + Sh B. influenzæ + + + B. influenzæ + + Gram + diplococci + + Pneumococcus IV + + + Wal Gram + diplostrep + + + S. viridans + + B. influenzæ + B. influenzæ + + CLF B. influenzæ + + + + + B. influenzæ Gram + diplococci + Pneumococcus IV NCC B. influenzæ + + B. influenzæ + + + B. influenzæ Gram − micrococcus + M. catarrhalis + + M. catarrhalis Gram + diplostrep. + S. viridans + + JCM B. influenzæ + + + B. influenzæ + + + + B. influenzæ Gram + streptococcus + S. hemolyticus + S. hemolyticus Gram − micrococcus + M. catarrhalis + Pneumococcus IV Gram + diplococcus + Bl B. influenzæ + B. influenzæ Gram + diplococcus + Pneumococcus IIa Bu B. influenzæ + + + + B. influenzæ + + + B. influenzæ Gram + diplococcus + + + + Pneumococcus IV + + + Pneumococcus IV From the data presented in Table XIII it is evident that a mixed infection existed in all cases. The results obtained by stained sputum films and by direct culture on blood agar plates are of special significance. B. influenzæ was present in all cases, being the predominant organism in 6 cases, abundantly present in others, and few in number in 2. Of other organisms the pneumococcus was most frequently found, occurring in 11 of the 13 cases, in all but 2 instances being present in considerable numbers. S. viridans was encountered twice, once in association with a Gram- negative micrococcus resembling M. catarrhalis culturally. S. hemolyticus was found once, together with M. catarrhalis and a few pneumococci, Type IV, coming
- 16. through in the mouse only and of doubtful significance. The stained sputum films and direct cultures always showed these organisms present in sufficient abundance to indicate that they were present in the bronchial sputum and were not merely contaminants from the buccal mucosa. It seems quite probable from these results that purulent bronchitis following influenza is, in most cases at least, due to mixed infection of the bronchi and should be looked upon as a complication of influenza. Whether the condition may be caused by infection with B. influenzæ alone is difficult to say. No evidence that it may be caused by B. influenzæ alone was obtained in the cases studied. It is not intended to enter here into a discussion as to whether B. influenzæ should be regarded as a secondary invader or not; the other organisms encountered certainly are. It would seem most probable that purulent bronchitis is caused by the mixed infection of B. influenzæ and various other organisms, commonly the pneumococcus, but that the condition is initiated by the invasion of the bronchi by these other organisms in the presence of a preceding infection with B. influenzæ. Clinical Features.—Purulent bronchitis following influenza began insidiously without any prominent symptoms to mark its onset. About the third or fourth day of influenza, when recovery from the primary disease might be looked for, the patient would begin to cough more frequently, raising increasing amounts of mucopurulent sputum. This sputum was yellowish green in color, copious in amount, and often somewhat nummular in character, sometimes streaked with blood. These symptoms were accompanied by the appearance of coarse, medium and fine moist râles more or less diffusely scattered throughout the chest and usually most numerous over the lower lobes. The percussion note, breath and voice sounds, and vocal and tactile fremitus remained normal. There was no increase in the respiratory rate or pulse rate, and cyanosis did not develop in the absence of a beginning pneumonia. Many such cases, of course, developed bronchopneumonia; in this event areas showing diminished resonance, suppressed breath sounds, and fine crepitant râles with the “close to the ear” quality would appear, the respiratory rate would become increased and cyanosis would become evident. In those cases of purulent bronchitis not developing pneumonia, a moderate elevation of temperature, rarely above 101° F., and irregular in character usually occurred and persisted for a few days or a week. Many cases maintained a persistent cough, raising considerable amounts of sputum throughout the period of their convalescence in the hospital, which was often considerably prolonged when this complication of influenza occurred. Although no clinical data are available on such cases over a prolonged period of observation, it seems probable that some of them, at least, had developed some degree of bronchiectasis. This would seem all the more probable, since many cases of pneumonia following influenza showed at autopsy extensive purulent bronchitis with well-developed bronchiectasis. Bronchiectasis will be discussed in greater detail in another section of this report. It is this group of cases with more or less
- 17. permanent damage to the bronchial tree that makes this type of bronchitis following influenza a serious complication of the disease.
- 18. Pneumonia The opportunity presented for a correlated study of the clinical features, bacteriology, and pathology of pneumonia following influenza throughout the period of the epidemic at Camp Pike from September 6, 1918, to December 15, 1918, made it evident that this pneumonia could be regarded as an entity in only one respect, namely, that influenza was the predisposing cause. Clinically, bacteriologically, and pathologically it presented a very diversified picture ranging all the way from pneumococcus lobar pneumonia to hemolytic streptococcus interstitial and suppurative pneumonia with the picture modified to a varying extent by the preceding or concomitant influenzal infection. One hundred and eleven consecutive cases in which careful clinical and bacteriologic studies were made form the basis of the material presented. Of these cases, 38 came to necropsy so that ample opportunity was presented to correlate the clinical and bacteriologic studies made during life with the pathology and bacteriology at necropsy. It has seemed advisable to group the cases primarily on an etiologic basis with secondary division according to clinical features in so far as this can be done. Bacteriologic studies showed that at the time of onset these pneumonias were either pneumococcus pneumonias or mixed pneumococcus and influenza bacillus pneumonias in nearly all instances. Certain of these cases later became complicated by a superimposed hemolytic streptococcus or a staphylococcus infection. In a few instances hemolytic streptococcus pneumonia directly followed influenza without an intervening pneumococcus infection. B. influenzæ was present in varying numbers in nearly all cases. In only 2 instances however, was it found unassociated with pneumococci or hemolytic streptococci, once alone and once with S. viridans. Clinically the cases fell into four main groups: (1) Lobar pneumonia; (2) lobar pneumonia with purulent bronchitis; (3) bronchopneumonia (pneumococcus); (4) bronchopneumonia (streptococcus). It should be borne in mind, however, that the picture was a complex one and that correct clinical interpretation was not always possible, since many cases did not conform sharply to any one type and superimposed infections during the course of the disease often modified the picture. Pneumococcus Pneumonia Following Influenza.—Bacteriologic examination of selected and washed specimens of sputum coughed from the lungs at time of onset of pneumonia showed the various immunologic types of pneumococcus to be present in 105 cases. The incidence of the different types is shown in Table XIV.
- 19. Table XIV Types of Pneumococcus in 105 Cases of Pneumococcus Pneumonia Following Influenza LOBAR PNEUMONIA BRONCHOPNEUMONIA TOTAL PER CENT Pneumococcus, Type I 8 0 8 7.6 Pneumococcus, Type II 3 1 4 3.8 Pneumococcus, II atyp. 12 7 9 18.1 Pneumococcus, Type III 3 3 6 5.7 Pneumococcus, Group IV 32 36 68 64.8 The most noteworthy feature of the figures in Table XIV is the high proportion of pneumonias due to types of pneumococci found in the mouths of normal individuals, 93 cases or 88.6 per cent, being caused by Pneumococcus Types II atypical, III, and IV. This is in harmony with the results generally reported and is in all probability due to the fact that in patients with influenza pneumococci, which under normal conditions would fail to cause pneumonia, readily gain access to the respiratory tract and produce the disease. It is also of interest that with one exception the highly parasitic pneumococci of Types I and II were associated with pneumonias clinically lobar in type. Superimposed infection of the lungs with other types of pneumococci than those primarily responsible for the development of pneumonia occurred not infrequently in this group of cases either during the course of the disease or shortly after recovery from the first attack of pneumonia. Pneumococcus Type II infection was superimposed upon or shortly followed pneumonia caused by Group IV pneumococci in 4 instances, by Pneumococcus II atypical in 1 instance. In 1 case pneumonia due to Pneumococcus II atypical occurred three days after recovery from a Pneumococcus Type I pneumonia, in another case Pneumococcus Type III infection was superimposed upon a pneumonia originally due to a pneumococcus of Group IV. These cases are presented in detail in another section of this report, and in several instances were shown to be directly due to contact infection from patients in neighboring beds. In a similar manner, superimposed infection with S. hemolyticus at some time during the course of the pneumonia occurred in 13 cases in this group, with fatal result in all but one. Streptococcus infection occurred in pneumonia due to Pneumococcus II atypical once, to Pneumococcus Type III once, and to pneumococci of Group IV eleven times. Nine of these cases were free from hemolytic streptococci at the time of onset of the pneumonia, 4 showed a very few colonies of hemolytic streptococci in the first sputum culture made. B. influenzæ was found in the sputum coughed from the deeper air passages in the majority of cases, being present in 80, or 76.2 per cent, of the 105 cases. In the 58 cases of lobar pneumonia it was found 41 times, or 70.7 per cent, in the 47 cases of bronchopneumonia 39 times, or 82.9 per cent. The abundance of B.
