Part 8

════════════════════════════╤══════════════════════════════════════════ │ Total (All Types) (82) ────────────────────────────┼────────────────────────────────────────── │ │ │ │ Sero- │ Sero- fibrino- │Fibrinous fibrinous purulent Empyema Total ────────────────────────────┼────────────────────────────────────────── Strep. hemolyticus │ 5 8 6 2 21 Strep. non-hemolyticus │ 2 2 3 7 Strep. “viridans” │ 1 1 2 Strep. mucosus capsulatus │ 1 1 Pneumococcus Type II. │ 4 2 3 1 10 Pneumococcus Type III. │ 2 3 5 Pneumococcus Type IV. │ 6 7 4 1 18 Pneumococcus (Type │ undetermined) │ 1 1 2 4 B. influenzæ │ 7 5 5 17 Staphylococci │ 4 4 7 1 16 B. mucosus capsulatus │ 1 1 2 Number of cases of pleurisy │ 17 20 21 2 60 Percent of cases showing │ excess of Pleural fluid. │ 52.4% ════════════════════════════╧══════════════════════════════════════════

════════════════════════════╤════════╤════════ │ │ ────────────────────────────┼────────┼──────── │ Total │ │ number │ │of cases│ │ with │Effusion │positive│present │cultures│percent. ────────────────────────────┼────────┼──────── Strep. hemolyticus │ 29│ 55% Strep. non-hemolyticus │ 12│ 42% Strep. “viridans” │ 2│ 50% Strep. mucosus capsulatus │ 1│ 100% Pneumococcus Type II. │ 11│ 54% Pneumococcus Type III. │ 7│ 71% Pneumococcus Type IV. │ 18│ 67% Pneumococcus (Type │ │ undetermined) │ 8│ 37.5% B. influenzæ │ 19│ 52% Staphylococci │ 19│ 63% B. mucosus capsulatus │ 3│ 67% Number of cases of pleurisy │ │ Percent of cases showing │ │ excess of Pleural fluid. │ │ 52.4% ════════════════════════════╧════════╧════════

TABLE III.—_Bacteriology in Relation to the Pneumonia._ ═════════════════════════════════╤═══════════════════════════════ │ Acute Fulminating (34) ─────────────────────────────────┼─────────────────────────────── │ Pseu- Peri- │ do- bron- │Lobar lobar chial Lobular Total ─────────────────────────────────┼─────────────────────────────── Strep. hemolyticus │ 1 4 5 Strep. hemolyticus and │ Pneumococcus II │ 0 Strep. hemolyticus and │ Pneumococcus IV │ 1 1 Strep. hemolyticus and │ Pneumococcus IV and │ staphylococci │ 0 Strep. hemolyticus and Strep. │ non-hemolyticus │ 1 1 Strep. hemolyticus and B. │ influenzæ │ 1 1 2 Strep. hemolyticus, B. influenzæ │ and Strep. non-hemolyticus │ 0 Strep. hemolyticus, B. influenzæ │ and staphylococci │ 0 Strep. hemolyticus and │ staphylococci │ 2 2 Strep. hemolyticus and M. │ catarrhalis │ 0 Strep. hemolyticus, M. │ catarrhalis and B. mucosus │ capsulatus │ 1 1 Strep. non-hemolyticus │ 3 3 Strep. non-hemolyticus, │ Pneumococcus II and │ staphylococci │ 0 Strep. non-hemolyticus, │ Pneumococcus IV and │ staphylococci │ 1 1 Strep. non-hemolyticus and │ staphylococci │ 0 Strep. non-hemolyticus and B. │ mucosus capsulatus │ 0 Strep. non-hemolyticus and M. │ catarrhalis │ 1 1 Strep. non-hemolyticus and │ diphtheroids │ 1 1 Strep. mucosus capsulatus │ 0 Strep. “viridans” and │ Pneumococcus IV │ 0 Strep. “viridans,” Pneumococcus │ IV and staphylococci │ 0 Pneumococcus Type II │ 3 3 Pneumococcus Type III │ 4 4 Pneumococcus Type IV │ 2 2 Pneumococcus (Type undetermined) │ 3 3 Pneumococcus Type II and B. │ influenzæ │ 1 1 Pneumococcus Type II and B. │ mucosus capsulatus │ 0 Pneumococcus Type II and │ staphylococci │ 0 Pneumococcus Type III and B. │ influenzæ │ 0 Pneumococcus Type III and │ staphylococci │ 0 Pneumococcus Type IV and B. │ influenzæ │ 2 2 Staphylococci │ 0 Staphylococci and B. influenzæ │ 0 Staphylococci, B. influenzæ and │ M. catarrhalis │ 0 B. influenzæ and Pneumococcus │ (Type undetermined) │ 0 B. influenzæ and a pleomorphic │ diplococcus │ 0 Enterococcus │ 1 1 ═════════════════════════════════╧═══════════════════════════════

