═══════╤═══════╤════════════╤═════════╤═_Epidemic Respiratory Disease The pneumonias and other infections of the repiratory tract accompanying influenza and measles

NO. OF │ABSCESS│INTERSTITIAL│MULTIPLE │EMPYEMA│BRONCHIECTASIS

AUTOPSY│ │SUPPURATIVE │ABSCESSES│ │

│ │ PNEUMONIA │ IN │ │

│ │ │CLUSTERS │ │

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432 │ │ │ │ E │

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433 │ │ + │ │ E │

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434 │ │ + │ │ E │

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435 │ │ │ │ │

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436 │ │ │ │ │

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437 │ │ │ │ │ +

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440 │ │ │ │ │ +

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445 │ │ │ │ │ +

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485 │ │ + │ │ E │

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487 │ + │ │ │ E │ +

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488 │ + │ │ │ E │ +

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489 │ │ │ │ │ +

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───────┴───────┴────────────┴─────────┴───────┴──────────────

═══════╤════════════════╤══════════╤════════╤════════╤════════╤════════

NO. OF │ UNRESOLVED │ORGANIZING│BACTERIA│BACTERIA│BACTERIA│BACTERIA

AUTOPSY│BRONCHOPNEUMONIA│BRONCHITIS│ IN │ IN │IN LUNG │IN BLOOD

│ │ │ SPUTUM │BRONCHUS│ │OF HEART

│ │ │ │ │ │

───────┼────────────────┼──────────┼────────┼────────┼────────┼────────

229 │ │ │ Pn. I. │ │ │ 0

│ │ │B. inf. │ │ │

231 │ │ │ │ │ │

232 │ │ │Pn. IIa.│ │Pn. IIa.│Pn. IIa.

│ │ │B. inf. │ │ │

233 │ │ │Pn. IIa.│ │ │ Pn.

236 │ │ │Pn. IV. │ │B. inf. │ 0

│ │ │B. inf. │ │ Staph. │

237 │ │ │ St. h. │ │ │ St. h.

238 │ │ │Pn. IV. │ │ │ Pn. IV

│ │ │B. inf. │ │ │

239 │ │ │Pn. II. │ │Pn. II. │Pn. II.

│ │ │ │ │B. inf. │

240 │ │ │Pn. IV. │B. inf. │ │Pn. IV.

241 │ │ │Pn. IV. │ │ │Pn. IV.

│ │ │B. inf. │ │ │

242 │ │ │Pn. IIa.│ │ │Pn. IIa.

│ │ │B. inf. │ │ │

243 │ │ │ │ │ │Pn. IV.

244 │ │ │ │Pn. IV. │Pn. IV. │ 0

│ │ │ │B. inf. │B. inf. │

246 │ │ │Pn. IIa.│ │ │ 0

│ │ │B. inf. │ │ │

247 │ │ │Pn. IV. │ │ │Pn. IV.

│ │ │B. inf. │ │ │

248 │ │ │ │ St. h. │ St. h. │ St. h.

249 │ │ │ │ │ │Pn. III.

250 │ │ │Pn. IIa.│ │ │Pn. IIa.

│ │ │B. inf. │ │ │

251 │ │ │ │ │ St. h. │ St. h.

252 │ │ │ │Pn. II. │Pn. II. │ 0

│ │ │ │B. inf. │B. inf. │

│ │ │ │ St. v. │ │

253 │ │ │Pn. Ia. │Pn. II. │Pn. II. │Pn. II.

│ │ │ │B. inf. │B. inf. │

│ │ │ │ Staph. │ │

254 │ │ │ │ Pn. I. │ Pn. I. │ 0

│ │ │ │B. inf. │ Staph │

255 │ │ │ │ St. h. │ St. h. │ St. h.

│ │ │ │Pn. IIa.│ │

│ │ │ │ Staph. │ │

256 │ │ │ │ Pn. │Pn. IIa.│Pn. IIa.

│ │ │ │ Staph. │ │

257 │ │ │ │B. inf. │ │ Pn. I.

│ │ │ │ Staph │ │

258 │ │ │ │ │ St. h. │ St. h.

│ │ │ │ │Pn. IV. │

│ │ │ │ │B. inf. │

259 │ │ │ │ │ St. h. │ St. h.

│ │ │ │ │Pn. III.│

│ │ │ │ │ Staph. │

260 │ │ │ │ │ │ 0

261 │ │ │ │B. inf. │ │ 0

│ │ │ │Pn. IV. │ │

262 │ │ │ │ St. h. │ St. h. │ St. h.

│ │ │ │B. inf. │ │

263 │ │ │ │ │ St. h. │ St. h.

│ │ │ │ │B. inf. │ Staph.

│ │ │ │ │ Staph. │

264 │ │ │Pn. IV. │ St. h. │ St. h. │ St. h.

│ │ │ Staph. │ Staph. │ │

265 │ │ │ │ St. h. │Pn. IV. │ St. h.

│ │ │ │ Staph. │B. inf. │

│ │ │ │ inf. │ │

266 │ │ │ St. h. │ St. h. │ St. h. │ St. h.

│ │ │ │B. inf. │ │

267 │ │ │Pn. IV. │Pn. II. │Pn. II. │Pn. II.

│ │ │ │B. inf. │ │

268 │ │ │Pn. III.│Pn. III.│Pn. III.│ 0

│ │ │ B. │B. inf. │B. inf. │

│ │ │ │ St. h. │ St. h. │

269 │ │ │Pn. IV. │Pn. IV. │Pn. IV. │ 0

│ │ │ B. │ Staph. │ │

270 │ │ │ │ St. h. │ St. h. │ St. h.

│ │ │ │B. inf. │ Staph. │

│ │ │ │ Staph. │ │

271 │ │ │ │ St. h. │ St. h. │ St. h.

│ │ │ │Pn. IV. │ │

│ │ │ │B. inf. │ │

272 │ │ │ │ │ │ St. h.

273 │ │ │ │ St. h. │ St. h. │ St. h.

│ │ │ │B. inf. │Pn. IV. │

│ │ │ │ Staph. │ Staph. │

274 │ │ │Pn. IV. │ St. h. │ St. h. │ St. h.

│ │ │ │ Staph. │ │

275 │ │ │ │ St. h. │ St. h. │ St. h.

│ │ │ │B. inf. │B. inf. │Pn. IV.

│ │ │ │ Staph. │ Staph. │

276 │ │ │ │ St. h. │ St. h. │ St. h.

│ │ │ │Staph B.│Pn. IV. │

│ │ │ │ inf. │B. inf. │

277 │ │ │ │ St. h. │ St. h. │ St. h.

│ │ │ │ Staph │ Staph │

278 │ │ │ │ St. h. │ St. h. │ St. h.

│ │ │ │B. inf. │ │

279 │ │ │ │ │ Pn. IV │Pn. IV.

280 │ │ │ │ St. h. │ St. h. │ St. h.

│ │ │ │B. inf. │ │

│ │ │ │ Staph. │ │

281 │ │ │ │ │ St. h. │ St. h.

│ │ │ │ │B. inf. │

282 │ │ │Pn. IV. │ St. h. │ St. h. │ St. h.

│ │ │B. inf. │B. inf. │Pn. II. │Pn. II.

│ │ │ │ Pn. II │ │

│ │ │ │ Staph. │ │

283 │ │ │ │B. inf. │ Staph. │Pn. IV.

│ │ │ │Pn. IV. │B. inf. │

│ │ │ │ Staph. │ │

284 │ │ │ │ St. h. │ St. h. │ St. h.

│ │ │ │B. inf. │ │

│ │ │ │ Staph. │ │

285 │ │ │Pn. IIa.│ St. h. │ St. h. │ St. h.

│ │ │B. inf. │B. inf. │ │

286 │ │ │ │Pn. IV. │ 0 │Pn. IV.

│ │ │ │B. inf. │ │

│ │ │ │ Staph. │ │

287 │ │ │ │Pn. IV. │Pn. IV. │Pn. IV.

│ │ │ │B. inf. │ B inf. │

│ │ │ │ Staph. │ Staph. │

288 │ │ │ St. h. │ St. h. │ St. h. │ St. h.

│ │ │B. inf. │B. inf. │ │

289 │ │ │ │Pn. IV. │Pn. IV. │Pn. IV.

│ │ │ │B. inf. │ │

│ │ │ │ Staph. │ │

290 │ │ │ │ St. h. │ St. h. │ St. h.

│ │ │ │B. inf. │ │

291 │ │ │Pn. IV. │B. inf. │ 0 │ 0

│ │ │B. inf. │ Staph. │ │

292 │ │ │ │ │ St. h. │ St. h.

│ │ │ │ │B. inf. │

293 │ │ │ │Pn. III.│Pn. III.│Pn. III.