- 20. influenzæ in the sputum varied greatly in different cases. Microscopic examination of stained sputum films and direct culture of the sputum on blood agar plates showed that in general it was more abundant in the mucopurulent sputum from cases of bronchopneumonia than in the mucoid rusty sputum from cases of lobar pneumonia. This was by no means an invariable rule, however, since in the former the bacilli were sometimes very few in number, in the latter quite abundant. Whether B. influenzæ shared in the production of the actual pneumonia in these cases is difficult to decide and cannot be stated on the basis of the bacteriologic and clinical observations which have been made. Clinical Features.—One of the most striking aspects of pneumococcus pneumonia following influenza was the diversity of clinical pictures presented. These varied all the way from the classical picture of lobar pneumonia to that of bronchopneumonia of all grades of severity from the rapidly fatal coalescing type to that of very mild character with very slight signs of consolidation. For this reason it is questioned whether there is any real justification for speaking of a typical influenzal pneumonia, an opinion that seems well supported by the diversified picture found at the necropsy table. For purposes of presentation, pneumococcus pneumonia following influenza may be divided into three clinical groups: (1) Lobar pneumonia; (2) lobar pneumonia with purulent bronchitis; (3) bronchopneumonia. No accurate data are available as to the relative frequency with which these three types occurred at Camp Pike. In the group of 105 cases studied there were 58 cases of lobar pneumonia, 11 of which had purulent bronchitis, and 47 cases of bronchopneumonia. The majority of these cases, however, occurred during the early days of the epidemic of influenza and probably show a considerably higher proportion of lobar pneumonias than actually occurred in the total number of pneumonias throughout the epidemic. This is indicated by the fact that of 100 consecutive cases of influenza selected for observation at the height of the epidemic, 3 developed clinical evidence of lobar pneumonia and 12 of bronchopneumonia. (1) Lobar pneumonia presenting the typical clinical picture with sudden onset, tenacious rusty sputum, sustained temperature, and physical signs of complete consolidation of one or more lobes occurred in 47 cases; 36 cases in this group definitely followed influenza. In 11 cases no certain clinical evidence of a preceding influenza was obtained, and it is probable that some of these represent cases of pneumonia occurring independently of the epidemic of influenza. The onset of pneumonia in this group of cases occurred from four to nine days after the onset of influenza and with few exceptions was ushered in by a chill and pain in the chest. In several instances the patient had apparently recovered from influenza as evidenced by fall of temperature to normal. After twenty-four to seventy-two hours of normal temperature the patient would have a chill and develop lobar pneumonia. In the majority of cases, however, lobar pneumonia developed while the patient was still sick with influenza. The course of the disease,
- 21. symptomatology and physical signs were quite characteristic of lobar pneumonia and require no special comment. Recovery by crisis occurred in 21 cases, by lysis in 8. Pneumococcus empyema developed in 3 cases, fibrinopurulent pericarditis in 3 and all but 1 of these 6 cases terminating fatally. In Table XV 5 fatal cases of lobar pneumonia, which illustrate some of the unusual features of the disease when it follows influenza, have been summarized. The first 2 cases represent examples of recurring attacks of pneumonia which developed shortly after recovery from the first attack, in both instances being due to types of pneumococci different from those causing the first attack. The third case represents an example of superimposed infection of the lungs with hemolytic streptococci and staphylococci during the course of a pneumonia due to Pneumococcus IV and disappearance of the latter organism from the tissues so that it was not found at time of necropsy. The last 2 cases are examples of fulminating rapidly fatal cases of lobar pneumonia associated with mixed infections of pneumococci and hemolytic streptococci, the streptococci probably being secondary in both cases. Cases like the few examples cited above, which occurred not infrequently throughout the epidemic of influenza, serve to illustrate the difficulties which may be met in attempting to correlate the clinical, bacteriologic and pathologic features of pneumonia following influenza unless careful bacteriologic examinations are made both during life and at the necropsy table in the same group of cases.
- 22. Table XV Cases of Lobar Pneumonia Following Influenza CASE ONSET OF INFLUENZA ONSET OF PNEUMONIA SPUTUM EXAMINATION COURSE OF PNEUMONIA NECROPSY DATE BACTERIOLOGY DIAGNOSIS BACTERIOLOGY Pul Sept. 7 Sept. 9 1st attack bronchopn. Sept. 10 Pn. IV ++++ B. inf. +++ Recovery by crisis on Sept. 14. On Sept. 21 developed lobar pneumonia. Died Sept. 30 Lobar pneumonia. Gray hepatization L.L, L.U, R.L. H.B. Pn. II Br. Pn. II ++++ B. inf. +++ R.L. Pn. II + + Lew Sept. 16 Sept. 20 chill Sept. 22 Pn. I +++ B. inf. + Lobar pn., recovery by crisis Sept. 29. Developed 2nd attack lobar pn. on Oct. 2. Died Oct. 8 Lobar pneumonia. Gray hepatization R.U. Fibrinopurulent pleurisy H.B. Pn. II atyp. Br. B. inf. ++++ Pn. IIa +++ S. hem. + Staph. + R.U. Pn. IIa ++++ Col Sept. 20 Sept. 24 Sept. 27 Pn. IV ++ Severe lobar pneumonia. Died on Sept. 30 Lobar pneumonia. Red hepatization all lobes. Serofibrinous pl., rt. 125 c.c. H.B. S. hem. Br. S. hem. ++++ Staph. + L.L. S. hem. ++++ Staph. + Gar Sept. 23 Sept. 28 Sept. 30 Pn. IV ++ S. hem. + B. inf. + Fulminating rapidly fatal lobar pneumonia. Died Sept. 30 Lobar pneumonia. Engorgement and red hepatization L.U., R.U. H.B. S. hem. Br. S. hem. ++++ B. inf. +++ L.U. S. hem. ++++ Hol Sept. 25 Sept. 30 Sept. 30 Pn. III ++ B. inf. ++ Fulminating rapidly fatal lobar pneumonia. Died Oct. 1. Lobar pneumonia. Engorgement all lobes H.B. sterile Br. B. inf. ++++ Pn. III ++ S. hem. + R.L. Pn. III ++++ B. inf. ++ S. hem. + L.L. R.L., etc., indicates lobes involved. H. B. = Heart’s blood. Br. = bronchus. (2) There were 11 cases of lobar pneumonia with purulent bronchitis in the group studied. Clinically, they closely resembled the cases in the preceding group except in so far as the picture was modified by the presence of the purulent bronchitis. All directly followed influenza. The sputum, instead of being rusty and tenacious, was profuse and mucopurulent, usually streaked with blood. Stained films and direct culture on blood agar plates showed pneumococci in abundance and B. influenzæ in varying numbers, in only two instances the predominant organism. The physical signs were those of lobar pneumonia with, in addition, those of a diffuse bronchitis as manifested by medium and coarse moist râles throughout both chests. Five cases recovered by crisis; 6 terminated fatally and in all of them the clinical diagnosis of lobar pneumonia with purulent bronchitis was confirmed at necropsy.
