891
Letters
to
the Editor
BACTERIA AND INFLUENZA SIR,—With the cooperation of many hospital pathologists, the Public Health Laboratory Service is collecting records of cases of fatal pneumonia associated with influenza-like illness. The reports received so far enable us to add a few figures to your leading article last week. We have had complete records of 36 fatal cases. In 31 Staphylococcus aureus was the major or only pathogen isolated from the lung ; in 2 of these cases group-A hæmolytic streptococci and in 2 others Hœmophilus influenza? were also found. Of the 5 cases yielding no staphylococci, 3 gave coliform organisms, 1 a group-A and 1 a group-C streptococcus. Of the 31 strains of staphylococci, 19 were sensitive 12 were resistant to to all the common antibiotics. 4 but of these were resistant to tetraonly penicillin, 1 of them was to us as showing only reported cyclines ; any degree of resistance to erythromycin. 2 of the 12
penicillin-resistant staphylococci were certainly, and 1 probably, acquired in hospital ; and 2 of the 4 tetracycline-resistant strains were among the hospital infec-
tions. The
staphylococci belonged
phage-types, the
the
to
a
strains
drug-resistant in hospitals.
great variety being mostly
of of
types commonly found
Incomplete
records for another 50
cases
show
a
similar
frequency of drug-resistant strains. Central Public Health
Laboratory,
Colindale, London, N.W.9.
M. PATRICIA JEVONS C. E. D. TAYLOR R. E. O. WILLIAMS.
INFLUENZA COMPLICATING HEART-DISEASE IN PREGNANCY
SIR,—We should like
to draw attention to the serious influenza in pregnancy complicated by of consequences valvular disease of the heart. We have had experience of this condition in 9 patients, 4 of whom died. Clinically, these patients presented with signs of an acute febrile illness, and within twelve hours of the onset there was an obviously fulminating bronchopneumonia, accompanied by a distressing unproductive cough. A peculiar " blue " cyanosis was a characteristic feature. Despite the fact that all had signs of mitral stenosis, there was little evidence of cardiac failure although tachycardia The blood-pressure remained was a constant finding. normal throughout. Signs of bronchopneumonia with tachypncea were prominentand a considerable degree of ketosis developed. All the patients had a high temperature (102-103° F.) and examination of the blood showed a low white-cell count. 5 patients went into labour during the acute stage of the infection. (Of the 4 patients who died, 3 came into this category.) 2 babies were stillborn and 3 died within forty-eight hours. Post-mortem examination confirmed the clinical impressions. Despite cyanosis there was little evidence. of cardiac failure. Œdema was absent and there was no chronic venous congestion of the organs. The heart showed mitral stenosis, but there was an absence of the fresh vegetations usually associated with fatal cardiac failure in pregnancy. A widespread bronchopneumonic consolidation was present in both lungs, and the cut surface showed irregular areas of haemorrhage through the parenchyma. Histologically there was only a mild cellular reaction, partly polymorph, partly rnononuclear. In treating these cases, attention was paid to four aspects. In an attempt to control secondary infection, antibiotics were given from the beginning. ’Sigmamycin’ (tetracycline and oleandomycin) was apparently the most effective. To control the tachycardia, intravenous ’Lanoxin’ (lanat,oside C) was administered. Since
ketosih
was
sucrose
solution
was
small intravenous infusion of 50% given. The rernainder of treatment symptomatic; pethidine and atropine were given for
marked,
a
was
to reduce sec;retions, and minimise the effects right-heart stress. The cough was controlled by
sedation, of
, Benylin.’ In view of the severity of this infection and the frequently fatal outcome in the pregnant cardiac patient, we feel that adequate supplies of the specific vaccine should be made readily available for the inoculation of these patients. A. D. TELFORD GOVAN Glasgow Royal Maternity and H. R. F. MACDONALD. Women’s Hospital. INFLUENZAL PNEUMONIA TREATED WITH CORTISONE AND ANTIBIOTICS
SIR,—I was extremely interested in the letter by Dr. Plaza de los Reyes and his colleagues last week. I lost my mother a few days ago from innuenzal bronchopneumonia confirmed by radiographs of the chest. Antibiotic therapy was pushed to the limit, the antibiotics used being determined by culture and sensitivity of the purulent sputum. Three predominant
cultured—Staphylococcus aureus (coaguli and II) and Hcsmophihcs influenzœ. Unfortunately a profound circulatory failure developed five days before death, associated with an intense pulmonary oedema. Neptal’ injections,Omnopon,’ continuous oxygen, intravenous digoxin, &c., produced organisms
were
age-positive
strains
’
little clinical response. The heart condition was assessed by repeated electrocardiograms, the overall picture suggesting a toxic myocarditis. The use of cortisone was considered but it was not given, since Friedberg, in his classical book, Diseases of the Heart, states that in heartfailure " cortisone and hydrocortisone cause an early renal retention of sodium, despite the fact that there is a rise in glomerular filtration. Unless sodium intake is sharply restricted, their administration may cause oedema, pulmonary oedema, and in fact many of the haemodynamic disturbances associated with congestive heart failure." It is suggested that " the secretion of these corticoid hormones may actually represent an intermediate mechanism in heart failure." The problem was-should cortisone be administered if pulmonary oedema complicates the pictureQ Is it beneficial in cases of toxic myocarditis ? What exactly is its mode of action in cases of profound circulatory failure with increasing cyanosis ?Is it anti-inflammatory or antitoxic ? Lastly, it would be interesting to know the age-groups of the cases which survived in Dr. Plaza de los Reyes’ series. ISAAC ROSE. ’
NORADRENALINE IN SHOCK
SIR,—The recent extensive use of noradrenaline in the treatment of various forms of shock does not appear to have led, as it might have done, to a very much clearer understanding of the mechanisms involved in the production and control of the circulatory failures concerned. The work reported by Dr. Littler and Dr. McKendrick in your issue of Oct. 26 is exceptional in this respect, since their demonstration of the profound effects of the drug on heart rhythm may well explain its failure to restore the circulation in their cases of cardiac infarction. The significance of these observations is emphasised by their further observation that the action of noradrenaline on the cardiac rhythm is abolished by atropine. From the clinical point of view this would suggest that atropine might be given simultaneously with noradrenaline when the latter is employed in cardiac shock, in order to combat its potentially dangerous action on the cardiac rhythm. Although their " prophylactic use against the possible development of atrial and ventricular arrhythmias "