diphtheria. · diphtheria: read before the richmond academy of medicine and surgery, february 16th,...

DIPHTHERIA.

READ BEFORE THE

RICHMOND ACADEMY OF MEDICINE AND SURGERY,

February i6th, 1892,

Dr J. W WILLIAMS.

diphtheria:

READ BEFORE THE RICHMOND ACADEMY OF MEDICINEAND SURGERY, FEBRUARY 16th, 1892,

Dr. J. W. WILLIAMS, v/

THE human body is covered by skin ; and the disgestive tract, urethra,vagina, &c., by mucous membrane. Both skin and mucous mem-

brane are covered by a layer of epithelium that is so arranged that solu-tion of continuity must take place before bacteria or germs can have accessto the tissues within. Hence, a wound of this epithelium is absolutelynecessary to infection—to sepsis. In other words, septicaemia or pyaemiacannot take place without a wound in this epithelial layer, through whichwound the bacteria enter the blood and systemic intoxication follows as aconsequence. In case HI2 below, Mr. C. had a minute scratch near thenostril, so small as to escape my notice, and in using a towel that I hadused in opening an abscess upon his brother’s face, who was sufferingfrom erysipelas, he inoculated himself with the same disease with whichhis brother was suffering. The streptococci entered the blood throughthis microscopic wound, and septic intoxication followed. Case IV affordsanother example. Mr. R. was suffering from pyaemia. The streptococcuswas found in the pus from an abscess near the outer middle ofright thigh.From this abscess the streptococci entered the general circulation throughthe disintegrated or broken walls of the neighboring blood-vessels, andpyaemia resulted.

A few words upon the process of

INFLAMMATIONinvolved in diphtheria may not be out of place. All injuries causingwounds, whether the keen edge of the flashing stiletto or the jagged andrough section of a shell, destroy the life of those cells that lie in the pathof the cutting or lacerating object. The blood and lymph exuding from

1. The old Roman physicians called it Angina, and the GreeksCynanche—“ Nostri anginam vocant:Graecos nomen cynauche."—Celsus, caput IV, p. 257. Its present name (Diphtheria) wasgiven by M.Bretennou, of France in 1818. It is thought that descriptions of this disease can be traced to atime anterior to Hippocrates (460 B. C.), and that Aretanes, of Cappadocia, described it (100 A. D.).One of the earliest treatises was by Hecker, who described an epidemic that prevailed in Holland in1337. Dr. Fothergill gives a description of the epidemic that appeared in London in 1745, and Dr.Samuel Bard, of New York, describes the epidemic that swept this country in 1771.

2. For cases 111, IV. see paper on Pyogenesis.

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the vessels coagulate, and necrosis follows. If a number of active micro-cocci from the surrounding air or dirt attack this wound, they find a con-genial soil for their development and multiplication. The fermentativedecomposition here set up produces certain chemical alkaloids or extremelypoisonous substances—the ptomaines. The adjacent vaso-motor nervescome under their toxic influence, causing active hyperaemia, and we havethe first symptom of inflammation—“rubor.” The dilated capillaries in-volved, in virtue of this very dilatation, invite a larger volume of blood,which now rushing through them with greater velocity, the red blood-corpuscles become packed and finally stagnate (stasis) in the smaller arte-ries. The walls of these vessels give way, and the white blood-corpusclesand serum are extravasated into the surrounding tissues, infiltrating theirinterstices, and the characteristic swelling ensues (“turgor"'), the secondsymptom of inflammation. As a consequence of increased blood supply,marked oxydation takes place, a rise of the local temperature follows, andwe have “calor" (heat), the third symptom of the inflammatory action.The action, perhaps, of the ptomaines, the direct pressure caused by theswelling, combined with the actual destruction of the nerve tissue duringthe resulting suppuration, accounts for the pain (“dolor ”) which com-pletes the classical cycle of the four cardinal symptoms of inflammation—

rubor, calor, turgor, dolor.The infiltrated tissue, devitalized by the shutting off of the normal cir-

culation, falls a prey to the millions of micro-organisms, and necrosis logi-cally follows. This last step in the textual destruction results in the lique-faction of the tissues. A cavity or abscess is formed, filled with lymph-serum exuded from the injured blood-vessels in the neighborhood, mil-lions of dead white blood-corpuscles (pus cells), and shreds of necrosedtissue. The great tension surrounding a large abscess necessarily causesan overflow of its liquid contents into the surrounding efferent vessels—

