series of cases.

The operation is basically a transthoracic that short esophagus is a structural defect that cannot
reduction of the stomach, with alteration in the dia- be reduced by conservative measures. Although the
phragmatic hiatus and phrenic paralysis (Figs. 4 and 5). symptoms may be relieved in many cases by intensive
Although the esophagus itself is not appreciably length- medical therapy, the program must be continued through
ened, the vertical diameter of the thoracic cavity is life, since the underlying cause of the symptoms remains.
shortened. We feel that there is an excellent possibility that surgery
The technic parallels the procedure described by Mer- will offer permanent relief in selected cases.
endino, Vareo, and Wangensteen in correction of para-
10
Cleveland Clinic (Dr. Effier).
esophageal hiatus hernia. A thoracotomy is performed
at the level of the eighth left rib, and the pulmonary liga-
ment divided. The terminal esophagus and thoracic
stomach are completely mobilized from within the
mediastinum. The phrenic nerve is crushed, and the dia- CLINICAL NOTES
phragm is allowed to elevate. A site is selected for the
new hiatus, and the diaphragm is incised from this
point through the anatomic hiatus. Care must then APLASTIC ANEMIA COMPLICATING
be taken to free the stomach from its posterior and me- STREPTOMYCIN TREATMENT OF
dial attachments along the crura of the diaphragm. PULMONARY TUBERCULOSIS
Emphasis is placed on the necessity for complete
mobilization of the terminal esophagus and thoracic REPORT OF A CASE, WITH RECOVERY
stomach, with separation of the mediastinal and sub-
diaphragmatic attachments. It is not necessary for Milton S. Sacks, M.D., George T. Bradford, M.D.
one to divide the gastrohepatic or gastrolienal liga- and
ments. After mobilization is accomplished, the cardia of Carroll L. Spurling, M.D., Baltimore
the stomach is brought laterally to the site of new hiatus;
the right and left crura are approximated with inter- The major toxic manifestations accompanying pro-
rupted double silk sutures, with resultant obliteration of longed streptomycin therapy are well known. Renal
the original hiatus medially and posteriorly to the cardia. damage, vestibular dysfunction, dermatitis, and other
The stomach is reduced below the diaphragm, and the sensitivity reactions have all been observed. The reported
tendinous portion is closed around the cardiac esoph- incidence of blood dyscrasias, however, has been very
agus. One should observe care in tacking the new hiatus low. The initial report of the Streptomycin Committee of
completely around the esophagus by means of inter- the Veterans Administration and offices of the Surgeons
rupted silk sutures to prevent sliding or herniation. When General of the Army and Navy,1 stated that of 800 pa-
the repair is accomplished, the cardiac stomach is at the tients treated with streptomycin, in five (0.7%) relatively
highest point under the dome of the diaphragm, the posi- mild leukopenia with neutropenia developed. One case of
tion normally occupied by the fundus. Because the dia- agranulocytosis occurred in a patient with miliary
phragm is paralyzed, the dome is considerably elevated. tuberculosis. These reactions were felt to be quite def-
The combination of new hiatus, plus phrenic paralysis, initely caused by streptomycin in the sense that they were
greatly diminishes the distance traversed by the esopha- alleviated by its withdrawal. Deyke and Wallace rec- 2