═════════════════════════════════╤═══════════════════════════════ │ Necrotizing (36) ─────────────────────────────────┼─────────────────────────────── │ Pseu- Peri- │ do- bron- │Lobar lobar chial Lobular Total ─────────────────────────────────┼─────────────────────────────── Strep. hemolyticus │ 4 4 Strep. hemolyticus and │ Pneumococcus II │ 0 Strep. hemolyticus and │ Pneumococcus IV │ 1 1 Strep. hemolyticus and │ Pneumococcus IV and │ staphylococci │ 0 Strep. hemolyticus and Strep. │ non-hemolyticus │ 0 Strep. hemolyticus and B. │ influenzæ │ 0 Strep. hemolyticus, B. influenzæ │ and Strep. non-hemolyticus │ 1 1 Strep. hemolyticus, B. influenzæ │ and staphylococci │ 0 Strep. hemolyticus and │ staphylococci │ 2 2 Strep. hemolyticus and M. │ catarrhalis │ 1 1 Strep. hemolyticus, M. │ catarrhalis and B. mucosus │ capsulatus │ 0 Strep. non-hemolyticus │ 1 1 Strep. non-hemolyticus, │ Pneumococcus II and │ staphylococci │ 1 1 Strep. non-hemolyticus, │ Pneumococcus IV and │ staphylococci │ 0 Strep. non-hemolyticus and │ staphylococci │ 1 1 Strep. non-hemolyticus and B. │ mucosus capsulatus │ 1 1 Strep. non-hemolyticus and M. │ catarrhalis │ 0 Strep. non-hemolyticus and │ diphtheroids │ 0 Strep. mucosus capsulatus │ 0 Strep. “viridans” and │ Pneumococcus IV │ 1 1 Strep. “viridans,” Pneumococcus │ IV and staphylococci │ 1 1 Pneumococcus Type II │ 1 1 Pneumococcus Type III │ 1 1 Pneumococcus Type IV │ 1 1 2 Pneumococcus (Type undetermined) │ 3 3 Pneumococcus Type II and B. │ influenzæ │ 0 Pneumococcus Type II and B. │ mucosus capsulatus │ 1 1 Pneumococcus Type II and │ staphylococci │ 1 1 Pneumococcus Type III and B. │ influenzæ │ 1 1 Pneumococcus Type III and │ staphylococci │ 0 Pneumococcus Type IV and B. │ influenzæ │ 3 3 6 Staphylococci │ 0 Staphylococci and B. influenzæ │ 1 1 Staphylococci, B. influenzæ and │ M. catarrhalis │ 1 1 B. influenzæ and Pneumococcus │ (Type undetermined) │ 2 2 B. influenzæ and a pleomorphic │ diplococcus │ 1 1 Enterococcus │ 0 ═════════════════════════════════╧═══════════════════════════════ ═════════════════════════════════╤═══════════════════════════════╤═════ │ Organizing (12) │(82) ─────────────────────────────────┼───────────────────────────────┼───── │ Pseu- Peri- │ │ do- bron- │ │Lobar lobar chial Lobular Total│Total ─────────────────────────────────┼───────────────────────────────┼───── Strep. hemolyticus │ 1 1 2│ 11 Strep. hemolyticus and │ │ Pneumococcus II │ 1 1 2│ 2 Strep. hemolyticus and │ │ Pneumococcus IV │ 0│ 2 Strep. hemolyticus and │ │ Pneumococcus IV and │ │ staphylococci │ 1 1│ 1 Strep. hemolyticus and Strep. │ │ non-hemolyticus │ 0│ 1 Strep. hemolyticus and B. │ │ influenzæ │ 0│ 2 Strep. hemolyticus, B. influenzæ │ │ and Strep. non-hemolyticus │ 0│ 1 Strep. hemolyticus, B. influenzæ │ │ and staphylococci │ 1 1│ 1 Strep. hemolyticus and │ │ staphylococci │ 1 1 2│ 6 Strep. hemolyticus and M. │ │ catarrhalis │ 0│ 1 Strep. hemolyticus, M. │ │ catarrhalis and B. mucosus │ │ capsulatus │ 0│ 1 Strep. non-hemolyticus │ 0│ 4 Strep. non-hemolyticus, │ │ Pneumococcus II and │ │ staphylococci │ 0│ 1 Strep. non-hemolyticus, │ │ Pneumococcus IV and │ │ staphylococci │ 0│ 1 Strep. non-hemolyticus and │ │ staphylococci │ 0│ 1 Strep. non-hemolyticus and B. │ │ mucosus capsulatus │ 0│ 1 Strep. non-hemolyticus and M. │ │ catarrhalis │ 0│ 1 Strep. non-hemolyticus and │ │ diphtheroids │ 0│ 1 Strep. mucosus capsulatus │ 1 1│ 1 Strep. “viridans” and │ │ Pneumococcus IV │ 0│ 1 Strep. “viridans,” Pneumococcus │ │ IV and staphylococci │ 0│ 1 Pneumococcus Type II │ 0│ 4 Pneumococcus Type III │ 0│ 5 Pneumococcus Type IV │ 0│ 4 Pneumococcus (Type undetermined) │ 0│ 6 Pneumococcus Type II and B. │ │ influenzæ │ 1 1│ 2 Pneumococcus Type II and B. │ │ mucosus capsulatus │ 0│ 1 Pneumococcus Type II and │ │ staphylococci │ 0│ 1 Pneumococcus Type III and B. │ │ influenzæ │ 0│ 1 Pneumococcus Type III and │ │ staphylococci │ 1 1│ 1 Pneumococcus Type IV and B. │ │ influenzæ │ 0│ 8 Staphylococci │ 1 1│ 1 Staphylococci and B. influenzæ │ 0│ 1 Staphylococci, B. influenzæ and │ │ M. catarrhalis │ 0│ 1 B. influenzæ and Pneumococcus │ │ (Type undetermined) │ 0│ 2 B. influenzæ and a pleomorphic │ │ diplococcus │ 0│ 1 Enterococcus │ 0│ 1 ═════════════════════════════════╧═══════════════════════════════╧═════

