Chapter 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.

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FIG. LIII. AUTOPSY NO. 163. PULMONARY EMBOLUS.
]

FIG. LIV. (AUTOPSY NO. 20. U. S. GENERAL HOSPITAL.) ILLUSTRATES THE
CHANGE IN THE BRONCHIAL LYMPH GLANDS. NOTE THE PHAGOCYTOSIS WITHIN
THE SINUSOIDS AS WELL AS THE MEGALOKARYOCYTES AND THE MITOTIC
FIGURES IN THE CELLS LINING THE CHANNELS.
]

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FIG. LVI. AUTOPSY NO. 135. ACUTE HEMORRHAGIC MYOSITIS (ZENKER’S
NECROSIS).

COMPARE FIG. LVII.

HELIOTYPE CO. BOSTON
]

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99. McMeekin: The Present Epidemic of Influenza;—Med. J. Australia,
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101. Menetrier, M. P.: Bronchopneumonia à B. de Pfeiffer; Bull. de
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103. Moore, Sir John: Influenza from a Clinical
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109. Opie, Freeman, Blake, Small, and Rivers: Pneumonia at Camp
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111. Orteconi, Barbie, et LeClerc: Contribution à l’Etude de la Flore
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125. Rosenow: Prophylactic Inoculation against Respiratory
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126. Rosenow: Studies in Influenza and Pneumonia;—J. A. M. A., 1919,
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127. Schinz: Die Influenza Epidemie bei der Guiden-Abteilung 5;—Corr.
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128. Schmorl: Pathologische-anatomische Beobachtungen bei der jetzt
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129. Schorer, E. H.: Influenza at the Port of Embarkation
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130. Shera: Influenza Epidemic of Spring of 1915;—Lancet, 1917, 192,
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132. Slye, Holmes, and Wells: Primary Spontaneous Tumors of the Lung
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133. Smith: Influenzal Intra-abdominal Catastrophies;—Lancet, 1919,
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134. Soper: Pandemic in the Army Camps;—J. A. M. A., 1918, 71, 1899.

135. Speares: Influenza;—Boston Med. & Surg. J., 1919, 180, 212.

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137. Spooner, Sellards, and Wyman: Serum Treatment of Type I
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138. Stone and Swift: Influenza and Bronchopneumonia at Fort Riley;—J.
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139. Strouse and Bloch: Notes on Present Epidemic of Respiratory
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140. Symmers: A Note on the Pathology of the Prevailing Pandemic
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141. Symmers: Pathologic Similarity between Pneumonia of Bubonic
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142. Symmonds, C. P.: Nephritis in Relation to the Recent Epidemic of
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143. Synnot and Clark: The Influenza Epidemic at Camp Dix;—J. A. M.
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144. Talbot: Influenza among Children;—Boston Med. & Surg. J., 1918,
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145. Thayer: Discussion on Influenza;—Proc. Roy. Soc. Med., 1919, 12,
28 & 61.

146. Thomas, H. M., Jr.: Rupture of Encapsulated Empyema into Pleural
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147. Thompson: Influenza as it Affects the Air Passages;—Practitioner,
1919, 102, 12.

148. Titus and Jamison: Pregnancy Complicated by Epidemic
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FIG. LVII. AUTOPSY NO. 150. ORGANIZATION OF THE INFLAMMATORY EXUDATE
AND REGENERATION OF THE MUSCLE FIBERS AFTER AN ACUTE HEMORRHAGIC
MYOSITIS. COMPARE FIGURE LVI.

HELIOTYPE CO. BOSTON
]

149. Torry and Grosch: Acute Pulmonary Emphysema Observed during the
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1919, 157, 170.

150. Uhlenhuth: Zur Bacteriologie der Influenza;—Med. Klin., 1918, 14,
777.

151. U. S. Pub. Health Reports, 1919, 34, 1.

152. Valentine: Study of Agglutination Reactions of B.
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153. Vaughan: The Bacteriology of Influenza (Editorial);—J. Lab. &
Clin. Med., 1918, 4, 83.

154. Wadsworth, A. B.: A Study of Experimental Organizing
Pneumonia;—J. Med. Res., 1918, 39, 147.

155. Wanner, F.: La Grippe à l’Hôpital d’isolement de Vevey en
Juillet-Août, 1918;—Corr. Blatt f. Schweizer Aerzte, 1918, 48, 1729.