gus. In this way, a previously short esophagus may be cently reported two cases of aplastic anemia, one of which
adequate in length. Although the esophagus itself is not terminated fatally, during streptomycin therapy of 400
lengthened, the required span is shortened. patients with tuberculosis at Fitzsimons General Hos-
COMMENT
pital. Autopsy of the fatal case revealed pronounced
Greater emphasis must be placed on the recognition hypoplasia of the bone marrow. In reviewing the toxic
manifestations encountered during the treatment of 57
of short esophagus and its associated complications.
patients in the Cornell-New York Hospital series,
Special technics used by the experienced roentgenologist, McDermott8 reported that relative granulocytopenia
including examinations in the Trendelenburg position, had been observed in a few cases with acute hematogen-
are of paramount importance. Inadequacy of medical ous tuberculosis. The total leukocyte counts eventually
therapy for short esophagus is largely due to the frequent rose to within normal range despite the continuation
erroneous diagnosis of duodenal ulcer. With early recog- of streptomycin therapy. In one patient with acute
nition of the entity and adequate medical therapy, the brucellosis, who had been receiving 6 gm. of streptomycin
patient may be spared prolonged discomfort and serious daily, thrombocytopenia developed. Recovery was
complication. prompt and complete after the discontinuation of
When serious complications have ensued and the dis-
ease is refractory to therapy, the possibilities of surgical Dr. Lawrence M. Serra kindly permitted us to study this patient.
Baltimore Rh Laboratory Fellows in Medicine (Drs. Bradford and
relief must be considered. Whereas the outright indica- Spurting).
tions for surgery are by no means crystallized in our From the Department of Medicine, University of Maryland School of
Medicine.
minds, we believe that a more radical approach will be 1. The Effect of Streptomycin upon Pulmonary Tuberculosis: Pre-
employed in the future. It must always be borne in mind liminary Report of a Cooperative Study of 223 Patients by the Army, Navy
and Veterans Administration, Am. Rev. Tuberc. 56: 485-605 (Dec.) 1947.
2. Deyke, V. F., and Wallace, J. B.: Development of Aplastic Anemia
10. Merendino, K. A.; Vareo, R. L., and Wangensteen, O. H.: Displace- During the Use of Streptomycin: Report of 2 Cases, J. A. M. A. 136:
ment of Esophagus into New Diaphragmatic Orifice in Repair of Para- 1098 (April 24) 1948.
Esophageal and Esophageal Hiatus Hernia, Ann. Surg. 139: 185 (Feb.) 3. McDermott, W.: Toxicity of Streptomycin, Am. J. Med. 2: 491-500
1949. (May) 1947.
/

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 streptomycin. A recent report4 of the Veterans Admin- The patient was readmitted to the hospital on Aug. 5, 1948.
istration Streptomycin Committee stated that in 5.2% The significant physical findings consisted of marked pallor of
the skin and mucous membranes, numerous petechiae over the
of 1,751 patients treated with streptomycin some type extremities and trunk, several large ecchymotic areas on the
of blood dyscrasia developed. extremities, a right pneumothorax, and a systolic and rumbling
We wish to report a case of aplastic anemia, which presystolic murmur over the mitral area. Remainder of the
occurred as a complication of streptomycin therapy of physical examination was essentially noncontributory.
Admission laboratory studies revealed a red blood cell count
pulmonary tuberculosis. The patient eventually re- of 2,980,000, a hemoglobin value of 10.2 gm., 4,850 leukocytes
covered. with a differential count of 34% neutrophils and 66% lympho-
REPORT OF A CASE cytes, and platelets, 23,840 (counted by Olef's method). All blood
H. W., white housewife, aged 35, was first admitted to the
a chemical studies were within normal limits. The bleeding time
University Hospital on Aug. 27, 1945. She had been in good was 2 min. 45 sec; the coagulation time (Lee-White), IVi min.;
health until four months prior to admission, when she noted the clot retraction was not complete in 24 hr. The prothrombin time
onset of dyspnea, nervousness, anorexia, and weight loss. Two was 18 sec. with a control of 18 sec. The capillary fragility test
months prior to admission she had been seen by a physician who was markedly positive. Several blood cultures and sputum exami-

suspected the existence of hyperthyroidism and advised hospital- nations were negative. X-ray of the chest revealed a right
ization. pneumothorax with an excellent degree of collapse. There was
The family history revealed that her father had died of tuber- slight patchy infiltration demonstrable in the upper left lung.
culosis. Review of her past history disclosed an episode of pneu- No specific cavitation was present.
monia at 1 yr. of age. At the age of 9 yr. she had an acute bout She was given 2,000 cc. of whole blood, and, although the red
of fever and painful swollen knee joints. No diagnosis was made blood cell count and hemoglobin value returned to normal levels,
at that time, but she was later told she had rheumatic heart dis- the leukopenia and thrombocytopenia persisted (chart). The
ease with valvular damage. The patient had two attacks of acute
pyelitis in 1929 and in 1931. There were two uneventful preg- _THERAPY
vitamin
liver extract, B complex,
nancies. A review of systems revealed frequent acute respiratory folie acid, rutiji and ascorbic acid I
infections.
tpoo cc blood ï,ooo cc blood
On physical examination the patient appeared poorly nour-
THOUSANDS OF WHITE » ^
ished and chronically ill. There was a slight generalized enlarge- ,o