- 23. (3) Forty-seven cases in the group studied presented the clinical picture of bronchopneumonia. The onset of pneumonia in these cases was in most instances insidious and appeared to occur as a continuation of the preceding influenza. The temperature, instead of falling to normal after from three to four days, remained elevated or rose higher, the respiratory rate began to rise, a moderate cyanosis appeared, the cough increased, and the sputum became more profuse, usually being mucopurulent and blood streaked, sometimes mucoid with fresh blood. The pulse showed little change at first, being only moderately accelerated. Pleural pain, so characteristic of the onset of lobar pneumonia, was rarely complained of, but a certain amount of substernal pain was common, probably due to the severe tracheobronchitis. Physical examination at this time revealed small areas showing relative dullness, diminished or nearly absent breath sounds, and fine crepitant râles. These areas usually appeared first posteriorly over the lower lobes. The subsequent course of the disease showed the widest variation from mild cases with limited pulmonary involvement going on to prompt recovery in four or five days with defervescence by lysis or crisis to those presenting the picture of a rapidly progressive and coalescing pneumonia with fatal outcome. In the milder cases the diagnosis of pneumonia depended in considerable part upon the general symptoms of continued fever, increased respiratory rate, and slight cyanosis. Definite pulmonary signs were always present if carefully looked for, though sometimes not outspoken. Areas of bronchial breathing and bronchophony often appeared late, sometimes not until the patient was apparently recovering. In the severe cases cyanosis became intense and an extreme toxemia dominated the picture. In certain of these cases there was an intense pulmonary edema. The respiratory rate showed wide variation, the breathing in some cases being rapid and gasping, in others comparatively quiet. Progressive involvement of the lungs occurred with the development of marked dullness, loud bronchial breathing and bronchophony. Abundant medium and coarse moist râles were heard throughout the chest, probably due in considerable part to the extensive bronchitis almost universally present. An active delirium was not uncommon. Signs of pleural involvement, even in the most severe and extensive cases, rarely occurred, except in those cases in which a hemolytic streptococcus infection supervened. Of the 47 cases in this group, 29 recovered; 14 by crisis, 15 by lysis. The average duration of illness from the onset of influenza until recovery from the pneumonia was ten days, the majority of these cases being relatively mild in character with pneumonia of three to six days’ duration. Empyema with ultimate recovery occurred in 1 of these cases, Pneumococcus Type II being the causative organism. There were 18 fatal cases in the group. Nine of these are summarized in Table XVI as illustrative of the frequently complex character of bronchopneumonia following influenza and because of the interest attaching to the bacteriologic examinations made during life and at necropsy. Case 70 is a typical instance of the rapidly progressive type of confluent lobular pneumonia with extensive purulent
- 24. bronchitis, intense cyanosis, and appearance of suffocation, with which pneumococci, in this case Pneumococcus IV, and B. influenzæ are commonly associated. Case 59 is illustrative of the small group of bronchopneumonias following influenza which die, often unexpectedly, after a long drawn out course, in this instance three weeks after onset. Examination of the sputum at the time the pneumonia began, showed Pneumococcus Type IV and B. influenzæ. At necropsy there was a lobular pneumonia with clustered small abscesses, probably due to a superimposed infection with S. aureus. There was a well-developed bronchiectasis in the left lower lobe. Cultures taken at autopsy showed a sterile heart’s blood, which is not infrequently the case in cases of pneumococcus lobular pneumonia after influenza. Cultures from the consolidated portions of the lung showed no growth, the pneumococcus having disappeared as might be expected from the duration of the case. B. influenzæ together with staphylococci were found in the bronchi. In Cases 50 and 56 a second attack of pneumonia caused by a different type of pneumococcus from that responsible for the first attack occurred, the second attack in both instances being due to contact infection with Pneumococcus Type II from a patient in a neighboring bed suffering with Pneumococcus Type II pneumonia. Both cases showed at necropsy the type of confluent lobular pneumonia so commonly found in pneumococcus pneumonias following influenza. Case 107 illustrates well the extent to which mixed infections may occur, especially when cases are treated in crowded hospital wards. The sputum at time of onset showed Pneumococcus IV in abundance and a few staphylococci. At necropsy there was a confluent lobular pneumonia with clustered abscesses, purulent bronchitis, and bronchiectasis in the left lower lobe. The heart’s blood was sterile, the lungs showed Pneumococcus Type III and staphylococci. B. influenzæ was not found, but through oversight, no cultures were taken from the bronchi. Cases 92, 99, 102, and 104 are all examples of superimposed hemolytic streptococcus infection occurring in the presence of a Pneumococcus Type IV pneumonia, with the picture of interstitial suppuration, abscess formation, and empyema due to S. hemolyticus on the background of a pneumococcus lobular pneumonia found at necropsy. All showed abundant pneumococci and B. influenzæ in the sputum and were free from hemolytic streptococci at time of onset of pneumonia, except Case 92 which showed 2 colonies of S. hemolyticus in the first sputum culture made. At time of death the pneumococci had disappeared in all cases and were replaced by hemolytic streptococci.
- 25. Table XVI Cases of Bronchopneumonia Following Influenza CASE ONSET OF INFLUENZA ONSET OF PNEUMONIA SPUTUM EXAMINATION COURSE OF PNEUMONIA NECROPSY DATE BACTERIOLOGY DIAGNOSIS BACTERIOLOGY 70 Sept. 18 Sept. 21 Sept. 22 B. inf. ++++ Pn. IV ++ Diffuse bronchitis with rapidly progressive confluent bronchopneumonia. Died Sept. 24 Nodular and diffuse confluent lobular pneumonia. Purulent bronchitis. Bronchiectasis H.B. sterile Br. B. inf. ++++ Pn. IV ++ Lun. B.inf. +++ Pn. IV +++ 59 Sept. 13 Sept. 18 Sept. 19 Pn. IV +++ B. inf. + Bronchopneumonia with long drawn out course. Died Oct. 4 Lobular pneumonia, with clustered abscesses. Bronchiectasis H.B. sterile Br. B.inf. +++ Staph. ++ R.L. no growth. 50 Sept. 14 Sept. 17 Sept. 18 Pn. IV +++ Mild bronchopneumonia improving on Sept. 24. On Sept. 26 became suddenly worse and died on Sept. 30 Nodular and confluent lobular pneumonia. Purulent bronchitis H.B. sterile Br. B.inf. +++ Staph + R.L. Pn. II +++ B.inf. + L.U. Pn. II +++ 56 Sept. 10 Sept. 17 Sept. 18 Pn. IIa +++ Bronchopneumonia with recovery by crisis on Sept. 19. Developed a second attack of pneumonia and died Sept. 29 Confluent lobular pneumonia H.B. Pn. II Br. Pn. II +++ B.inf. ++ L.L. Pn. II +++ B.inf. + 107 Sept. 27 Sept. 29 Oct. 1 Pn. IV +++ B. inf. + Staph. + Diffuse bronchitis and severe bronchopneumonia. Died Oct. 5 Confluent lobular pneumonia with clustered abscesses. Pur. bronchitis and bronchiectasis H.B. sterile R.L. Pn. III ++ Staph. ++ L.L. Staph. ++ 92 Sept. 23 Sept. 28 Oct. 1 B. inf. +++++ Pn. IV +++ S. hem. 2 col. Severe bronchopneumonia with empyema. Died Oct. 5 Lobular pneumonia. Empyema. Purulent bronchitis H.B. S.hem. Br. B.inf. +++ S.hem. +++ R.L. S.hem. +++ B.inf. ++ Emp. S.hem. 99 Sept. 24 Sept. 29 Oct. 1 B. inf. ++++ Pn. IV ++ S. vir. + Diffuse purulent bronchitis with bronchopneumonia. Died Oct. 7 Bronchopneumonia. Purulent bronchitis H.B. S.hem. Br. B.inf. +++ Lun. S.hem. +++ S.hem. ++ B. inf. + 102 Sept. 24 Sept. 28 Oct. 1 Pn. IIa +++ B. inf. ++ Severe bronchopneumonia with empyema. Died Oct. 4 Lobular pneumonia with interstitial suppuration. Pur. bronchitis. Empyema H.B. S.hem. Br. B.inf. +++ S.hem. +++ R.L. S.hem. +++ 104 Sept. 26 Oct. 1 Oct. 1 B. inf. ++++ Pn. IV +++ Diffuse purulent bronchitis with severe bronchopneumonia. Developed streptococcus empyema. Died Oct. 11 Nodular bronchopneumonia with interstitial suppuration. Pur. bronchitis and bronchiectasis. Empyema. H.B. S.hem. R.L. S.hem. ++++ Emp S.hem.