│ │ │ │B. inf. │B. inf. │

295 │ │ │Pn. IV. │ St. h. │ │ St. h.

│ │ │ St. h. │B. inf. │ │

296 │ │ │ │ St. h. │ St. h. │ St. h.

│ │ │ │B. inf. │B. inf. │

297 │ │ │ │B. inf. │Pn. IV. │ 0

│ │ │ │Pn. IV. │B. inf. │

│ │ │ │ St. h. │ │

298 │ │ │ │Pn. IIa.│Pn. IIa.│

│ │ │ │B. inf. │ │

299 │ │ │ │B. inf. │ │

│ │ │ │Pn. IV. │ │

│ │ │ │ Staph. │ │

│ │ │ │ St. h. │ │

300 │ │ │Pn. IIa.│Pn. IIa.│Pn. IIa.│

│ │ │B. inf. │B. inf. │ │

301 │ │ │ │Pn. IV. │Pn. IV. │

│ │ │ │B. inf. │ │

│ │ │ │ Staph. │ │

│ │ │ │ St. h. │ │

302 │ │ │ │Pn. IV. │Pn. IV. │

│ │ │ │B. inf. │ │

303 │ │ │ │ Staph. │Pn. IV. │

│ │ │ │Pn. IV. │B. inf. │

│ │ │ │B. inf. │ │

304 │ │ │ │ St. h. │ St. h. │

│ │ │ │B. inf. │B. inf. │

305 │ │ │ │B. inf. │B. inf. │

│ │ │ │ St. h. │ St. h │

│ │ │ │Pn. IV. │Pn. IV. │

│ │ │ │ Staph. │ Staph. │

306 │ │ │ │B. inf. │ 0 │ 0

│ │ │ │Pn. IV. │ │

│ │ │ │ Staph. │ │

308 │ │ │ │Pn. IV. │ St. h. │Pn. IV.

│ │ │ │B. inf. │ │

│ │ │ │ St. h. │ │

│ │ │ │ Staph. │ │

309 │ │ │ │ │ St. h. │ St. h.

310 │ │ │ │Pn. III.│Pn. III.│

│ │ │ │B. inf. │Pn. IV. │

│ │ │ │ Staph. │B. inf. │

312 │ │ │Pn. IV. │ St. h. │ St. h. │ St.

│ │ │B. inf. │B. inf. │B. inf. │

│ │ │ St. h. │ Staph. │ │

313 │ │ │ │ St. h. │ St. h. │ St. h.

│ │ │ │B. inf. │ │

│ │ │ │ Staph. │ │

314 │ │ │ │Pn. IV. │Pn. IV. │Pn. IV.

│ │ │ │B. inf. │ │

│ │ │ │ Staph. │ │

315 │ │ │ │ │Pn. IV. │Pn. IV.

│ │ │ │ │B. inf. │

│ │ │ │ │ Staph. │

316 │ │ │ │B. inf. │Pn. III.│Pn. III.

│ │ │ │ │B. inf. │

317 │ │ │ │Pn. IV. │Pn. IV. │

│ │ │ │B. inf. │ │

318 │ │ │ │Pn. IV. │Pn. IV. │

│ │ │ │B. inf. │B. inf. │

319 │ │ │ │ St. h. │ St. h. │ St. h.

│ │ │ │ Staph. │B. inf. │

│ │ │ │ │ Staph. │

320 │ │ │ │Pn. IIa.│Pn. IIa.│Pn. IIa.

321 │ │ │ │B. inf. │Pn. IV. │Pn. IV.

│ │ │ │ │B. inf. │

322 │ │ │Pn. IV. │ │Pn. III.│ 0

│ │ │ │ │ Staph. │

│ │ │ │ │ aur. │

323 │ │ │ │Pn. IV. │ │ 0

│ │ │ │B. inf. │ │

│ │ │ │ Staph. │ │

324 │ │ │ │ Pn. I. │ 0 │ Pn. I.

│ │ │ │B. inf. │ │

325 │ │ │ │ St. h. │ St. h. │ St. h.

│ │ │ │B. inf. │ │

│ │ │ │ Staph. │ │

326 │ │ │ │ St. h. │ St. h. │ St. h.

│ │ │ │B. inf. │B. inf. │

│ │ │ │ Staph. │ │

327 │ │ │ │ │ │

328 │ │ │ │Pn. III.│Pn. III.│ Pn.

│ │ │ │Pn. IV. │Pn. IV. │ III.

│ │ │ │B. inf. │B. inf. │

│ │ │ │ Staph. │ │

330 │ │ │ │ │Pn. IV. │Pn. IV.

331 │ │ │ │ │ │Pn. IV.

332 │ │ │ │ │ │ 0

333 │ │ │ │ Staph. │ Staph. │Pn. IIa.

│ │ │ │aur. B. │aur. Pn.│

│ │ │ │inf. St.│IIa. St.│

│ │ │ │ h. │ h. │

334 │ │ │ │ │ St. h. │ St. h.

│ │ │ │ │ Staph │

335 │ │ │ │ │ St. v. │Pn. IV.

│ │ │ │ │B. inf. │

│ │ │ │ │ Staph. │

│ │ │ │ │Pn. IV. │

336 │ │ │ │ │ │ 0

337 │ │ │ │ │ │Pn. IV.

338 │ │ │ │ │ │Pn. IV.

339 │ │ │ │ │ │Pn. IV.

340 │ │ │ │ │ │ 0

341 │ │ │ │ │ │ 0

342 │ │ │ │ │ │

343 │ │ │ │ │Pn. IV. │Pn. IV.

344 │ │ │ │ │ │ St. h.

345 │ │ │ │ │Pn. III.│

│ │ │ │ │ St. h │

│ │ │ │ │ Staph. │

346 │ │ │B. inf. │ St. h. │ St. h. │ St. h.

│ │ │Pn. IV. │B. inf. │B. inf. │

347 │ │ │ │ │ │ St. h.

348 │ │ │ │ │ │Pn. IIa.

349 │ │ │ │ │Pn. III │ Pn. I.

│ │ │ │ │ St. h │

350 │ │ │ │ │ │ St. h.

351 │ │ │ │ │ │

352 │ │ │ │ │ │Pn. IIa.

353 │ │ │ Pn. I. │B. inf. │Pn. IIa.│Pn. IIa.

│ │ │B. inf. │ Pn. │ │

354 │ │ │ │ St. h. │ St. h. │ St. h.

│ │ │ │B. inf. │ │

│ │ │ │ Staph. │ │

355 │ │ │ │ St. h. │ St. h. │ 0

│ │ │ │B. inf. │B. inf. │

│ │ │ │Pn. IV. │ Staph. │

│ │ │ │ Staph. │ │

356 │ │ │ │ │ │Pn. IV.

357 │ │ │ │ │Pn. IV. │Pn. IV.

│ │ │ │ │B. inf. │

358 │ │ │ │ │ │Pn. IIa.

359 │ │ │ │ │ │Pn. IV.

360 │ │ │ │ │ │ 0

361 │ │ │ │ │ │Pn. IV.

362 │ │ │ │ │ │ St. h.

363 │ │ │ │ │ │Pn. IV.

364 │ │ │ │ │ │ St. h.

365 │ │ │ │ │Pn. IV. │Pn. IV.

366 │ │ │ │ │ │Pn. IV.

367 │ │ │ │ │ │Pn. IV.

368 │ │ │ │ │ │ Pn. I.

369 │ │ │ St. h. │ │ St. h. │ St. h.

370 │ + │ + │[No. St.│ Staph. │ Staph. │ 0

│ │ │ h.] │aur. Pn.│ aur │

│ │ │ │ IV. B. │ │

│ │ │ │ inf. │ │

372 │ │ │ │ │ │

373 │ │ │ │ │ │ St. h.

374 │ │ │ │ │ │Pn. IV.

375 │ │ │ │ │ │ 0

376 │ │ │[No. St │ St. h. │ St. h. │ St. h.

│ │ │ h.] │B. inf. │ │

│ │ │ │ Staph. │ │

│ │ │ │ aur. │ │

377 │ │ │ │ │ │Pn. IV.

378 │ │ │ │ St. h. │ St. h. │Pn. IIa.

│ │ │ │B. inf. │B. inf. │

│ │ │ │Pn. IIa.│Pn. IIa.│

379 │ │ │ │B. inf. │ ? │Pn. IIa.

│ │ │ │ + │ │

380 │ │ │ │ │Pn. III.│Pn. III.

381 │ │ │ │ │ St. h. │ St. h.

│ │ │ │ │Pn. II. │

│ │ │ │ │Pn. IV. │

│ │ │ │ │ Staph. │

│ │ │ │ │ aur. │

382 │ │ │ │ │ │ 0

383 │ │ │ │ │B. inf. │Pn. III.