ment of the thyroid gland. A harsh blowing systolic murmur

was heard in the mitral area. The heart was not enlarged. Exami-
nation of the chest revealed limitation of motion on the right
side. There was marked dullness to percussion at the right apex
posteriorly from the first to the fourth ribs. Breath sounds were
decreased and tactile fremitus was increased over this area. No
rales were heard. The left lung was normal. The remainder of
the physical examination was essentially normal.
Admission laboratory studies revealed the following data: red
blood cell count, 4,250,000 per cubic millimeter; hemoglobin
value, 13 gm.; leukocytes, 10,200 per cubic millimeter, with a dif-
ferential count of 60% neutrophils, 28% lymphocytes, and 12%
monocytes; platelets, 310,000 per cubic millimeter. Routine
urine and stool examinations were noncontributory. All blood
chemical studies were within normal limits. An electrocardio-
gram did not indicate any deviations from normal. Repeated
basal metabolism rates were normal. An x-ray of the chest re-
vealed a large amount of patchy infiltration involving the right
lung from the apex to the anterior end of the sixth rib. Similar MTtLUID
ERYTHROID
& isa
AUG. SEPT. OCT N0V DEC. JAN. FEB. MAR. APRIL MAY
infiltration was present in the left lung, from the first to the LYMPHOID »4« i»>» it/7/«
fourth interspaces. No definite cavities were noted. The cardiac
Summary of patient's course and treatment.
shadow was normal. On Aug. 31 sputum examination was posi-
tive for tubercle bacilli.
The patient did not receive any therapy while hospitalized. differential count continued to show a high percentage of mature
She was discharged on Sept. 6, 1945, arrangements having been lymphocytes. Sternal bone marrow examination was done on
made for her to be treated at home by a chest specialist. A right Aug. 18, 1948. The smears showed a marked decrease in cellu-
pneumothorax was performed and maintained. The patient was larity, the predominant cells being small mature lymphocytes.
kept on strict bed rest for 12 mo. Sputum examinations became Ditferential count was as follows: myeloblasts 3%, promyelo-
negative and moderate activity was allowed. The patient gained cytes 2%, myelocytes 2%, metamyelocytes 12%, segmented
weight and improved over a two-year period. Serial x-rays of neutrophils 17%, mature lymphocytes 58%, and erythroid ele-
the chest revealed no change in the left lung. The pneumothorax ments 6%. Megakaryocytes were not observed. A diagnosis of
was constantly maintained on the right. hypoplastic anemia with secondary thrombocytopenia was made.
On Feb. 20, 1948, her sputum again became positive for acid- A therapeutic regimen consisting of liver extract, intramuscu-
fast organisms. Because of this finding, the patient was placed lar vitamin B complex, folie acid, rutin, and ascorbic acid was
on strict bed rest and started on intramuscular streptomycin, initiated. The patient was discharged from the hospital on Aug.
0.8 gm. daily (16 mg. per kilogram). She continued to receive 24, 1948, by which time the fever had subsided and the hemor-
this dose until June 20, 1948, a period of 122 days. The total rhage tendency had become less marked. The blood studies on
dose of streptomycin given was 98 gm. During this period that day were as follows: red blood cell count, 4,050,000;
the lesion in her left lung cleared considerably and she felt hemoglobin value, 11.6 gm.; 3,000 leukocytes with a differen-
much improved. Sputum examinations became negative and tial count of 70% lymphocytes, 27% neutrophils, 2% eosinophils
other routine laboratory studies were said to have been within and 1% monocytes; platelets, 35,000.
normal limits. Periodic blood studies were made during the next six weeks
In July 1948, she contracted an acute respiratory infection and therapy was continued as before. Occasional spontaneous
after which she noted the appearance of marked pallor, recur- epistaxis and small showers of petechiae occurred. Menstrual
rent elevations of temperature, and numerous petechiae and periods were somewhat prolonged and profuse. Slight hematuria
purpuric spots on the extremities. Several episodes of spon-
taneous epistaxis occurred. She was seen by her physician, and 4.Streptomycin in the Treatment of Tuberculosis, report of the Council
hospitalization was again advised. on Pharmacy and Chemistry, J. A. M. A. 138: 584-593 (Oct. 23) 1948.