- 26. The cases cited in the preceding paragraph are illustrative examples from a series of over 250 necropsies which are described in another section of this report. They serve to indicate clearly the extent to which mixed and superimposed infections of the lungs may occur in pneumonia following influenza and leave little doubt that a considerable proportion of the deaths from influenzal pneumonia are due to this circumstance.
- 27. Hemolytic Streptococcus Pneumonia Following Influenza But 4 cases of hemolytic streptococcus pneumonia directly following influenza without an intervening pneumococcus infection of the lungs occurred in the group of cases studied clinically. Superimposed infection with S. hemolyticus, however, occurred not infrequently during the course of pneumococcus pneumonia following influenza, as has been stated above. This occurred 3 times in lobar pneumonia and 10 times in bronchopneumonia, with fatal outcome in all but 1 case. Bacteriology.—Bacteriologic examination of the sputum in the 4 cases of streptococcus pneumonia directly following influenza showed S. hemolyticus present in abundance. B. influenzæ was also present in large numbers in 3 cases, but was not found in the fourth. In 1 case a Gram-negative micrococcus resembling M. catarrhalis was also present in large numbers in the sputum. Pneumococci were not found either by direct culture on blood agar plates or by inoculation of the sputum intraperitoneally in white mice. In the 13 cases of superimposed hemolytic streptococcus infection occurring during the course of pneumococcus pneumonia, bacteriologic examination of the sputum by direct culture and by mouse inoculation shortly after onset of the pneumonia showed Pneumococci (atypical II once, Type III once, Group IV eleven times) B. influenzæ present in large numbers, and no hemolytic streptococci except in 4 instances in which a very few organisms were present. Subsequent invasion of the lower respiratory tract by S. hemolyticus was shown to occur by means of cultures of empyema fluids or by cultures made at necropsy. Clinical Features.—The 4 cases of hemolytic streptococcus pneumonia following influenza that occurred in this series resembled in all respects the secondary streptococcus pneumonias of the winter and spring of 1918 and presented no features requiring special comment. The onset resembled that of pneumococcus bronchopneumonia, the disease appearing to develop as a continuation of the preceding influenza. The sputum was profuse and mucopurulent in 3 cases, mucoid and bloody in the other. Two cases ran a severe and rapid course with the development of empyema early in the disease and fatal outcome. The other 2 cases ran only moderately severe courses without developing empyema and recovered by lysis in twenty and fifteen days, respectively, after the onset of influenza. Clinical differentiation between streptococcus and pneumococcus bronchopneumonia following influenza did not seem possible without bacteriologic examination of the sputum except in those cases of the streptococcus group which developed an extensive pleural effusion early in the disease.
- 28. The advent of superimposed hemolytic streptococcus infection of the lower respiratory tract during the course of pneumococcus pneumonia following influenza presented no clinical features that made diagnosis certain without bacteriologic examination. The sudden occurrence of a pleural exudate during the course of the disease seemed of particular significance, especially since empyema in the bronchopneumonias following influenza was exceedingly rare in the absence of hemolytic streptococcus infection. Other suggestive symptoms were a chill during the course of the disease, a sudden turn for the worse in cases apparently doing well, or the development of a cherry red cyanosis. None of these features, however, was sufficiently constant or distinctive of streptococcus invasion to be depended upon and when they occurred, were merely indications for further bacteriologic examination.
- 29. Bacillus Influenzæ Pneumonia Following Influenza Bacteriologic evidence that cases of pneumonia following influenza might be due to B. influenzæ alone was very meager in the group of cases studied clinically at Camp Pike; in fact, no convincing evidence was obtained that such cases occurred. In one case B. influenzæ alone was found in the sputum coughed from the deeper air passages, and in another case B. influenzæ with a few colonies of S. viridans was found. Both were cases of bronchopneumonia, mild in character, and recovered promptly. They presented no clinical features by which they could be distinguished from cases of pneumococcus bronchopneumonia. It has been previously stated that B. influenzæ was found in all early uncomplicated cases of influenza somewhere in the respiratory tract; that it was present together with other organisms, notably pneumococcus in the sputum from cases of purulent bronchitis following influenza; and that it was found in the sputum coughed from the lung in approximately 80 per cent of cases of pneumonia complicating influenza. In 35 cases it was very abundant, often being the predominating organism. In all these cases, however, pneumococci or hemolytic streptococci were also present in considerable numbers at the time of onset of the pneumonia. It is impossible to say merely from the clinical and bacteriologic data under consideration what part B. influenzæ played in the development of the actual pneumonia in these cases. Discussion of this subject is therefore reserved for the section of this report dealing with the pathology and bacteriology of pneumonia following influenza.