│ │ │ │ │Pn. III.│

│ │ │ │ │ St. h. │

384 │ │ │ │ │ │Pn. IV.

385a │ │ │ │ │ St. h. │ St. h.

385b │ │ │ │ │ │Pn. IV.

385c │ │ │ │ │ St. h. │ St. h.

│ │ │ │ │B. inf. │

386 │ │ │ │ │Pn. III.│Pn. III.

│ │ │ │ │B. inf. │

│ │ │ │ │ Staph. │

│ │ │ │ │ aur. │

387 │ │ │ │ St. h. │ Staph. │ St. h.

│ │ │ │B. inf. │alb Pn. │

│ │ │ │ Staph. │ II. B. │

│ │ │ │aur. Pn.│ inf. │

388 │ │ │ │ │ │Pn. IV.

389 │ │ │ │ │ St. h. │ St. h.

391 │ │ │ │ │Pn. IV. │Pn. IV.

392 │ │ │ │ │ │Pn. II.

393 │ │ │ │ │ │Pn. IV.

394 │ │ │ │ │ │ St. h.

395a │ + │ │ │ │ St. h. │ St. h.

│ │ │ │ │B. inf. │

395b │ │ │ │ │Pn. IIa.│Pn. IIa.

396 │ │ │ │ │ │ 0

397 │ │ │ │ │ St. h. │ St. h.

│ │ │ │ │B. inf. │

398 │ + │ │ │ │ │ 0

399 │ │ │ │ │ │Pn. IIa.

400 │ │ │ │ │ │Pn. IV.

401 │ │ │ │ │ │Pn. IV.

402 │ + │ + │ │ │ │Pn. IV.

│ │ │ │ │ │ St. h.

404 │ │ │ │ │ │

405 │ │ │ │ │ │ Pn.

406 │ │ │ │ │ │Pn. IV.

408 │ │ │ │ │ │ 0

409 │ │ │ │ │ │ 0

410 │ │ │ │ │ St. h. │

│ │ │ │ │B. inf. │

│ │ │ │ │ Staph. │

│ │ │ │ │ aur. │

411 │ │ │ │ │Pn. IIa.│Pn. IIa.

│ │ │ │ │B. inf. │

412 │ │ │ │Pn. II. │ │Pn. II.

│ │ │ │B. inf. │ │

413 │ │ │ │ │Pn. III.│Pn. III.

│ │ │ │ │B. inf. │

414 │ │ │ │ │Pn. IIa.│Pn. IIa.

│ │ │ │ │B. inf. │

415 │ │ │ │ │ St. h. │ 0

416 │ │ │ │Pn. IV. │Pn. IV. │Pn. IV.

418 │ │ │ │ │Pn. IIa.│Pn. IIa.

│ │ │ │ │ St. v. │

│ │ │ │ │B. inf. │

419 │ │ │ │Pn. II. │Pn. II. │ 0

│ │ │ │B. inf. │B. inf. │

420 │ + │ + │ │ │ St. h. │ St. h.

│ │ │ │ │B. inf. │

│ │ │ │ │ Staph. │

│ │ │ │ │ aur. │

421 │ + │ + │ │ │Pn. IV. │ St. h.

│ │ │ │ │ St. h. │

422 │ + │ │ │ │Pn. IIa.│ 0

│ │ │ │ │B. inf. │

423 │ + │ │ │ │ St. h. │ St. h.

│ │ │ │ │B. inf. │

424 │ │ │ │ │Pn. IV. │

425 │ + │ │ │ │ St. h. │ St. h.

│ │ │ │ │B. inf. │

│ │ │ │ │ Staph. │

│ │ │ │ │ alb. │

426 │ │ │ │ │Pn. IIa.│Pn. IIa.

│ │ │ │ │B. inf. │

427 │ │ │ │ │ St. h. │ St. h.

428 │ + │ │ │ St. h. │ St. h. │ St. h.

│ │ │ │B. inf. │B. inf. │

429 │ │ │ │ │B. inf. │ 0

│ │ │ │ │ Staph. │

│ │ │ │ │ alb │

430 │ │ │ │ │ St. h. │ St. h.

│ │ │ │ │B. inf. │

│ │ │ │ │ Staph. │

│ │ │ │ │ aur. │

431 │ + │ │ │ │ 0 │ 0

432 │ │ │ │ │B. inf. │Pn. IIa.

│ │ │ │ │Pn. IIa.│

433 │ + │ │ │ │ St. h. │ 0

│ │ │ │ │B. inf. │

│ │ │ │ │ Staph. │

│ │ │ │ │ aur. │

434 │ │ │ │ St. h. │ St. h. │ St. h.

│ │ │ │B. inf. │ Staph. │

│ │ │ │ Staph. │ aur. │

│ │ │ │ aur. │ │

435 │ │ │ │ St. h. │B. inf. │ St. h.

│ │ │ │B. inf. │ + │

436 │ │ │ │Pn. IIa.│Pn. IIa.│Pn. IIa.

│ │ │ │B. inf. │ │

│ │ │ │ Staph. │ │

│ │ │ │ aur. │ │

437 │ │ │ │ │ │ 0

440 │ + │ │ │B. inf. │B. inf. │ 0

│ │ │ │ Staph. │ Staph. │

│ │ │ │ aur. │ aur. │

445 │ │ + │ │ Staph. │ Staph. │ St. h.

│ │ │ │ aur. │aur. Pn.│

│ │ │ │ │ IV. │

446 │ │ │ │ │ 0 │

447 │ │ │ │ Staph. │B. coli.│ 0

│ │ │ │ aur. │ Staph. │

│ │ │ │ │ aur. │

448 │ │ │ │ 0 │ 0 │ 0

449 │ + │ │ │ St. h. │ St. h. │ St. h.

│ │ │ │B. coli.│B. coli.│

452 │ │ │ │ St. h. │ St. h. │ St. h.

│ │ │ │B. inf. │B. inf. │

451 │ │ │ │B. coli.│Pn. IIa.│Pn. IIa.

│ │ │ │ Staph. │B. inf. │

│ │ │ │ St. v. │ │

455 │ │ │ │ St. h. │ St. h. │ St. h.

│ │ │ │B. inf. │ │

456 │ │ │ │B. coli.│ │ St. h.

457 │ + │ + │ │Pn. IV. │ │

│ │ │ │B. inf. │ │

458 │ │ │ │Pn. IV. │ │ 0

│ │ │ │B. inf. │ │

│ │ │ │ St. v. │ │

459 │ │ │ │ Staph. │ │ 0

│ │ │ │aur. Pn.│ │

│ │ │ │ IV. │ │

460 │ │ │ │ St. h. │ St. h. │ St. h.

│ │ │ │B. inf. │B. inf. │

│ │ │ │ Staph. │ │

461 │ │ │ │ Staph. │ │ Pn. I.

│ │ │ │aur. Pn.│ │

│ │ │ │ I. St. │ │

│ │ │ │ h. │ │

462 │ │ │ │ │ │ 0

463 │ + │ │ │B. inf. │B. inf. │ 0

│ │ │ │ Staph. │ Staph. │

464 │ │ │ │B. inf. │B. inf. │ 0

│ │ │ │ Pn. I. │ Pn. I. │

│ │ │ │ Staph. │ │

465 │ │ │ │ St. h. │ St. h. │ St. h.

│ │ │ │B. inf. │ │

│ │ │ │ Staph. │ │

│ │ │ │ St. v. │ │

466 │ │ │ │Pn. IIa.│Pn. IIa.│Pn. IIa.

467 │ │ │ │ St. h. │ 0 │ St. h.

│ │ │ │B. inf. │ │

468 │ │ │ │ Staph. │B. inf. │ 0

│ │ │ │aur. B. │ St. v. │

│ │ │ │inf. St.│ │

│ │ │ │ v. │ │

469 │ + │ │ │ │ │

471 │ │ │ │Pn. IV. │ Pn. I. │ 0

│ │ │ │B. inf. │Pn. IV. │

│ │ │ │ Staph. │B. inf. │

│ │ │ │ aur. │ │

472 │ + │ │ │B. coli.│ St. h. │ St. h.

│ │ │ │ │B. coli.│

473 │ + │ + │ │B. inf. │ St. v. │Pn. III.

│ │ │ │ St. v. │ │

│ │ │ │ Staph. │ │

│ │ │ │M. cat. │ │

474 │ │ │ │ St. v. │ St. h. │ St. h.

│ │ │ │B. inf. │ │B. inf.

│ │ │ │M. cat. │ │

476 │ │ │ │ │ │ 0

477 │ │ │ │ St. h. │ St. h. │ St. h.

│ │ │ │B. coli.│B. coli.│

478 │ │ │ │ │ St. h. │ St. h.

479 │ │ │ │B. inf. │ St. h. │ St. h.