The type of the pneumonic process, as well as the invading organism, has varied widely in different localities. From the foregoing brief survey, it will be seen that before the associations suggested above can be proven, much more definite evidence must be presented.

An attempt has been made to correlate the bacteriological findings in this series with the distribution and type of pneumonic process. These are tabulated in Table III. It will be seen at a glance that no relationship is demonstrable between the type of single or associated organisms and the distribution of the pneumonia, whether it is lobar, pseudolobar, peribronchial or lobular and whether acute fulminating, necrotizing or organizing. (See Table No. III.)

D. SUMMARY AND DISCUSSION

The confusion which exists in associating different bacterial types with well defined and characteristic anatomical lesions is true, not only for the disease as it occurs spontaneously in man, but also for its reproduction in experimental animals. A review of the literature teaches that not all of the factors concerned in producing the different anatomical types are known.

Pertinent experimental studies were reported recently by Blake and Cecil from the Army Medical School in Washington. One cubic centimeter of a very virulent pneumococcus (M. L. D. for a mouse in forty-eight hours equals one-millionth of 1 cubic centimeter) inoculated in monkeys through the skin of the neck into the trachea just beneath the larynx has uniformly produced a lobar pneumonia, clinically as well as anatomically the nearest experimental approach to spontaneous lobar pneumonia of man. This work indicates, not only the possible importance the species may play, but also points to the rôle of the infecting organism which, when sufficiently virulent, incites a characteristic reaction even when inoculated in a minimal quantity into the trachea as distinct from the bronchioles or lung tissue.

Pneumonia unassociated with a simultaneous or preliminary incapacitation of the mechanism of the upper respiratory tract, differs from the pulmonary lesions encountered after measles, gas poisoning, influenza, etc., and those experimentally produced by intrabronchial insufflations. In the lobar type the virulence of the infecting organism, combined perhaps with species variation,—implying as this does different capacities for reaction on the part of the host,—seems to be the fundamental principle. It remains to be determined whether other organisms of equal virulence with that of the pneumococcus are capable of producing characteristic anatomical reactions when inoculated in a similar manner.