veins and lymphatics. The ptomaines at once enter the general circula-lation, systemic intoxication ensues, manifested by a marked rise of tem-perature, rigors, nausea, headache, delirium, and asthenia—septic fever.This systemic intoxication is caused, not by the absorption of the bacilli,but its ptomaines—a very poisonous substance, a white powder, solublein water, whose chemistry is Cas-ss,The extension of septic material is twofold : First, by infiltrating thetissue interstices by columns of micrococci; and secondly, by way of thelymphatics. It seems probable that in diphtheria the Klebs-Hoefflerbacillus utilize both of these ways. If the parts affected are loose tissues,as the tonsils and cervical glands, the infection will be rapid ; if the partsare dense, the inflammation is localized so long as the tissue-density re-sists the pressure of the imprisoned secretions. Inflammation has threestages:

First stage. Dilatation of the blood-vessels, the increased flow ofblood

3

and lymph to the part, slowing of the circulation, and finally inflammatorystasis, with extravasation of blood-plasma and corpuscles. In this stagethe vital activity of the tissue is suspended, the functions of the part are,so to speak, paralyzed; in other words, the tissue has, to a certain extent,become devitalized, and therefore unable to resist the entrance of bacteria.

Second stage. Here this weak tissue has been removed and healthygranulations have taken its place. This healthy granulation seems to havepower to resist attacking organisms.

Third stage. Here the irritating agent no longer acts. The first effectof this irritant was to damage the part, and under its damaging influencedilatation of the blood-vessels resulted ; and as a consequence of this dila-tation an increased flow of blood and lymph took place. Nature is heretrying to overcome the irritating cause by flushing the part. with blood—

by washing away the obstruction. • Probably this process is often goingon in our bodies unnoticed by us. If the irritant continues to act, andthese measures are ineffectual, nature removes the irritating cause by ne-crosis and sloughing.

The tonsils and cervical glands being vascular bodies, and loose in theiranatomical structure, they become easily infiltrated by columns of micro-cocci, which burrow down to the depth of a quarter of an inch in thetissue and below the surface (Prudden-Seibert). Here inflammation takesplace, which results in an exudation of serum and leucocytes accumulatingin the upper epithelial layer of the mucosa, thus producing the false mem-brane of diphtheria. In view of this pathological fact, all washes andgar-gles are useless, just because they do not and cannot reach down to themicrobe burrowing beneath the surface. The mortality from diphtheria inthe city of New York during ten months of the year 1890 amounted to1,725 out of4,340 cases, and nowhere is the bichloride treatment more ex-tensively used than in New York; yet here is frightful mortality. “Of thestrength of 1-500, thousands of micrococci remained alive at the end offifteen minutes.”—(Pruden.) Givenof this strength you kill your patient,and in weak solutions you fail to kill the streptococcus; and in either caseyou fail to reach the microbe. This treatment is not efficient, because itdoes not reach the bacilli at work below the mucosa. It does not penetratethe false membrane, but glides off its surface into the oesophagus; it isnot local, because the seat of the disease is not reached ; and it is notgermicidal, because the solution is not strong enough to destroy the diph-theritic germs. Chlorate of potassa, benzoate of soda, boric acid, et omnegemis, may at once be struck from the list as topical agents useful in diph-theria. In the very nature of diphtheria the only scientific treatment mustbe a germicidal one. Carbolic acid and corrosive sublimate solutions,when used of sufficient strength, will inevitably produce systemic intoxi-cation. The sooner local treatment is commenced the better the chancesof preventing the general infection. An early diagnosis is therefore in-

4

dispensable. A bit of the pseudo-membrane should at once be removed,dried on a cover-glass, stained with fuschin, or gentian vjolet, and placedunder the microscope for examination. 3 The microscope was inventedabout the latter part of the sixteenth century, and Kircher suggested in1646 that disease might be due to minute organisms. Van Leuwenhorck,of Holland, pushed his investigations still further (1680-1723); Andy in1701, Muller in 1786, Ehrenburg in 1833. But it was not until 1863 thatDavani established a connection between bacteria and disease. And thefirst complete study of a contagious affection was made by Pasteur in 1869;then Koch in 1875; and finally Klebs-Loeffler differentiated the bacteriaof diphtheria in 1884: “Small, slightly-curved rods, about as long as thetubercle bacilli and twice as broad; the ends are at times swollen.’’ Dr.Plfeifer .discovered the bacillus ofla grippe in 1891.