- 30. Summary Influenza as observed at Camp Pike presented itself as a highly contagious infectious disease, the principal clinical manifestations of which were, sudden onset with high fever, profound prostration with severe aching pains in the head, back and extremities, erythema of the face, neck and upper chest with injection of the conjunctivæ, and a rapidly progressive attack upon the mucous membranes of the respiratory tract as evidenced by coryza, pharyngitis, tracheitis and bronchitis with their accompanying symptoms. In the majority of cases it ran a short self-limited course, rarely of more than four days’ duration, and was never fatal in the absence of a complicating pneumonia. Bacteriologic examination in early uncomplicated cases of the disease showed the B. influenzæ of Pfeiffer to be present in all cases, often in predominating numbers. It was found more abundantly present during the acute stage of the disease than during convalescence in uncomplicated cases. No other organisms of significance were encountered by the methods employed. Purulent bronchitis of varying extent developed in approximately 35 per cent of the cases and often prolonged the course of the illness to a considerable extent. Bacteriologic studies showed that it was invariably associated with a mixed infection of the bronchi with B. influenzæ and other bacteria, in most instances the pneumococcus, and indicated that it should be regarded as a complication rather than as an essential part of influenza. Its clinical features consisted of a mild febrile reaction, frequent cough with the raising of considerable amounts of purulent sputum, and the physical signs of a more or less diffuse bronchitis. It led to a varying degree of bronchiectasis in at least some instances. Pneumonia complicating influenza presented a very diversified picture and appeared to have only one constant character, namely, that influenza was the predisposing cause. It may be best classified on an etiologic basis since the clinical features to some extent and the pathology to a much greater extent depended upon the infecting bacteria in a given case. Bacteriologic examination showed that a very large proportion of the cases was due to infection with the different immunologic types of pneumococci or to a mixed infection with B. influenzæ and pneumococci. The types of pneumococci commonly found in normal mouths, namely, II atypical, III, and IV, comprised approximately 88 per cent of these, the highly parasitic Pneumococci Types I and II, but 12 per cent. A small number of cases were due to hemolytic streptococci or to mixed infection with B. influenzæ and S. hemolyticus. No certain evidence was obtained that pneumonia was due to B. influenzæ alone. This organism was present in varying numbers, however, in approximately 80 per cent of the sputums examined, and it seems fairly certain that it must have played at least a part in the
- 31. development of the pneumonia in many of the cases in which it was found. Superimposed infections with other types of pneumococci than those primarily responsible for the development of pneumonia, with hemolytic streptococci and with Staphylococcus aureus occurred frequently in cases of pneumococcus or mixed pneumococcus and B. influenzæ pneumonia and undoubtedly contributed to a considerable extent in increasing the number of deaths. Three clinical types of pneumococcus pneumonia following influenza occurred: lobar pneumonia, lobar pneumonia with purulent bronchitis, and bronchopneumonia. Lobar pneumonia was usually sudden in onset and ran the characteristic course of the primary disease. Lobar pneumonia with purulent bronchitis similarly ran the characteristic course of the primary disease but presented the unusual picture of lobar pneumonia with mucopurulent rather than rusty, tenacious sputum and numerous moist râles throughout the unconsolidated portions of the lungs. The cases of bronchopneumonia ran a very variable course from mild cases of a few days’ duration and meager signs of consolidation to rapidly progressive cases with signs of extensive pulmonary involvement. Purulent bronchitis was very frequently associated with bronchopneumonia. Hemolytic streptococcus pneumonia following influenza presented the clinical picture of bronchopneumonia and was not readily distinguished on clinical grounds from pneumococcus bronchopneumonia except in those cases which developed a pleural exudate early in the disease. The advent of tertiary infection of the lower respiratory tract with hemolytic streptococci in cases of secondary pneumococcus pneumonia presented no symptoms sufficiently constant or certain to make clinical diagnosis easy. The development of empyema in pneumococcus bronchopneumonia usually meant streptococcus infection. Pure B. influenzæ pneumonia, if such cases existed, presented no diagnostic features by which it could be distinguished from pneumococcus bronchopneumonia following influenza. It was impossible to determine on clinical and bacteriologic grounds alone what part the prevalent influenza bacilli played in the causation of the actual pneumonia.
- 32. Discussion That wide variations in the conception of influenza have arisen during the recent pandemic, even a hasty review of the literature makes clear. In its essence this divergence of opinion seems to depend upon whether pneumonia is considered an essential part of influenza or a complication due either to the primary cause of influenza or to secondary infection. One extreme is expressed by Dunn[30] who says “the so-called complication is the disease,” the other by Fantus[31] who finds influenza a relatively mild disease with pneumonia a relatively infrequent and largely preventable complication. A similar divergence of opinion prevails with respect to the bacteriology of influenza. There is fairly general agreement that the members of the pneumococcus and streptococcus groups and to a less extent other organisms are responsible for a large proportion of the secondary pneumonias, and but few observers hold that they possess any etiologic relationship to influenza. No such uniformity of opinion exists, however, with respect to the relation of B. influenzæ to influenza and to the complicating pneumonia. By some it is considered the primary cause of influenza, by others it is regarded as a secondary invader responsible for a certain proportion of the secondary pneumonias, and by still others it is not considered to bear any relation either to influenza or its complications. A limited number of references to the extensive literature of the recent pandemic will amply serve to illustrate the various points of view that have developed. Keegan[32] regards pneumonia as a complication and considers that B. influenzæ, the probable cause of influenza, is the primary cause of the pneumonia which may or may not be still further complicated by pneumococcus or streptococcus infection as a terminal event. Christian[33] states that epidemic influenza causes a clinically demonstrable bronchitis and bronchopneumonia in the larger proportion of cases, and lays particular emphasis upon the fact that it is quite incorrect to consider fatalities in the epidemic as due to influenza uncomplicated by bronchopneumonia. Blanton and Irons[34] speak of influenza as an “antecedent respiratory infection” of undetermined etiology, and believe that pneumonia when it occurs is due to autogenous infection by a variety of secondary invaders, principally of the pneumococcus and streptococcus groups. Hall, Stone, and Simpson[35] regard pneumonia strictly as a complication and quite distinct from influenza itself. Synnott and Clark[36] believe that the infection is characterized by a progressive intense exudative inflammation of the respiratory tract often terminating in an aspiration pneumonia with a variety of conditions found at autopsy and a multiplicity of secondary organisms responsible for the fatal termination. B. influenzæ was usually found but always with other organisms. Friedlander and his collaborators[37] speak of a fulminating fatal type of influenza with acute inflammatory pulmonary edema,
- 33. but regard true bronchopneumonia as secondary, due to infection with pneumococcus or S. hemolyticus. B. influenzæ was not found more frequently than under normal conditions. Brem[38] and his collaborators present a clear cut clinical picture both of influenza and the secondary pneumonia to which it predisposes, regarding the latter as definitely due to secondary infection with pneumococcus, streptococcus or B. influenzæ, the virus of influenza being unknown. Ely[39] and his collaborators make no distinction between influenza and pneumonia, and apparently consider the epidemic due to a hemolytic streptococcus of indefinite and inconstant characters. The Camp Lewis Pneumonia Unit[40] states “the process [influenza], whether mild or severe, is etiologically and pathologically the same; * * *.” B. influenzæ was not found. In a report of The American Public Health Association[41] it is stated that deaths resulting from influenza are commonly due to pneumonias resulting from an invasion of the lungs by one or more forms of streptococci, by one or more forms of pneumococci, or by the so-called influenza bacillus. This invasion is apparently secondary to the initial attack. Wolbach[42] found B. influenzæ in a high proportion of cases, not infrequently in pure culture in the lung, and believes that there is a true influenzal pneumonia whether B. influenzæ is the cause of the primary disease or not. Spooner, Scott and Heath[43] isolated B. influenzæ in a high percentage of cases and consider it reasonable to suppose that it was the prime factor in the epidemic. Kinsella[44] found B. influenzæ infrequently and regards it as a secondary invader. MacCallum[45] regards B. influenzæ as a secondary invader and believes that it is responsible for a form of purulent bronchitis and bronchopneumonia following certain cases of influenza. Pritchett and Stillman[46] found B. influenzæ in 93 per cent of cases of influenza and bronchopneumonia. Hirsch and McKinney[47] state that B. influenzæ played no rôle in the epidemic at Camp Grant and apparently consider it due to a specially virulent pneumococcus. No further references to the extensive literature of the recent pandemic seem necessary, since those cited above serve to illustrate the various points of view that exist. A similar diversity of opinion may be found in the reports from foreign sources. It would appear that much of the divergence of opinion that has been formed has depended to a considerable extent upon the conditions under which cases have been observed. This is clearly brought out by contrasting the experience of Fantus[39] dealing with private cases in civilian practice, where pneumonia was relatively uncommon, with that of others dealing only with cases in large hospitals, where those admitted have been in large part selected seriously ill patients with a high incidence of pneumonia, the milder cases comprising from 60 to 90 per cent of those attacked by influenza never reaching the hospital. Variations in opinion with respect to the bacteriology of the epidemic, especially in regard to B. influenzæ, would appear to be due for the most part to differences in bacteriologic technic, in some degree to differences in interpretation. Accumulating evidence can leave little doubt that B. influenzæ was at least extraordinarily and universally