In the other group, where there is not only a free ingress to the pulmonary parenchyma by the bacteria of the mouth, but where there is, in all probability, also a simultaneous or preliminary pulmonary damage furnishing a proper medium for relatively innocuous organisms, the lesion of response will surely depend upon other factors as much as upon the infecting organism. Among these obscure factors, the most important, unquestionably, is the extent of the damage to the lung tissue before the entry of the organisms, or simultaneously with it, into this area. The systemic capacity to compensate also must be considered.

VIII. CONCLUSIONS

The etiology of influenza is unknown.

The portal of entry of the inciting cause is likewise undetermined.

The respiratory lesions, whether primary or secondary, are responsible for the high mortality of the disease.

The lesions of the respiratory tract peculiar to this disease and most frequently encountered are:

An acute tracheobronchitis associated with diffuse involvement of the pulmonary parenchyma.

Hyalinization of the epithelium of the air passages, and necrosis of the alveolar walls with extensive interstitial emphysema and occasionally with pneumothorax.

Dilatation of the terminal bronchioles.

Aplastic serofibrinous, and hemorrhagic, pneumonic exudates.

Necrotizing and organizing bronchiolitis, and pneumonia: lobar, lobular, peribronchial, interstitial.

The sequelæ—obliterating bronchiolitis and bronchiolectasis.

Proliferation of alveolar and bronchiolar epithelium.

The extrarespiratory lesions of influenza are neither constant nor characteristic. Irrespective of localization, they have the same fundamental pathology characterized by:

Vascular damage.

Hemorrhage.

Organization with or without infection.

A basis for the interpretation of the respiratory lesions of influenza is offered by the analogous changes in the respiratory tract initiated by the inhalation of poisonous gases.

The respiratory lesions are dependent primarily upon the damage produced by the true etiological agent and the systemic capacity to compensate, and only secondarily upon invasion by the bacterial flora of the mouth and inspired air.

BIBLIOGRAPHY

1. Abrahams, Hallows, Eyre, and French: Purulent Bronchitis; Its Influenzal and Pneumococcal Bacteriology;—Lancet, 1917, 193, 377.

2. Abrahams, Hallows, and French: A Further Investigation into Influenzo-Pneumococcal and Influenzo-Streptococcal Septicæmia;—Lancet, 1919, 196, 1.

3. Askanazy: Über die Veränderungen der grossen Luftwege, besonders ihre Epithel-Metaplasie bei der Influenza;—Corr. Blatt f. Schweizer Aerzte, 1919, 49, 465.

4. Averill, Young, and Griffiths: The Influenza Epidemic in a Camp;—Brit. Med. J., 1918, 2, 111.

5. Avery, Chickering, Cole, and Dochez: Acute Lobar Pneumonia;—Monograph of the Rockefeller Institute, No. 7.

6. Ballin: Empyema Following Influenzal Pneumonia;—J. A. M. A., 1919, 72, 335.

7. Beals, Blanton, and Eisendrath: Abdominal Complications of the Influenza Epidemic at Camp Custer;—J. A. M. A., 1919, 72, 850.

8. Berkley and Coffen: Generalized Interstitial Emphysema and Spontaneous Pneumothorax;—J. A. M. A., 1919, 72, 535.

9. Bernhardt: Zur Aetiologie der Grippe, 1918;—Med. Klin., 1918, 14, 683.

10. Bircher: Zur Grippe Epidemie;—Corr. Blatt f. Schweizer Aerzte, 1918, 48, 1338.

11. Bland: Influenza in Relation to Pregnancy;—Am. J. of Obs., 1919, 79, 184.

12. Blanton and Irons: Recent Epidemic Respiratory Disease at Camp Custer;—J. A. M. A., 1918, 71, 1988.

13. Blanton, Burhans, and Hunter: Studies in Streptococcic Infections at Camp Custer;—J. A. M. A., 1919, 72, 1520.

14. Bloomfield and Harrop: Clinical Observations on Epidemic Influenza;—Bull. Johns Hopk. Hosp., 1919, 30, 1.

15. Borst: Pathologisch-anatomische Beobachtungen zur “spanischen Grippe” 1918;—Mün. med. Wchnschr., 1918, 65, 1342.

16. Bradford, Bashford, and Wilson: Preliminary Report on the Presence of “Filter Passing” Virus in Certain Diseases;—Brit. Med. J., 1919, 1, 127.