│ │ │ │ St. h. │ Staph. │

│ │ │ │ Staph. │ aur. │

│ │ │ │M. cat. │ │

480 │ │ │ │ Staph. │ Staph. │B. coli.

│ │ │ │aur. St.│aur. B. │ St.

│ │ │ │ v. │inf. St.│

│ │ │ │ │ v. │

482 │ │ │ │B. inf. │B. inf. │ 0

│ │ │ │Pn. IV. │Pn. IV. │

│ │ │ │ St. h. │ │

485 │ │ │ │ St. h. │ St. h. │ St. h.

│ │ │ │B. inf. │ │

│ │ │ │ Staph. │ │

│ │ │ │aur. B. │ │

│ │ │ │ coli. │ │

487 │ + │ │ │B. inf. │B. inf. │ St. h.

│ │ │ │ St. h. │ │

488 │ │ │ │ St. h. │ St. h. │ St. h.

│ │ │ │Pn. IIa.│ │

489 │ │ │ │B. inf. │Pn. IV. │ 0

│ │ │ │Pn. IV. │B. inf. │

494 │ │ │ │ St. h. │ St. h. │ St. h.

│ │ │ │B. inf. │B. inf. │

498 │ │ │ │ St. v. │ St. v. │ St. v.

│ │ │ │ │ Staph. │

│ │ │ │ │ aur. │

│ │ │ │ │ Staph. │

│ │ │ │ │ alb. │

499 │ │ + │ │ St. h. │ 0 │ St. h.

│ │ │ │B. inf. │ │

504 │ │ │ │ St. h. │ St. h. │ St. h.

│ │ │ │B. inf. │ │

│ │ │ │ Staph. │ │

506 │ │ │ │Pn. IV. │Pn. IV. │Pn. IV.

│ │ │ │B. inf. │ Staph. │

│ │ │ │ Staph. │ aur. │

│ │ │ │aur. M. │ │

│ │ │ │ cat. │ │

───────┴────────────────┴──────────┴────────┴────────┴────────┴────────

In successive columns the table gives the autopsy number, race, and

length of military service. These factors have had an important

influence upon the incidence of influenza and pneumonia and have been

discussed in a preliminary report.[79] The duration of illness (4th

column of table), counted from the date of onset of symptoms of

influenza or in some instances, when the earliest symptoms were those of

pneumonia, from onset of pneumonia, can usually be determined

accurately. The duration of pneumonia (5th column of table) is much more

uncertain, because its determination dates from the first recognition of

the physical signs of pneumonia.

=Clinical Diagnosis.=—The clinical diagnosis recorded upon the clinical

history of the patient is given in column 6. Many clinicians have been

impressed with the difficulty of determining during life the type of

pneumonia associated with influenza. The occurrence of purulent

bronchitis, the frequent coexistence of lobar and bronchopneumonia and

an atypical onset often make the recognition of lobar pneumonia more

difficult than usual. The diffuse consolidation of confluent lobular

pneumonia increases the difficulty of recognizing bronchopneumonia. In

the table (column 6) lobar pneumonia is indicated by L.,

bronchopneumonia by B. Among 227 autopsies the clinical diagnosis agreed

with the condition found at autopsy in 109 instances (48 per cent); in

35 instances (15.4 per cent) both lobar and bronchopneumonia were found

at autopsy and a diagnosis of one or other was made during life. In 83

instances (36.6 per cent) the diagnosis made during life was incorrect.

Cases admitted to the base hospital at Camp Pike were as carefully

studied as the conditions in a base hospital during an epidemic

permitted and diagnosis of pneumonia was doubtless as accurate as in

other base hospitals. Statistics from military and other hospitals based

upon clinical diagnosis of the pneumonias of influenza are probably

subject to an error of at least 1 in 3 cases, and conclusions based upon

them are almost valueless.

The inaccuracy of clinical diagnosis of the pneumonia of influenza is

further illustrated by a consideration of lobar pneumonia. This

diagnosis on the one hand was made 136 times and was correct 67 times

and incorrect 69 times; on the other hand, lobar pneumonia was found at

autopsy 98 times and had been diagnosed in only 67 of these cases (68.4

per cent).

=Classification of the Pulmonary Lesions of Influenza.=— Influenzal

pneumonia exhibits the following noteworthy characters:

1. Acute bronchitis with injury or destruction of lining epithelium and

accumulation of inflammatory exudate within the lumen.

2. Hemorrhagic pneumonia with accumulation of blood within the alveoli

and within and about the bronchi.

3. Susceptibility of bronchi and pulmonary tissue to secondary pyogenic

infection with necrosis and suppuration.

4. Bronchiectasis.

5. Tendency to the occurrence of chronic pneumonia following failure of

pneumonia to undergo resolution.

All these changes are doubtless referable to the severity of the primary

injury to the lower air passages.

In the presence of destructive changes in the bronchi many bacterial

species, including B. influenzæ, pneumococci of various types,

streptococci (notably hemolytic streptococci) and staphylococci may

invade the lungs and produce acute inflammation. The anatomic characters

of the pneumonic lesions following influenza are equally varied.

In order to obtain insight into the pathogenesis of these lesions, it is

desirable to imitate the historical development of knowledge concerning

the characters and causes of disease, namely, first to define accurately

the lesions concerned and later to determine with what microorganisms

these lesions are associated. The difficulties of this undertaking are

increased by the multiplicity of the microorganisms concerned and by the

well-known truth that the same microorganism, _e. g._, the tubercle

bacillus, may produce widely different anatomic lesions.

In the table of autopsies the following lesions are listed:

=Column 7. Purulent bronchitis.=—“P” indicates that the small

bronchi contain mucopurulent fluid.

=Column 8. Lobar pneumonia.=—The occurrence of the lesion is

indicated by the plus sign (+).

=Column 9. Peribronchiolar consolidation.=—The presence of nodular

patches of consolidation about respiratory bronchioles is indicated

by the plus sign (+) when the lesion has been recognized at the time

of autopsy. When the lesion has been first recognized by microscopic

examination the letter “M” is used.

=Column 10. Hemorrhagic peribronchiolar consolidation.=—The

occurrence of this lesion which represents the preceding on a

background of hemorrhage is indicated by the plus sign (+).

=Column 11. Lobular consolidation.=—The presence of the lesion is

indicated by the plus sign (+).

=Column 12. Peribronchial consolidation.=—Peribronchial pneumonia

recognized at the time of autopsy is indicated by the plus sign (+).

Peribronchial pneumonia recognized microscopically is indicated by

“M.” The presence of peribronchial hemorrhage without consolidation

is indicated by “h.”

=Column 13. Abscess formation with pneumonia.=—Suppuration with

abscess formation almost invariably just below the pleura is

indicated by the plus sign (+). Necrosis of lung tissue recognized

microscopically and unaccompanied by suppuration is indicated by

“N.”

=Column 14. Suppurative interstitial pneumonia.=—This lesion

invariably associated with suppurative lymphangitis is indicated by

the plus sign (+).

=Column 15. Multiple abscess in clusters.=—Abscesses in clusters

about a bronchus of medium size are indicated by the plus sign (+).

=Column 16. Empyema.=—The presence of the lesion is indicated by

“E.”

=Column 17. Bronchiectasis.=—“B” indicates the lesion.

=Column 18. Unresolved bronchopneumonia.=—Presence of the lesion is

indicated by the plus sign (+).

=Column 19. Organizing bronchitis and bronchiolitis.=—“O” indicates

the lesion.

The lesions of columns 7 to 12 are acute inflammatory processes, columns

9 to 12 represent different types of bronchopneumonia. Columns 13 to 15

represent suppurative lesions. Columns 17 to 19 represent chronic

lesions. A survey of the table shows the predominance of acute lesions

in the early period of the study and the gradual increase of chronic

lesions.

The last four columns of the table of autopsies give the bacteriology of

the sputum during life and the bacteria found in the bronchi, in the

lungs, and in the blood of the heart after death.

=Mortality of Pneumonia Following Influenza.=—From September 6 to

December 15, 250 autopsies were performed on patients who had died with

pneumonia at the base hospital at Camp Pike, and with few exceptions

bacteriologic cultures were made from them. Although it was not possible

to perform autopsies on all who died, those which were performed afford

a fair index of all deaths, for throughout the epidemic of influenza and

its outbreak of pneumonia approximately one half of all who died were

examined after death. The relation of autopsies to deaths is shown by a

comparison by weeks of the number of deaths and number of autopsies

during the months of September and October.