- 34. prevalent throughout the period of the epidemic and thereafter, and that earlier reports of failure to find it were due to the use of methods unsuitable for its detection and isolation. The opportunity afforded the commission at Camp Pike to devote their full time to a systematic and correlated group study of the epidemic simultaneously from many aspects throughout its whole course made it apparent that influenza per se is in the large majority of instances, in spite of the initial picture of profound prostration, a relatively mild disease which tends to rapid spontaneous recovery. This opinion is supported by the fact that the disease during the first waves of the epidemic in this country, which it is now recognized occurred pretty generally in the army camps during the spring of 1918, was so mild that it attracted only passing attention, since the disease at that time was not sufficiently virulent to predispose to any alarming amount of pneumonia. With the return of the epidemic in the late summer and early fall, however, the disease had attained such a high degree of virulence that it predisposed to an appalling amount of severe and often rapidly fatal pneumonia, which often detracted attention from the real nature of the preceding disease. Yet even during the fall epidemic from 60 to 90 per cent of the cases of influenza proceeded to rapid recovery without developing complications. On this ground alone it would seem only logical to regard pneumonia strictly as a complication of influenza rather than as an essential part of the disease, irrespective of whether the pneumonia may be caused by the primary cause of influenza or not. The complexity of the clinical features, the bacteriology and pathology of the pneumonias following influenza lend further support to this opinion. It seems better, therefore, to consider influenza first as a disease by itself and subsequently to take up the question of pneumonia and the relation of influenza to it. The most striking clinical features of influenza are its epidemic character, its involvement of the respiratory tract, its extremely prostrating effect, and the often surprising rapidity with which the individual cures himself. These features strongly suggest that the etiologic agent of the disease is an organism subject to rapid changes in virulence; that it is confined to the respiratory tract where it produces a superficial inflammatory reaction giving rise to the characteristic symptoms of coryza, pharyngitis and tracheitis; that it elaborates a poison, possibly a true toxin, readily absorbed by the lymphatics, the effect of which is manifested in the profound prostration, severe aching pains, erythema, and leucopenia; and that it may either disappear promptly from the respiratory mucous membrane at time of recovery or may persist, leading a relatively saprophytic existence for an indefinite period of time, being no longer harmful to the individual, at least more than locally, because of an acquired immunity. Furthermore, in our opinion, the very brief incubation period suggests that the disease is bacterial in origin, rather than that it
- 35. is analogous to the exanthemata, the majority of which present a comparatively long, fairly constant, incubation period. B. influenzæ has characteristics in accord with the clinical features of influenza. It is an organism of very labile virulence; it is always present in our experience on the mucous membranes of the respiratory tract in early uncomplicated cases of influenza, often in overwhelming numbers; in only very exceptional instances, in adults at least, does it invade the body producing a general infection, as the numerous reports of negative blood cultures testify; recent investigations by Parker[48] and others indicate that it is capable of producing a toxin quickly fatal for rabbits; it is predominantly present in the respiratory tract during the active stage of the disease and disappears in a considerable proportion of cases at time of recovery, while in others, more particularly those that develop an extensive secondary bronchitis and bronchiectasis it may persist for an indefinite period of time. It is, of course, fully appreciated that the foregoing is in the main merely argumentative reasoning and it is put forth only to suggest that B. influenzæ merits a much closer scrutiny with respect to its etiologic relationship to influenza than the trend of present opinion has awarded it. Although there remains some difference of opinion as to the relation of influenza to pneumonia, the majority of observers concur in regarding pneumonia as a complication and this would seem to be the only logical interpretation of the facts available. The same may be said with respect to purulent bronchitis and bronchiectasis. It is of considerable significance in this connection that pneumonia following influenza presents no uniform clinical picture, no uniform bacteriology and no uniform pathology. Whether the predisposition of patients with influenza to contract pneumonia is preponderantly due to lowering of general resistance to infection by the extremely prostrating effect of the disease and the inhibition of leucocytic defense, or to a destruction of local resistance against bacterial invasion by reason of profound injury to the bronchial mucosa, or to a combination of both factors, is difficult to say. It seems most probable that both are concerned. At any rate it seems clear that in the presence of influenza a considerable variety of organisms which under ordinary conditions do not find lodgement in the lungs are able to gain access to the lower respiratory tract and produce pneumonia.
- 36. CHAPTER III SECONDARY INFECTION IN THE WARD TREATMENT OF INFLUENZA AND PNEUMONIA Eugene L. Opie, M.D.; Francis G. Blake, M.D.; James C. Small, M.D.; and Thomas M. Rivers, M.D. One of the most pressing problems that presented itself in the care of influenza and pneumonia patients in the army cantonments during the recent epidemic was the danger of secondary contact infection because of the overcrowding of the base hospitals, nearly all of which were taxed far beyond the limits of their capacity. That this danger was very real was fully demonstrated by certain studies in ward infection that this commission was able to make at Camp Pike[49] . It is the purpose of the present section of the report to present these studies and to discuss the means whereby this danger may be most successfully met. It is perhaps well, first to define exactly what is meant by secondary contact infection in influenza and pneumonia. In our experience at Camp Pike it was found that a very large percentage of the pneumonias following influenza were accompanied by secondary infection with pneumococcus, some few being caused by hemolytic streptococcus. The types of pneumococcus encountered were almost entirely those that are found normally in the mouths of healthy men, approximately 85 per cent being Types II atypical, III, and IV. It has been generally accepted that infection with these types of pneumococci is usually autogenous—that is, that under the proper conditions of lowered resistance an individual becomes infected with the pneumococcus that he carries in his own mouth. Many observations made during the course of the present work have suggested that this is probably not so in many instances and that the influenza patient may not be so much in danger from the pneumococcus that he normally carries in his own mouth as he is from that carried by his neighbor, in other words, he is in danger from contact infection. The same considerations hold true with
- 37. respect to hemolytic streptococcus infection. Secondary contact infection in cases of already existing pneumonia following influenza were found to occur frequently. These were for the most part caused by hemolytic streptococcus infection superimposed upon a pneumococcus pneumonia. Many instances of double pneumococcus infection, however, either coincident with or following one another were encountered.
- 38. Secondary Infection with S. Hemolyticus in Pneumonia Pneumonia caused by streptococci was repeatedly observed[50] during the pandemic of influenza which occurred in 1889–90. With clearer recognition of the characters which distinguish varieties of streptococci several observers have shown that secondary infection with hemolytic streptococci may occur during the course of pneumonia and though definite evidence has been lacking have suggested that it may be acquired within hospital wards. That a similar secondary infection with S. hemolyticus in pneumococcus pneumonias following influenza occurred not infrequently at Camp Pike during the epidemic was shown by bacteriologic studies made during life and at autopsy in a considerable series of cases. During the early days of the epidemic of influenza, secondary streptococcus infection was almost entirely limited to certain wards which were opened for the care of the rapidly increasing number of patients with pneumonia. During this period these wards were overcrowded, organization was incomplete, and the opportunities for transfer of infection from patient to patient were almost unlimited. The spread of streptococcus contagion and its fatal effect may be clearly brought out by comparison of these wards with wards that had long been organized for the care of patients with pneumonia. Ward 3 had been in use for the care of patients with pneumonia for some time prior to the outbreak of influenza. It was provided with sheet cubicles and conducted by medical officers, nurses and enlisted men accustomed to the care of patients with pneumonia, ordinary precautions being taken against transfer of infection from one patient to another. The data in Table XVII show the average number of patients in the ward, the number of new cases of pneumonia admitted, and the number of deaths among patients admitted during the corresponding period, for three periods of ten days each from September 6 to October 5. The types of infection in fatal cases as determined by cultures taken at autopsy are also shown.