INOCULATION.Breiger and Frankel, by injecting ten to twenty per cent, of a three-

weeks’ -old culture of diphtheria bacilli, produced an immunity in guinea-pigs against the virulent form. Drs. Wood and Formad, of the Universityof Pennsylvania, have been invited by the National Board of Health “todetermine whether it is possible to produce diphtheria in the lower ani-mals by inoculation.” Seibert has inoculated eighty animals. Here,stretching out before us, is a new and most inviting field for the scientificphysician. The day will come soon and shortly when children4 will be in-oculated to insure immunity against diphtheria as well as from small-pox.Where is the Jenner who will immortalize himself and hand down to pos-terity a name more precious than a monument of diamonds?

TREATMENT.Submembraneous and Tonic. —Diphtheria is a local disease, and the con-

stitutional symptoms are due to the absorption of the ptomaines from thelocal lesion. The treatment is essentially germicidal and tonic. Both thepathology and etiology of the disease teach this. Besides, it is the mostscientific and successful. “It should be clearly held in mind—by thoseeager to draw from experimental studies on the etiology of this disease suchpractical lessons as shall be ofvalue in treatment—that it seems to be fullyestablished that in all of the cases the seat ofinfection and the origin of the

3. “ There are only two germs to be considered in studying the etiology of diphtheria—the strepto-coccusand the rod-shapedbacillus'frith rounded extremities.”—(Oertel.) Afterall that has been writ-ten upon this qestion, I think it is conservative to say that the identification of the specific microbeand its ptomaines will be the work of the future.

4. The important discovery made by Behring and Kitasato in 1890, that blood-serum taken fromanimals that had beenrendered immune to tetanus and to diphtheriacould cure otheranimals affectedwith these diseases, and the further discovery made by the Drs. Klemperer, that serum taken froman animal that had pneumonia containsthe anti-pneumotoxin, by means of which an immunity againstpneumonic septicaemia is secured in other animals, should stimulate my medical brethren to pushtheir investigations in this new field under a brighter light—encouragedby a stronger hope.

5

mischief is always a local one.” —(Prudden’s “ Studies on the Etiology ofDiphtheria.”)

The pseudo-membrane is an exudate from the deeper layer of the mucousmembrane, coagulated in the epithelium, and not the disease, but the re-sult of it. If it is removed, mopped, or torn, the points of infection willbe multiplied. Let it alone. Geppert has shown that ‘ ‘ bacilli will livein a 7 per cent, solution of carbolic acid, and in a 1-1000 solution ofthe bichloride of mercury for twenty minutes.” He also showed that theanthrax bacillus died in ten seconds if brought in contact with a 0.2 percent, solution of aqua chlori. ‘‘The obvious lesson taught by a definiteconception ofthe nature of the germ which causes diphtheria is not to dallywith fancy mixtures, which have at least a moderate germicidal power,but to get at the growing germ, as directly as the seat of the lesion willpermit, with some agent that we know will kill it. ”—(Prudden).

Traube first made intratonsular injections in diphtheria, and after himHuebner. Traube used a3to 5 per cent, solution of carbolic acid twicedaily, and reduced the mortality from 35.5 per cent, to 10 per cent. Sei-bert, in 1891, treated thirty-five cases hypodermically, and only lost two. Itreated lately eleven cases, wifh one death. Case six recovered and wasout on the streets for eight or ten days, but was stricken with paralysis,and died on the forty-second day. The hypodermic syringe I use has fivetubes or needles fixed to a plate, which is screwed to the barrel, making theinstrument eight inches long. These five needles are one-fourth of aninch in length. The plate is firmly held against the tonsil or pharynx, theneedles boldly pressed through the false membrane down to the sub-mucous tissue where the bacilli are at their deadly work, and the aquachlori at once, by injection, brought in contact with them. In the meantime, however mild the case, I at once put the patient upon tonics :

R. Best beef . . 1 lb.Aqua Oij.

Boil down to one pint, strain, and season with salt and pepper, and take daily.

Should the constitutional symptoms announce the general systemic in-fection, the patient being stronger, will be the more readily tided over it.

Case I. Mr. R., age 26, October 2d, 7 P. M.: Fever 104° for two daysprevious ; false-membrane on both tonsils and infiltration of cervical glands.