═══════════════════════╤═══════════════════════╤═══════════════════════

WEEK │ DEATHS │ AUTOPSIES

───────────────────────┼───────────────────────┼───────────────────────

Sept. 1–7 │ 1│ 1

Sept. 8–14 │ 1│ 1

Sept. 15–21 │ 4│ 3

Sept. 22–28 │ 15│ 14

Sept. 29–Oct. 5 │ 121│ 67

Oct. 6–12 │ 191│ 78

Oct. 13–19 │ 78│ 43

Oct. 20–27 │ 22│ 15

Oct. 28–31 │ 8│ 6

│ ———│ ———

│ 441│ 228

───────────────────────┴───────────────────────┴───────────────────────

For most of these autopsies there is a record of the date of onset of

the illness, namely, influenza, which finally resulted in pneumonia and

death. Comparison of the number of cases of influenza which developed on

any day with the number of fatal cases which had their onset on the same

day will determine the mortality of influenza at different periods of

the epidemic. Chart 1 shows the number of cases of influenza which had

their onset on each day from September 1 to October 31 and the number of

fatal cases with autopsy which had their origin on corresponding days.

The comparison by weeks between autopsies and total number of deaths

shows that the autopsies represent with considerable accuracy the

deaths. If there is any error it occurs at the height of the outbreak of

pneumonia from September 29th to October 5th and not at its beginning,

or end. The chart shows that the highest mortality occurred among cases

of influenza which had their origin at the beginning of the epidemic

from September 21 to October 1, whereas after October 1, though the

maximum number of cases of influenza occurred on October 3, very few

developed fatal pneumonia.

=Mortality from Pneumococcus and Streptococcus Pneumonias.=—By referring

fatal cases of streptococcus pneumonia back to their date of origin it

is possible to determine what proportion of the cases of influenza,

which developed on any day, died with infection by hemolytic

streptococcus. The accompanying chart (Chart 1) shows that infection

with hemolytic streptococci has been very frequent at the beginning of

the epidemic of influenza (shown by area with double hatch in chart)

that is, from September 20 to 30 and subsequently has gradually

diminished so that few cases have had their onset in the second half of

the epidemic from September 30 to October 15.

Pneumococcus pneumonia uncomplicated by streptococcus infection (shown

by area with single hatch in chart) pursued a course which more closely

conformed to the curve representing influenza. The cases of influenza

which resulted fatally bore a fairly constant ratio to the total number

of cases of influenza from the onset of the epidemic until October 1,

but subsequently few cases of influenza developed fatal pneumococcus

pneumonia.

These charts arranged with reference to the onset of fatal pneumonias

dissociate very clearly the outbreak of streptococcus pneumonia, which

reached its height at the beginning of the influenza epidemic, from the

uncomplicated pneumococcus pneumonia which reached its maximum at the

midpart of the influenza epidemic and then abruptly abated.

[Illustration:

Chart 1—Showing the relation of (_a_) onset of cases of pneumonia

shown by autopsy to be uncomplicated by secondary infection with

hemolytic streptococcus, indicated by upper continuous line with

single hatch, and of (_b_) onset of fatal cases of streptococcus

pneumonia, indicated by the lower continuous line with double hatch,

to (_c_) the occurrence of influenza, indicated by the broken line.

The onset of each case of fatal pneumonia is represented by a single

square.

]

Our study of ward infection in pneumonia furnishes an explanation of the

outbreak of fatal streptococcus pneumonia coincident with the initial

stage of the influenza epidemic. This outbreak is a true epidemic of

streptococcus infection superimposed, in many instances at least, upon

preexisting pneumococcus pneumonia, but in some instances, doubtless, a

primary streptococcus pneumonia, following the bronchitis of influenza.

In the absence of secondary streptococcus infection a very large

proportion of these individuals would have recovered. This epidemic of

streptococcus pneumonia, it has been shown, was the result of

unfavorable conditions produced by great overcrowding of the hospital

and in the early part of the epidemic by inadequate separation of those

with streptococcus infection from those with none. With control of these

conditions, streptococcus pneumonia rapidly diminished.

Greater susceptibility to pneumococcus pneumonia in the early than in

the late period of the epidemic is perhaps explained by differences in

the severity of influenza; the more susceptible individuals were

attacked by influenza in the early period, whereas the less susceptible

did not acquire the disease until they had been exposed to an immensely

increased number of infected individuals. A better explanation is

furnished by the greater opportunity at the beginning of the epidemic

for the transmission of microorganisms causing pneumonia, for at this

time patients with influenza were crowded together and methods to

prevent the transmission of infection were little used.

Bronchitis

Clinical study has shown that purulent bronchitis (see Fig. 2) occurs in

about one-third of the cases of influenza. In a large proportion of

cases of bronchitis there is no clinical evidence of pneumonia. The

bronchial lesions found in association with the pneumonia of influenza

are an index of the ability of the agent, which causes influenza, to

injure the bronchi.

In those who have died with pneumonia following influenza the large

bronchi (with cartilage) are intensely injected, so that the mucosa has

a deep red color which on cross section contrasts very sharply with the

pearly white of the cartilage. Superficial injury to the bronchi is not

infrequently evident in the larger bronchial branches; superficial loss

of epithelium is indicated by erosion of the surface, whereas somewhat

deeper destructive changes are occasionally evident. Microscopic

examination accurately determines the degree of destructive change.

Purulent bronchitis was noted in 134 autopsies (55.6 per cent of

autopsies). From the small bronchi, in many instances, purulent fluid

welled up upon the cut surface of the lung, whereas in other instances

tenacious mucopurulent fluid could be squeezed from small, cut bronchi

by pressure upon lung tissue. The consistency of the material within the

bronchi varied greatly, ranging from a viscid and tenacious mucus of

creamy, yellow color to a thin, turbid, gray fluid. The coexistence of

local inflammatory or of general edema of the lungs modifies the

character of the material found in the bronchi at autopsy; with edema

the purulent exudate is in some instances diluted so that a thin cloudy

fluid flows from the small bronchi. In the presence of advanced edema of

the lungs the bronchi rarely if ever contain purulent exudate. The

underlying changes in the bronchi are more significant than the

character of the exudate found at autopsy. Nevertheless, the group of

cases in which the diagnosis of purulent bronchitis has been made,

because small and medium sized bronchi have contained purulent or

mucopurulent exudate, represents instances of readily recognizable

bronchitis of considerable severity.

With few exceptions, purulent bronchitis was diffusely distributed in

the lungs; occasionally it was observed in one lung alone, and in

several instances was limited to the bronchi at the base of a lung,

usually of the left lung.

In a considerable proportion of instances of purulent bronchitis

abnormal distention of the lungs was noted. On removal from the chest

the lungs fail to collapse and retain the size and shape of the thorax.

Even after section is made through the organ, parts of the lung fail to

collapse and have a resistant cushion-like consistency. This condition

is present where the lung tissue is air containing and dry, and occurs

when very small bronchi contain tenacious mucous exudate which becomes

apparent upon the cut surface after the sectioned lung is squeezed.

Microscopic examination shows that the alveolar ducts and infundibula

are distended with air, though the respiratory bronchioles contain

inflammatory exudate. Complete obstruction of the bronchi is followed by

absorption of air from the tributary pulmonary tissue with atelectasis.

It is not improbable that partial obstruction, permitting the

penetration of air with inspiration, produces distention of air

containing tissue.

It is furthermore probable that cyanosis, which is a conspicuous feature

of many instances of pneumonia following influenza, is referable, in

part at least, to obstruction of the bronchi by mucopurulent exudate.

The term pneumonia will refer to those inflammatory changes in the lung

which are found within the alveoli; it will include inflammatory changes

in the alveoli surrounding the respiratory bronchioles, in the alveolar

ducts and infundibula and in their tributary alveoli. Bronchitis will be

described by defining the changes which occur (a) in the small bronchi

with no cartilage or mucous glands, and (b) in the large bronchi

including the primary branches of the trachea.

For convenience of description those bronchi may be designated small,

which have no cartilaginous plates in their wall. Larger bronchi have

cartilage and mucous glands, the latter situated in considerable part

outside the cartilaginous plates. These bronchi, of which the largest

are the right and left bronchi formed by bifurcation of the trachea,

diminish with repeated branching to a caliber of about 1 mm. Small

bronchi are lined by columnar ciliated epithelium; their wall consists

of very vascular connective tissue containing a layer of smooth muscle

and their caliber varies approximately from 1 to 0.5 mm. It is

convenient to designate as respiratory bronchioles[80] the terminal

ramifications of the bronchi; they are lined by a single layer of

columnar ciliated cells passing over into cuboidal nonciliated

epithelium and are beset with small air sacs lined by flat cells or

epithelial plates similar to those of the alveoli elsewhere. Not

infrequently these alveoli occur along only one side of the bronchiole,

the remainder of the circumference being covered by a continuous layer

of cubical epithelium. The respiratory bronchiole by branching along its

course or at its end is continued into several alveolar ducts which

unlike the respiratory bronchioles have no cubical or columnar

epithelium but are closely beset by alveoli lined by flat epithelial

plates. The alveolar duct is recognized by the absence of cubical

epithelium and the presence of bundles of smooth muscle which occur in

the wall. The infundibula or alveolar sacs arise as branches from the

alveolar ducts and like them are beset with alveoli, but smooth muscle

does not occur in their walls. The base of the infundibulum is wider

than its orifice, which Miller states is surrounded by a sphincter-like

bundle of smooth muscle.