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 wasalso observed on several occasions in September. On Oct. 1, corded blood counts. Several weeks after discontinuance
1948, marked pallor of the skin and mucous membranes was of the drug, purpuric manifestations appeared. On ad-
again noted. Laboratory studies revealed a red blood cell count mission to the hospital, detailed study revealed a picture
of 2,390,000, hemoglobin value of 7.4 gm., 3,050 leukocytes,
with a differential count of 44% neutrophils, 48% lymphocytes, compatible with the diagnosis of aplastic anemia. There
6% monocytes, and 2% eosinophils, and 27,600 platelets. was no history of exposure to other agents or drugs which
She was readmitted to the hospital on Oct. 16, 1948. Marked have been reported to produce hypoplasia of the bone
pallor, petechiae, and several ecchymotic areas were
numerous
marrow, nor was there any evidence of miliary spread
noted on the extremities. The red blood cell count was 1,910,000
and the hemoglobin value was 6.6 gm. The patient was again of the tuberculous infection.
given 2,000 cc. of whole blood over a period of four days. Bone During the first six months after streptomycin had
marrow examination on Oct. 18 revealed a moderate increase been discontinued, very little hematological improvement
in cellularity as compared to the marrow previously examined. occurred in spite of supportive therapy. The leukocyte
The differential count was as follows: myeloblasts 3.5%, pro-
count and differential pattern became essentially normal
myelocytes 4.0%, myelocytes 9.5%, metamyelocytes 17.0%,
segmented neutrophils 23.5%, mature lymphocytes 25%, mono- by December, 1948, approximately six months after on-
cytes 1%, plasma cells 1%, and erythroid elements 15.5%. set of illness. The hemoglobin and red blood cell values
The patient was discharged from the hospital on Oct. 19, 1948, rose to normal during the next three months. The plate-
somewhat improved. She continued on the therapeutic regimen
noted above. For a period of several months thereafter there
lets, on the other hand, did not reach normal until ap-
was gradual clinical and hematological improvement. The proximately 16 mo. after onset. It is interesting to note
hemorrhagic manifestations diminished. The red blood cell count that during the last hospital admission (August, 1949)
was maintained between "iVi and 4 million without further when exacerbation of the tuberculous process had oc-
transfusions. The white blood cell count fluctuated between curred, no hematological regression was observed. The
4,000 and 6,000, and the differential counts became normal in most recent blood studies indicate an essentially normal
December, 1948. However, the thrombocytopenia persisted. In
February, 1949, blood studies were as follows: red blood cell picture.
count 3,500,000; hemoglobin value 11.4 gm.; 6,600 leukocytes The evidence incriminating streptomycin as the agent
with a differential count of 74% neutrophils, 18% lymphocytes,
6% monocytes, and 2% eosinophils; platelets 3,300.
responsible for the aplastic anemia in this case is, of
course, only circumstantial. One must consider first the
The vitamin B complex and folie acid were discontinued in
February. From February to April, 1949, there was further influence of tuberculosis itself on the hematopoietic
hématologie improvement. The platelet level rose steadily. Liver system. It is well known that anemia, granulocytopenia,
extract was discontinued in March, 1949. Blood studies on April and/or thrombocytopenia have been observed in acute
27, 1949, revealed a red blood cell count of 4,480,000; hemo- hematogenous tuberculosis with bone marrow involve-
globin value of 13.8 gm.; 7,300 leukocytes with a differen- ment. A decrease in granulocytes and/or platelets has
tial count of 59% neutrophils, 39% lymphocytes, and 2%
monocytes, and 140,800 platelets. On May 25, 1949, another also been observed following the injection of tuberculin
bone marrow aspiration was performed. Examination of the in patients with active pulmonary tuberculosis.5 The lat-
smears revealed normal cellularity. The differential count was ter observation led to the suggestion that perhaps a
as follows: myeloblasts 1.0%, premyelocytes 5.0%, myelocytes similar mechanism may be responsible for the granulo-
10%, neutrophilic metamyelocytes 31%, segmented neutrophils
19.5%, lymphocytes 13.0%, and erythroid elements 20.5%. cytopenia and thrombocytopenia occasionally seen in
Several megakaryocytes were seen. Peripheral blood studies were such patients. However, a careful search of the literature
as follows: red blood cell count, 4,520,000; hemoglobin value, failed to reveal typical cases of aplastic anemia due to
3.3 gm., 5,700 leukocytes with a differential count of 61% tuberculosis per se except when miliary spread was pres-
segmented neutrophils, 32% lymphocytes, 4% monocytes, 2% ent. The case presented here displayed no evidence of
eosinophils, and 1% basophils; platelets, 200,000. miliary dissemination.
In Aug. 1949, progression of the tuberculous process in the
left apex necessitated readmission to the hospital for performance The mechanism of the development of hypoplasia of
of a lucite plumbage. The patient withstood the procedure well the bone marrow during streptomycin therapy is un-
and had no unusual hemorrhagic phenomena. The blood picture known. No evidence exists for a direct toxic effect on
was essentially normal at this time except for moderate thrombo-
the hematopoietic system. However, bone marrow hypo-
cytopenia (260,000 per cubic millimeter). When last seen on Dec.
7, 1949, she was completely asymptomatic, had gained weight, plasia can occur as a result of the creation of a folie acid
and presented the following blood picture: red blood cell count, deficiency." Lucherini and Schiavetti observed that
"