6

Injection of 30gtt. of aqua chlori at 7:15 P. M. into both tonsils throughthe pseudo-membrane down to the depth of a quarter of an inch. Octo-ber 3d, 9A.M. ; CEdaema of both tonsils continue. Intense redness ofthroat; voice changed. Injection at 9:15 A. M.; injection again the nextday. False membrane becoming detached. October 7th, dischargedcured. Beaf tea, one pint daily, was given this case.

Case 11. Mr. C., age 18 years, October 9th: Fever high; false membraneon right tonsil, smaller patch on left; oedaema and infiltration of cervicalglands. Injections. October 10th, 9A. M.: Patient worse ; oedaema in-creasing, especially of the left cervical glands. Seven P. M.: Injection,each time into both tonsils. October 11th: No fever; false membrane aninch long; patient worse. Nine A. M.: Injectin; antiseptic gargle toclear throat; injections daily; beaf-tea (1 lb.). October 12th, dischargedcured.

Case 111. Mr. C., age 21: High fever; false membrane on both tonsils;injection in both tonsils as before ; liver torpid.

R. Euonymin grs. ivLeptandrin grs. iiiPodophyllin (neutral) • grs. ij

M. Sig. Ft. pil. ix. Dosis : Unus omni tri hora.

This corrected all hepatic trouble, cleaned off the tongue, and cleared upthe complexion. First saw this man November 24th. Made daily injec-tions for three days. November 27th: Membrane came away. Dischargedcured.

Case IV. Boy, age 10 years. High fever; false membrane on righttonsil, and on second day on left tonsil also. Injection through falsemembrane into both tonsils to the depth of a quarter of an inch. On thirdday false membrane came off. Discharged cured.

Case V. Boy, age 41 years. (In consultation.) False membrane onboth tonsils and over nearly the whole of the pharynx ; systemic intoxica-tion ; the septicaemia well developed ; heart feeble. First saw him Octo-ber 15th. Injection at 11 A. M.; injection at 6P. M. October 16th, 10:30A. M.: Three injections; at 6P. M. coughed up tube cast. False mem-brane loose and a piece came away an inch long and one eighth ofan inchin thickness. Sent this fine specimen to Dr. Billings, at Washington.October 17th: CEdaema of cervical glands continues ; croupy symptoms ;

bronchi involved ; pulse failing.R . Peroxid. of hydrogen if ij.

Tr. digitalis £iFI. ext. sanguinaria cand sij

Dosis : Coch. parv. omni tri hora.

Septicaemia no doubt caused by absorption of the ptomaines. Beef tea.Alimentary tract disinfected with thymol. Patient gradually growing

7worse. October 18th, 2P. M.: Died of septic infection. Ido not thinkany local treatment will avail after systemic septic intoxication sets in.

Case VI. Boy, age 3 > years; Tonsils covered with false membrane;five or six ulcers on leg ; had been exposed to the disease ; false membranecovered each ulcer. This boy recovered; was out on the streets for aweek or so; fattened rapidly, but died on the forty-second day of paraly-sis, 5 as mentioned above.

Case VII. Lady, age 26 ; false membrane on both tonsils ; injection atonce through the necrosed membrane down to the mucosa beneath wherethe microbes are burrowing; injections daily; discharged cured on thefifth day.

HISTOLOGY.Prudden found the streptococcus pyogenes in twenty-two out of twenty-

four cases of diphtheria examined by him. We have reasons for believing,on biological and experimental grounds, that not only is the streptococcuspyogenes the etiological factor in diphtheria, but that erysipelas and someforms of phlegmonous inflammations are cognate 6 diseases with diphtheria.Pruden carried cultures of streptococci from cases of diphtheria along sideby side with cultures of streptococci made from various cases of acuteerysipelas and phlegmonous inflammation, week after week; over andover again has he measured and compared the growth from these threesources. Pie has repeatedly inoculated duplicate sets of animals with thedifferent cultures, and has never found a single, constant feature of differ-ence between them. The close relationship existing between these threeforms of inflammation has long since been pointed out by Baumgarten.

In the above cases I had the bedding, napkins, towels, &c., boiled inwater for two hours in the same rooms in which I treated the cases! Thecity should establish a disinfecting-house,7 well equipped, for this purpose,to which all clothing, bedding, &c., from infectious diseases should besent. All exudates should be received into vessels containing a 5 per cent,solution of carbolic acid.