Changes in the main bronchi and their primary branches are usually less

severe than those in bronchi of smaller size. The epithelium is often

intact, the superficial cells being columnar and ciliated, but not

infrequently desquamation of superficial cells has occurred and the

lower layers alone remain. Occasionally (Autopsy 471) there is necrosis

of epithelium with which, although the architecture of cells is

preserved, nuclei have disappeared. Accumulation of blood or serum may

separate epithelium from the underlying basement membrane (Fig. 1).

Complete loss of epithelium occurs, usually in small patches.

Polynuclear leucocytes are numerous upon the surface of the epithelium

and are sometimes fixed in process of migration through epithelium and

basement membrane.

[Illustration:

Fig. 1.—Acute bronchitis showing engorgement of blood vessels of

mucosa and elevation of epithelium by serum and blood. Autopsy 352.

]

The blood vessels of the mucosa are engorged. There is sometimes edema

or hemorrhage, and in the superficial part of the mucosa polynuclear

leucocytes are often fairly abundant. When superficial epithelium has

been lost, polynuclears are numerous immediately below the surface of

the exposed tissue. Fibrin is often present upon the denuded surface and

extends for a short distance into the tissue below. In the deeper part

of the mucosa, about the muscularis and especially about and between the

acini of the mucous glands, the tissue is infiltrated with lymphoid and

plasma cells.

Changes in the mucous glands are invariably present. These changes are

distention of ducts and acini with mucous, degenerative changes

occasionally ending in necrosis of cells, disappearance of acini, dense

infiltration of interstitial tissue with lymphoid and plasma cells and

finally proliferation of this interstitial tissue. The duct of a mucous

gland, dilated and filled with mucus, may be surrounded by lymphoid and

plasma cells in great number. Acini, similarly dilated, contain mucus

and are composed of cubical cells which have discharged their mucous

content. In some instances (_e. g._, Autopsy 257) the cells of the acini

have undergone necrosis; the cytoplasm stains homogeneously and the

nuclei have disappeared. Where necrosis has occurred, polynuclear

leucocytes may penetrate into the dead cells. In association with

degenerative changes in the acini there is abundant infiltration of the

interstitial tissue within and about the glands with lymphoid and plasma

cells. When the acini have disappeared there is proliferation of

fibroblasts and new formation of fibrous tissue, and mucous glands are

found in which a few atrophied acini are separated by newly formed

fibrous tissue.

With the bronchitis of influenza the small bronchi (with no cartilage or

mucous glands) show every stage of transition from early acute

inflammation characterized by accumulation of polynuclear leucocytes

within the lumen, engorgement of blood vessels, and infiltration of the

wall with polynuclear leucocytes, through various stages of destructive

changes to complete disappearance of the bronchial wall and formation of

an abscess cavity at the site of the bronchus. In the early stages of

acute bronchitis, hemorrhage is frequently associated with the lesion.

Blood may be abundant within the lumen of the bronchus, and in the

mucosa red blood corpuscles often infiltrate the tissue around greatly

distended blood vessels, or accumulating below the epithelium, separate

it from its basement membrane. Hemorrhage is not limited to the wall of

the bronchus, but frequently occurs into the alveoli in a zone

encircling the bronchus.

With acute bronchitis there may be desquamation of epithelial cells with

partial or complete loss of epithelial lining. In the smallest bronchi

the single layer of columnar cells may be separated in places from the

underlying tissue, so that intact rows of cells are found within the

lumen. In somewhat larger bronchi, lined by epithelium in multiple

layers, superficial columnar ciliated cells may be lost. In some

instances superficial epithelial cells appear to have lost their

cohesion and are separated by narrow spaces; in these instances,

polynuclear leucocytes are often numerous between epithelial cells.

Epithelium is occasionally separated from its basement membrane by small

accumulations of serum or blood. Occasionally necrosis of epithelial

cells with disappearance of nuclei is seen and is doubtless caused by

the action of bacteria; the affected cells may be raised from the

underlying tissue by accumulated serum (Autopsy 253). The changes which

have been described bring about partial or complete loss of the ciliated

lining of the bronchial tube.

The severity of changes in the bronchial wall is in direct relation to

the extent of destruction of the lining epithelium: when the epithelium

remains intact polynuclear leucocytes may be found in considerable

number immediately below it, but as the lesion progresses, cells in

great part mononuclear, namely, lymphoid and plasma cells, accumulate in

large number throughout the wall of the bronchus. There is often

abundant cellular infiltration within and about the bundles of the

muscular coat. The changes assume the character of chronic inflammation.

When the lining epithelium of the bronchus is lost, fibrin tends to

accumulate over the surface of the defect, to which it is firmly

attached. It remains separated by a conspicuous space from adjacent

intact epithelium over which it may project. This superficial network of

fibrin merges with a similar network, extending to a variable depth

within the tissue. What may well be described as coagulative necrosis

has often occurred, and structures, such as white fibrous bundles or

wall of blood vessels, are marked out by hyaline material which merges

with fibrin. When the walls of the blood vessels which are invariably

engorged are involved, the lumen is plugged by a fibrinous thrombus.

Little patches of fibrin adherent to the inner surface of the bronchus

may occur in spots where epithelium has been lost; with uniform loss of

epithelium the entire circumference may be lined with fibrin forming a

circular zone occasionally quite uniform in thickness.

Accumulations of polynuclear leucocytes doubtless bring about conditions

which cause solution of fibrin or prevent its formation (when

disintegration of leucocytes sets free leucoprotease in abundance). The

activity of the infecting microorganisms, usually hemolytic streptococci

or staphylococci, may cause complete necrosis of a part or all of the

bronchial wall. The cavity which is formed may penetrate into lung

tissue that has previously undergone pneumonic consolidation.

Further changes caused by the bronchitis of influenza will be considered

under peribronchial hemorrhage and edema, peribronchial pneumonia and

bronchiogenic abscess. Purulent bronchitis is almost invariably

associated with dilatation of the bronchi, the affected bronchi being

distended with pus. With increasing dilatation bronchiectasis becomes

evident upon gross examination of the tissue, and is much more advanced

in the small bronchi than in the larger cartilaginous passages. This

subject will be further considered under bronchiectasis.

In association with the acute bronchitis of influenza the epithelium of

bronchi not infrequently looses its superficial columnar ciliated cells

and assumes some of the characters of a squamous epithelium being

covered by polygonal or flat cells (Figs. 17 and 18). The condition is

often described a “squamous metaplasia,” although it doubtless

represents a stage of regeneration following injury rather than a true

metaplasia. The basal cells of the epithelium have a cubical or columnar

form; above them the cells become polygonal and as the surface is

approached, cells are flat and even scale-like. The nuclei of these

superficial cells are often lost. There is no close resemblance to the

squamous epithelium of the skin, for intercellular bridges are not seen.

This change may occur within six days after onset of influenza, though

in most instances the duration of illness has been two weeks or more. It

may affect either large or small bronchi, but it is more frequently

found in the latter. Whenever ciliated columnar cells are lost,

superficial cells tend to become flat. Epithelium on one side of a

bronchus may have a squamous character, whereas that elsewhere is

columnar and ciliated. The flat epithelium may undergo thickening so

that it is 0.1 mm. or more in thickness. It is noteworthy that

regenerating epithelium growing over a denuded surface has the squamous

character which has been described (Plate XIV, Fig. 22).