4,970,000; hemoglobin value, 14.1 gm.; 6,600 leukocytes with

differential count of 58% neutrophils, 33% lymphocytes, 6%
streptomycin administered orally to rats and chickens
a

monocytes, 2% eosinophils, and 1% myelocytes; platelets,

produced a macrocytic anemia, granulocytopenia, and
470,400. hypoplasia of the bone marrow. The peripheral blood
COMMENT picture as well as the bone marrow was rapidly restored
to normal by the oral or parenteral administration of folie
When first seen in 1945, prior to streptomycin therapy,
the patient's peripheral blood picture was essentially acid. The experiments seemed to indicate that, at least in
rats and chickens, the bacterial flora of the intestinal tract
normal. During the four-month period of streptomycin
administration she was at home, and there were no re- plays an important part in the synthesis of folie acid. It
was suggested that the toxic hematopoietic effect of
5. Muller, G. L.: Clinical Significance of the Blood in Tuberculosis, streptomycin was due to its bactericidal action on the
New York, Commonwealth Fund, 1943, chap. 2. intestinal flora. The possibility that prolonged adminis-
6. (a) Jukes, T H., and Stokstad, E. L. R.: Pteroylglutamic Acid and
Related Compounds, Physiol. Rev. 28: 51-106 (Jan.) 1948. (b) Sacks, tration of streptomycin may, as a result of its effect on the
M. S.; Bradford, G. T., and Schoenbach, E. B.: The Response of Acute
Leukemia to the Administration of Folic Acid Antagonists Aminopterin
bacterial flora of the human intestinal tract, produce a
and Amethopterin: Report of 14 Cases, Ann. Int. Med. 32: 80-115 (Jan.) folie acid deficiency must be considered. This could re-
1950.
7. Lucherini, T., and Schiavetti, L.: Experimental Macrocytic Anemia
sult in hypoplasia of the bone marrow.
from Oral Administration of Streptomycin, and Restoration of Blood In the treatment of acute leukemia with the folie acid
Picture to Normal by Administration of Folic Acid, Policlinico (Sez. prat.)
55: 65-73 (Jan. 19) 1948. antagonists, some authors 6b have observed hypoplasia of

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 the bone marrow, ulcerative stomatitis, alopecia, and details were given, the case presumably was fairly mild.
diarrhea. Beham and Perr s have reported the develop- To our knowledge there has been no instance in the
ment of an ulcerative aphthous stomatitis in three patients American literature of severe thrombopenic purpura
with pulmonary and extrapulmonary tuberculosis during developing during or after streptomycin therapy. It may,
streptomycin therapy. The hematological picture was not therefore, be of interest to report one such case occurring
discussed, but the description and photographs of the in a patient treated with streptomycin, bringing to the
ulcerative stomatitis appeared quite similar to that ob- attention of the medical profession the possibility of such
served by us in patients with a folie acid deficiency in- a reaction, especially when a
patient has a history of
duced by the therapeutic use of folie acid antagonists. previous administration of this antibiotic.
Since streptomycin therapy has become widespread in REPORT OF A CASE
the treatment of many human infections, the minor toxic
History.—B. S., white man aged 32, gave a history suggestive
a
manifestations will probably assume greater importance. of pulmonary tuberculosis since July, 1946, that was confirmed
At the present time, it would seem advisable to consider bacteriologically and by x-ray studies a month later when a
anemia, granulocytopenia, and thrombocytopenia col- diagnosis of active pulmonary tuberculosis of the right upper
lobe made. Pneumothorax was started on the right side in
lectively as a manifestation of streptomycin toxicity and was
September, 1946. and was followed by pneumonolysis. The pa-
an indication for the immediate discontinuation of tient responded well to therapy; smears and cultures of his
therapy. sputum and gastric contents became negative for acid-fast bacilli.
SUMMARY During April, 1947, a course of streptomycin was started, but
A of aplastic anemia following prolonged admin- after the administration of only 2 gm. over a period of two days,
case
further antibiotic therapy was refused by the patient because of
istration of streptomycin is presented. Gradual recovery
took place over a period of 16 mo. after the discontinu-
ation of the drug.
It is suggested that prolonged courses of streptomycin,
by virtue of an effect upon the bacterial flora of the
human intestinal tract, may produce a folie acid defi-
ciency with subsequent hypoplasia of the bone marrow.
8. Beham, H., and Perr, H.: Stomatitis Due to Streptomycin, J. A.
M. A. 138: 495-496 (Oct. 16) 1948.