The following mortuary table shows the alarming mortality of the cityof Richmond—a death-rate of over 44 per cent. It will be seen that ofthe forty-one leading cities of the United States Richmond exceeds themall probably in her death-rate—125 deaths out of 279 cases of diphtheria:

5. “ Paralysis occurs in 40 per cent, of the cases.”— Btower.6. The uniform presenceof the streptococcus in these three diseases, as an etiological factor, indi-

cates a closer relationship than had been supposed, and suggests that future biological studies maydemonstrate their identity.

7. The sulphur fumigation of infectious houses is under the ban of a more advanced science. Alarge and well-arranged disinfecting plant is now being planned for the city of New York.

MONTHLY RETURNS OF MORTALITYOF

Forty-two Cities of the United States.

PLACES AND

POPULATION. Diphtheriaj

andCroup,j

PLACES AND

POPULATION. Diphtheria andCroup. PLACES AND

POPULATION. Diphtheria andCroup.

Jan. 156 Jan. 30 Jan. 42New York. Feb. 185 Baltimore. Feb. 31 Buffalo. Feb. 25

Mar. 194 Mar. 23 Mar. 131,687,072. Apr. 166 455,427. Apr. 14 255,664. Apr. 19

May 131 May. 28 May. 19Jun. 333 Jun. 24 Jun. 13J uly. 134 July. 14 July. 13Aug, 111 Aug. 18 Aug. 16Sep. 139 Sep. 35 Sep. 26Oct. 176 Oct. 49 Oct. 39Jan. 133 Jan. 22 Jan. 4

Chicago. Feb. 117 Boston. Feb. 21 New Orleans. Feb. 3Mar. 118 Mar. 18 Mar. 4

1,200,000. Apr. 75 459,062. Apr. 254,000. Apr. 10May. 88 May. 30 May. 2Jun 69 Jun. 17 Jun. 1July. 58 July. 7 July. 2Aug. 93 Aug. 10 Aug. 1Sep. 107 Sep. 12 Sep. 3Oct. 151 Oct. 33 Oct. 17

4 jan. 86 Jan. 34 Jan. 24Philadelphia. Feb. 83 Cincinnati. Feb. 26 Wash- 5 Feb. 16

4 Mar. 79 Mar. 17 ington. 4 Mar. 81,069,264. 5 Apr. 91 300,000. Apr. 16 Apr. 13

4 May. 71 May. 20 250,000. May. 104 Jun. 54 Jun. 15 4 J un. 135 July. 54 July. 26 5 J uly. 214 Aug. 52 Aug. 18 4 Aug. 165 Sep. 94 Sep. 17 5 Sep. 344 Oct. 188 Oct. 29 4 Oct. 344 Jan. 130 Jan. 45 Jan. 19

Brooklyn. F eb. 102 San Francisco. Feb. 61 Pittsburgh. Feb. 304 Mar. 90 Mar. 63 4 Mar. 17

871,723. 5 Apl. 121 330,000. Apr. 39 247,000. 5 Apr. 124 May. 93 May. 26 4 May. 114 Jun. 81 Jun. 28 4 Jun. 145 July. 78 July. 17 5 July. 204 Aug. 47 Aug. 19 4 Aug. 245 Sep. 82 Sep. 24 5 Sep. 494 Oct. 96 Oct. 37 Oct.

Jan. 30 Jan. 5 4 Jan. 15St. Louis. Feb. 30 New Haven, Feb. 7 Louisville. Feb. 9

Mar. 29 Conn. Mar. 7 5 Mar. 7460,000. Apr. 29 Apr, 1 227,000. 4 Apr. 11

May. 26 86,000. May. 9 4 May. 1jun. 26 Jun. 6 4 Jun. 8July. 19 July. 1 5 July. 7Aug. 16 Aug. 5 4 Aug. 7Sep. Sep. 5 Sep. 9Oct. Oct. 4 Oct. 41

MONTHLY RETURNS OF MORTALITY.

PLACES AND

POPULATION. Diphtheria andCroup.1

PLACES AND



Jan.Detroit. Feb.

Mar.220,000. A pr.

May.Jun.July.Aug.Sep.Oct.

41274824311516192734

Jan.Rochest- r. Feb.

Mar.138,327 Apr.