=Bacteriology of the Bronchitis of Influenza.=—With the pneumonia of

influenza, bronchitis is invariably present. Cultures have been made

from the right or left main bronchus or from the very small bronchi

which contained purulent exudate. A routine method of making the culture

has been adopted. The right main bronchus, exposed by drawing the right

lung out of the chest and toward the midline, was widely seared with a

hot knife; the bronchus was partially cut across through the seared

surface with a heated knife and a platinum needle inserted into the

lumen. The bacteria obtained named in the approximate order of their

relative frequency have been: B. influenzæ, pneumococci, hemolytic

streptococci, staphylococci (aureus and albus), B. coli, S. viridans, M.

catarrhalis, and diphthoid bacilli which have not been identified. Mixed

infections occurred in most instances. The following list arranged by

grouping bacteria in the order cited above, shows how varied have been

the combinations which occur:

B. influenzæ 3

Pneumococci 5

S. hemolyticus 3

Staphylococci 3

B. coli 3

S. viridans 1

B. influenzæ, pneumococci 17

B. influenzæ, S. hemolyticus 18

B. influenzæ, staphylococci 4

Pneumococci, S. hemolyticus 1

Pneumococci, staphylococci 3

S. hemolyticus, staphylococci 4

S. hemolyticus, B. coli 2

Staphylococci, S. viridans 1

B. influenzæ, pneumococci, S. hemolyticus 6

B. influenzæ, pneumococci, staphylococci 15

B. influenzæ, pneumococci, S. viridans 2

B. influenzæ, S. hemolyticus, staphylococci 16

B. influenzæ, S. hemolyticus, M. catarrhalis 1

B. influenzæ, staphylococci, S. viridans 1

Pneumococci, S. hemolyticus, staphylococci 3

Staphylococci, B. coli, S. viridans 1

B. influenzæ, pneumococci, S. hemolyticus, staphylococci 7

B. influenzæ, pneumococci, staphylococci, M. catarrhalis 1

B. influenzæ, S. hemolyticus, staphylococci, B. coli 1

B. influenzæ, S. hemolyticus, staphylococci, S. viridans 1

B. influenzæ, S. hemolyticus, staphylococci, M. catarrhalis 1

B. influenzæ, staphylococci, S. viridans, M. catarrhalis 1

B. influenzæ has been present in the bronchi in 79.3 per cent of

instances of pneumonia referable to influenza. Combinations which have

been found most frequently are B. influenzæ and pneumococci (17

instances), B. influenzæ and hemolytic streptococci (18 instances), or

the same combinations with staphylococci, namely, B. influenzæ,

pneumococci and staphylococci (15 instances), and B. influenzæ,

hemolytic streptococci and staphylococci (16 instances). There is little

doubt that B. influenzæ was not identified in some instances in which it

was present; when other microorganisms are very numerous its

inconspicuous colonies may be overgrown even though the presence of

pneumococci, streptococci or staphylococci tends to increase the size of

its colonies. Moreover, it is not improbable that the microorganism may

disappear from the bronchi. Comparison with observations made upon

influenza suggests that multiple methods of examination might have

demonstrated a much higher incidence of B. influenzæ. Throat cultures

alone made during life demonstrated the presence of B. influenzæ in only

65.7 per cent of patients with acute influenza, whereas when cultures

were made from the nose, throat and sputum, and a mouse was inoculated

with sputum from each patient, B. influenzæ was found in every instance.

After the acute stage of the disease had passed, the number of

microorganisms diminished, and in many instances B. influenzæ

disappeared from the upper air passages. In some of our autopsies B.

influenzæ doubtless present during life has similarly disappeared before

death due to pneumonia caused by pneumococci or streptococci. In view of

these considerations it is not improbable that B. influenzæ demonstrated

by a single culture in 80 per cent of instances has been constantly

present.

Table XXVIII represents the incidence of pneumococci, hemolytic

streptococci, staphylococci, and B. influenzæ in the bronchi, lungs and

blood of those individuals with pneumonia in whom bacteriologic

examination has been made at autopsy. The number of cultures made from

the bronchi, lungs or blood of the heart is given in the second column

of the table and in other columns are given the incidence in number and

percentage of the microorganisms which have been mentioned.

TABLE XXVIII

════════╤════════╤═════════════════╤═════════════════

│ NO. OF │ │ HEMOLYTIC

│CULTURES│ PNEUMOCOCCI │ STREPTOCOCCI

────────┼────────┼────────┬────────┼────────┬────────

│ │ NO. │PER CENT│ NO. │PER CENT

│ │POSITIVE│POSITIVE│POSITIVE│POSITIVE

────────┼────────┼────────┼────────┼────────┼────────

Bronchus│ 121│ 56│ 46.3│ 58│ 47.9

Lung │ 153│ 68│ 44.4│ 77│ 50.3

Blood │ 218│ 87│ 39.9│ 85│ 39.0

────────┴────────┴────────┴────────┴────────┴────────

════════╤═════════════════╤═════════════════

│ │

│ STAPHYLOCOCCI │ B. INFLUENZÆ

────────┼────────┬────────┼────────┬────────

│ NO. │PER CENT│ NO. │PER CENT

│POSITIVE│POSITIVE│POSITIVE│POSITIVE

────────┼────────┼────────┼────────┼────────

Bronchus│ 61│ 50.4│ 96│ 79.3

Lung │ 37│ 24.2│ 70│ 45.7

Blood │ 1│ 0.5│ 1│ 0.5

────────┴────────┴────────┴────────┴────────

Cultures from the bronchus represent the bacteriology of the bronchitis

of influenza. Infection of the lung following influenza doubtless occurs

by way of the bronchi, so that the bacteria which cause pneumonia are

present in the bronchi before they enter the lung tissue. The figures in

Table XXVIII, similar to those previously cited, show the high incidence

of B. influenzæ, and the occurrence of pneumococci, hemolytic

streptococci and staphylococci each present in approximately half of all

autopsies.

The figures in Table XXVIII are an index of the capacity of the

microorganisms which enter the bronchi to invade the lungs and finally

the blood. Pneumococci were present in the bronchi in 46.3 per cent of

instances, in the lungs in only slightly less, and in approximately 40

per cent of autopsies they had penetrated into the blood. Hemolytic

streptococci enter the bronchi with the same frequency and exhibit an

equal ability to penetrate into the lungs and blood. Staphylococci enter

the bronchi in half of these individuals, but penetrate into the lungs

in only a fourth of the instances. They have entered the blood only once

(Autopsy 263) in this instance in association with hemolytic

streptococci. B. influenzæ has been present in the bronchi in

approximately 80 per cent of autopsies. It is noteworthy that it has

been found in the lung in little more than half this percentage of

instances and has entered the blood only once (Autopsy 474), in this

instance in association with hemolytic streptococci.

In a limited number of autopsies there was purulent bronchitis

recognized by the presence of mucopurulent exudate in small bronchi. It

has been stated that this group of cases is not sharply separable from

other instances of bronchitis, because in some cases death has occurred

before a purulent exudate has accumulated or in other instances a

purulent exudate has been displaced by edema. Table XXIX shows the

bacteriology of instances of purulent bronchitis:

TABLE XXIX

════════╤════════╤═════════════════╤═════════════════

│ NO. OF │ │ HEMOLYTIC

│CULTURES│ PNEUMOCOCCI │ STREPTOCOCCI

────────┼────────┼────────┬────────┼────────┬────────

│ │ NO. │PER CENT│ NO. │PER CENT

│ │POSITIVE│POSITIVE│POSITIVE│POSITIVE

────────┼────────┼────────┼────────┼────────┼────────

Bronchus│ 66│ 33│ 50.0│ 32│ 48.5

────────┴────────┴────────┴────────┴────────┴────────

════════╤═════════════════╤═════════════════

│ │

│ STAPHYLOCOCCI │ B. INFLUENZÆ

────────┼────────┬────────┼────────┬────────

│ NO. │PER CENT│ NO. │PER CENT

│POSITIVE│POSITIVE│POSITIVE│POSITIVE

────────┼────────┼────────┼────────┼────────

Bronchus│ 36│ 54.5│ 53│ 80.3

────────┴────────┴────────┴────────┴────────

The percentages of various bacteria with purulent bronchitis do not

differ essentially from those obtained from all autopsies with

pneumonia. B. influenzæ is found in approximately 80 per cent of

autopsies. In 16 instances cultures were made from the purulent fluid

contained in a small bronchus and the incidence of B. influenzæ (namely,

81.4 per cent) has not differed from that in the main bronchus. In 7 of

8 instances in which cultures were made, both from the right main

bronchus and from the purulent fluid in a small bronchus, B. influenzæ

was found in one or other in all but one autopsy (87.5 per cent); in

this instance (Autopsy 472) respiratory disease began thirty-seven days

before death and cultures from large and small bronchi at autopsy were

overgrown by B. coli. Since observations upon influenza made during life

have shown that B. influenzæ is constantly demonstrable when multiple

methods are employed for its detection, the figures just cited give

support to the suggestion that B. influenzæ is constantly present in the

bronchi with the bronchitis of influenza.

Lobar Pneumonia

The frequency with which the confluent lobular consolidation of

bronchopneumonia involving whole lobes or parts of lobes follows

influenza has emphasized the desirability of distinguishing carefully

between lobar and confluent lobular pneumonia. The pulmonary lesion has

been designated lobar pneumonia when it exhibited the well-known

characters of this lesion, namely, firm consolidation of large parts of

lobes, coarse granulation of the cut surface, fibrinous plugs in the

bronchi and, on microscopic examination, homogeneous consolidation and

fibrinous plugs within the alveoli. With confluent lobular consolidation

of bronchopneumonia the consolidated area is in most cases obviously

limited by lobule boundaries, and well-defined lobules of consolidation

occur elsewhere in the lungs.

Lobar pneumonia occurred in 98 among 241 instances of pneumonia

following influenza, namely, in 40.7 per cent of autopsies.