156. Wegelin: Pathologische-anatomische Beobachtungen bei der Grippe
Epidemie von 1918;—Corr. Blatt f. Schweizer Aerzte, 1919, 49, 65.

157. Whittingham and Sims: Bacteriology and Pathology of
Influenza;—Lancet, 1918, 195, 865.

158. Winternitz, M. C.: Anatomical Changes in the Respiratory Tract
Initiated by the Inhalation of Irritating Gases;—Military Surg.,
1919, 44, 476.

159. Winternitz, M. C.: Collected Studies in the Pathology of War Gas
Poisoning;—Yale University Press, 1919.

160. Winternitz, M. C., and Hirschfelder, A. D.: Studies upon
Experimental Pneumonia in Rabbits;—J. Exp. Med., 1913, 17, 657.

161. Winternitz, M. C., and Smith, G. H.: Intrapulmonary
Irrigation;—Proceed. Soc. Exp. Biology & Med., 1919, 16, 55.

162. Wolbach, S. B.: Comments on the Pathology and Bacteriology of
Fatal Influenza Cases Observed at Camp Devens, Massachusetts;—Bull.
Johns Hopk. Hosp., 1919, 30, 104.

163. Wollstein, Martha: An Immunological Study of Bacillus
influenzæ;—J. Exp. Med., 1915, 22, 445.

164. Wollstein and Goldbloom: Epidemic Influenza in Infants;—Am. J.
Dis. Children, 1919, 17, 165.

165. Woolston and Conley: Epidemic Pneumonia (Spanish Influenza) in
Pregnancy;—J. A. M. A., 1918, 71, 1898.

166. Yanagisawa: Experimental Study on the Mixed Injection of Bacillus
influenzæ and Various Species of Cocci;—Kitasato Arch. Exp. Med.,
1919, 3, 85.

FIG. LV. AUTOPSY NO. 146. ACUTE HEMORRHAGIC ENTERITIS ASSOCIATED WITH
MULTIPLE BACTERIAL EMBOLI IN THE CAPILLARIES OF THE INTESTINAL
MUCOSA.
]

PRINTED IN THE UNITED STATES OF AMERICA

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Footnote 1:

The history of the epidemics of influenza cannot but impress one with
the difficulties of medical progress. Beyond the fact that the
descriptions of the epidemics are such that the disease is
recognizable as being the same, there is little of real value in the
literature until the beginning of the 19th century.

In the 18th century the infectious nature of the malady had been
recognized. The results of study in the first half of the 19th century
are shown in the literature of the epidemic of 1847–49. In it,
exceptionally good clinical descriptions and epidemilogical studies
are published. In the next forty years great strides were made in
Pathology and in the essentially new science of Bacteriology. With
those two aids in the study of infectious disease, it is only
reasonable to expect an increase in knowledge of influenza after the
epidemic of 1889–90. Such is the fact and a comprehensive review of
both the Bacteriology and Pathology of this disease is offered in
Nothnagel’s Specielle Pathologie, 1896, Bd. IV, by O. Leichtenstern.

Footnote 2:

Early in the epidemic, Nicolle (106) and his co-workers described a
filterable virus as the probable etiological agent in influenza.
Several investigators have corroborated this work. Chief of these are:
Gibson, Bowman, and Connor (46); Bradford, Bashford, and Wilson (16).
The latter investigators independently isolated a filterable virus
which may be cultivated by the Noguchi method and which, when
inoculated into monkeys, produces a general reaction with specific
respiratory lesions which, they think, are comparable to those of man
in influenza. While these results must be confirmed, they offer
greater promise than any other.

Footnote 3:

A marked fibrinous exudate in the lower trachea with the formation of
a pseudomembrane was noted by Oberndorfer (108), Lubarsch (19), Coray
(28), Borst (15), and Schmorl (128). Schmorl studied the bacteria from
the trachea and found in sections streptococci, pneumococci, and
staphylococci, but not B. influenzæ or B. diphtheriæ.

Footnote 4:

Simmonds (131), Bernhardt and Meyer (19) note that perichondritis may
be present, but do not give a detailed description of the lesion.
Gruber and Schädel (50) found this perichondritis to be associated
with abscess formation.