- 39. Table XVII Pneumonia in Ward 3 AVERAGE NUMBER OF PATIENTS IN WARD NUMBER OF PATIENTS ADMITTED TOTAL DEATHS AMONG PATIENTS ADMITTED DURING THE CORRESPONDING PERIOD CULTURES AT AUTOPSY NUMBER PER CENT PNEUMOCOCCUS S. HEMOLYTICUS UNDETERMINED (NO AUTOPSY) Sept. 6–15 18.6 11 3 27.2 3 0 0 Sept. 16–25 46.1 52 16 30.7 13 1 2 Sept. 26– Oct. 5 58.6 23 8 34.7 5 1 2 During the period from September 6 to 15, just prior to the outbreak of influenza in epidemic proportions, the ward had an average population of 18.6 patients. The total number of new patients admitted was 11, of whom 3 died, a mortality of 27.2 per cent. All these cases were pneumococcus pneumonias as determined by bacteriologic examination of the sputum at time of admission. The 3 fatal cases showed pneumococcus infection at autopsy. During the second period, from September 16 to 25, with the outbreak of the epidemic of influenza, the ward rapidly filled with new cases of pneumonia, attaining an average population of 46.1 patients. Of the 52 new cases admitted 16 died, a mortality of 30.7 per cent. Again all the cases admitted during this period in which bacteriologic examination of the sputum was made, were found to be pneumococcus pneumonias with one exception. This case, admitted on September 21 and dying two days later, had a hemolytic streptococcus pneumonia. Fortunately, though quite by accident, he was placed in a bed at one end of the porch and no transmission of streptococcus infection to other cases in the ward took place. At autopsy 13 cases showed pneumococcus infection; the foregoing case, hemolytic streptococcus. During the third period from September 26 to October 5 the ward became even more crowded, having an average of 58.6 patients; 23 new cases were admitted, 8 of whom died, a mortality of 34.7 per cent. Autopsy showed that 5 of these were pneumococcus pneumonias and 1 was caused by hemolytic streptococcus infection. It is noteworthy that the death rate from pneumonia gradually increased as the ward became more and more crowded. This may possibly be attributed in part to the increasing severity of the pneumonia during the early days of the influenza epidemic. That it was in part directly due to secondary contact infection with
- 40. pneumococcus will be shown when the transmission of pneumococcus infection is discussed. In spite of the overcrowding of the ward the introduction of 2 cases of streptococcus pneumonia did not cause an outbreak of streptococcus infection. Whether this was due to precautions taken against the transfer of infection or was merely a matter of good luck is difficult to say, in view of the fact that a considerable amount of transfer of pneumococcus infection from one patient to another did occur. Ward 8 had long been used for the care of colored patients with pneumonia. As in Ward 3 cubicles were in use and ordinary precautions against the transfer of infection were used. The data are presented in Table XVIII. Table XVIII Pneumonia in Ward 8 AVERAGE NUMBER OF PATIENTS IN WARD NUMBER OF PATIENTS ADMITTED TOTAL DEATHS AMONG PATIENTS ADMITTED DURING THE CORRESPONDING PERIOD CULTURES AT AUTOPSY NUMBER PER CENT PNEUMOCOCCUS S. HEMOLYTICUS UNDETERMINED (NO AUTOPSY) Sept. 6–20 25.5 18 2 11.1 2 0 0 Sept. 21– Oct. 5 46.1 59 20 33.9 10 1 9 During the period from September 6 to 20, prior to the outbreak of influenza in epidemic proportions among the colored troops, the ward had an average population of 25.5 patients; 18 new cases of pneumonia were admitted during this period, all of whom were pneumococcus pneumonias as determined by bacteriologic examination of the sputum at time of admission to the ward. Only 2 died, a mortality of 11.1 per cent, autopsy cultures showing pneumococcus in both cases. All these patients were treated on the porch of the ward while they were acutely sick. During the second period from September 21 to October 5, when the influenza epidemic was at its height, the ward rapidly filled with active cases of pneumonia and became distinctly crowded. It contained an average of 46.1 patients, but had actually reached a population of 64 patients at the end of the period. Of the 59 new cases admitted, 20 died, a mortality of 33.9 per cent, 10 with pneumococcus pneumonia, one with hemolytic streptococcus pneumonia. In 9 there was no autopsy. The conditions in Ward 8 were quite analogous to those in Ward 3.
- 41. In spite of the overcrowding during the second period no outbreak of secondary infection with S. hemolyticus occurred, but secondary pneumococcus infection did occur as will be shown below. In contrast with these two wards are Wards 1 and 2 in which widespread secondary contact infection with S. hemolyticus took place. Ward 2 was opened September 26, at the beginning of the period when 20 new wards for pneumonia were organized. From September 26 to October 1 the cubicle system was not in use, the ward was crowded, organization was imperfect, and few precautions were taken to prevent transfer of infection from one patient to another. On October 2 the cubicle system was installed and precautions against transfer of infection were instituted. The data are shown in Table XIX. Table XIX Pneumonia in Ward 2 AVERAGE NUMBER OF PATIENTS IN WARD NUMBER OF PATIENTS ADMITTED TOTAL DEATHS AMONG PATIENTS ADMITTED DURING THE CORRESPONDING PERIOD CULTURES AT AUTOPSY NUMBER PER CENT PNEUMOCOCCUS S. HEMOLYTICUS UNDETERMINED (NO AUTOPSY) Sept. 26 10 10 40 27 67.5 0 23 4 Sept. 27 27 17 Sept. 28 40 13 Sept. 29 51 12 17 6 35.3 2 2 2 Sept. 30 49 1 Oct. 1 43 4 Oct. 2 47 6 10 4 40.0 2 1 1 Oct. 3 42 0 Oct. 4 41 4 During the first three days 40 patients with pneumonia were admitted to the ward. Of these 40 patients, 27 died, a mortality of 67.5 per cent. Cultures at autopsy showed that 23 of these died with hemolytic streptococcus infection, none of pneumococcus infection. In four there was no autopsy. To appreciate the full significance of these figures it must be emphasized that these patients at time of admission to the ward in no way differed from those admitted to Ward 3 during the corresponding period and were not in any sense selected cases. The type of infection in 9 of these patients had been
- 42. determined by bacteriologic examination of the sputum just prior to or immediately after admission to the ward before opportunity for secondary contact infection in this ward had occurred. All 9 were shown to have pneumococcus pneumonia free from hemolytic streptococci at that time. All 9 died, 7 with secondary streptococcus infection as shown by cultures taken at autopsy, 1 with a secondarily acquired Pneumococcus Type III infection— sputum showed a Pneumococcus Type IV on admission—and in 1 there was no autopsy. In view of the fact that bacteriologic examination of the sputum in cases of pneumonia following influenza had shown that the large majority of them were due to pneumococcus infection, it is probable that most of the other cases of pneumonia admitted to this ward were pneumococcus pneumonias at time of admission, and that they acquired the streptococcus infection after admission. During the next three days 17 new patients were admitted, of whom 6 died, a mortality of 35.3 per cent. Cultures at autopsy showed pneumococcus infection in 2, streptococcus in 2. It is noteworthy that the porch was first put into use on September 29. Of the 12 patients admitted on this date, 8 were treated throughout the acute stage of their illness on the porch. Of these 8 patients but one died, of a Pneumococcus Type IV infection and none became infected with S. hemolyticus. From