The difficulty of separating lobar and bronchopneumonia following

influenza has been increased by the frequent combination of the two

lesions in the same individual. There were 34 instances in which lobar

and bronchopneumonia occurred together. The anatomic diagnosis of lobar

pneumonia was made only when lobes or parts of lobes were firmly

consolidated and exhibited the characters of the lesion enumerated

above; in several instances, in which there was some doubt concerning

the nature of the lesion, microscopic examination was decisive. The

associated bronchopneumonic lesions represented all the types which have

been associated with influenza. In the group of 34 cases of coexisting

lobar and bronchopneumonia, lobular consolidation occurred 10 times,

peribronchiolar consolidation 14 times (recognized in all but 4

instances by microscopic examination), hemorrhagic peribronchiolar

consolidation 9 times, peribronchial pneumonia 4 times. The intimate

relation of these lesions to changes in the bronchi is well shown by the

frequent presence of purulent bronchitis. The associated lesions of the

bronchi in these cases were as follows: purulent bronchitis in 23

instances; peribronchial hemorrhage in 6; bronchiectasis in 11. The

frequency of purulent bronchitis and other bronchial lesions in

association with coexisting lobar and bronchopneumonia is in sharp

contrast with the occurrence of these lesions in association with lobar

pneumonia alone; with 69 instances of lobar pneumonia alone purulent

bronchitis occurred 17 times and bronchiectasis once.

Lobar pneumonia following influenza passes through the usual stages of

red and gray hepatization. Red hepatization was found 16 times, combined

red and gray hepatization 28 times, and gray hepatization 20 times. The

average duration of pneumonia with red hepatization was 3.7 days, with

combined red and gray hepatization 5.1 days and with gray hepatization

7.5 days. These figures, it will be shown later, have some importance in

relation to the stage at which hemolytic streptococcus infects lungs the

site of lobar pneumonia.

=Bacteriology of Lobar Pneumonia.=—Table XXX is compiled with the

purpose of determining the bacteriology of the bronchi, lungs and

heart’s blood in autopsies performed on individuals with lobar

pneumonia. In some instances bacteriologic examination of one or other

of these organs was omitted; the percentage incidence is an index of the

presence of pneumococci, hemolytic streptococci, staphylococci or B.

influenzæ in the bronchi, lungs or heart’s blood and measures the

invasive power of these microorganisms during the course of lobar

pneumonia following influenza.

TABLE XXX

════════╤════════╤═════════════════╤═════════════════

│ NO. OF │ │ HEMOLYTIC

│CULTURES│ PNEUMOCOCCI │ STREPTOCOCCI

────────┼────────┼────────┬────────┼────────┬────────

│ │ NO. │PER CENT│ NO. │PER CENT

│ │POSITIVE│POSITIVE│POSITIVE│POSITIVE

────────┼────────┼────────┼────────┼────────┼────────

Bronchus│ 44│ 56.9│ 14│ 31.8│ 22

Lung │ 53│ 77.3│ 13│ 24.5│ 8

Blood │ 87│ 65.5│ 11│ 12.6│

────────┴────────┴────────┴────────┴────────┴────────

════════╤═════════════════╤═════════════════

│ │

│ STAPHYLOCOCCI │ B. INFLUENZÆ

────────┼────────┬────────┼────────┬────────

│ NO. │PER CENT│ NO. │PER CENT

│POSITIVE│POSITIVE│POSITIVE│POSITIVE

────────┼────────┼────────┼────────┼────────

Bronchus│ 37│ 84.1│ 96│ 79.3

Lung │ 26│ 49.1│ 70│ 45.7

Blood │ │ │ 1│ 0.5

────────┴────────┴────────┴────────┴────────

Pneumococci, the recognized cause of lobar pneumonia, were found in the

lungs in 73.3 per cent of autopsies; failure to find the microorganism

in all instances is doubtless the result of its disappearance from the

lung, which, it is well known, occurs not infrequently particularly

during the later stages of the disease. In 65.5 per cent of instances of

fatal lobar pneumonia pneumococci have entered the heart’s blood.

Hemolytic streptococci unlike pneumococci were found more frequently in

the bronchi than in the lungs; this microorganism which exhibits little

tendency to disappear, once it has established itself within the body,

found entrance into the bronchi in 31.8 per cent of instances of lobar

pneumonia and in 24.5 per cent entered the lungs. Its invasive power is

further illustrated by its penetration into the heart’s blood

approximately in half this proportion of autopsies.

Staphylococci enter the bronchi in many instances (50 per cent), but

relatively seldom (15.1 per cent) invade the lung and rarely if ever

penetrate into the blood.

The high incidence, namely, 84.1 per cent, of B. influenzæ in the

bronchi is particularly noteworthy; it exceeds that of pneumococci, the

well-recognized cause of lobar pneumonia, within the lung. It is found

much less frequently within consolidated lung tissue and shows no

tendency to invade the heart’s blood. B. influenzæ finds the most

favorable conditions for its multiplication within the bronchi.

In view of the frequent occurrence of coexisting lobar and

bronchopneumonia it has appeared desirable to determine how far the

existence of obvious bronchopneumonia modifies the bacteriology of lobar

pneumonia. In Table XXXI the incidence of pneumococci, hemolytic

streptococci, staphylococci and B. influenzæ after death with lobar

pneumonia on the one hand is compared with their incidence after

combined lobar and bronchopneumonia on the other.

Pneumococci are found in the lung more frequently with lobar than with

combined lobar and bronchopneumonia. The incidence of hemolytic

streptococci and of staphylococci in the lung is on the contrary higher

when bronchopneumonia is associated with lobar pneumonia. It is not

improbable that these microorganisms have a part in the production of

associated bronchopneumonia. The frequency with which microorganisms

invade the blood is almost identical in the two groups.

TABLE XXXI

WITH LOBAR PNEUMONIA ALONE

════════╤════════╤═════════════════╤═════════════════

│ NO. OF │ │ HEMOLYTIC

│CULTURES│ PNEUMOCOCCI │ STREPTOCOCCI

────────┼────────┼────────┬────────┼────────┬────────

│ │ NO. │PER CENT│ NO. │PER CENT

│ │POSITIVE│POSITIVE│POSITIVE│POSITIVE

────────┼────────┼────────┼────────┼────────┼────────

Bronchus│ 30│ 20│ 66.6│ 9│ 30

Lung │ 34│ 29│ 85.2│ 7│ 20.6

Blood │ 54│ 36│ 66.7│ 7│ 13

────────┴────────┴────────┴────────┴────────┴────────

════════╤═════════════════╤═════════════════

│ │

│ STAPHYLOCOCCI │ B. INFLUENZÆ

────────┼────────┬────────┼────────┬────────

│ NO. │PER CENT│ NO. │PER CENT

│POSITIVE│POSITIVE│POSITIVE│POSITIVE

────────┼────────┼────────┼────────┼────────

Bronchus│ 15│ 50│ 26│ 86.7

Lung │ 3│ 8.8│ 18│ 52.9

Blood │ │ │ │

────────┴────────┴────────┴────────┴────────

WITH COMBINED LOBAR AND BRONCHOPNEUMONIA

════════╤════════╤═════════════════╤═════════════════

│ NO. OF │ │ HEMOLYTIC

│CULTURES│ PNEUMOCOCCI │ STREPTOCOCCI

────────┼────────┼────────┬────────┼────────┬────────

│ │ NO. │PER CENT│ NO. │PER CENT

│ │POSITIVE│POSITIVE│POSITIVE│POSITIVE

────────┼────────┼────────┼────────┼────────┼────────

Bronchus│ 14│ 9│ 64.3│ 5│ 34.3

Lung │ 19│ 12│ 63.2│ 6│ 31.6

Blood │ 33│ 21│ 63.1│ 4│ 12.1

────────┴────────┴────────┴────────┴────────┴────────

════════╤═════════════════╤═════════════════

│ │

│ STAPHYLOCOCCI │ B. INFLUENZÆ

────────┼────────┬────────┼────────┬────────

│ NO. │PER CENT│ NO. │PER CENT

│POSITIVE│POSITIVE│POSITIVE│POSITIVE

────────┼────────┼────────┼────────┼────────

Bronchus│ 7│ 50│ 11│ 78.6

Lung │ 5│ 26.3│ 8│ 42.1

Blood │ │ │ │

────────┴────────┴────────┴────────┴────────

The relative frequency with which different types of pneumococci produce

lobar pneumonia under the conditions existing when Camp Pike was

attacked by an epidemic of influenza is indicated by Table XXXII in

which instances of lobar pneumonia alone and of combined lobar and

bronchopneumonia are listed separately.

Epidemic Respiratory Disease The pneumonias and other infections of the repiratory tract accompanying influenza and measles · 第 5 / 10 章

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