116

6139437

25

Jan.Albany. Feb.M ar.

100,000. Apr.May.Jun.July.Aug.Sep.Oct.

6118115315

Jan. 45 Jan. 5 Jan. 2Milwaukee. Feb. 48 Providence, Feb. 6 Syracuse, Feb 3

Mar. 41 R. I. Mar. 9 N. Y. Mar. 2220,000 Apr. 44 Apr. Apr. 2

May. 30 135,000. May. 6 88,000. May.Jun. 22 Jun. 4 Jun. 3July. 22 July. 4 July. 1Aug. 35 Aug. 3 Aug.Sep. 23 Sep. Sep. 3Oct. 53 Oct. 11 Oct.Jan. 15 Ian. 7 Jan. 21

Minneapolis. Feb. 12 Kansas City. Feb. 3 Toledo. Feb. 7M ar. 9 Mar. Mar. 7

164,738. Apr. 3 132,416. Apr. 82,652. Apr. 7May. 14 May. 4 May. 10Jun. 7 Jun. Jun. 4July. 8 July. July. 7Aug. 4 Aug. Aug. 3Sep. 9 Sep. 3 Sep. 2Oct. 14 Oct. 7 Oct. 16Jan. 22 fan. 12 Jan. 14

Jersey City. Feb. 18 Columbus. Feb. 9 Scranton, Feb. 13Mar. 14 M ar. 8 Penn. Mar. 10

67,237. Apr. 14 101,945. Apr. 3 Apr. 8May. 10 May. 6 | 100,000. May. 6jun. 31 Jun. 5 Jun. 1

July. 23 July. 5 1 July.Aug. 17 Aug. 4 Avig. 3Sep. Sep. 3 Sep. 4Oct. Oct. 11 Oct. 5Jan. 23 Jan. 3 Jan. 9

St. Paul. Feb. 8 Richmond, F'eb. 6 Grand Rapids, Feb. 4Mar. 9 Va. Mar. 1 Mich. Mar. 9

150,000. Apr. Apr. Apr. 6May. 4 100,000. May. 3 85,000. May. 3Jun. c 3 Jun. 3 fun. 4July. Julv. 38 July.Aug. 4 Total: Aug. 48 1 Aug. 11Sep. 3 Cases, 279. Sep. 79 | Sep. 12Oct. Deaths, 125. Oct. 75 Oct. 12

Nov. 15Dec. 8

10

MONTHLY RETURNS OF MORTALITY

PLACES AND


POPULATION. Diphtheria andCroup PLACES AND


Jan.Lowell, Mass. Feb.

Mar.80,400. Apr.


21

41115

Jan.Nashville, Feb,

Tenn. Mar.Apr

76.369. May.Jun.July.Aug.Sep.Oct.

31

11

2

3

Jan.Dayton, Ohio. Feb.

Mar,60,000. Apr


1266757561

5Jan. 18 Jan 4 4 J an.

Paterson, N. J. Feb. 3 Los Angeles, Feb 2 Charleston, Feb. 2Mar. 14 Cal. Mar. 1 S. C. Mar.

800,000. Apr. 20 Apr. 3 5 AprMay. 11 65,000. May. 2 65,145. 4 May.Jun. 4 Jun. 2 4 Jun.July 19 July 4 5 JulyAug. 5 Aug. 4 Aug.Sep. 24 Sep. 1 5 Sep.Oct. 15 Oct. 4 Oct.Jan. 5 Jan. Jan. 8

Fall River, Feb. 2 Troy, N. Y. Feb. 2 Memphis, Feb. 1Mass. Mar Mar. 3 Tenn. Mar 2

Apr. 1 60,605. Apr. 3 Apr.75,000. May. 1 May. 1 60,000. May. 1

Jun. Jun. 4 Jun. oJuly. 2 July. 2 July 3Aug. Aug 4 Aug. 8Sep. Sep. 3 Sep. 7Oct. Oct. Oct. iJan. 28 Jun. 2 Aug n

Denver. Feb. 19 Wilmington, July. 9 Worcester, Sep. 4Mar. 12 Del. Aug. 6 Mass. Oct.

106,713. Apr. 6 Sep. 10 Nov.May. 12 62,000. Oct. 84,655. Decjun 26July. 14Aug. 14Sep.Oct.

diphtheria. · diphtheria: read before the richmond academy of medicine and surgery, february 16th,...

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