October 4 to October 6, 10 patients were admitted, of whom 4 died. Cultures at autopsy showed pneumococcus infection in 2, hemolytic streptococcus in 1. The widespread prevalence of hemolytic streptococcus infection in this ward as compared with its almost entire absence in Wards 3 and 8 is very striking. Cultures made during life and at autopsy have shewn clearly that it was due to rapid spread of contagion throughout the ward. The almost unlimited opportunities for transfer of infection from patient to patient, during the first six days the ward was in use, undoubtedly greatly facilitated this spread. From the data available it is impossible to state exactly when and by which patients hemolytic streptococcus infection was introduced into the ward, but it must have been very early since the death rate was very high from the beginning, and the first 23 cases coming to autopsy died with streptococcus infection. Ward 1 was opened on September 24. From that date until October 2 no cubicles were in use and few precautions were taken against transfer of infection. On October 2 cubicles were installed and ordinary precautions to prevent transfer of infection were instituted. On October 6 the ward was closed to further admissions. The data presented in Table XX are divided into
- 43. two periods, because on September 29 and 30, 4 patients with streptococcus pneumonia were admitted to the ward. Table XX Pneumonia in Ward 1 AVERAGE NUMBER OF PATIENTS IN WARD NUMBER OF PATIENTS ADMITTED TOTAL DEATHS AMONG PATIENTS ADMITTED DURING THE CORRESPONDING PERIOD CULTURES AT AUTOPSY NUMBER PER CENT PNEUMOCOCCUS S. HEMOLYTICUS UNDETERMINED (NO AUTOPSY) Sept. 24–29 35.8 34 11 32.3 5 3 3 Sept. 30– Oct. 5 55.3 40 24 60.0 6 14 4 During the first period from September 24 to 29 the ward contained an average of 35.8 patients, being only moderately crowded; 34 cases of pneumonia were admitted, of whom 11 died, a mortality of 32.3 per cent. It is noteworthy that deaths among this group which occurred prior to September 30 were due to pneumococcus infection with one exception, a patient entering the ward on September 26 and dying the following day. Of the other 2 patients in this group who died with hemolytic streptococcus pneumonia, 1 was admitted to the ward on September 25, was shown to be free from S. hemolyticus on September 30, and died on October 12 with a secondarily acquired streptococcus pneumonia and empyema; the other was admitted on September 29 with streptococcus pneumonia and died the following day. During the second period from September 30 to October 5 the ward contained an average of 55.3 patients, being very overcrowded; 40 new cases of pneumonia were admitted of whom 24 died, a mortality of 60 per cent. Cultures taken at autopsy showed that 6 died of pneumococcus pneumonia, 14 with hemolytic streptococcus infection. As in Ward 2, patients admitted to this ward were in no way selected and were probably, as experience has shown, in large part pneumococcus pneumonias at time of admission. The widespread dissemination of hemolytic streptococcus and its fatal effect following the introduction of the organism on September 29 and 30 is only too evident.
- 44. Table XXI Secondary Infection with Pneumococcus Type II NAME BED OCCUPIED ADMITTED PNEUMOCOCCUSIN SPUTUM ON ADMISSION SECONDARY INFECTION DATE PNEUMOCOCCUS AT AUTOPSY Pvt. Wolfe No. 6 Sept. 17 IV Sept. 23 II[51] Pvt. Pullam No. 5 Sept. 9 IV Sept. 24 II Pvt. Swain No. 3 Sept. 16 II
- 45. Secondary Infection with Pneumococcus in Pneumonia The foregoing studies have shown that hemolytic streptococcus infection may spread by contagion throughout an entire ward with great rapidity. Other observations have demonstrated that pneumococcus infection may be transmitted in the same way. Only three instances of this nature will be cited. The first occurred in Ward 3 (Table XXI). Between September 6 and 16 no cases of pneumonia caused by Pneumococcus Type II had been admitted to the ward. On September 16 Pvt. Swain was admitted to the ward and placed in Bed 3. Bacteriologic examination of his sputum showed that his pneumonia was caused by Pneumococcus Type II. At this time Pvt. Pullam, who had been admitted to the ward on September 9 with a pneumococcus Type IV pneumonia, occupied Bed 5 separated from Bed 3 by one intervening bed. He had had his crisis on September 14 and was doing well, his temperature being normal. On September 24 he developed a second attack of pneumonia and died on September 30. Cultures at autopsy showed Pneumococcus Type II in heart’s blood and lung, Pneumococcus Type II and B. influenzæ in the right bronchus. Pvt. Wolfe was admitted to the ward with bronchopneumonia on September 17 and placed in Bed 6 next to Pvt. Pullam. Pneumococcus Type IV and B. influenzæ were found in his sputum. His temperature had fallen to normal by lysis on September 21 and he was doing well. On September 23 his temperature suddenly rose and he developed a second attack of pneumonia. Pneumococcus Type II was isolated by blood culture on this date. He recovered. In both instances Pneumococcus Type II was acquired after the admission of a patient with a Pneumococcus Type II pneumonia, the opportunity for contact infection having been favored by the association of these patients in adjoining beds.
- 46. Table XXII Secondary Infection with Pneumococcus Type II NAME BED OCCUPIED ADMITTED PNEUMOCOCCUS IN SPUTUM ON ADMISSION SECONDARY INFECTION DATE PNEUMOCOCCUS AT AUTOPSY Pvt. Smith No. 26 Sept. 18 II II Pvt. Thompson No. 28 Sept. 17 Atyp. II Sept. 21 II Pvt. Linehan No. 30 Sept. 16 IV Sept. 26 II The second instance is almost identical and occurred on the opposite side of Ward 3 at about the same time (Table XXII). Pvt. Linehan was admitted on September 16 and placed in Bed 30. Pneumococcus Type IV was found in his sputum. Pvt. Thompson was admitted the following day with a Pneumococcus II atypical pneumonia and placed in Bed 28. The next day Pvt. Smith was admitted and placed in Bed 26. Pneumococcus Type II was found in his sputum. On September 19 Pvt. Thompson recovered by crisis and was doing well. On September 21 he had a chill, his temperature rose to 104.4° F. and he developed a second attack of pneumonia. He died on September 29; cultures at autopsy showing Pneumococcus Type II in heart’s blood and left pleural cavity, Pneumococcus Type II and B. influenzæ in bronchus and lung. Pvt. Linehan had begun to improve on September 24 and his temperature was falling by lysis. On September 26 he became worse, developed signs of pericarditis and died on September 30. Cultures from lungs and bronchus at autopsy showed Pneumococcus Type II and B. influenzæ. In both instances the fatal secondary infection with Pneumococcus Type II was undoubtedly acquired from Pvt. Smith in the nearby bed. The third instance occurred in Ward 8 (Table XXIII). Pvts. Lewis and Scott were admitted on September 21 and were placed in adjoining beds, 50 and 51. Lewis showed Pneumococcus Type I in his sputum, Scott Pneumococcus II atypical. The following day Pvts. Pighee, Jones, and Columbus were admitted and given Beds 48, 49 and 53 respectively. All showed Pneumococcus II atypical in the sputum. Pvt. Lewis with Pneumococcus Type I pneumonia recovered by crisis on September 29. His temperature remained normal until October 2 when it suddenly rose to 104.2° F. He developed a second attack of pneumonia and died on October 8. Cultures at autopsy from heart’s blood and lung showed Pneumococcus II atypical, from the bronchus
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