Footnote 5:

Two examples of fresh endocarditis are reported by Malloch (95) and
one by Dietrich (34), all of which were due to B. influenzæ. Acute
myocarditis was observed by Blanton and Irons (12) and Gruber and
Schädel (50). Glaus and Fritzsche (47) report a case with multiple
hemorrhages, necrosis, and leucocytic infiltration of the heart muscle
and also one of Zenker’s degeneration of the myocardium. Cases of both
myocarditis and endocarditis are included by Leichtenstern (82) in a
review of the epidemic of 1889–1890.

Footnote 6:

The picture is not unlike that of the interstitial pneumonia after
measles as described by MacCallum (93).

Footnote 7:

Pneumothorax as a complication following influenzal pneumonia is
mentioned in association with marked emphysema in the epidemic of
1889–90 by Leichtenstern (82). It has been found by X-ray examination
in two cases of interstitial emphysema by Berkley and Coffen (8) and
also has occurred at Camp Dix according to the report of Synnot and
Clark (143).

Footnote 8:

The rarity of empyema has been commented upon by LeCount (78) and
Torry and Grosch (149). The condition was found in a small number of
cases by Wegelin (156), Malloch (95), Lyon (90), Chickering (25), and
Thomas (146), while Goodpasture (48) described it in eleven out of
sixteen cases of streptococcus hemolyticus pneumonia.

Footnote 9:

Fibrinopurulent pericarditis has been described by Simmonds (131),
Stone and Swift (138), Lyon (90), Fildes et al (40), Jaffé (66), Glaus
and Fritzsche (47).

Footnote 10:

The types of consolidation described as having been encountered at the
post-mortem table apparently vary somewhat with the locality and the
interpretation of the observers. The lobar type has been frequently
found by Opie et al (110), Wollstein and Goldbloom (164), Stone and
Swift (138), and others. The pseudolobar pneumonia has been mentioned
by Abrahams et al (2), Keegan (67), and Speares (135), while the
peribronchial type has been well described by Hubschman, Glaus and
Fritzsche (47), and MacCallum (92). Lobular pneumonia has been noted
by all observers. The type of consolidation in this series has been
tabulated in relation to the inflammatory reaction.

Acute Fulminating Pneumonia Necrotization Organization Total Lobar 0 2 3 5 Pseudolobar 2 4 3 9 Peribronchial 0 1 4 5 Lobular 42 32 2 76 ———— ———— ———— ———— Total 44 39 12 95

Footnote 11:

No particular search was made for such lesions until the epidemic was
nearly half over. At that time word was received from Camp Devens that
hemorrhagic lesions in the rectus muscle were being found. Thereafter,
the recti were examined with care.

Footnote 12:

Abscesses supervening upon the rectus hemorrhages are reported by
Beals, Blanton and Eisendrath (7), and by Glaus and Fritzsche (47).
Generalized abscesses are reported by the latter and by Dietrich (34).
Abrahams, Hallows and French (2) report subcutaneous abscesses; Beals,
Blanton and Eisendrath, abscesses of the kidneys.

Footnote 13:

The sinuses of the head and middle ears were examined in a number of
cases with negative findings. Suppuration of these areas is, however,
reported by others.

Stone and Swift (138) found pus in the sphenoidal sinus in 68 per cent
of their cases with pneumococci, streptococci and B. influenzæ
present. Wolbach (162) found twenty cases of infection of the sphenoid
sinus from twelve of which B. influenzæ alone or combined with
pneumococci or streptococci were isolated. Lacy (74) reports four
cases of influenzal sinusitis.

Footnote 14:

Acute nephritis has been reported by many observers, but the
histological descriptions have been so meager that judgment regarding
it must be suspended.

Footnote 15:

This condition has been met with more frequently in other localities.
Stone and Swift (138) report it in a high percentage of their cases.
Lamb and Brannin (77) encountered it seven times, and Blanton and
Irons (12) report two cases. Borst (15) and Jaffé (66) also have found
this complication.

Footnote 16:

Cheesman and Meltzer (24) demonstrated as early as 1898 the importance
of primary injury for the localization and development of secondary
infecting bacteria.

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TRANSCRIBER’S NOTES

1. The illustrations are not numbered in the order they appear. 2. Silently corrected typographical errors and variations in spelling. 3. Retained anachronistic, non-standard, and uncertain spellings as printed. 4. Footnotes have been re-indexed using numbers and collected together at the end. 5. Enclosed italics font in _underscores_.