THROMBOPENIC PURPURA DURING

STREPTOMYCIN TREATMENT OF
TUBERCULOUS EMPYEMA
REPORT OF A CASE

Herman Rudensky, M.D., Ft. Wayne, Ind.

and
Seymour Fisher, M.D., Phoenix, Ariz.
Incidence of severe toxic reactions in the hemato-
poietic systems of patients treated with streptomycin has Roentgenogram of chest, Sept. 2. 1948. showing tuberculous empyema.
been very small. The Central Streptomycin Committee
of the Veterans Administration reported only 0.6%\x=req-\ local burning pain. About May, 1948, a tuberculous empyema
2.3% of blood dyscrasias in 1,751 patients treated under developed on the right side; the patient was treated by repeated
streptomycin regimens in the federal hospitals.1 The great aspirations and irrigations of the pleural cavity with chloroazodin
(azochloramid8) solution. There was some improvement in his
majority of these reactions consisted of relatively mild condition.
leukopenia and granulocytopenia; however, two cases of Physical Examination and Laboratory Data.—On Aug. 31,
aplastic anemia apparently caused by streptomycin were 1948, he was admitted to Billings Veterans Administration Hos-

reported by Deyke and Wallace.2 A. M. Walker,3 secre- From the Chest and Tuberculosis Service, Billings Veterans Adminis-
tary of the Central Streptomycin Committee, informed tration Hospital, Ft. Benjamin Harrison, Ind.
us that he knew of no case of thrombopenic purpura Chief, Medical Service, Veterans Administration Hospital, Ft. Wayne
(Dr. Rudensky) and manager, Veterans Administration Hospital, Phoenix,
occurring during the administration of streptomycin in Ariz. (Dr. Fisher).
Reviewed in the Veterans Administration and published with the
any patient treated in the United States. In one patient approval of the Chief Medical Director. The statements and conclusions
with miliary tuberculosis treated with streptomycin published by the authors are the result of their own study and do not nec-
essarily reflect the opinion or policy of the Veterans Administration.
by Feld4 agranulocytosis developed. Benhamou and 1. Streptomycin in Treatment of Tuberculosis, Report of the Council
on Pharmacy and Chemistry, J. A. M. A. 138: 584 (Oct. 23) 1948.
others5 reported that in one child with tuberculous 2. Deyke, V. F., and Wallace, J. B.: Development of Aplastic Anemia
meningitis, treated with 2 gm. of streptomycin daily, During the Use of Streptomycin: Report of 2 Cases, J. A. M. A. 136:
1098 (April 24) 1948.
agranulocytosis with purpura developed on the 30th day 3. Walker, A. M.: Personal communication to the authors.
of therapy, and the child died within 48 hr. Keefer and 4. Feld, D. D.: Agranulocytosis During the Streptomycin Treatment of
Miliary Tuberculosis, Am. Rev. Tuberc. 59: 317, 1949.
others,6 in a report of 1,000 cases treated with streptomy- 5. Benhamou, E.; Destaing, F., and Cholal, A.: Blood Accidents in
cin, mentioned one case of purpura hemorrhagica occur- Course of Treatment with Streptomycin, Presse m\l=e'\d.56: 517, 1948.
6. Keefer, C. S., and others: Streptomycin in Treatment of Infections:
ring in a patient treated with streptomycin. Since no A Report of 1,000 Cases, J. A. M. A. 132: 70, 1946.

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